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    Guidelines Guidelines Document Transcript

    • Journal of Cardiac Failure Vol. 16 No. 6 2010 HFSA 2010 Guideline Executive Summary Executive Summary: HFSA 2010 Comprehensive Heart Failure Practice Guideline HEART FAILURE SOCIETY OF AMERICA St. Paul, Minnesota Guideline Committee Members JoAnn Lindenfeld, MD1 (Chair) Nancy M. Albert, RN, PhD Debra K. Moser, RN, DNSc John P. Boehmer, MD Joseph G. Rogers, MD Sean P. Collins, MD, MSc Randall C. Starling, MD, MPH Justin A. Ezekowitz, MBBCh William G. Stevenson, MD Michael M. Givertz, MD W. H. Wilson Tang, MD Stuart D. Katz, MD John R. Teerlink, MD Marc Klapholz, MD Mary N. Walsh, MD Executive Council Douglas L. Mann, MD, President Inder S. Anand, MD Steven R. Houser, PhD J. Malcolm O. Arnold, MD Mariell L. Jessup, MD John C. Burnett, Jr., MD Barry M. Massie, MD John Chin, MD Mandeep R. Mehra, MD Jay N. Cohn, MD Mariann R. Piano RN, PhD Thomas Force, MD Clyde W. Yancy, MD Barry H. Greenberg, MD Michael R. Zile, MD ABSTRACT Heart failure (HF) is a syndrome characterized by high mortality, frequent hospitalization, reduced quality of life, and a complex therapeutic regimen. Knowledge about HF is accumulating so rapidly that individ- ual clinicians may be unable to readily and adequately synthesize new information into effective strategies of care for patients with this syndrome. Trial data, though valuable, often do not give direction for indi- vidual patient management. These characteristics make HF an ideal candidate for practice guidelines. The 2010 Heart Failure Society of America comprehensive practice guideline addresses the full range of eval- uation, care, and management of patients with HF. Key Words: Heart failure, practice guidelines. From the 1Department of Cardiology, University of Colorado Health A copy of the HFSA Comprehensive Heart Failure Practice GuidelineSciences Center, Denver, CO. can be found at www.onlinejcf.com The document should be cited as follows: Lindenfeld J, Albert NM, See page 506 for disclosure information.Boehmer JP, Collins SP, Ezekowitz JA, Givertz MM, Klapholz M, Moser 1071-9164/$ - see front matterDK, Rogers JG, Starling RC, Stevenson WG, Tang WHW, Teerlink JR, Ó 2010 Elsevier Inc. All rights reserved.Walsh MN. Executive Summary: HFSA 2010 Comprehensive Heart Fail- doi:10.1016/j.cardfail.2010.04.005ure Practice Guideline. J Card Fail 2010;16:475e539. 475
    • 476 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 Table of Contents Section 1: Development and Implementation of a Comprehensive Heart Failure Practice Guideline.......476 Section 2: Conceptualization and Working Definition of Heart Failure ......................................................479 Section 3: Prevention of Ventricular Remodeling, Cardiac Dysfunction, and Heart Failure......................480 Section 4. Evaluation of Patients for Ventricular Dysfunction and Heart Failure.......................................481 Section 5: Management of Asymptomatic Patients with Reduced Left Ventricular Ejection Fraction...........................................................................................................................484 Section 6: Nonpharmacologic Management and Health Care Maintenance in Patients with Chronic Heart Failure ..........................................................................................................485 Section 7: Heart Failure in Patients with Reduced Ejection Fraction .........................................................486 Section 8: Disease Management, Advance Directives, and End-of-Life Care in Heart Failure .................492 Section 9: Electrophysiology Testing and the Use of Devices in Heart Failure .........................................494 Section 10: Surgical Approaches to the Treatment of Heart Failure.............................................................495 Section 11: Evaluation and Management of Patients with Heart Failure and Preserved Left Ventricular Ejection Fraction ...............................................................................................496 Section 12: Evaluation and Management of Patients with Acute Decompensated Heart Failure................497 Section 13: Evaluation and Therapy for Heart Failure in the Setting of Ischemic Heart Disease ..............500 Section 14: Managing Patients with Hypertension and Heart Failure...........................................................502 Section 15: Management of Heart Failure in Special Populations ................................................................502 Section 16: Myocarditis: Current Treatment ..................................................................................................503 Section 17: Genetic Evaluation of Cardiomyopathy* ....................................................................................503 Acknowledgement.............................................................................................................................................505 References .........................................................................................................................................................506 Section 1: Development and Implementation of driving the development of HF guidelines are presenteda Comprehensive Heart Failure Practice Guideline in Table 1.1. The first HF guideline developed by the Heart Failure Heart failure (HF) is a syndrome characterized by high mor- Society of America (HFSA) had a narrow scope, concen-tality, frequent hospitalization, poor quality of life, multiple trating on the pharmacologic treatment of chronic, symp-comorbidities, and a complex therapeutic regimen. Knowl- tomatic left ventricular dysfunction.1 It did not consideredge about HF is accumulating so rapidly that individual clini- subsets of the clinical syndrome of HF, such as acute de-cians may be unable to readily and adequately synthesize new compensated HF and ‘‘diastolic dysfunction,’’ or issuesinformation into effective principles of care for patients with such as prevention. The subsequent comprehensive clinicalthis syndrome. Trial data, though valuable, often do not give practice guideline published in 2006 addressed a full rangeadequate direction for individual patient management. of topics including prevention, evaluation, disease manage- Given the complex and changing picture of HF and the ac- ment, and pharmacologic and device therapy for patientscumulation of evidence-based HF therapy, it is not possible with HF.2 The 2010 guideline updates and expands eachfor the clinician to rely solely on personal experience and ob- of these areas and adds a section on the Genetic Evaluationservation to guide therapeutic decisions. The situation is ex- of Cardiomyopathy published separately in 2009.3 Theacerbated because HF is now a chronic condition in most discussion of end of life management has also been consid-patients, meaning that the outcome of therapeutic decisions erably expanded. Appendix A is a comparison of the 2006might not be apparent for several years. The prognosis of in- Table 1.1. Assumptions Underlying HFSA Practicedividual patients differs considerably, making it difficult to Guidelinegeneralize. Treatments might not dramatically improvesymptoms of the disease process, yet might provide impor- Clinical decisions must be made. Correct course of action may not be readily apparent.tant reductions or delays in morbid events and deaths. The as- Multiple non-pharmacologic, pharmacologic, and device therapies aresessment of specific therapeutic outcomes is complicated by available.the potential differential impact of various cotherapies. Reasonably valid methods exist to address knowledge base and evaluate medical evidence. The complexity of HF, its high prevalence in society, and Data beyond randomized clinical trials exist that enhance medical decisionthe availability of many therapeutic options make it an ideal making.candidate for practice guidelines. Additional assumptions Uncertainties remain concerning approaches to treatment after review of totality of medical evidence. * Expert opinion has a role in management decisions when Strength of Reprinted with edits and permission from Hershberger RE, Linden- Evidence A data are not available to guide management.feld J, Mestroni L, Seidman C, Taylor MRG, Towbin JA. Genetic evalua- A consensus of experts remains the best method of managementtion of cardiomyopathy: a Heart Failure Society of America practice recommendations when Strength of Evidence A data are not availableguideline. J Card Fail 2009;15:83-97.
    • Executive Summary: Heart Failure Practice Guideline  HFSA 477and 2010 guideline, summarizing the modifications, addi- and robust outcomes. However, randomized clinical trialtions, and deletions in the guideline recommendations. data, whether derived from one or multiple trials, haveAppendix B is a list of acronyms (including clinical trials) not been taken simply at face value. They have been eval-used in the 2010 guideline. uated for: (1) endpoints studied, (2) level of significance, (3) reproducibility of findings, (4) generalizability of studyHFSA Guideline Approach to Medical Evidence results, and (5) sample size and number of events on which outcome results are based. Two considerations are critical in the development ofpractice guidelines: assessing strength of evidence and de- Strength of Evidence B. The HFSA guideline processtermining strength of recommendation. Strength of evi- also considers evidence arising from cohort studies or smallerdence is determined both by the type of evidence clinical trials with physiologic or surrogate endpoints. Thisavailable and the assessment of validity, applicability, and level B evidence is derived from studies that are diverse in de-certainty of a specific type of evidence. Following the sign and may be prospective or retrospective in nature. Theylead of previous guidelines, strength of evidence in this may involve subgroup analyses of clinical trials or haveguideline is heavily dependent on the source or type of a case control or propensity design using a matched subsetevidence used. The HFSA guideline process has used three of trial populations. Dose-response studies, when available,grades (A, B, or C) to characterize the type of evidence may involve all or a portion of the clinical trial population. Ev-available to support specific recommendations (Table 1.2). idence generated from these studies has well-recognized, in- It must be recognized, however, that the evidence sup- herent limitations. Nevertheless, their value is enhancedporting recommendations is based largely on population re- through attention to factors such as pre-specification of hy-sponses that may not always apply to individuals within the potheses, biologic rationale, and consistency of findings be-population. Therefore, data may support overall benefit of tween studies and across different populations.one treatment over another but cannot exclude that some in- Strength of Evidence C. The present HFSA guidelinedividuals within the population may respond better to the makes extensive use of expert opinion, or C-level evidence.other treatment. Thus, guidelines can best serve as The need to formulate recommendations based on level Cevidence-based recommendations for management, not as evidence is driven primarily by a paucity of scientific evi-mandates for management in every patient. Furthermore, dence in many areas critical to a comprehensive guideline.it must be recognized that trial data on which recommenda- For example, the diagnostic process and the steps used totions are based have often been carried out with background evaluate and monitor patients with established HF havetherapy not comparable to therapy in current use. There- not been the subject of clinical studies that formally testfore, physician decisions regarding the management of in- the validity of one approach versus another. In areas suchdividual patients may not always precisely match the as these, recommendations must be based on expert opinionrecommendations. A knowledgeable physician who inte- or go unaddressed.grates the guidelines with pharmacologic and physiologic The value of expert opinion as a form of evidence re-insight and knowledge of the individual being treated mains disputed. Many contend that expert opinion isshould provide the best patient management. a weak form of observational evidence, based on practiceStrength of Evidence A. Randomized controlled clinical experience and subject to biases and limitations. Advocatestrials provide what is considered the most valid form of believe expert opinion represents a complex synthesis ofguideline evidence. Some guidelines require at least 2 pos- observational insights into disease pathophysiology anditive randomized clinical trials before the evidence for a rec- the benefits of therapy in broad populations of patients.ommendation can be designated level A. The HFSA They stress the value of the interchange of experienceguideline committee has occasionally accepted a single ran- and ideas among colleagues, who collectively treat thou-domized, controlled, outcome-based clinical trial as suffi- sands of patients. Through contact with numerous individ-cient for level A evidence when the single trial is large ual health care providers who may discuss patients withwith a substantial number of endpoints and has consistent them, experts are exposed to rare safety issues and gain insight into the perceptions of practitioners concerning the efficacy of particular treatments across a wide spectrum Table 1.2. Relative Weight of Evidence Used to Develop HFSA Practice Guideline of HF. Despite the case that can be made for its value, recom-Hierarchy of Types of Evidence mendations based on expert opinion alone have been lim-Level A Randomized, Controlled, Clinical Trials ited to those circumstances when a definite consensus May be assigned based on results of a single trial could be reached across the guideline panel and reviewers.Level B Cohort and Case-Control Studies Post hoc, subgroup analysis, and meta-analysis HFSA Guideline Approach to Strength of Prospective observational studies or registries RecommendationLevel C Expert Opinion Observational studies-epidemiologic findings Safety reporting from large-scale use in practice Determining Strength. Although level of evidence is im- portant, the strength given to specific recommendations is
    • 478 Journal of Cardiac Failure Vol. 16 No. 6 June 2010critical. The process used to determine the strength of indi- Table 1.4. Steps in the Development of the 2010 HFSAvidual recommendations is complex. The goal of guideline Practice Guidelinedevelopment is to achieve the best recommendations for Determine the scope of the practice guidelineevaluation and management, considering not only efficacy, Form subcommittees with expertise for each guideline sectionbut the cost, convenience, side effect profile, and safety of Perform literature search relevant to each guideline section and distribute to subcommittee and committee membersvarious therapeutic approaches. The HFSA guideline com- Solicit additional relevant information from subcommittee and committeemittee often determined the strength of a recommendation members for each subsectionby the ‘‘totality of evidence,’’ which is a synthesis of all Formulate new recommendations and revise previous recommendations assigning Strength of Recommendation and Strength of Evidencetypes of available data, pro and con, about a particular ther- Form consensus of subcommittee for each section by conference callapeutic option. Assign writing of additional or revised background by subcommittee Full committee review of each section with revisions by subcommitteeTotality of Evidence. Totality of evidence includes not Review of each completed section by Executive Council with revisionsonly results of clinical trials, but also expert opinion and made by full committee and returned to Executive Council for final approval.findings from epidemiologic and basic science studies. Disseminate documentAgreement among various types of evidence, especially Update document as changes are necessaryfrom different methodologies, increases the likelihoodthat a particular therapy is valuable. Although many equateevidence-based medicine with the results of a few individ- subcommittees and the full Guideline Committee. Membersual clinical trials, the best judgment seems to be derived of each subcommittee were asked to review the search andfrom a careful analysis of all available trial data combined identify any additional relevant medical evidence for eachwith integration of results from the basic laboratory and the assigned section. Changes in recommendation and back-findings of epidemiologic studies. ground were carried out by each subcommittee with confer- ence calls directed by the Guideline Committee chair. EachScale of Strength. The HFSA guideline employs the cat- section was presented for comments and consensus ap-egorization for strength of recommendation outlined in proval to the Guideline Committee. Once subsectionsTable 1.3. There are several degrees of favorable recom- were complete, the Executive Council reviewed and com-mendations and a single category for therapies felt to be mented on each section and these comments were returnednot effective. The phrase ‘‘is recommended’’ should be to the Guideline Committee for changes and once complete,taken to mean that the recommended therapy or manage- for final approval by the Executive Council.ment process should be followed as often as possible in in-dividual patients. Exceptions are carefully delineated. Consensus. The development of a guideline involves the‘‘Should be considered’’ means that a majority of patients selection of individuals with expertise and experience toshould receive the intervention, with some discretion in- drive the process of formulating specific recommendationsvolving individual patients. ‘‘May be considered’’ means and producing a written document. The role of these ex-that individualization of therapy is indicated (Table 1.3). perts goes well beyond the formulation of recommenda-When the available evidence is considered to be insufficient tions supported by expert opinion.or too premature, or consensus fails, issues are labeled un- Experts involved in the guideline process must functionresolved and included as appropriate at the end of the rele- as a collective, not as isolated individuals. Expert opinionvant section. is not always unanimous. Interpretations of data vary. Dis- agreements arise over the generalizability and applicability Table 1.3. HFSA System for Classifying the Strength of of trial results to various patient subgroups. Experts are Recommendations influenced by their own experiences with particular thera- pies, but still generally agree on the clinical value of trial‘‘Is recommended’’ Part of routine care Exceptions to therapy should be minimized data. Discomfort with the results of trials reported as posi-‘‘Should be Majority of patients should receive the tive or negative generally focus on factors that potentially considered’’ intervention compromise the evidence. Unfortunately, there are no abso- Some discretion in application to individual patients should be allowed lute rules for downgrading or upgrading trial results or for‘‘May be considered’’ Individualization of therapy is indicated deciding that the limitations of the trial are sufficient to ne-‘‘Is not recommended’’ Therapeutic intervention should not be used gate what has been regarded as a traditionally positive or negative statistical result. The HFSA Guideline Committee sought resolution ofProcess of Guideline Development difficult cases through consensus building. An open, dy- Key steps in the development of this guideline are listed namic discussion meant that no single voice was allowedin Table 1.4. Having determined the broad scope of the cur- to dominate. Written documents were essential to this pro-rent guideline, subcommittees of the guideline committee cess, because they provided the opportunity for feedbackwere formed for each section of the guideline. A literature from all members of the group. On occasion, consensussearch with relevant key words and phrases for each of opinion was sufficient to override positive or negative re-guideline section were provided to members of the sults of almost any form of evidence. The HFSA process
    • Executive Summary: Heart Failure Practice Guideline  HFSA 479had a strong commitment to recommendations based on ob- basis by physicians and other health care providers in thejective evidence rigorously reviewed by a panel of experts. field. The development and utilization of practice guidelines Issues that caused difficulty for the HFSA guideline pro- has emerged as an alternative strategy. The methodology ofcess were some of the more important ones faced by the guideline development needs improvement, but when thesecommittee, because they mirrored those that are often documents are properly conceived and formulated, their im-most challenging to clinicians in day-to-day practice. The portance to patient care seems evident. This HFSA guidelinefoundation of the HFSA guideline process was the belief on HF is designed as a ‘‘living document,’’ which will con-that the careful judgment of recognized opinion leaders tinue to serve as a resource for helping patients with HF.in these controversial areas is more likely to be correctthan ad hoc decisions made ‘‘on the spot’’ by physicians Section 2: Conceptualization and Working Defini-in practice. tion of Heart Failure The involvement of many groups in the development ofthis guideline helped avoid the introduction of bias, which HF remains a major and growing societal problem de-can be personal, practice-based, or based on financial inter- spite advances in detection and therapy.4-7 However, thereest. Committee members and reviewers from the Executive is no widely accepted characterization and definition ofCouncil received no direct financial support from the HFSA HF, probably because of the complexity of the syndrome.or any other source for the development of the guideline. The conceptualization and working definition of HF pre-Support was provided by the HFSA administrative staff, sented here emerged as these guidelines were developed.but the writing of the document was performed on a volun- They are critical to understanding HF and approaching itsteer basis primarily by the Committee. Financial relation- treatment appropriately.ships that might represent conflicts of interest were Conceptual Background. HF is a syndrome rather thancollected annually from all members of the Guideline Com- a primary diagnosis. It has many potential etiologies, di-mittee and the Executive Council. Current relationships are verse clinical features, and numerous clinical subsets. Pa-shown in Appendix C. tients may have a variety of primary cardiovascularDissemination and Continuity. The value of a practice diseases and never develop cardiac dysfunction, and thoseguideline is significantly influenced by the scope of its dis- in whom cardiac dysfunction is identified through testingsemination. The first and second HFSA guidelines were may never develop clinical HF. In addition to cardiac dys-available on the Internet, and thousands of copies were function, other factors, such as vascular stiffness, dyssyn-downloaded. The current document will be implemented chrony, and renal sodium handling, play major roles inon the Internet both for file transfer and as a hypertext the manifestation of the syndrome of HF.source of detailed knowledge concerning HF. Patients at risk for many cardiovascular diseases are at An important final consideration is the continuity of the risk for HF. Early identification and treatment of risk fac-guideline development process. The intent is to create tors is perhaps the most significant step in limiting the pub-a ‘‘living document’’ that will be updated and amended lic health impact of HF.8-10 Emphasis on primary andas necessary to ensure continuing relevance. The rapid de- secondary prevention is particularly critical because ofvelopment of new knowledge in HF from basic and clinical the difficulty of successfully treating left ventricular (LV)research and the continuing evolution of pharmacologic and dysfunction, especially when severe.8 Current therapeuticdevice therapy for this condition provides a strong mandate advances in the treatment of HF do not make preventionfor timely updates. The HFSA intends to undertake targeted any less important.reviews and updates in areas where new research has impli- Although HF is progressive, current therapy may providecations for practice. Section 17: The Genetic Evaluation of stability and even reversibility. The inexorable progressionCardiomyopathy is an example of this policy. of HF from LV remodeling and dysfunction is no longer inevitable. Prolonged survival with mild to moderate LVSummary dysfunction is now possible. Therapy with angiotensin- converting enzyme (ACE) inhibitors or angiotensin receptor Practice guidelines have become a major part of the clini- blockers (ARBs), beta blockers, and cardiaccal landscape and seem likely to become more rather than resynchronization therapy (CRT) can lead to slowing or toless pervasive. Some may perceive guidelines as another partial reversal of remodeling.mechanism for process management or as another instrument Because of this prolonged survival, comorbid conditions,for cost control. But there is a more patient-centered rationale such as coronary artery disease (CAD) or renal failure, canfor their development, especially for a common, potentially progress, complicating treatment. Given this prolonged sur-debilitating, and often fatal syndrome such as HF. Despite ad- vival, considerable attention is devoted in this guideline tovances in clinical trial methodology and the extensive use of disease management, the use of multidrug therapy, and thestudies to evaluate therapeutics and the care process, essen- management of patients with HF at the end of life.tial elements of the management process remain undefinedfor many clinical problems. HF is no exception. Tradition- Working Definition. Although HF may be caused byally, management guidelines were determined on an ad hoc a variety of disorders, the following comprehensive
    • 480 Journal of Cardiac Failure Vol. 16 No. 6 June 2010guideline and this working definition focus on HF primarily Table 2.1. Additional HF Definitionsfrom the loss or dysfunction of myocardial muscle or ‘‘HF With Reduced Left A clinical syndrome characterizedinterstitium. Ventricular Ejection Fraction by signs and symptoms of HF (LVEF)’’ Sometimes: ‘‘HF and reduced LVEF. Most HF is a syndrome caused by cardiac dysfunction, With a Dilated Left Ventricle’’ commonly associated with LV generally resulting from myocardial muscle dys- chamber dilation. ‘‘HF With Preserved LVEF’’ A clinical syndrome characterized function or loss and characterized by either LV di- Sometimes: ‘‘HF With by signs and symptoms of HF lation or hypertrophy or both. Whether the a Nondilated LV’’ with preserved LVEF. Most dysfunction is primarily systolic or diastolic or commonly associated with a nondilated LV chamber. May mixed, it leads to neurohormonal and circulatory be the result of valvular disease abnormalities, usually resulting in characteristic or other causes (Section 11). symptoms such as fluid retention, shortness of ‘‘Myocardial Remodeling’’ Pathologic myocardial hypertrophy or dilation in breath, and fatigue, especially on exertion. In the response to increased absence of appropriate therapeutic intervention, myocardial stress. These HF is usually progressive at the level of both car- changes are generally accompanied by pathologic diac function and clinical symptoms. The severity changes in the cardiac of clinical symptoms may vary substantially dur- interstitium. Myocardial ing the course of the disease process and may remodeling is generally a progressive disorder. not correlate with changes in underlying cardiac function. Although HF is progressive and often fa- tal, patients can be stabilized and myocardial dys- function and remodeling may improve, either infarction (MI) in patients with atherosclerotic cardiovascu- spontaneously or as a consequence of therapy. In lar disease is a critical intervention, since occurrence of MI physiologic terms, HF is a syndrome characterized confers an 8- to 10-fold increased risk for subsequent HF.30 by either or both pulmonary and systemic venous Other modifiable risk factors include anemia, diabetes, hy- congestion and/or inadequate peripheral oxygen perlipidemia, obesity, valvular abnormalities, alcohol, cer- delivery, at rest or during stress, caused by cardiac tain illicit drugs, some cardiotoxic medications, and dysfunction. diet.37,38Additional Definitions Recommendations for Patients With Risk Factors for HF is often classified as HF with reduced systolic func- Ventricular Remodeling, Cardiac Dysfunction, andtion versus HF with preserved systolic function. Myocardial Heart Failureremodeling often precedes the clinical syndrome of HF.Additional definitions are provided in Table 2.1. 3.1 A careful and thorough clinical assessment, with ap- propriate investigation for known or potential risk fac- tors, is recommended in an effort to preventSection 3: Prevention of Ventricular Remodeling, development of LV remodeling, cardiac dysfunction, Cardiac Dysfunction, and Heart Failure and HF. These risk factors include, but are not limited to, hypertension, hyperlipidemia, atherosclerosis, dia- HF is an all-too-frequent outcome of hypertension and betes mellitus, valvular disease, obesity, physical inac-arterial vascular disease, making it a major public health tivity, excessive alcohol intake, dietary choices, andconcern.11,12 Epidemiologic, clinical, and basic research smoking. (Strength of Evidence 5 A)have identified a number of antecedent conditions that pre-dispose individuals to HF and its predecessors, LV remod- 3.2 The recommended goals for the management of spe-eling and dysfunction.13-21 Recognition that many of these cific risk factors for the development of cardiac dys-risk factors can be modified and that treating HF is difficult function and HF are shown in Table 3.1.and costly has focused attention on preventive strategies for 3.3 ACE inhibitors are recommended for prevention of HFHF. in patients at high risk of this syndrome, including Development of both systolic and diastolic dysfunction those with CAD, peripheral vascular disease, orrelated to adverse ventricular remodeling may take years stroke. Patients with diabetes and another major riskto produce significant ill effects.22-28 Although the precise factor or patients with diabetes who smoke or havemechanisms for the transition to symptomatic HF are not microalbuminuria are also at high risk and should re-clear, many modifiable factors have been identified that pre- ceive ACE inhibitors. (Strength of Evidence 5 A)dispose or aggravate the remodeling process and the devel-opment of cardiac dysfunction. Treatment of systemic 3.4 Beta blockers are recommended for patients with priorhypertension, with or without LV hypertrophy, reduces MI to reduce mortality, recurrent MI, and the develop-the development of HF.8,29-36 Prevention of myocardial ment of HF. (Strength of Evidence 5 A)
    • Executive Summary: Heart Failure Practice Guideline  HFSA 481 Table 3.1. Goals for the Management of Risk Factors for the Development of Heart FailureRisk Factor Population Treatment Goal Strength of EvidenceHypertension No diabetes or renal disease !140/90 mmHg A Diabetes !130/80 mmHg A Renal insufficiency and O1g/day of 127/75 A proteinuria Renal insufficiency and #1 g/day of 130/85 A proteinuria Everyone with hypertension Limit sodium to #1500 mg/day ADiabetes See American Diabetes Association (ADA) GuidelineHyperlipidemia See National Cholesterol Education Program (NCEP) GuidelinePhysical Inactivity Everyone Sustained aerobic activity 20-30 minutes, 3- B 5 times weeklyObesity BMI O30 Weight reduction to achieve BMI !30 CExcessive alcohol intake Men Limit alcohol intake to 1-2 drink equivalents C per day Women 1 drink equivalent per day Those with propensity to abuse alcohol or Abstention with alcoholic cardiomyopathySmoking Everyone Cessation AVitamin/mineral deficiency Everyone Diet high in Kþ/calcium BPoor diet Everyone 4 or more servings of fruit and vegetables B per day; One or more servings of breakfast cereal per week Section 4. Evaluation of Patients for Ventricular concentration as part of a screening evaluation for Dysfunction and Heart Failure structural heart disease in asymptomatic patients is not recommended. (Strength of Evidence 5 B) Patients undergoing evaluation for ventricular dysfunc-tion and HF fall into 3 general groups: (1) patients at risk Table 4.1. Indications for Evaluation of Clinicalof developing HF, (2) patients suspected of having HF Manifestations of HFbased on signs and symptoms or incidental evidence of ab- Conditions Hypertensionnormal cardiac structure or function, and (3) patients with Diabetes Obesityestablished symptomatic HF. CAD (eg, after MI, revascularization) Peripheral arterial disease or cerebrovascularPatients at Risk for Heart Failure disease Valvular heart disease Patients identified to be at risk for HF require aggressive Family history of cardiomyopathy in a first-management of modifiable risk factors as outlined in Sec- degree relative History of exposure to cardiac toxinstion 3 of this guideline. Patients with risk factors may Sleep-disordered breathinghave undetected abnormalities of cardiac structure or func- Test Findings Sustained arrhythmiastion. In addition to risk factor reduction, these patients re- Abnormal ECG (eg, LVH, left bundle branch block, pathologic Q waves)quire careful assessment for the presence of symptoms of Cardiomegaly on chest X-rayHF and, depending on their underlying risk, may warrantnoninvasive evaluation of cardiac structure and function.Recommendations for Evaluation of Patients at Risk for Table 4.2. Assess Cardiac Structure and Function inHeart Failure Patients with the Following Disorders or Findings CAD (eg, after MI, revascularization)4.1 Evaluation for clinical manifestations of HF with a rou- Valvular heart disease tine history and physical examination is recommended Family history of cardiomyopathy in a first-degree relative Atrial fibrillation or flutter in patients with the medical conditions or test findings Electrocardiographic evidence of LVH, left bundle branch block, or listed in Table 4.1. (Strength of Evidence 5 B) pathologic Q waves Complex ventricular arrhythmia4.2 Assessment of Cardiac Structure and Function. Echo- Cardiomegaly cardiography with Doppler is recommended to deter- mine cardiac structure and function in asymptomatic patients with the disorders or findings listed in Table 4.2. (Strength of Evidence 5 B) Patients Suspected of Having HF4.3 Routine determination of plasma B-type natriuretic The evaluation of patients suspected of having HF fo- peptide (BNP) or N-terminal pro-BNP (NT-proBNP) cuses on interpretation of signs and symptoms that have
    • 482 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 Table 4.3. Symptoms Suggesting the Diagnosis of HF 4.7 Differential Diagnosis. The differential diagnoses inSymptoms Dyspnea at rest or on exertion Table 4.5 should be considered as alternative explana- Reduction in exercise capacity tions for signs and symptoms consistent with HF. Orthopnea (Strength of Evidence 5 B) Paroxysmal nocturnal dyspnea (PND) or nocturnal cough Edema Ascites or scrotal edema Table 4.5. Differential Diagnosis for HF Symptoms andLess specific Early satiety, nausea and vomiting, abdominal Signs presentations of HF discomfort Myocardial ischemia Wheezing or cough Pulmonary disease (pneumonia, asthma, chronic obstructive pulmonary Unexplained fatigue disease, pulmonary embolus, primary pulmonary hypertension) Confusion/delirium Sleep-disordered breathing Depression/weakness (especially in the elderly) Obesity Deconditioning Malnutrition Anemialed to the consideration of this diagnosis. Careful history Hepatic failureand physical examination, combined with evaluation of car- Chronic kidney disease Hypoalbuminemiadiac structure and function, should be undertaken to deter- Venous stasismine the cause of symptoms and to evaluate the degree of Depressionunderlying cardiac pathology. Anxiety and hyperventilation syndromes Hyper or hypo-thyroidismRecommendations for Evaluation of PatientsSuspected of Having HF Patients With Established HF4.4 Symptoms Consistent with HF. The symptoms listed The evaluation of patients with an established diagnosis in Table 4.3 suggest the diagnosis of HF. It is recom- of HF is undertaken to identify the etiology, assess symp- mended that each of these symptoms be elicited in all tom nature and severity, determine functional impairment, patients in whom the diagnosis of HF is being consid- and establish a prognosis. Follow-up of patients with HF ered. (Strength of Evidence 5 B) or cardiac dysfunction involves continuing reassessment4.5 Physical Examination. It is recommended that patients of symptoms, functional capacity, prognosis, and therapeu- suspected of having HF undergo careful physical ex- tic effectiveness. amination with determination of vital signs and care- ful evaluation for signs shown in Table 4.4. (Strength of Evidence 5 B) Recommendations for the Evaluation of Patients With Established HF Table 4.4. Signs to Evaluate in Patients Suspected of 4.8 It is recommended that patients with a diagnosis of HF Having HF undergo evaluation as outlined in Table 4.6. (Strength of Evidence 5 C)Cardiac Abnormality Sign 4.9 Symptoms. In addition to symptoms characteristic ofElevated cardiac Elevated jugular venous pressure filling pressures S3 gallop HF (dyspnea, fatigue, decreased exercise tolerance, and fluid overload Rales fluid retention), evaluation of the following symptoms Hepatojugular reflux should be considered in the diagnosis of HF: Ascites Edema  AnginaCardiac enlargement Laterally displaced or prominent apical impulse  Symptoms suggestive of embolic events Murmurs suggesting valvular dysfunction  Symptoms suggestive of sleep-disordered breathingReduced cardiac output Narrow pulse pressure Cool extremities Tachycardia with pulsus alternansArrhythmia Irregular pulse suggestive of atrial Table 4.6. Initial Evaluation of Patients With a Diagnosis of fibrillation or frequent ectopy HF Assess clinical severity of HF by history and physical examination Assess cardiac structure and function Determine the etiology of HF, with particular attention to reversible causes Evaluate for coronary disease and myocardial ischemia4.6 It is recommended that BNP or NT-proBNP levels be Evaluate the risk of life-threatening arrhythmia assessed in all patients suspected of having HF, espe- Identify any exacerbating factors for HF cially when the diagnosis is not certain. (Strength of Identify comorbidities which influence therapy Identify barriers to adherence Evidence 5 A)
    • Executive Summary: Heart Failure Practice Guideline  HFSA 483  Symptoms suggestive of arrhythmias, including  Assess electrical dyssynchrony (wide QRS or palpitations bundle branch block), especially when left ven-  Symptoms of possible cerebral hypoperfusion, in- tricular ejection fraction (LVEF) !35% cluding syncope, presyncope, or lightheadedness  Detect LV hypertrophy or other chamber enlarge- (Strength of Evidence 5 B) ment  Detect evidence of myocardial infarction (MI) or4.10 Functional Capacity/Activity Level. It is recommen- ischemia ded that the severity of clinical disease and functional limitation be evaluated and recorded and the ability to  Assess QTc interval, especially with drugs that perform typical daily activities be determined. This prolong QT intervals (Strength of Evidence 5 B) evaluation may be graded by metrics such as New 4.14 Chest X-Ray. It is recommended that all patients with York Heart Association (NYHA) functional class HF have a postero-anterior and lateral chest X-ray (Table 4.7) (Strength of Evidence 5 A) or by the 6- examination for determination of heart size, evidence minute walk test. (Strength of Evidence 5 C) of fluid overload, detection of pulmonary and other diseases, and appropriate placement of implanted Table 4.7. Criteria for NYHA Functional Classification in cardiac devices. (Strength of Evidence 5 B) Patients With HFClass I No limitation of physical activity. Ordinary physical 4.15 Additional Laboratory Tests. It is recommended that activity does not cause undue fatigue, palpitation, or patients with no apparent etiology of HF or no spe- dyspnea. cific clinical features suggesting unusual etiologiesClass II Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, undergo additional directed blood and laboratory palpitations, or dyspnea. studies to determine the cause of HF. (Strength ofClass III IIIA: Marked limitation of physical activity. Evidence 5 B) Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea. IIIB: Marked 4.16 Evaluation of myocardial ischemia is recommended limitation of physical activity. Comfortable at rest, but minimal exertion causes fatigue, palpitation, or in those who develop new-onset LV systolic dysfunc- dyspnea. tion especially in the setting of suspected myocardialClass IV Unable to carry on any physical activity without ischemia or worsening symptoms with pre-existing discomfort. Symptoms of cardiac insufficiency present at rest. If any physical activity is undertaken, CAD. The choice of testing modality should depend discomfort is increased. on the clinical suspicion and underlying cardiac risk factors. Coronary angiography should be considered when pre-test probability of underlying ischemic4.11 Volume Status. The degree of volume excess is a key cardiomyopathy is high and an invasive coronary consideration during treatment. It is recommended intervention may be considered. (See Section 13 that it be routinely assessed by determining: for specific clinical situations and Strength of  Presence of paroxysmal nocturnal dyspnea or or- Evidence) thopnea 4.17 Exercise testing for functional capacity is not recom-  Presence of dyspnea on exertion mended as part of routine evaluation in patients with  Daily weights and vital signs with assessment for HF. Specific circumstances in which maximal exercise orthostatic changes testing with measurement of expired gases should be  Presence and degree of rales, S3 gallop, jugular considered include (Strength of Evidence 5 C): venous pressure elevation, hepatic enlargement and tenderness, positive hepatojugular reflux,  Assessing disparity between symptomatic limita- edema, and ascites (Strength of Evidence 5 B) tion and objective indicators of disease severity  Distinguishing non HF-related causes of func-4.12 Standard Laboratory Tests. It is recommended that tional limitation, specifically cardiac versus pul- the following laboratory tests be obtained routinely monary in patients being evaluated for HF: serum electro-  Considering candidacy for cardiac transplantation lytes, blood urea nitrogen, creatinine, glucose, cal- or mechanical circulatory support cium, magnesium, fasting lipid profile (low-density  Determining the prescription for cardiac rehabili- lipoprotein cholesterol, high-density lipoprotein cho- tation lesterol, triglycerides), complete blood count, serum albumin, uric acid, liver function tests, urinalysis,  Addressing specific employment capabilities and thyroid function. (Strength of Evidence 5 B) 4.18 Routine endomyocardial biopsy is not recommended4.13 Electrocardiogram (ECG). It is recommended that all in cases of new-onset HF. Endomyocardial biopsy patients with HF have an ECG performed to: should be considered in patients with rapidly pro-  Assess cardiac rhythm and conduction (in some gressive clinical HF or ventricular dysfunction, de- cases, using Holter monitoring or event monitors) spite appropriate medical therapy. Endomyocardial
    • 484 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 biopsy also should be considered in patients sus- 4.21 It is recommended that reevaluation of electrolytes and pected of having myocardial infiltrative processes, renal function occur at least every 6 months in clini- such as sarcoidosis or amyloidosis, or in patients cally stable patients and more frequently following with malignant arrhythmias out of proportion to LV changes in therapy or with evidence of change in vol- dysfunction, where sarcoidosis and giant cell ume status. More frequent assessment of electrolytes myocarditis are considerations. (Strength of Evi- and renal function is recommended in patients with se- dence 5 C) vere HF, those receiving high doses of diuretics, those on aldosterone antagonists, and those who are clini-4.19 It is recommended that clinical evaluation at each cally unstable. (Strength of Evidence 5 C) follow-up visit include determination of the elements listed in Table 4.9. (Strength of Evidence 5 B) See Section 7 for recommendations for patients on an aldosterone receptor antagonist. These assessments should include the same symp- toms and signs assessed during the initial evaluation. (Strength of Evidence 5 B) Section 5: Management of Asymptomatic Patients Table 4.9. Elements to Determine at Follow-Up Visits of HF Patients With Reduced Left Ventricular Ejection FractionFunctional capacity and activity level LV remodeling and reduced LVEF should be distin-Changes in body weightPatient understanding of and compliance with dietary sodium restriction guished from the syndrome of clinical HF. When LVEF isPatient understanding of and compliance with medical regimen reduced (!40%), but there are no signs and symptoms ofHistory of arrhythmia, syncope, presyncope, palpitation or ICD discharge HF, the condition frequently is referred to as asymptomaticAdherence and response to therapeutic interventionsThe presence or absence of exacerbating factors for HF, including LV dysfunction (ALVD). It is important to distinguish be- worsening ischemic heart disease, hypertension, and new or worsening tween ALVD and patients categorized as NYHA Class I valvular disease HF. Although patients with NYHA Class I HF do not cur- rently have HF symptoms, they may have ALVD currently, or they may have clinical systolic HF with symptoms in the4.20 In the absence of deteriorating clinical presentation, past. In contrast, patients with ALVD have no past history repeat measurements of ventricular volume and of HF symptoms. It is now well recognized that there LVEF should be considered in these limited circum- may be a latency period when the LVEF is reduced before stances: the development of symptomatic HF. Although most atten-  When a prophylactic implantable cardioverter de- tion in the HF literature has centered on patients with symp- fibrillator (ICD) or cardiac resynchronization toms, evidence now indicates that ALVD is more common therapy (CRT) device and defibrillator (CRT-D) than previously assumed. The recent realization that thera- placement is being considered in order to deter- pies aimed at symptomatic HF may improve outcomes in mine that LVEF criteria for device placement patients with ALVD has increased the importance of recog- are still met after medical therapy (Strength of nizing and treating patients with this condition. Evidence 5 B) The management of patients with ALVD focuses on con-  When patients show substantial clinical improve- trolling cardiovascular risk factors and on the prevention or ment (for example, in response to beta blocker reduction of progressive ventricular remodeling. Exercise, treatment or following pregnancy in patients smoking cessation, hypertension control, as well as treat- with peripartum cardiomyopathy). Such change ment with ACE inhibitors (or ARBs) and beta blockers, may denote improved prognosis, although it all have a potential role in the treatment of this syndrome. does not in itself mandate alteration or discontin- uation of specific treatments (see Section 7). Recommendations for the Management of (Strength of Evidence 5 C) Asymptomatic Patients With Reduced LVEF  In alcohol and cardiotoxic substance abusers who have discontinued the abused substance. (Strength 5.1 It is recommended that all patients with ALVD exercise of Evidence 5 C) regularly according to a physician-directed prescription to avoid general deconditioning; to optimize weight,  In patients receiving cardiotoxic chemotherapy. blood pressure, and diabetes control; and to reduce car- (Strength of Evidence 5 B) diovascular risk. (Strength of Evidence 5 C) Repeat determination of LVEF is usually unnecessary 5.2 Smoking cessation is recommended in all patients in- in patients with previously documented LV dilatation cluding those with ALVD. (Strength of Evidence 5 B) and low LVEF who manifest worsening signs or symp- toms of HF, unless the information is needed to justify 5.3 Alcohol abstinence is recommended if there is current a change in patient management (such as surgery or de- or previous history of excessive alcohol intake. vice implantation). (Strength of Evidence 5 C) (Strength of Evidence 5 C)
    • Executive Summary: Heart Failure Practice Guideline  HFSA 4855.4 It is recommended that all patients with ALVD with (cardiac cachexia). Measurement of nitrogen balance, hypertension achieve optimal blood pressure control. caloric intake, and prealbumin may be useful in deter- (Strength of Evidence 5 B) mining appropriate nutritional supplementation. Calo- ric supplementation is recommended. Anabolic5.5 ACE inhibitor therapy is recommended for asymptom- steroids are not recommended for cachexic patients. atic patients with reduced LVEF (!40%). (Strength of (Strength of Evidence 5 C) Evidence 5 A) 6.5 Patients with HF, especially those on diuretic therapy5.6 ARBs are recommended for asymptomatic patients with and restricted diets, should be considered for daily reduced LVEF who are intolerant of ACE inhibitors from multivitamin-mineral supplementation to ensure ade- cough or angioedema. (Strength of Evidence 5 C) quate intake of the recommended daily value of essen- Routine use of the combination of ACE inhibitors and tial nutrients. Evaluation for specific vitamin or ARBs for prevention of HF is not recommended in this nutrient deficiencies is rarely necessary. (Strength of population. (Strength of Evidence 5 C) Evidence 5 C)5.7 Beta blocker therapy should be considered in asymp- 6.6 Documentation of the type and dose of naturoceutical tomatic patients with reduced LVEF. (post-MI, products used by patients with HF is recommended. Strength of Evidence 5 B; non post-MI, Strength of (Strength of Evidence 5 C) Evidence 5 C) Naturoceutical use is not recommended for relief of Section 6: Nonpharmacologic Management and symptomatic HF or for the secondary prevention ofHealth Care Maintenance in Patients With Chronic cardiovascular events. Patients should be instructed Heart Failure to avoid using natural or synthetic products containing ephedra (ma huang), ephedrine, or its metabolites be- Nonpharmacologic management strategies represent an cause of an increased risk of mortality and morbidity.important contribution to HF therapy. They may signifi- Products should be avoided that may have significantcantly impact patient stability, functional capacity, mortal- drug interactions with digoxin, vasodilators, betaity, and quality of life. These strategies include diet and blockers, antiarrhythmic drugs, and anticoagulants.nutrition, oxygen supplementation, and management of (Strength of Evidence 5 B)concomitant conditions such as sleep apnea, insomnia, de- Recommendations for Other Therapiespression, and sexual dysfunction. Exercise training mayalso play a role in appropriate patients. Attention should 6.7 Continuous positive airway pressure to improve dailybe focused on the appropriate management of routine functional capacity and quality of life is recommendedhealth maintenance issues. in patients with HF and obstructive sleep apnea docu- mented by approved methods of polysomnography.Recommendations for Diet and Nutrition (Strength of Evidence 5 B)6.1 Dietary instruction regarding sodium intake is recom- 6.8 Supplemental oxygen, either at night or during exer- mended in all patients with HF. Patients with HF and tion, is not recommended for patients with HF in the diabetes, dyslipidemia, or severe obesity should be absence of an indication of underlying pulmonary dis- given specific dietary instructions. (Strength of Evi- ease. Patients with resting hypoxemia or oxygen desa- dence 5 B) turation during exercise should be evaluated for residual fluid overload or concomitant pulmonary dis-6.2 Dietary sodium restriction (2-3 g daily) is recommen- ease. (Strength of Evidence 5 B) ded for patients with the clinical syndrome of HF and preserved or depressed left ventricular ejection frac- 6.9 The identification of treatable conditions, such as tion (LVEF). Further restriction (!2 g daily) may sleep-disordered breathing, urologic abnormalities, be considered in moderate to severe HF. (Strength of restless leg syndrome, and depression should be con- Evidence 5 C) sidered in patients with HF and chronic insomnia. Pharmacologic aids to sleep induction may be neces-6.3 Restriction of daily fluid intake to !2 L is recommen- sary. Agents that do not risk physical dependence ded in patients with severe hyponatremia (serum so- are preferred. (Strength of Evidence 5 C) dium !130 mEq/L) and should be considered for Recommendations for Specific Activity and Lifestyle all patients demonstrating fluid retention that is diffi- Issues cult to control despite high doses of diuretic and so- dium restriction. (Strength of Evidence 5 C) 6.10 It is recommended that screening for endogenous or6.4 It is recommended that specific attention be paid to prolonged reactive depression in patients with HF be nutritional management of patients with advanced conducted following diagnosis and at periodic inter- HF and unintentional weight loss or muscle wasting vals as clinically indicated. For pharmacologic
    • 486 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 treatment, selective serotonin reuptake inhibitors are setting of reduced renal function or ACE-inhibitor preferred over tricyclic antidepressants, because the therapy. (Strength of Evidence 5 B) latter have the potential to cause ventricular arrhyth- 6.17 It is recommended that patients with new- or recent- mias, but the potential for drug interactions should be onset HF be assessed for employability following considered. (Strength of Evidence 5 B) a reasonable period of clinical stabilization. An6.11 Nonpharmacologic techniques for stress reduction may objective assessment of functional exercise capacity be considered as a useful adjunct for reducing anxiety is useful in this determination. (Strength of Evi- in patients with HF. (Strength of Evidence 5 C) dence 5 B)6.12 It is recommended that treatment options for sexual 6.18 It is recommended that patients with chronic HF who dysfunction be discussed openly with both male are employed and whose job description is compati- and female patients with HF. (Strength of Evi- ble with their prescribed activity level be encouraged dence 5 C) to remain employed, even if a temporary reduction in hours worked or task performed is required. Retrain- The use of phosphodiasterase-5 inhibitors such as sil- ing should be considered and supported for patients denafil may be considered for use for sexual dysfunc- with a job demanding a level of physical exertion tion in patients with chronic stable HF. These agents exceeding recommended levels. (Strength of Evi- are not recommended in patients taking nitrate prepa- dence 5 B) rations. (Strength of Evidence 5 C) Recommendations for Exercise Testing/ExerciseRecommendations for Routine Health Care TrainingMaintenance 6.19 It is recommended that patients with HF undergo ex-6.13 It is recommended that patients with HF be advised ercise testing to determine suitability for exercise to stop smoking and to limit alcohol consumption training (patient does not develop significant ische- to #2 standard drinks per day in men or #1 standard mia or arrhythmias). drink per day in women. Patients suspected of having an alcohol-induced cardiomyopathy should be ad- If deemed safe, exercise training should be consid- vised to abstain from alcohol consumption. Patients ered for patients with HF in order to facilitate under- suspected of using illicit drugs should be counseled standing of exercise expectations (heart rate ranges to discontinue such use. (Strength of Evidence 5 B) and appropriate levels of exercise training), to in- crease exercise duration and intensity in a supervised6.14 Pneumococcal vaccine and annual influenza vaccina- setting, and to promote adherence to a general exer- tion are recommended in all patients with HF in the cise goal of 30 minutes of moderate activity/exercise, absence of known contraindications. (Strength of Ev- 5 days per week with warm up and cool down exer- idence 5 B) cises. (Strength of Evidence 5 B)6.15 Endocarditis prophylaxis is not recommended based Section 7: Heart Failure in Patients With Reduced on the diagnosis of HF alone. Consistent with the Ejection Fraction AHA recommendation, ‘prophylaxis should be given for only specific cardiac conditions, associated with There are 3 primary issues that must be considered the highest risk of adverse outcome from endocardi- when treating HF patients with reduced LVEF: (1) im- tis.’39 These are: ‘prosthetic cardiac valves; previous proving symptoms and quality of life, (2) slowing the infective endocarditis; congenital heart disease progression or reversing cardiac and peripheral dysfunc- (CHD)’ such as: ‘unrepaired cyanotic CHD, includ- tion, and (3) reducing mortality. General measures, such ing palliative shunts and conduits; completely re- as salt restriction, weight loss, lipid control, and other paired congenital heart defect with prosthetic nonpharmacologic measures are addressed in Section 6. material or device, whether placed by surgery or by Pharmacologic approaches to symptom control, including catheter intervention, during the first six months after diuretics, vasodilators, intravenous inotropic drugs, antico- the procedure; repaired CHD with residual defects at agulants, and antiplatelet agents are discussed at the end the site or adjacent to the site of a prosthetic patch or of this section. prosthetic device (which inhibit endothelialization); Two classes of agents have become the recommended cor- cardiac transplantation recipients who develop car- nerstone of therapy to delay or halt progression of cardiac diac valvulopathy.’ (Strength of Evidence 5 C) dysfunction and improve mortality: ACE inhibitors and6.16 Nonsteroidal anti-inflammatory drugs, including beta blockers. Even while these agents are underused in the cyclooxygenase-2 inhibitors, are not recommended treatment of HF, new classes of agents have been added in patients with chronic HF. The risk of renal failure that show an impact on mortality, complicating decisions and fluid retention is markedly increased in the about optimal pharmacologic therapy. These include
    • Executive Summary: Heart Failure Practice Guideline  HFSA 487 Table 7.1. ACE-inhibitor, Angiotensin Receptor Blocker, and Beta-Blocker Therapy in Heart Failure with Low Ejection Fraction Mean Dose Achieved inGeneric Name Trade Name Initial Daily Dose Target Dose Clinical TrialsACE-inhibitorsCaptopril Capoten 6.25 mg tid 50 mg tid 122.7 mg/day160Enalapril Vasotec 2.5 mg bid 10 mg bid 16.6 mg/day42Fosinopril Monopril 5-10 mg qd 80 mg qd n/aLisinopril Zestril, Prinivil 2.5-5 mg qd 20 mg qd *4.5 mg/day (low dose ATLAS) 33.2 mg/day (high dose ATLAS)161Quinapril Accupril 5 mg bid 80 mg qd n/aRamipril Altace 1.25-2.5 mg qd 10 mg qd n/aTrandolapril Mavik 1 mg qd 4 mg qd n/aAngiotensin Receptor BlockersCandesartan Atacand 4-8 mg qd 32 mg qd 24 mg/day162Losartan Cozaar 12.5-25 mg qd 150 mg qd 129 mg/day163Valsartan Diovan 40 mg bid 160 mg bid 254 mg/day164Beta-blockersBisoprolol Zebeta 1.25 mg qd 10 mg qd 8.6 mg/day47Carvedilol Coreg 3.125 mg bid 25 mg bid 37 mg/day165Carvedilol Coreg CR 10 mg qd 80 mg qdMetoprolol succinate CR/XL Toprol XL 12.5-25 mg qd 200 mg qd 159 mg/day48Aldosterone AntagonistsSpironolactone Aldactone 12.5 to 25 mg qd 25 mg qd 26 mg/day60Eplerenone Inspra 25 mg qd 50 mg qd 42.6 mg/day61Other VasodilatorsFixed dose Hydralazine/ BiDil 37.5 mg hydralazine/20 mg 75 mg hydralazine/40 mg 142.5 mg hydralazine/76 mg Isosorbide dinitrate isosorbide dinitrate tid isosorbide dinitrate tid isosorbide dinitrate/day166Hydralazine Apresoline 37.5 mg qid 75 mg qid 270 mg/day167Isosorbide dinitrate Isordil 20 mg qid 40 mg qid 136 mg/day167 *No difference in mortality between high and low dose groups, but 12% lower risk of death or hospitalization in high dose group vs. low dose group.ARBs, aldosterone antagonists, and the combination of 7.2 It is recommended that other therapy be substituted forhydralazine and an oral nitrate (Table 7.1). ACE inhibitors in the following circumstances:  In patients who cannot tolerate ACE inhibitors dueRecommendations for ACE-inhibitors to cough, ARBs are recommended. (Strength of There is compelling evidence that ACE inhibitors should Evidence 5 A)be used to inhibit the renin-angiotensin-aldosterone system The combination of hydralazine and an oral nitrate(RAAS) in all HF patients with reduced LVEF, whether or may be considered in such patients not toleratingnot they are symptomatic (Table 7.1). A number of large ARB therapy. (Strength of Evidence 5 C)clinical trials have demonstrated improvement in morbidityand mortality in HF patients with reduced LVEF, both  Patients intolerant to ACE inhibitors from hyperka-chronically and post-MI.40-42 lemia or renal insufficiency are likely to experience the same side effects with ARBs. In these cases, the7.1 ACE inhibitors are recommended for routine adminis- combination of hydralazine and an oral nitrate tration to symptomatic and asymptomatic patients should be considered. (Strength of Evidence 5 C) with LVEF # 40%. (Strength of Evidence 5 A) ACE inhibitors should be titrated to doses used in 7.3 ARBs are recommended for routine administration to clinical trials, as tolerated during concomitant up- symptomatic and asymptomatic patients with an titration of beta blockers. (Strength of Evidence 5 C) LVEF # 40% who are intolerant to ACE inhibitors for reasons other than hyperkalemia or renal insuffi-Recommendations for Alternatives to ACE-inhibitors ciency. (Strength of Evidence 5 A) ACE inhibitors can have some troublesome side effects, in- 7.4 ARBs should be considered in patients experiencingcluding cough and angioedema, which may limit therapy with angioedema while on ACE inhibitors based on theirthese agents. ARBs have been demonstrated to be well toler- underlying risk and with recognition that angioedemaated in randomized trials of patients judged to be intolerant has been reported infrequently with ARBs. (Strengthof ACE inhibitors.43,44 Both drugs have similar effects on of Evidence 5 B)blood pressure, renal function, and potassium.43 Thus, patientsintolerant of ACE-inhibitors for these reasons may also be in- The combination of hydralazine and oral nitrates maytolerant of ARBs, and the combination of hydralazine and oral be considered in such patients not tolerating ARBnitrates should be considered for these patients. therapy. (Strength of Evidence 5 C)
    • 488 Journal of Cardiac Failure Vol. 16 No. 6 June 2010Recommendations for Angiotensin Receptor Blockers intravenous diuretics and vasoactive agents, including inotropic support. Whenever possible, beta blocker Both ACE inhibitors and ARBs inhibit the RAAS, but by dif- therapy should be initiated in the hospital setting atferent mechanisms. ACE inhibitors block an enzyme responsi- a low dose prior to discharge in stable patients.ble for converting angiotensin I to angiotensin II and for (Strength of Evidence 5 B)degrading various kinins. However, during chronic therapy,angiotensin II levels are not completely suppressed by ACE in- 7.9 Beta blocker therapy is recommended in the great ma-hibitors. ARBs block the effects of angiotensin II on the ATI jority of patients with HF and reduced LVEF, even ifreceptor, independent of the source of angio- there is concomitant diabetes, chronic obstructivetensin II production. ARBs have been compared to lung disease, or peripheral vascular disease. BetaACE-inhibitors in several clinical trials, in both chronic HF blocker therapy should be used with caution in pa-and in post-MI HF populations. tients with diabetes with recurrent hypoglycemia, with asthma, or with resting limb ischemia. Consider-7.5 Individual ARBs may be considered as initial therapy able caution should be used if beta blockers are initi- rather than ACE inhibitors for patients with the fol- ated in patients with marked bradycardia (!55 beats/ lowing conditions: min) or marked hypotension (systolic blood pressure  HF Post-MI (Strength of Evidence 5 A) !80 mm Hg). Beta blockers are not recommended  Chronic HF and reduced LVEF (Strength of Evi- in patients with asthma with active bronchospasm. dence 5 B) (Strength of Evidence 5 C) 7.10 It is recommended that beta blockade be initiated atRecommendations for Beta Adrenergic Receptor low doses and uptitrated gradually, typically at 2-Blockers week intervals in patients with reduced LVEF, and after 3-10 day intervals in patients with reduced Beta blocker therapy, advocated for HF by some investiga- LVEF following newly diagnosed MI. (Strength oftors since the 1970s, remains a major advance in the treatment Evidence 5 B)of patients with HF and reduced LVEF. Several large-scaleclinical trials, involving more than 10,000 patients, have pro- 7.11 It is recommended that beta blocker therapy be con-vided unequivocal evidence of important reductions in both tinued in most patients experiencing a symptomaticmortality and morbidity.45-51 The marked beneficial effects exacerbation of HF during chronic maintenanceof beta blockade has been well demonstrated in large-scale treatment, unless they develop cardiogenic shock, re-clinical trials of symptomatic patients with NYHA class II- fractory volume overload, or symptomatic bradycar-IV HF and reduced LVEF using carvedilol, bisoprolol, and me- dia (Strength of Evidence 5 C)toprolol controlled release/extended release (CR/XL). 47-51 A temporary reduction of dose (generally by one-These trials added beta blockade to background therapy that half) in this setting may be considered. Abrupt dis-included ACE inhibitors and diuretics in more than 90% of pa- continuation in patients with symptomatic exacerba-tients. The trial results support benefit from both beta1 selec- tion should be avoided, unless the situation is life-tive and nonselective beta blockers, whether ancillary threatening. (Strength of Evidence 5 C)properties are present or not. beta blocking agents with intrin-sic sympathomimetic activity are likely to worsen survival and If discontinued or reduced, beta blockers should beshould be avoided in patients with HF.52 The beta-blockers reinstated before the patient is discharged. In general,studied in clinical trials are now established as routine therapy doses should be uptitrated to the previous well-in patients with reduced LVEF. This therapy is well tolerated tolerated dose as soon as safely possible (Strengthby a large majority of patients with HF, even those with comor- of Evidence 5 B)bid conditions like diabetes mellitus,53,54 chronic obstructivelung disease,55 and peripheral vascular disease.56 Recommendations for Combination ACE-inhibitor,7.6 Beta blockers shown to be effective in clinical trials of ARB, and Beta Adrenergic Receptor Blocker Therapy patients with HF are recommended for patients with an LVEF #40%. (Strength of Evidence 5 A) 7.12 The routine administration of an ARB is not recom-7.7 The combination of a beta blocker and an ACE inhib- mended in addition to ACE inhibitor and beta itor is recommended as routine therapy for asymptom- blocker therapy in patients with a recent acute MI atic patients with a LVEF #40% and reduced LVEF. (Strength of Evidence 5 A)  Post-MI (Strength of Evidence 5 B) 7.13 The addition of an ARB should be considered in pa-  Non Post-MI (Strength of Evidence 5 C) tients with HF due to reduced LVEF who have persis-7.8 Beta blocker therapy is recommended for patients tent symptoms or progressive worsening despite with a recent decompensation of HF after optimization optimized therapy with an ACE inhibitor and beta of volume status and successful discontinuation of blocker. (Strength of Evidence 5 A)
    • Executive Summary: Heart Failure Practice Guideline  HFSA 489Recommendations for Aldosterone Antagonists  NYHA II HF (Strength of Evidence 5 B) (See Section 15: Special Populations) Sustained activation of aldosterone appears to play animportant role in the pathophysiology of HF.57 Although 7.20 A combination of hydralazine and isosorbide dini-ACE inhibition may transiently decrease aldosterone secre- trate may be considered in non-African-Americantion, there are diverse stimuli other than angiotensin II for patients with HF and reduced LVEF who remainthe production of this hormone.58 Studies suggest a rapid symptomatic despite optimized standard therapy.return of aldosterone to levels similar to those before (Strength of Evidence 5 C)ACE inhibition.59 Aldosterone antagonists have demon-strated efficacy in both severe HF and in post-MI HF.60,61 Recommendations for Optimal Use of Multi-DrugHyperkalemia is a serious adverse effect associated with Therapyboth non-selective (i.e. spironolactone) and selective (i.e. Multi-drug therapy is required for optimal management toeplerenone) aldosterone antagonists. In addition to hyper- slow progression and improve outcome in patients with HFkalemia, gynecomastia or breast pain may be important and reduced LVEF. An ACE inhibitor plus a beta blocker isside effects of spironolactone, but not eplerenone. standard background therapy. An ARB can be substituted7.14 Administration of an aldosterone antagonist is rec- for an ACE inhibitor if clinically indicated. An ARB can be ommended for patients with NYHA class IV (or class added to an ACE inhibitor in individuals in whom beta III, previously class IV) HF from reduced LVEF blocker is contraindicated or not tolerated. The optimal (!35%) while receiving standard therapy, including choice of additional drug therapy to further improve outcome diuretics. (Strength of Evidence 5 A) in patients already treated with 2 of these 3 drugs is not firmly established. An aldosterone inhibitor, an ARB (if the patient7.15 Administration of an aldosterone antagonist should be is already on an ACE inhibitor) and the combination of iso- considered in patients following an acute MI, with sorbide dinitrate and hydralazine have all been shown to exert clinical HF signs and symptoms or history of diabetes further benefit in controlled trials, but have not been the sub- mellitus, and an LVEF !40%. Patients should be on ject of comparative trials. The choice among these agents standard therapy, including an ACE inhibitor (or may be influenced by the patient’s age, renal function, serum ARB) and a beta blocker. (Strength of Evidence 5 A) potassium, racial background, and severity of the clinical7.16 Aldosterone antagonists are not recommended when syndrome. Certain combinations require careful monitoring. creatinine is O2.5 mg/dL (or creatinine clearance is 7.21 Additional pharmacologic therapy should be consid- !30 ml/min) or serum potassium is O5.0 mmol/L ered in patients with HF and reduced LVEF who or in conjunction with other potassium-sparing di- have persistent symptoms or progressive worsening uretics. (Strength of Evidence 5 A) despite optimized therapy with an ACE inhibitor and7.17 It is recommended that serum potassium concentra- beta blocker. The choice of specific agent will be influ- tion be monitored frequently following initiation or enced by clinical considerations, including renal func- change in an aldosterone antagonist. Monitoring tion status, chronic serum potassium concentration, should reflect protocols followed in clinical trials. blood pressure, and volume status. The triple combina- (Strength of Evidence 5 A) tion of an ACE inhibitor, an ARB, and an aldosterone antagonist is not recommended because of the high7.18 In the absence of persistent hypokalemia (!4.0 risk of hyperkalemia. (Strength of Evidence 5 C) mmol/L), supplemental potassium is not recommen-  Addition of an ARB. (Strength of Evidence 5 A) ded in patients taking an aldosterone antagonist. (Strength of Evidence 5 A)  Addition of an aldosterone antagonist: B for severe HF (Strength of Evidence 5A) B for moderate HF (Strength of Evidence 5 C)Recommendations for Oral Nitrates and Hydralazine B for post-MI HF (Strength of Evidence 5 A) The combination of hydralazine and isosorbide dinitrate  Addition of the combination of hydralazine/iso-has shown efficacy in several trials and plays a role in HF sorbide dinitrate:therapy as an alternative to ACE-inhibitors. Based on the B for African Americans (Strength of Evidenceresults of the African American Heart Failure Trial 5 A)(A-HeFT), it also is part of standard HF therapy in African B for others (Strength of Evidence 5 C)Americans with HF and reduced LVEF. 7.22 Additional pharmacological therapy should be consid-7.19 A combination of hydralazine and isosorbide dini- ered in patients with HF and reduced LVEF who are un- trate is recommended as part of standard therapy in able to tolerate a beta blocker and have persistent addition to beta blockers and ACE inhibitors for symptoms or progressive worsening despite optimized African Americans with HF and reduced LVEF. therapy with an ACE inhibitor. The choice of specific  NYHA III or IV HF (Strength of Evidence 5 A) agent will be influenced by clinical considerations,
    • 490 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 including renal function status, chronic serum potassium Diuretic refractoriness may represent patient nonad- concentration, blood pressure and volume status. The tri- herence, a direct effect of diuretic use on the kidney, ple combination of an ACE inhibitor, an ARB, and an al- or progression of underlying cardiac dysfunction. dosterone antagonist is not recommended due to the 7.25 Addition of chlorothiazides or metolazone, once or high risk of hyperkalemia. (Strength of Evidence 5 C) twice daily, to loop diuretics should be considered in patients with persistent fluid retention despite high-  Addition of an ARB. (Strength of Evidence 5 C) dose loop diuretic therapy. But chronic daily use, espe-  Addition of an aldosterone antagonist: cially of metolazone, should be avoided if possible be- B for severe HF (Strength of Evidence 5 C) cause of the potential for electrolyte shifts and volume B for moderate HF (Strength of Evidence 5 C) depletion. These drugs may be used periodically (ev-  Addition of the combination of hydralazine/iso- ery other day or weekly) to optimize fluid manage- sorbide dinitrate: ment. Metolazone will generally be more potent and B for African Americans (Strength of Evidence much longer-acting in this setting and in patients 5 C) with chronic renal insufficiency, so administration B for others (Strength of Evidence 5 C) should be adjusted accordingly. Volume status and electrolytes must be monitored closely when multipleRecommendations for Diuretic Therapy diuretics are used. (Strength of Evidence 5 C) Loop and distal tubular diuretics are necessary adjuncts 7.26 Careful observation for the development of sidein the medical therapy for HF when symptoms are the result effects, including electrolyte abnormalities, symp-of sodium and water retention. Diuretics reduce congestive tomatic hypotension, renal dysfunction, or worseningsymptoms and signs and can be titrated as needed to restore renal function, is recommended in patients treatedeuvolemia and to reach an estimated ‘‘dry’’ weight goal for with diuretics, especially when used at high dosesthe patient. Relief of signs and symptoms must be achieved and in combination. Patients should undergo routinewithout causing side effects, particularly symptomatic hy- laboratory studies and clinical examination as dic-potension or worsening renal function. tated by their clinical response. (Strength of Evi- dence 5 B)7.23 Diuretic therapy is recommended to restore and maintain normal volume status in patients with clin- 7.27 Patients requiring diuretic therapy to treat fluid reten- ical evidence of fluid overload, generally manifested tion associated with HF generally require chronic by congestive symptoms (orthopnea, edema, and treatment, although often at lower doses than those shortness of breath), or signs of elevated filling pres- required initially to achieve diuresis. Decreasing or sures (jugular venous distention, peripheral edema, even discontinuing diuretics may be considered in pulsatile hepatomegaly, and, less commonly, rales). patients experiencing significant improvement in (Strength of Evidence 5 A) Loop diuretics rather clinical status and cardiac function or in those who than thiazide-type diuretics are typically necessary successfully restrict dietary sodium intake. These pa- to restore normal volume status in patients with tients may undergo cautious weaning of diuretic dose HF. (Strength of Evidence 5 B) and frequency with careful observation for recurrent fluid retention. (Strength of Evidence 5 C)7.24 The initial dose of diuretic may be increased as neces- sary to relieve congestion. Restoration of normal vol- 7.28 It is recommended that patients and caregivers be given ume status may require multiple adjustments over education that will enable them to demonstrate under- many days and occasionally weeks in patients with se- standing of the early signs of fluid retention and the vere fluid overload evidenced by massive edema or as- plan for initial therapy. (Strength of Evidence 5 C) cites. After a diuretic effect is achieved with short- Selected patients may be educated to adjust daily dose acting loop diuretics, increasing administration fre- of diuretic in response to weight gain from fluid over- quency to twice or even 3 times per day will provide load (typically short-term weight gain of 2 to 4 lb). more diuresis with less physiologic perturbation than (Strength of Evidence 5 C) (See Section 6 for more in- larger single doses. (Strength of Evidence 5 B) formation on this topic) Oral torsemide may be considered in patients in whom poor absorption of oral medication or erratic Recommendations for Digoxin diuretic effect may be present, particularly those Data from the Digitalis Investigation Group (DIG) trial with right-sided HF and refractory fluid retention de- and the combined databases of several other large trials pro- spite high doses of other loop diuretics. (Strength of vide evidence of digoxin’s efficacy.62-68 Digoxin is a drug Evidence 5 C) that is inexpensive and can be given once daily, and it con- Intravenous administration of diuretics may be neces- tinues to have a therapeutic role in symptomatic patients sary to relieve congestion. (Strength of Evidence 5 A) with HF from reduced LVEF.
    • Executive Summary: Heart Failure Practice Guideline  HFSA 4917.29 Digoxin may be considered to improve symptoms in (goal INR 2.0-3.0) for the initial 3 months post-MI patients with reduced LVEF (LVEF #40%) who (Strength of Evidence 5 B) unless contraindicated. have signs or symptoms of HF while receiving stan- Other patients with ischemic or nonischemic car- dard therapy, including ACE inhibitors and beta diomyopathy and LV thrombus should be consid- blockers: ered for chronic anticoagulation, depending on the  NYHA class II-III (Strength of Evidence 5 B) characteristics of the thrombus, such as its size,  NYHA class IV (Strength of Evidence 5 C) mobility, and degree of calcification. (Strength of7.30 It is recommended that the dose of digoxin, which Evidence 5 C) should be based on lean body mass, renal function, 7.35 Long-term treatment with an antiplatelet agent, gen- and concomitant medications, should be 0.125 mg erally aspirin in doses of 75 to 81 mg, is recommen- daily in the majority of patients and the serum ded for patients with HF due to ischemic digoxin level should be !1.0 ng/mL, generally cardiomyopathy, whether or not they are receiving 0.7-0.9 ng/mL. (Strength of Evidence 5 B) ACE inhibitors. (Strength of Evidence 5 B)7.31 Digoxin should be considered for achieving adequate Warfarin (goal INR 2.0-3.0) and clopidogrel (75 mg) control of the ventricular response to atrial fibrilla- also have prevented vascular events in post-MI pa- tion in patients with HF. (Strength of Evidence 5 B) tients and may be considered as alternatives to aspi-7.32 High doses of digoxin (maintenance dose O0.25 mg rin. (Strength of Evidence 5 B) daily) for the purpose of rate control are not recom- 7.36 Routine use of aspirin is not recommended in pa- mended. (Strength of Evidence 5 C) tients with HF without atherosclerotic vascular dis- ease. (Strength of Evidence 5 C)Recommendations for Anticoagulation and AntiplateletDrugs Recommendations for Amiodarone Therapy Patients with HF are recognized to be at increased risk forarterial or venous thromboembolic events. In addition to Ventricular arrhythmias are common in HF patients, andatrial fibrillation and poor ventricular function, which sudden cardiac death (SCD) continues to account for a signif-promote stasis and increase the risk of thrombus formation, icant proportion of the mortality in this syndrome. Many an-patients with HF have other manifestations of hypercoagula- tiarrhythmic drugs have adverse hemodynamic effectsbility. Evidence of heightened platelet activation, increased sufficient to have negative consequences in patients withplasma and blood viscosity, and increased plasma levels of fi- HF. Patients with HF are at higher risk for proarrhythmic ef-brinopeptide A, betadthromboglobulin, D-dimer, and von fects of antiarrhythmic agents. The major role for the use ofWillebrand factor have been found in many patients.69-71 De- these agents in HF is to reduce recurrences of symptomaticspite a predisposition, estimates regarding the incidence of arrhythmias, usually in patients who have an ICD.75thromboemboli in patients with HF vary substantially be- 7.37 Antiarrhythmic agents, including amiodarone, aretween 1.4% and 4.2% per 100 patient years.72-74 Although not recommended for the primary prevention ofvariability in the reported incidence likely results from differ- sudden death in patients with HF. (Strength of Evi-ences in the populations studied and the methodology used to dence 5 A).identify these events, the consensus is that pulmonary andsystemic emboli are not common in HF patients in sinus 7.38 In patients with HF and an ICD, amiodarone may berhythm. Traditionally, discussion of anticoagulation in pa- considered to reduce the frequency of recurrenttients with HF has centered on warfarin. Antiplatelet agents symptomatic arrhythmias causing ICD shocks.are often used in patients with HF from ischemic heart (Strength of Evidence 5 C)disease. 7.39 It is recommended that when amiodarone therapy is7.33 Treatment with warfarin (goal international normal- initiated, the potential for interactions with other ized ratio [INR] 2.0-3.0) is recommended for all pa- drugs be reviewed. The maintenance doses of di- tients with HF and chronic or documented goxin, warfarin, and some statins should be reduced paroxysmal, persistent, or long-standing atrial fibril- when amiodarone is initiated and then carefully mon- lation (Strength of Evidence 5 A) or a history of sys- itored. Adjustment in doses of these drugs and labo- temic or pulmonary emboli, including stroke or ratory assessment of drug activity or serum transient ischemic attack (Strength of Evidence 5 concentration after initiation of amiodarone is rec- C), unless contraindicated. ommended. (Strength of Evidence 5 A)7.34 It is recommended that patients with symptomatic or 7.40 Routine use of amiodarone therapy for asymptomatic asymptomatic ischemic cardiomyopathy and docu- arrhythmias that are not felt to contribute to HF or mented recent large anterior MI or recent MI with ventricular dysfunction is not recommended. documented LV thrombus be treated with warfarin (Strength of Evidence 5 B)
    • 492 Journal of Cardiac Failure Vol. 16 No. 6 June 20107.41 n-3 polyunsaturated fatty acids (PUFA) may be con- sessions should address specific issues (eg, medication sidered to reduce mortality in HF patients with nonadherence) and their causes (eg, lack of knowledge NYHA class II-IV symptoms and reduced LVEF. vs cost vs forgetting) and employ strategies that pro- (Strength of Evidence 5 B) mote behavior change, including motivational ap- proaches. (Strength of Evidence 5 B) Section 8: Disease Management, Advance Direc- tives, and End-of-Life Care in Heart Failure 8.4 It is recommended that the frequency and intensity of patient education and counseling vary according to The majority of HF care is performed at home by the pa- the stage of illness. Patients in advanced HF or with per-tient and family or caregiver. If these individuals do not sistent difficulty adhering to the recommended regimenknow what is required, fail to see its importance, or face require the most education and counseling. Patientsbarriers to engagement in self-care, they will not participate should be offered a variety of options for learning abouteffectively. For this reason, comprehensive education and HF according to their individual preferences:counseling are the foundation for all HF management.  VideotapeThe goals of education and counseling are to help patients,  One-on-one or group discussiontheir families, and caregivers acquire the knowledge, skills,  Reading materials, translators, telephone calls,strategies, problem solving abilities, and motivation neces- mailed informationsary for adherence to the treatment plan and effective par-  Internetticipation in self-care. The inclusion of family members  Visitsand other caregivers is especially important, because HFpatients often suffer from cognitive impairment, functional Repeated exposure to material is recommendeddisabilities, multiple comorbidities and other conditions because a single session is never sufficient. (Strengththat limit their ability to fully comprehend, appreciate, or of Evidence 5 B)enact what they learn.76-82 8.5 It is recommended that during the care process pa-Recommendations for Education and Counseling tients be asked to:  Demonstrate knowledge of the name, dose, and purpose of each medication8.1 It is recommended that patients with HF and their family members or caregivers receive individualized  Sort foods into high- and low-sodium categories education and counseling that emphasizes self-care.  Demonstrate their preferred method for tracking This education and counseling should be delivered medication dosing by providers using a team approach in which nurses  Show provider daily weight log with expertise in HF management provide the majority  Reiterate symptoms of worsening HF of education and counseling, supplemented by physi-  Reiterate when to call the provider because of cian input and, when available and needed, input specific symptoms or weight changes. (Strength from dietitians, pharmacists, and other health care pro- of Evidence 5 B) viders. (Strength of Evidence 5 B) 8.6 During acute care hospitalization, only essential edu- Teaching is not sufficient without skill building and spec- cation is recommended, with the goal of assisting pa- ification of critical target behaviors. It is recommended tients to understand HF, the goals of its treatment, and that essential elements of patient education (with the post-hospitalization medication and follow-up reg- associated skills) are utilized to promote self-care with imen. Education begun during hospitalization should associated skills shown in Table 8.1. (Strength of be supplemented and reinforced within 1-2 weeks af- Evidence 5 B) ter discharge, continued for 3-6 months, and reas- sessed periodically. (Strength of Evidence 5 B)8.2 It is recommended that patients’ literacy, cognitive sta- tus, psychological state, culture, and access to social Recommendations for Disease Management Programs and financial resources be taken into account for optimal Practitioners who care for patients with HF are challenged education and counseling. Because cognitive impair- daily with preventing common, recurrent rehospitalizations ment and depression are common in HF and can seri- for exacerbations. Disease management is "a comprehensive, ously interfere with learning, patients should be integrated system for managing patients.by using best prac- screened for these. Patients found to be cognitively im- tices, clinical practice improvement.and other resources paired need additional support to manage their HF. and tools to reduce overall cost and improve measurable out- (Strength of Evidence 5 B) comes in the quality of care.’’83 A number of disease manage-8.3 It is recommended that educational sessions begin ment programs have been studied, including HF clinics,84-100 with an assessment of current HF knowledge, issues care delivered in the home or to patients who are at home,101- 117 about which the patient wants to learn, and the pa- and telemonitoring.118-124 These programs focus on mul- tient’s perceived barriers to change. Education tiple aspect of patient care, including optimization of drug
    • Executive Summary: Heart Failure Practice Guideline  HFSA 493 Table 8.1. Essential Elements of Patient Education With Associated Skills and Target BehaviorsElements of Education Skill Building and Critical Target BehaviorsDefinition of HF (linking disease, symptoms, and treatment) and cause of  Discuss basic HF information, cause of patient’s HF, and how symp- patient’s HF toms relate to HF statusRecognition of escalating symptoms and concrete plan for response to  Identify specific signs and symptoms (eg, increasing fatigue or particular symptoms shortness of breath with usual activities, dyspnea at rest, nocturnal dyspnea or orthopnea, edema)  Perform daily weights and know how to respond to evidence of volume overload  Develop action plan for how and when to notify the provider, changes to make in diet, fluid and diureticsIndications and use of each medication  Reiterate medication dosing schedule, basic reason for specific med- ications, and what to do if a dose is missedModify risks for HF progression  Smoking cessation  Maintain blood pressure in target range  Maintain normal HgA1c, if diabetic  Maintain specific body weightSpecific diet recommendations: individualized low-sodium diet;  Understand and comply with sodium restriction recommendation for alcohol intake  Demonstrate how to read a food label to check sodium amount per serving and sort foods into high- and low-sodium groups  Reiterate limits for alcohol consumption or need for abstinence if history of alcohol abuseSpecific activity/exercise recommendations  Comply with prescribed exerciseImportance of treatment adherence and behavioral strategies to promote  Plan and use a medication system that promotes routine adherence  Plan for refillstherapy, patient and family/caregiver education and counsel- based on patient characteristics and needs. (Strengthing, emphasis on self-care, vigilant follow-up, early attention of Evidence 5 B)to signs and symptoms of fluid overload, coordination of care 8.9 It is recommended that HF disease management in-with other providers, quality assessment, and increased ac- clude integration and coordination of care betweencess to the health care provider. the primary care physician and HF care specialists8.7 Patients recently hospitalized for HF and other patients and with other agencies, such as home health and car- at high risk for HF decompensation should be consid- diac rehabilitation. (Strength of Evidence 5 C) ered for comprehensive HF disease management. 8.10 It is recommended that patients in a HF disease manage- High-risk patients include those with renal insuffi- ment program be followed until they or their family/ ciency, low output state, diabetes, chronic obstructive caregiver demonstrate independence in following the pulmonary disease, persistent NYHA class III or IV prescribed treatment plan, adequate or improved adher- symptoms, frequent hospitalization for any cause, mul- ence to treatment guidelines, improved functional ca- tiple active comorbidities, or a history of depression, pacity, and symptom stability. Higher risk patients cognitive impairment, inadequate social support, poor with more advanced HF may need to be followed perma- health literacy, or persistent nonadherence to therapeu- nently. Patients who experience increasing episodes of tic regimens. (Strength of Evidence 5 A) exacerbation or who demonstrate instability after dis-8.8 It is recommended that HF disease management pro- charge from a program should be referred again to the grams include the components shown in Table 8.3 service. (Strength of Evidence 5 B) Table 8.3. Recommended Components of a HF Disease Recommendations for Advance Directives and End-of- Management Program Life Care  Comprehensive education and counseling individualized to patient HF has a worse prognosis than many common cancers,125 needs and premature death from progressive acute decompensated  Promotion of self care, including self-adjustment of diuretic therapy in heart failure (ADHF) or SCD is frequent. Recent advances in appropriate patients (or with family member/caregiver assistance) HF treatment have resulted in substantial reductions in an-  Emphasis on behavioral strategies to increase adherence  Vigilant follow-up after hospital discharge or after periods of nual mortality from these modes of death. Nevertheless, the instability mortality rate in HF remains high, making advance directives  Optimization of medical therapy and end-of-life care important issues for patients with this  Increased access to providers condition. Hospice services or other end-of-life care should  Early attention to signs and symptoms of fluid overload only be implemented after full and appropriate application  Assistance with social and financial concerns of evidence-based pharmacologic and cardiac device
    • 494 Journal of Cardiac Failure Vol. 16 No. 6 June 2010therapies, unless documentation of intolerance or contra-  Need for continuous intravenous inotropic ther-indication to such treatments is present. For critically ill apy support 128,129 (Strength of Evidence 5 B)patients, clinicians should acknowledge to the patient 8.14 It is recommended that end-of-life care strategies beand their family the potentially life-threatening nature individualized and include core HF pharmacologicof their condition, and supportive care for them should therapies, effective symptom management and com-be implemented as indicated. In most cases, adequate fort measures, while avoiding unnecessary testing.time (weeks to months) must be given to allow medical New life-prolonging interventions should be dis-therapies to exert a beneficial therapeutic effect. In addi- cussed with patients and care-givers with careful dis-tion, issues such as access to care, adherence to medica- cussion of whether they are likely to improvetions and other self care behaviors, and knowledge about symptoms. (Strength of Evidence 5 C)HF must be addressed. End-of-life care most often in-cludes continuing HF therapies, which may effectively 8.15 It is recommended that a specific discussion about re-ease symptoms and stabilize or improve quality of life. suscitation be held in the context of planning for overallA discussion about HF course and prognosis should be care and for emergencies with all patients with HF. Theconducted with all patients to the extent that they are possibility of SCD for patients with HF should be ac-willing to participate in such a conversation. Discussion knowledged. Specific plans to reduce SCD (for exampleof end-of-life care can occur when the patient has pro- with an ICD) or to allow natural death should be basedgressed to a state of severe, refractory HF. on the individual patient’s risks and preferences for an attempt at resuscitation with specific discussion of risks8.11 It is recommended that patient and family or care- and benefits of inactivation the ICD. Preferences for at- giver discussions about quality of life and prognosis tempts at resuscitation and plans for approach to care be included in the disease management of HF. should be readdressed at turning points in the patient’s (Strength of Evidence 5 C) course or if potentially life-prolonging interventions8.12 It is recommended that: are considered. (Strength of Evidence 5 C) a. Seriously ill patients with HF and their families 8.16 It is recommended that, as part of end-of-life care, be educated to understand that patients with HF patients and their families/caregivers have a plan to are at high risk of death, even while aggressive manage a sudden decompensation, death, or progres- efforts are made to prolong life. sive decline. Inactivation of an implantable defibrilla- b. Patients with HF be made aware that HF is po- tion device should be discussed in the context of tentially life-limiting, but that pharmacologic allowing natural death at end of life. A process for and device therapies and self-management can deactivating defibrillators should be clarified in all prolong life. In most cases, chronic HF pharma- settings in which patients with HF receive care. cologic and device therapies should be optimized (Strength of Evidence 5 C) as indicated before identifying that patients are 8.17 Patients with HF receiving end-of-life care should be near end-of-life. considered for enrollment in hospice that can be de- c. Identification of end-of-life in a patient should be livered in the home, a nursing home, or a special hos- made in collaboration with clinicians experienced pice unit. (Strength of Evidence 5 C) in the care of patients with HF when possible. d. End-of-life management should be coordinated Section 9: Electrophysiology Testing and the Use with the patient’s primary care physician. of Devices in Heart Failure e. As often as possible, discussions regarding end- Device therapy has become an integral part of the treat- of-life care should be initiated while the patient ment for HF. Appropriate patient selection in terms of HF is still capable of participating in decision-mak- characteristics, severity, and other comorbidities is a key con- ing. (Strength of Evidence 5 C) sideration to ensure the optimal application of this therapy.8.13 End-of-life care should be considered in patients who Recommendations for General Electrophysiology have advanced, persistent HF with symptoms at rest Testing despite repeated attempts to optimize pharmacologic, cardiac device, and other therapies, as evidenced by 1 9.1 It is recommended that the decision to undertake elec- or more of the following: trophysiologic intervention, including implantable cardioverter defibrillator (ICD) implantation, be  HF hospitalization 126,127 (Strength of Evidence 5 B) made in light of functional status and prognosis based  Chronic poor quality of life with minimal or no on severity of underlying HF and comorbid ability to accomplish activities of daily living conditions. If an ICD is considered due to left ventric- (Strength of Evidence 5 C) ular (LV) dysfunction which is of recent onset, LV
    • Executive Summary: Heart Failure Practice Guideline  HFSA 495 function should be reassessed, ideally after 3-6 months of specialized conduction or by scarring of the myocar- of optimal medical therapy. (Strength of Evidence dium.136 CRT seeks to normalize depolarization to improve 5 C) the efficiency of ventricular contraction and ventricular sep- tal motion, decrease atrioventricular valve regurgitation,Recommendations for Electrophysiology Testing and and increase diastolic filling time.137Evaluation of Syncope 9.7 Biventricular pacing therapy is recommended for pa-9.2 Immediate evaluation is recommended in patients with tients in sinus rhythm with a widened QRS interval HF who present with syncope. In the absence of a clear ($120 ms) and severe LV systolic dysfunction identifiable noncardiac cause, consultation with an EP (LVEF # 35%) who have persistent, moderate to se- specialist should be obtained. (Strength of Evidence vere HF (NYHA III) despite optimal medical therapy. 5 C) (Strength of Evidence 5 A)9.3 Routine EP testing is not recommended in patients 9.8 Biventricular pacing therapy may be considered for with LV systolic dysfunction who have asymptomatic patients with atrial fibrillation with a widened QRS in- nonsustained ventricular tachycardia (VT) in the ab- terval ($120 ms) and severe LV systolic dysfunction sence of prior infarction. (Strength of Evidence 5 B) LVEF #35% who have persistent, moderate to severe HF (NYHA III) despite optimal medical therapy. (Strength of Evidence 5 B)Recommendations for Prophylactic ICD Placement 9.9 Selected ambulatory NYHA IV patients in sinus More than 80 percent of patients who experience a life- rhythm with QRS R120 ms and LV systolic dysfunc-threatening ventricular tachyarrhythmia do not survive to tion may be considered for biventricular pacing ther-benefit from an ICD. Thus, the concept of the ICD for pri- apy. (Strength of Evidence 5 B)mary prevention of SCD has received considerable atten- 9.10 Biventricular pacing therapy may be considered intion. Several large trials have demonstrated efficacy of patients with reduced LVEF and QRS R 150 msprophylactic ICDs in certain patient groups.130-135 who have NYHA I or II HF symptoms. (Strength of9.4a Prophylactic ICD placement should be considered in Evidence 5 B) patients with an LVEF #35% and mild to moderate 9.11 In patients with reduced LVEF who require chronic HF symptoms: pacing and in whom frequent ventricular pacing is ex-  Ischemic etiology (Strength of Evidence 5 A) pected, biventricular pacing may be considered.  Non-ischemic etiology (Strength of Evidence (Strength of Evidence 5 C) 5 B) See Recommendation 9.1 for additional criteria. Recommendations for Dual Chamber Pacemakers9.4b In patients who are undergoing implantation of a bi- ventricular pacing device according to the criteria in 9.12 The routine use of dual (atrioventricular [AV]) cham- recommendations 9.7-9.8, use of a device that pro- ber pacemakers for HF in the absence of symptomatic vides defibrillation should be considered. (Strength bradycardia or high-grade AV block is not recommen- of Evidence 5 B) ded. (Strength of Evidence 5 A) See Recommendation 9.1 for additional criteria.9.5 ICD placement is not recommended in chronic, severe Section 10: Surgical Approaches to the Treatment refractory HF when there is no reasonable expectation of Heart Failure for improvement or in patients with a life expectancy of less than 1 year. (Strength of Evidence 5 C) Despite advances in medical management of HF, there remain circumstances in which surgical procedures are9.6 ICD implantation is recommended for survivors of the only or the best treatment option. These include cardiac arrest from ventricular fibrillation or hemody- heart transplantation and procedures that (1) repair the namically unstable sustained VT that is not due to heart, (2) reshape it, or (3) replace all or part of heart a transient, potentially reversible cause, such as acute function. MI. (Strength of Evidence 5 A) Recommendations for Surgical ApproachesRecommendations for Biventricular ResynchronizationPacing 10.1 It is recommended that the decision to undertake sur- The majority of patients with HF have interventricular gical intervention for severe HF be made in light ofconduction delay, and up to 30% to 50% have manifest bun- functional status and prognosis based on severity ofdle branch block caused by direct pathologic involvement underlying HF and comorbid conditions. Procedures
    • 496 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 should be done at centers with demonstrable exper- document. The left ventricle in HF with preserved LVEF tise and multidisciplinary medical and surgical teams may be characterized by LV hypertrophy,141 concentric re- experienced in the selection, care, and perioperative modeling, increased extracellular matrix,142 abnormal cal- and long-term management of high risk patients cium handling, abnormal relaxation and filling and with severe HF. (Strength of Evidence 5 C) decreased diastolic distensibility.143,144 Activation of the neurohormonal milieu, including the RAAS and the sym-10.2 Evaluation for heart transplantation is recommended pathetic nervous system, is common in HF with and with- in selected patients with severe HF, debilitating re- out preserved LVEF.144 fractory angina, or ventricular arrhythmia that cannot be controlled despite drug, device, or alternative sur- Recommendations for Patients With Heart Failure and gical therapy. (Strength of Evidence 5 B) Preserved LVEF10.3 Isolated mitral valve repair or replacement for severe 11.1 Careful attention to differential diagnosis is recom- mitral regurgitation secondary to ventricular dilata- mended in patients with HF and preserved LVEF to tion in the presence of severe left ventricular (LV) distinguish among a variety of cardiac disorders, be- systolic dysfunction is not generally recommended. cause treatments may differ. These various entities (Strength of Evidence 5 C) may be distinguished based on echocardiography,10.4 Partial LV resection ("Batista procedure") is not rec- electrocardiography, and stress imaging (via exercise ommended in nonischemic cardiomyopathy. or pharmacologic means, using myocardial perfusion (Strength of Evidence 5 B) or echocardiographic imaging) and cardiac catheter- ization. See complete guideline Section 11 for10.5 Patients awaiting heart transplantation who have be- Figures 11.1, 11.2, and 11.3 for guidance to a differ- come refractory to all means of medical circulatory ential diagnosis. (Strength of Evidence 5 C) support should be considered for a mechanical support device as a bridge to transplant. (Strength 11.2 Evaluation for ischemic heart disease and inducible of Evidence 5 B) myocardial ischemia is recommended in patients with HF and preserved LVEF (see Section 13).10.6 Permanent mechanical assistance using an implant- (Strength of Evidence 5 C) able assist device may be considered in highly selected patients with severe HF refractory to conventional 11.3 Blood pressure monitoring is recommended in pa- therapy who are not candidates for heart transplanta- tients with HF and preserved LVEF (Section 14, Rec- tion, particularly those who cannot be weaned from in- ommendation 14.1). (Strength of Evidence 5 C) travenous inotropic support at an experienced HF 11.4 Counseling on the use of a low-sodium diet (Section center. (Strength of Evidence 5 B) 6) is recommended for all patients with HF, in-10.7 Patients with refractory HF and hemodynamic insta- cluding those with preserved LVEF. (Strength of bility, and/or compromised end-organ function, with Evidence 5 C) relative contraindications to cardiac transplantation 11.5 Diuretic treatment is recommended in all patients or permanent mechanical circulatory assistance ex- with HF and clinical evidence of volume overload, pected to improve with time or restoration of an im- including those with preserved LVEF. Treatment proved hemodynamic profile should be considered may begin with either a thiazide or loop diuretic. for urgent mechanical circulatory support as a ‘‘bridge In more severe volume overload or if response to to decision.’’ These patients should be referred to a cen- a thiazide is inadequate, treatment with a loop di- ter with expertise in the management of patients with uretic should be implemented. Excessive diuresis, advanced HF. (Strength of Evidence 5 C) which may lead to orthostatic changes in blood pres- sure and worsening renal function, should be Section 11: Evaluation and Management of avoided. (Strength of Evidence 5 C) Patients With Heart Failure and Preserved Left Ventricular Ejection Fraction 11.6 In the absence of other specific indications for these drugs, angiotensin receptor blockers (ARBs) or an- A substantial number of patients with HF have pre- giotensin converting enzyme (ACE) inhibitors mayserved LVEF, variably defined as an LVEF O40%, be considered in patients with HF and preservedO45%, or O50%.138,139 When these patients have inva- LVEF.sive or non-invasive evidence of abnormal diastolic func-  ARBs (Strength of Evidence 5 C)tion (either abnormal relaxation, filling or stiffness) they  ACE inhibitors (Strength of Evidence 5 C)are said to have ‘‘diastolic HF’’.140 Although the term‘‘HF with normal LVEF’’ is often used to denote this 11.7 ACE inhibitors should be considered in all patientsgroup, because ‘‘normal’’ is variously defined, ‘‘HF with with HF and preserved LVEF who have symptomaticpreserved LVEF’’ will be the active definition in this atherosclerotic cardiovascular disease or diabetes
    • Executive Summary: Heart Failure Practice Guideline  HFSA 497 and one additional risk factor. (Strength of Evi- poor compliance, and lack of education or an inadequate dence 5 C) medical regimen may lead to hospitalization without a wors- ening of underlying circulatory function. In patients who meet these criteria but are intolerant There is a paucity of controlled clinical trial data to de- to ACE inhibitors, ARBs should be considered. fine optimal treatment for patients with ADHF. The few tri- (Strength of Evidence 5 C) als have focused primarily on symptom relief, not11.8 Beta blocker treatment is recommended in patients outcomes, and have mainly enrolled patients with reduced with HF and preserved LVEF who have: LVEF who were not hypertensive. Clinical studies to deter- mine the best care processes to achieve the multiple goals  Prior myocardial infarction (Strength of Evidence for patients admitted with ADHF are lacking. The recom- 5 A) mendations in this section address the common therapeutic  Hypertension (see Section 14) (Strength of Evi- dilemmas associated with the broad group of patients with dence 5 B) ADHF using the best available evidence from clinical re-  Atrial fibrillation requiring control of ventricular search and consensus expert opinion. rate (Strength of Evidence 5 B)11.9 Calcium channel blockers should be considered in Recommendations for Acute Decompensated Heart patients with HF and preserved LVEF and: Failure  Atrial fibrillation requiring control of ventricular 12.1 The diagnosis of Acute Decompensated HF should rate and intolerance to beta blockers. In these pa- be based primarily on signs and symptoms. (Strength tients, diltiazem or verapamil should be consid- of Evidence 5 C) ered. (Strength of Evidence 5 C)  Symptom-limiting angina. (Strength of Evi- When the diagnosis is uncertain, determination of B- dence 5 A) type natriuretic peptide (BNP) or N-terminal pro-B-  Hypertension. (Strength of Evidence 5 C) type natriuretic peptide (NT-proBNP) concentration is recommended in patients being evaluated for dysp-11.10 Measures to restore and maintain sinus rhythm may nea who have signs and symptoms compatible with be considered in patients who have symptomatic HF. (Strength of Evidence 5 A) atrial flutter-fibrillation and preserved LVEF, but this decision should be individualized. (Strength The natriuretic peptide concentration should not be of Evidence 5 C) interpreted in isolation, but in the context of all avail- able clinical data bearing on the diagnosis of HF, and Section 12: Evaluation and Management of Pa- with the knowledge of cardiac and non-cardiac fac- tients With Acute Decompensated Heart Failure tors that can raise or lower natriuretic peptide levels. 12.2 Hospital admission is recommended for patients pre- Data from several studies have refined our understanding senting with ADHF when the clinical circumstancesof the clinical characteristics of patients hospitalized with listed in Table 12.1(a) are present. Patients presentingworsening HF.145-148 These studies demonstrate that the with ADHF should be considered for hospital admis-majority of patients hospitalized with HF have evidence sion when the clinical circumstances listed in Tableof systemic hypertension on admission and commonly 12.1(b) are present. (Strength of Evidence 5 C)have preserved LVEF. Most hospitalized patients have sig-nificant volume overload, and congestive symptoms pre- 12.3 It is recommended that patients admitted with ADHFdominate. Patients with severely impaired systolic be treated to achieve the goals listed in Table 12.3.function, reduced blood pressure, and symptoms from (Strength of Evidence 5 C)poor end-organ perfusion are in the distinct minority. Nat- 12.4 Patients admitted with ADHF should be carefullyural history studies have shown that ADHF represents a pe- monitored. It is recommended that the items listedriod of high risk for patients, during which their likelihood in Table 12.4 be assessed at the stated frequencies.of death and rehospitalization is significantly greater than (Strength of Evidence 5 C)for a comparable period of chronic, but stable HF.146 The clinical classification of patients with ADHF con- 12.5 It is recommended that patients admitted with ADHFtinues to evolve and reflects ongoing changes in our under- and evidence of fluid overload be treated initiallystanding of the pathophysiology of this syndrome.149 with loop diuretics - usually given intravenouslyWorsening renal function, persistent neurohormonal activa- rather than orally. (Strength of Evidence 5 B)tion, and progressive deterioration in myocardial function Ultrafiltration may be considered in lieu of diuretics.all seem to play a role. Decompensation also commonly oc- (Strength of Evidence 5 B)curs without a fundamental worsening of underlying car-diac structure or function. Failure to adhere to prescribed 12.6 It is recommended that diuretics be administered atmedications related to inadequate financial resources, doses needed to produce a rate of diuresis sufficient
    • 498 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 Table 12.1. Recommendations for Hospitalizing Patients Table 12.4. Monitoring Recommendations for Patients Presenting With ADHF Hospitalized With ADHFRecommendation Clinical Circumstances Frequency Value Specifics(a) Hospitalization Evidence of severe ADHF, including: At least daily Weight Determine after voiding in the Recommended Hypotension morning Worsening renal function Account for possible increased Altered mentation food intake due to improved Dyspnea at rest appetite Typically reflected by resting tachypnea At least daily Fluid intake Less commonly reflected by oxygen satu- and output ration !90% More than daily Vital signs Orthostatic blood pressure if indicated Hemodynamically significant arrhythmia Oxygen saturation daily until Including new onset of rapid atrial fibril- stable lation At least daily Signs Edema Acute coronary syndromes Ascites(b) Hospitalization Worsened congestion Pulmonary rales Should Be Even without dyspnea Hepatomegaly Considered Signs and symptoms of pulmonary or Increased JVP systemic congestion Hepatojugular reflux Even in the absence of weight gain Liver tenderness Major electrolyte disturbance At least daily Symptoms Orthopnea Associated comorbid conditions Paroxysmal nocturnal dyspnea Pneumonia (PND) or cough Pulmonary embolus Nocturnal cough Diabetic ketoacidosis Dyspnea Symptoms suggestive of transient ische- Fatigue, lightheadedness mic accident or stroke At least daily Electrolytes Potassium Repeated ICD firings Sodium Previously undiagnosed HF with signs and At least daily Renal function BUN symptoms of systemic or pulmonary Serum creatinine* congestion *See background section for additional recommendations on laboratory evaluations. to achieve optimal volume status with relief of signs 12.8 Monitoring of daily weights, intake, and output is and symptoms of congestion (edema, elevated JVP, recommended to assess clinical efficacy of diuretic dyspnea), without inducing an excessively rapid re- therapy. Routine use of a Foley catheter is not duction in 1) intravascular volume, which may result recommended for monitoring volume status. How- in symptomatic hypotension and/or worsening renal ever, placement of a catheter is recommended when function, or 2) serum electrolytes, which may precip- close monitoring of urine output is needed or if itate arrhythmias or muscle cramps. (Strength of Ev- a bladder outlet obstruction is suspected of contribut- idence 5 C) ing to worsening renal function. (Strength of Evi- dence 5 C)12.7 Careful repeated assessment of signs and symptoms of congestion and changes in body weight is recom- 12.9 Careful observation for development of a variety mended, because clinical experience suggests it is of side effects, including renal dysfunction, elec- difficult to determine that congestion has been ade- trolyte abnormalities, symptomatic hypotension, quately treated in many patients. (Strength of Evi- and gout is recommended in patients treated with dence 5 C) diuretics, especially when used at high doses and in combination. Patients should undergo routine laboratory studies and clinical examination as dic- Table 12.3. Treatment Goals for Patients Admitted for tated by their clinical response. (Strength of Evi- ADHF dence 5 C)Improve symptoms, especially congestion and low-output symptoms It is recommended that serum potassium and magne- Restore normal oxygenationOptimize volume status sium levels be monitored at least daily and maintainedIdentify etiology (see Table 4.6) in the normal range. More frequent monitoring mayIdentify and address precipitating factors be necessary when diuresis is rapid. (Strength of Evi-Optimize chronic oral therapyMinimize side effects dence 5 C)Identify patients who might benefit from revascularizationIdentify patients who might benefit from device therapy Overly rapid diuresis may be associated with severeIdentify risk of thromboembolism and need for anticoagulant therapy muscle cramps. If indicated, treatment with potas-Educate patients concerning medications and self management of HF sium replacement is recommended. (Strength of Ev-Consider and, where possible, initiate a disease management program idence 5 C)
    • Executive Summary: Heart Failure Practice Guideline  HFSA 49912.10 Careful observation for the development of renal dys- Venous thromboembolism prophylaxis with a me- function is recommended in patients treated with di- chanical device (intermittent pneumatic compres- uretics. Patients with moderate to severe renal sion devices or graded compression stockings) to dysfunction and evidence of fluid retention should prevent proximal DVT and PE should be considered continue to be treated with diuretics. In the presence for patients who are admitted to the hospital with of severe fluid overload, renal dysfunction may ADHF and who are not already anticoagulated and improve with diuresis. (Strength of Evidence 5 C) who have a contraindication to anticoagulation. (Strength of Evidence 5 C)12.11 When congestion fails to improve in response to diuretic therapy, the following options should be 12.17 In the absence of symptomatic hypotension, intrave- considered: nous nitroglycerin, nitroprusside or nesiritide may  Re-evaluating presence/absence of congestion be considered as an addition to diuretic therapy for  Sodium and fluid restriction, rapid improvement of congestive symptoms in pa-  Increasing doses of loop diuretic, tients admitted with ADHF. (Strength of Evidence  Continuous infusion of a loop diuretic, or 5 B)  Addition of a second type of diuretic orally (me- Frequent blood pressure monitoring is recommen- tolazone or spironolactone) or intravenously ded with these agents. (Strength of Evidence 5 B) (chlorothiazide). These agents should be decreased in dosage or Another option, ultrafiltration, may be considered. discontinued if symptomatic hypotension or wors- (Strength of Evidence 5 C) ening renal function develops. (Strength of Evi-12.12 A low sodium diet (2 g daily) is recommended dence 5 B) for most hospitalized patients. (Strength of Evidence Reintroduction in increasing doses may be consid- 5 C) ered once symptomatic hypotension is resolved. In patients with recurrent or refractory volume over- (Strength of Evidence 5 C) load, stricter sodium restriction may be considered. 12.18 Intravenous vasodilators (nitroglycerin or nitroprus- (Strength of Evidence 5 C) side) and diuretics are recommended for rapid symp-12.13 Fluid restriction (!2 L/day) is recommended in pa- tom relief in patients with acute pulmonary edema or tients with moderate hyponatremia (serum sodium severe hypertension. (Strength of Evidence 5 C) !130 mEq/L) and should be considered to assist in treatment of fluid overload in other patients. 12.19 Intravenous vasodilators (nitroprusside, nitroglyc- erin, or nesiritide) may be considered in patients (Strength of Evidence 5 C) with ADHF who have persistent severe HF despite In patients with severe (serum sodium !125 mEq/ aggressive treatment with diuretics and standard L) or worsening hyponatremia, stricter fluid restric- oral therapies. tion may be considered. (Strength of Evidence 5 C)  Nitroprusside (Strength of Evidence 5 B)12.14 Routine administration of supplemental oxygen in  Nitroglycerine, Nesiritide (Strength of Evi- the presence of hypoxia is recommended. (Strength dence 5 C) of Evidence 5 C) 12.20 Intravenous inotropes (milrinone or dobutamine) Routine administration of supplemental oxygen in may be considered to relieve symptoms and improve the absence of hypoxia is not recommended. end-organ function in patients with advanced HF (Strength of Evidence 5 C) characterized by LV dilation, reduced LVEF, and di- minished peripheral perfusion or end-organ dysfunc-12.15 Use of non-invasive positive pressure ventilation tion (low output syndrome), particularly if these may be considered for severely dyspneic patients patients have marginal systolic blood pressure with clinical evidence of pulmonary edema. (!90 mm Hg), have symptomatic hypotension de- (Strength of Evidence 5 A) spite adequate filling pressure, or are unresponsive12.16 Venous thromboembolism prophylaxis with low to, or intolerant of, intravenous vasodilators. dose unfractionated heparin (UFH), low molecular (Strength of Evidence 5 C) weight heparin (LMWH), or fondaparinux to pre- These agents may be considered in similar patients vent proximal deep venous thrombosis (DVT) and with evidence of fluid overload if they respond poorly pulmonary embolism (PE) is recommended for pa- to intravenous diuretics or manifest diminished or tients who are admitted to the hospital with ADHF worsening renal function. (Strength of Evidence 5 C) and who are not already anticoagulated and have no contraindication to anticoagulation. (Strength of When adjunctive therapy is needed in other pa- Evidence 5 B) tients with ADHF, administration of vasodilators
    • 500 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 should be considered instead of intravenous ino- Table 12.7. Discharge Criteria for Patients With HF tropes (milrinone or dobutamine). (Strength of Ev- Recommended for all HF patients  Exacerbating factors addressed. idence 5 C)  Near optimal volume status observed. Intravenous inotropes (milrinone or dobutamine)  Transition from intravenous to oral are not recommended unless left heart filling diuretic successfully completed.  Patient and family education pressures are known to be elevated or cardiac in- completed, including clear dex is severely impaired based on direct measure- discharge instructions ment or clear clinical signs. (Strength of Evidence  LVEF documented  Smoking cessation counseling 5 C) initiated  Near optimal pharmacologic It is recommended that administration of intrave- therapy achieved, including ACE nous inotropes (milrinone or dobutamine) in the inhibitor and beta blocker (for setting of ADHF be accompanied by continuous patients with reduced LVEF), or intolerance documented (Sections or frequent blood pressure monitoring and contin- 7 and 11) uous monitoring of cardiac rhythm. (Strength of  Follow-up clinic visit scheduled, Evidence 5 C) usually for 7-10 days Should be considered for patients  Oral medication regimen stable for If symptomatic hypotension or worsening tachyar- with advanced HF or recurrent 24 hours admissions for HF  No intravenous vasodilator or rhythmias develop during administration of these inotropic agent for 24 hours agents, discontinuation or dose reduction should be  Ambulation before discharge to considered. (Strength of Evidence 5 C) assess functional capacity after therapy12.21 The routine use of invasive hemodynamic monitor-  Plans for postdischarge management (scale present in ing in patients with ADHF is not recommended. home, visiting nurse or telephone (Strength of Evidence 5 A) follow up generally no longer than 3 days after discharge)12.22 Invasive hemodynamic monitoring should be con-  Referral for disease management, if sidered in a patient: available  who is refractory to initial therapy,  whose volume status and cardiac filling pres- 12.25 It is recommended that criteria in Table 12.7 be met sures are unclear, before a patient with HF is discharged from the hos- pital. (Strength of Evidence 5 C)  who has clinically significant hypotension (typi- cally SBP !80 mm Hg) or worsening renal In patients with advanced HF or recurrent admissions function during therapy, or for HF, additional criteria listed in Table 12.7 should be considered. (Strength of Evidence 5 C)  who is being considered for cardiac transplant and needs assessment of degree and reversibility 12.26 Discharge planning is recommended as part of the of pulmonary hypertension, or management of patients with ADHF. Discharge planning should address the following issues:  in whom documentation of an adequate hemody-  Details regarding medication, dietary sodium re- namic response to the inotropic agent is necessary striction, and recommended activity level when chronic outpatient infusion is being consid-  Follow-up by phone or clinic visit early after ered. (Strength of Evidence 5 C) discharge to reassess volume status12.23 It is recommended that patients admitted with  Medication and dietary compliance ADHF undergo evaluation for the following precip-  Alcohol moderation and smoking cessation itating factors: atrial fibrillation or other arrhyth-  Monitoring of body weight, electrolytes and mias (eg, atrial flutter, other supraventricular VT renal function or VT), exacerbation of hypertension, myocardial  Consideration of referral for formal disease man- ischemia/infarction, exacerbation of pulmonary agement. (Strength of Evidence 5 C) congestion, anemia, thyroid disease, significant drug interactions, and other less common factors. (Strength of Evidence 5 C) Section 13: Evaluation and Therapy for Heart Fail-12.24 It is recommended that every effort be made to use ure in the Setting of Ischemic Heart Disease the hospital stay for assessment and improvement of patient adherence via patient and family education The most common cause of chronic HF is no longer hy- and social support services (see Section 8). pertension or valvular heart disease; it is CAD.2 The chang- (Strength of Evidence 5 B) ing pattern in the risk factors for HF is evidenced in the
    • Executive Summary: Heart Failure Practice Guideline  HFSA 501Framingham Heart Study, which documents a decrease in angiography to assess severity of coronary diseasevalvular disease and LV hypertrophy and an increase in and the presence of ischemia. (Strength of EvidenceMI from 1950 to 1998.3 As survival from MI continues to 5 C)improve, it is expected that the number of patients with 13.5 It is recommended that patients with HF, no angina,CAD and HF will also increase. and unknown CAD status who are at high risk for HF in the setting of CAD is a heterogeneous condition CAD should undergo noninvasive stress imagingwith several factors contributing to LV systolic dysfunc- and/or coronary angiography to assess severity oftion and HF symptoms. After an MI, there is loss of coronary disease and the presence of ischemia.functioning myocytes, development of myocardial fibro- (Strength of Evidence 5 C)sis, and subsequent LV remodeling, resulting in chamberdilatation and neurohormonal activation - all leading to 13.6 In patients with HF, no angina, and unknown CADprogressive dysfunction of the remaining viable myocar- status who are at low risk for CAD noninvasivedium.49 evaluation should be considered and coronary angi- Several studies have shown that CAD is associated with ography may be considered. (Strength of Evidencean increase in mortality rates in patients with HF.30-36 Data 5 C)also suggest that the mechanism of sudden death may differ 13.7 Any of the following imaging tests should be consid-between ischemic and nonischemic HF patients, with acute ered to identify inducible ischemia or viable myocar-coronary events representing the major cause of sudden dium:death in HF patients with CAD.38 These findings further  Exercise or pharmacologic stress myocardial per-emphasize the importance of accurate differentiation be- fusion imagingtween ischemic and nonischemic causes of HF.  Exercise or pharmacologic stress echocardiogra- Managing HF in patients with CAD or a history of CAD phymay be significantly different than managing HF due to pri-mary cardiomyopathy. Antiplatelet agents, smoking cessa-  Cardiac magnetic resonance imaging (MRI)tion, and lipid-lowering therapy are particularly important  Positron emission tomography scanning (PET).interventions in patients with HF due to CAD.40 Trials of (Strength of Evidence 5 B)milrinone,41 amiodarone,18 amlodipine,15 and digoxin sug- 13.8 It is recommended that the following risk factors begest that patients with HF in the setting of CAD may have managed according to the indicated guidelines:a less favorable outcome than patients with HF from pri-  Lipids (see National Cholesterol Education Pro-mary cardiomyopathy. Revascularization in highly selected gram Adult Treatment Panel III) (http://patients with reduced LVEF and significant CAD, particu- www.nhlbi.nih.gov/guidelines/cholesterol) 92,93larly those with anginal symptoms, may be associated  Smoking (see Section 3)with improved survival and may be considered in addition  Physical activity (see Section 6)to risk modification.33,42-49  Weight (see Section 3)Recommendations for Heart Failure in the Setting of  Blood pressure (see Section 14 and JNC VIIIschemic Heart Disease Guidelines) (http://www.nhlbi.nih.gov/guide- lines/hypertension) 9413.1 Ongoing assessment for risk factors for CAD is rec- (See individual guidelines for Strength of Evidence). ommended in all patients with chronic HF regardless of LVEF. (Strength of Evidence 5 A) 13.9 Antiplatelet therapy is recommended to reduce vas- cular events in patients with HF and CAD unless13.2 It is recommended that the diagnostic approach for contraindicated. (aspirin, Strength of Evidence 5 A; CAD be individualized based on patient preference clopidogrel, Strength of Evidence 5 B) and comorbidities, eligibility, symptoms suggestive of angina and willingness to undergo revasculariza- 13.10 ACE inhibitors are recommended in all patients tion. (Strength of Evidence 5 C) with either reduced or preserved LVEF after an MI. (Strength of Evidence 5 A)13.3 It is recommended that patients with HF and symptoms suggestive of angina undergo cardiac catheterization 13.11 Beta blockers are recommended for the manage- with coronary angiography to assess for potential revas- ment of all patients with reduced LVEF or post- cularization. (Strength of Evidence 5 B) MI. (Strength of Evidence 5 B)13.4 It is recommended that, at the initial diagnosis of HF 13.12 It is recommended that ACE-inhibitor and beta and any time symptoms worsen without obvious blocker therapy be initiated early (!48 hours) dur- cause, patients with HF, no angina, and known ing hospitalization in hemodynamically stable post- CAD should undergo risk assessment that may in- MI patients with reduced LVEF or HF. (Strength of clude noninvasive stress imaging and/or coronary Evidence 5 A)
    • 502 Journal of Cardiac Failure Vol. 16 No. 6 June 201013.13 Nitrate preparations should be considered in pa- More than 1 drug may be required. Target resting tients with HF when additional medication is levels should be !130/!80 mm Hg, if tolerated. needed for relief of anginal symptoms. (Strength (Strength of Evidence 5 A) of Evidence 5 B)13.14 Calcium channel blockers may be considered in pa- Recommendations for Patients With Hypertension and tients with HF who have angina despite the optimal Asymptomatic LV Dysfunction With LV Dilation and use of beta blockers and nitrates. Amlodipine and fe- a Low LVEF lodipine are the preferred calcium channel blockers in patients with angina and decreased systolic func- 14.2 Prescription of an angiotensin converting enzyme tion. Based on available data, first generation calcium (ACE) inhibitor (dose equivalent to 20 mg daily ena- channel blockers (i.e. diltiazem, verapamil) should lapril) is recommended (Strength of Evidence 5 A) be avoided in patients with CAD, HF, and LVEF 14.3 Addition of a beta blocker (dose equivalent to HF tri- !40, unless necessary for heart rate control or other als) is recommended even if blood pressure is con- indications. (Strength of Evidence 5 C) trolled. (Strength of Evidence 5 C)13.15 It is recommended that coronary revascularization be 14.4 If blood pressure remains O130/80 mm Hg then the performed in patients with HF and suitable coronary addition of a thiazide diuretic is recommended, fol- anatomy for relief of refractory angina or acute coro- lowed by a dihydropyridine calcium antagonist (eg, nary syndrome. (Strength of Evidence 5 B) amlodipine or felodipine) or other antihypertensive13.16 Coronary revascularization with coronary artery by- drugs. (Strength of Evidence 5 C) pass surgery or percutaneous coronary intervention (PCI) as appropriate should be considered in pa- Recommendations for Patients With Hypertension and tients with HF and suitable coronary anatomy who Symptomatic LV Dysfunction With LV Dilation and Low have demonstrable evidence of myocardial viability LVEF in areas of significant obstructive coronary disease or the presence of inducible ischemia. (Strength of 14.5 Prescription of target doses of ACE inhibitors, angio- Evidence 5 C) tensin receptor blockers (ARBs), beta blockers, aldo- sterone inhibitors, and isosorbide dinitrate/ hydralazine in various combinations (with a loop di-Section 14: Managing Patients With Hypertension uretic if needed) is recommended, based on doses and Heart Failure used in large-scale outcome trials (see Table 7.1). (Strength of Evidence 5 A) Blood pressure is a simple measurement that assesses the 14.6 If blood pressure remains O130/80 mm Hg, a dihy-interaction of heart function with vascular impedance. dropyridine calcium antagonist (eg, amlodipine orWhen heart function is normal, the impedance is the main de- felodipine) may be considered or other antihyperten-terminant of blood pressure. Therefore, pressure (systolic sive medication doses increased. (Strength ofand mean) becomes a powerful risk factor for development Evidence 5 C)of LV hypertrophy, increased myocardial oxygen consump-tion, coronary atherosclerosis, and subsequent HF.150,151Control of blood pressure in this setting is critical to prevent Section 15: Management of Heart Failure in Specialthe development and progression of LV dysfunction.152 Populations When LV function is impaired, however, the relationshipbetween impedance and cardiac function becomes more HF is a prevalent condition in women, African Ameri-complex. Increases of impedance may impair LV emptying cans, and the elderly of both sexes and any race. In the ab-and thus not be reflected in a higher pressure. Under those sence of contradictory data, the clinical recommendationscircumstances therapy is aimed at the impedance, not at based on trial data derived from predominately youngerthe blood pressure. Indeed, blood pressure may rise in re- white male study populations have generally been appliedsponse to effective therapy that improves LV emptying or re- equally to these groups. However, there are etiologic andverses remodeling even if the impedance is reduced. pathophysiologic considerations specific to these groupsRecommendation for Patients With Hypertension and that warrant attention if care and outcomes are to be opti-Preserved LVEF and Asymptomatic LVH, or for Patients mized. Although a significant number of women and el-With Hypertension and HF With Preserved LVEF derly patients with HF have preserved LV systolic(Stage B) function there is little evidence-based data to guide therapy in this group. Other special populations - ethnic groups14.1 It is recommended that blood pressure be optimally such as Hispanics, Asians, American Indians, or Pacific Is- treated to lower systolic and usually diastolic levels. landers - are important special populations but there are
    • Executive Summary: Heart Failure Practice Guideline  HFSA 503inadequate data currently available about HF management 15.9 ACE inhibitors are recommended as part of standardto discuss these groups individually. Discussion in this sec- therapy for African-American patients with HF fromtion is based primarily on available data from subgroup symptomatic or asymptomatic LV systolic dysfunc-analyses of randomized HF trials and the results of cohort tion. (Strength of Evidence 5 C)studies. A substantial amount of the data on drug efficacy 15.10 ARBs are recommended as substitute therapy for HFcomes from studies of patients treated after a recent acute in African Americans intolerant of ACE inhibitors.MI. (Strength of Evidence 5 B)Recommendations 15.11 A combination of hydralazine and isosorbide dini- trate is recommended as part of standard therapy in15.1 As with younger patients, it is recommended that el- addition to beta blockers and ACE-inhibitors for derly patients, particularly those age O80 years, be African Americans with LV systolic dysfunction evaluated for HF when presenting with symptoms and: of dyspnea and fatigue. (Strength of Evidence 5 C)  NYHA class III or IV HF (Strength of Evi-15.2 Beta blocker and ACE inhibitor therapy is recom- dence 5 A) mended as standard therapy in all elderly patients  NYHA class II HF (Strength of Evidence 5 B) with HF due to LV systolic dysfunction. (Strength of Evidence 5 B) Section 16: Myocarditis: Current Treatment In the absence of contraindications, these agents are also recommended in the very elderly (age O80 Myocarditis is a distinct clinical entity with a wide va- years). (Strength of Evidence 5 C) riety of cardiac manifestations including HF. Potential eti-15.3 As in all patients, but especially in the elderly, care- ologies may include toxins, medications, physical agents ful attention to volume status, the possibility of and, most importantly, infections. The most common symptomatic cerebrovascular disease, and the pres- forms appear to be postviral in origin. The pathophysiol- ence of postural hypotension is recommended during ogy of myocarditis has been well established in animal therapy with ACE inhibitors, beta blockers and di- models with myocardial damage due not only to direct in- uretics. (Strength of Evidence 5 C) fection, but also consequent to postinfectious, autoimmune-mediated myocardial inflammatory damage.15.4 Beta blocker therapy is recommended for women In humans, ongoing myocardial inflammation may result with HF from: in dilated cardiomyopathy, restrictive cardiomyopathy, or  symptomatic LV systolic dysfunction (Strength of acute LV failure without dilatation (fulminant myocardi- Evidence 5 B) tis). Controversy continues to surround the best approach  asymptomatic LV systolic dysfunction (Strength to the management of patients considered to have myocar- of Evidence 5 C) ditis. The following recommendation is based on a review15.5 ACE inhibitor therapy is recommended as standard of available data from uncontrolled and controlled evalua- therapy in all women with symptomatic or asymp- tions of immunomodulatory therapy for the treatment of tomatic LV systolic dysfunction. (Strength of Evi- myocarditis. dence 5 B) Recommendations15.6 ARBs are recommended for administration to symp- tomatic and asymptomatic women with an LVEF # 16.1 Routine use of immunosuppressive therapies is not 40% who are intolerant to ACE inhibitors for reasons recommended for patients with myocarditis. other than hyperkalemia or renal insufficiency. (Strength of Evidence 5 A) (Strength of Evidence 5 A) 16.2 Endomyocardial biopsy should be considered in pa-15.7 The combination of hydralazine/isosorbide dinitrate tients with an acute deterioration of cardiac function is recommended as standard therapy for African of unknown etiology who are unresponsive to medi- American women with moderate to severe HF symp- cal therapy. (Strength of Evidence 5 B) toms who are on background neurohormonal inhibi- tion. (Strength of Evidence 5 B)15.8 Beta blockers are recommended as part of standard Section 17: Genetic Evaluation of Cardiomyopathy* therapy for African Americans with HF due to:  symptomatic LV systolic dysfunction (Strength of The evidence indicating that hypertrophic cardiomyopa- Evidence 5 B) thy (HCM) has a genetic basis is extensive: HCM is now  asymptomatic LV systolic dysfunction (Strength understood largely to be a genetic disease of contractile of Evidence 5 C) proteins, although less commonly, infiltrative etiologies
    • 504 Journal of Cardiac Failure Vol. 16 No. 6 June 2010may also be causative. The evidence supporting a genetic  Hypertrophic cardiomyopathy (Strength of Evi-basis for dilated cardiomyopathy (DCM), after other more dence 5 A)common causes have been excluded (eg, ischemic disease,  Dilated cardiomyopathy (Strength of Evidence 5 A)hypothyroidism, cardiotoxic agents such as Adriamycin),  Arrhythmogenic right ventricular dysplasiais now substantial for familial dilated cardiomyopathy (Strength of Evidence 5 A)(FDC), where FDC is defined as DCM of unknown cause  Left ventricular noncompaction (Strength of Evi-in 2 or more closely related family members. However, dence 5 A)whether sporadic DCM has a genetic basis remains an  Restrictive cardiomyopathy (Strength of Evi-open question, especially when detectable familial disease dence 5 B)has been clinically excluded by testing closely related  Cardiomyopathies associated with extracardiacfamily members. Thus, although some recommendations manifestations (Strength of Evidence 5 A)formulated for the genetic evaluation of cardiomyopathy,such as the need for family history, apply to all entities, 17.2 Clinical screening for cardiomyopathy in asymptom-other recommendations must be tailored to account for atic first-degree relatives is recommended.these differences. This is particularly relevant as these a. Cardiomyopathy Phenotypeguidelines use the generic term ‘‘cardiomyopathy’’ to im-  Hypertrophic cardiomyopathy (Strength ofply possible familial or genetic cause, assuming that all Evidence 5 A)other detectable causes of cardiomyopathy have been  Dilated cardiomyopathy (Strength of Evi-ruled out. This is particularly relevant for DCM where dence 5 A)multiple nongenetic causes are possible as noted previ-  Arrhythmogenic right ventricular dysplasiaously. Recent discoveries indicate that arrhythmogenic (Strength of Evidence 5 A)right ventricular dysplasia/cardiomyopathy (ARVD/C) is  Left ventricular noncompaction (Strength oflargely caused by mutations in genes encoding proteins Evidence 5 B)of the desmosome. Although initially recognized predom-  Restrictive cardiomyopathy (Strength of Evi-inantly in the right ventricle, LV involvement in 20% to dence 5 B)40% of patients has prompted the change in nomenclature  Cardiomyopathies associated with extracardiacfrom ARVD to ARVD/C.153 Discovering the genetic basis manifestations (Strength of Evidence 5 A)of restrictive cardiomyopathy (RCM) has been more chal-lenging, because RCM is much less common than DCM b. Clinical screening for cardiomyopathy is recom-or HCM, and less commonly presents with familial dis- mended at intervals (see below) in asymptomaticease. Left ventricular noncompaction (LVNC) is an ana-tomic abnormality of LV myocardial development: LVcompaction is incomplete, leaving deep trabeculations in Interval if geneticthe LV myocardium. LVNC was categorized as a specific testing is negative Screeningtype of cardiomyopathy by an expert panel in 2006,154 Cardio- and/or if clinical interval if myopathy family screening a mutation Strength ofand some genetic association has been observed. Although Phenotype is negative is present Evidenceinitially reported to be a rare condition associated with ad-verse outcome,155 more recent reports156-158 have called Hypertrophic Every 3 years Every 3 years B until 30 years until 30 yearsinto question those preliminary conclusions.159 Three dif- of age, except of age, exceptferent echocardiographic criteria have been used for diag- yearly during yearly duringnosis.156 These authors suggested that the diagnostic puberty; puberty; after 30 years, every 5 yearscriteria for LVNC might be too sensitive. Because of the if symptoms thereafteruncertainty of diagnostic standards leading to difficulty developclarifying its phenotype, we suggest that the LVNC rec- Dilated Every 3-5 years Yearly in B beginning in childhood;ommendations in this document be limited to those indi- childhood every 1-3viduals with only the most prominent disease. years in adults ARVD/C Every 3-5 years Yearly after age CRecommendations for the Genetic Evaluation of after age 10 10 to 50 years of ageCardiomyopathy LVNC Every 3 years Yearly in C beginning in childhood;17.1 A careful family history for $3 generations is rec- childhood every 1-3 years in ommended for all patients with cardiomyopathy. adults Restrictive Every 3-5 years Yearly in C beginning in childhood; *Reprinted with edits and permission from Hershberger RE, Lindenfeld adulthood every 1-3J, Mestroni L, Seidman C, Taylor MRG, Towbin JA. Genetic evaluating years incardiomyopathy: a Heart Failure Society of America Practice Guideline. adultsJ Card Fail 2009;15:83-97.
    • Executive Summary: Heart Failure Practice Guideline  HFSA 505 at-risk relatives who are known to carry the disease-causing mutation(s). (Strength of Evi- Cardiomyopathy Gene Tests Yield of dence 5 A) Phenotype Available* Positive Results HCM MYH7, MYBPC3, MYH7, MYBPC3 c. Clinical screening for cardiomyopathy is recom- TNNT2 TNNI3, each account for mended for asymptomatic at-risk first-degree rel- TPMI, ACTC, 30%-40% of atives when genetic testing has not been MYL2, MYL3 mutations, TNNT2 for 10%-20%. performed or has not identified a disease- Genetic cause can causing mutation. (Strength of Evidence 5 A) be identified in 35%-45% overall; d. It is recommended that clinical screening consist of: up to 60%-65%  History (with special attention to HF symp- when the family history is positive. toms, arrhythmias, presyncope, and syn- DCM LMNA, MYH7, 5.5%, 4.2%, 2.9%, for cope) TNNT2, SCN5A, LMNA, MYH7,  Physical examination (with special attention DES, MYBPC3, and TNNT2, TNNI3, TPMI, respectively. All to the cardiac and skeletal muscle systems) ACTC, PLN, data are from  Electrocardiogram LDB3 and TAZ research cohorts ARVD DSP, PKP2, DSG2, 6%-16%, 11%-43%,  Echocardiogram DSC2 12%-40%, for DSP,  CK-MM (at initial evaluation only) PKP2, and DSG2,  Signal-averaged electrocardiogram (SAECG) respectively LVNC Uncertain e see Uncertain e see in ARVD only discussion discussion  Holter monitoring in HCM, ARVD RCM Uncertain e see Uncertain e see discussion discussion  Exercise treadmill testing in HCM  Magnetic resonance imaging in ARVD *GeneTests (www.genetests.org) is a National Institutes of Health- (Strength of Evidence 5 B) funded resource that lists clinical (and research) molecular genetic testing laboratories for the cardiomyopathies. e. Clinical screening for cardiomyopathy should be considered at the following times and inter- vals or at any time that signs or symptoms b. Specific genes available for screening based on appear. cardiac phenotype f. At-risk first-degree relatives with any abnormal c. Screening for Fabry disease is recommended in clinical screening tests (regardless of genotype) all men with sporadic or non-autosomal domi- should be considered for repeat clinical screening nant (no male-to-male) transmission of unex- at 1 year. (Strength of Evidence 5 C) plained cardiac hypertrophy. (Strength of Evidence 5 B)17.3 Evaluation, genetic counseling, and genetic testing of cardiomyopathy patients are complex processes. Re- 17.5 Genetic and family counseling is recommended for ferral to centers expert in genetic evaluation and all patients and families with cardiomyopathy. family-based management should be considered. (Strength of Evidence 5 A) (Strength of Evidence 5 B) 17.6 Medical therapy based on cardiac phenotype is17.4 Genetic testing should be considered for the one recommended (see section 7). (Strength of Evi- most clearly affected person in a family to facilitate dence 5 A) family screening and management. 17.7 Device therapies for arrhythmia and conduction sys- a. Cardiomyopathy Phenotype tem disease based on cardiac phenotype are recom-  Hypertrophic cardiomyopathy (Strength of mended (see section 9). (Strength of Evidence 5 B) Evidence 5 A)  Dilated cardiomyopathy (Strength of Evi- 17.8 In patients with cardiomyopathy and significant ar- dence 5 B) rhythmia or known risk of arrhythmia an ICD may be considered before the LVEF falls below 35%.  Arrhythmogenic right ventricular dysplasia (Strength of Evidence 5 C) (Strength of Evidence 5 A)  Left ventricular noncompaction (Strength of Evidence 5 C) Acknowledgment  Restrictive cardiomyopathy (Strength of Evi- dence 5 C) The Guideline Committee would like to thank the Execu-  Cardiomyopathies associated with extracardiac tive Council for their review and comments and the following manifestations (Strength of Evidence 5 A) individuals for their input in revising specific sections;
    • 506 Journal of Cardiac Failure Vol. 16 No. 6 June 2010Jonathan G. Howlett (University of Calgary) and Richard 14. Grundy SM, Balady GJ, Criqui MH, Fletcher G, Greenland P,J. Rodeheffer (Mayo Clinic & Foundation), Prevention Sec- Hiratzka LF, et al. Primary prevention of coronary heart disease: guidance from Framingham: a statement for healthcare professionalstion; Marvin W. Kronenberg (Vanderbilt University), Non- from the AHA Task Force on Risk Reduction. American Heart Asso-pharmacologic Management and HF with Preserved LVEF ciation. Circulation 1998;97:1876e87.Sections; Alan B. Miller (University of Florida, Jackson- 15. Hellermann JP, Jacobsen SJ, Reeder GS, Lopez-Jimenez F,ville), Drug Therapy Section; Sarah J. Goodlin (Patient Cen- Weston SA, Roger VL. Heart failure after myocardial infarction:tered Research and Education, Salt Lake City, Utah), Disease prevalence of preserved left ventricular systolic function in the com- munity. Am Heart J 2003;145:742e8.Management, Advance Directives, and End-of-Life Care in 16. Howard BV. Blood pressure in 13 American Indian communities: theHeart Failure Section; Kenneth L. Baughman (deceased, Strong Heart Study. Public Health Rep 1996;111(Suppl. 2):47e8.Brigham & Women’s Hospital, Boston, Massachusetts), 17. Kenchaiah S, Evans JC, Levy D, Wilson PW, Benjamin EJ,Myocarditis Section; Michael R. Zile, MD, HF With Pre- Larson MG, et al. Obesity and the risk of heart failure. N Engl Jserved LVEF Section; Bart Galle, PhD and Wendy Gattis Med 2002;347:305e13. 18. Kjekshus J, Pedersen TR, Olsson AG, Faergeman O, Pyorala K. TheStough, PharmD for their scientific and editorial contribu- effects of simvastatin on the incidence of heart failure in patientstions; and Cheryl Yano for administrative support. with coronary heart disease. J Card Fail 1997;3:249e54. 19. Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progres- sion from hypertension to congestive heart failure. 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Effects of candesartan on mortality and morbid- risk of cardiovascular disease. N Engl J Med 2001;345:1291e7. ity in patients with chronic heart failure: the CHARM-Overall pro-152. Domanski MJ, Mitchell GF, Norman JE, Exner DV, Pitt B, gramme. Lancet 2003;362:759e66. Pfeffer MA. Independent prognostic information provided by sphyg- 163. Konstam MA, Neaton JD, Dickstein K, Drexler H, Komajda M, momanometrically determined pulse pressure and mean arterial pres- Martinez FA, et al. Effects of high-dose versus low-dose losartan sure in patients with left ventricular dysfunction. J Am Coll Cardiol on clinical outcomes in patients with heart failure (HEAAL study): 1999;33:951e8. a randomised, double-blind trial. Lancet 2009;374:1840e8.153. Sen-Chowdhry S, Syrris P, McKenna WJ. Role of genetic analysis in 164. Cohn JN, Tognoni G. Valsartan Heart Failure Trial Investigators. A the management of patients with arrhythmogenic right ventricular dys- randomized trial of the angiotensin-receptor blocker valsartan in plasia/cardiomyopathy. J Am Coll Cardiol 2007;50:1813e21. chronic heart failure. New England Journal of Medicine 2001;345:154. Maron BJ, Towbin JA, Thiene G, Antzelevitch C, Corrado D, 1667e75. Arnett D, et al. Contemporary definitions and classification of the 165. Packer M, Coats AJ, Fowler MB, Katus HA, Krum H, Mohacsi P, cardiomyopathies: an American Heart Association Scientific State- et al. Effect of carvedilol on survival in severe chronic heart failure. ment from the Council on Clinical Cardiology, Heart Failure and N Engl J Med 2001;344:1651e8. Transplantation Committee; Quality of Care and Outcomes Research 166. Taylor AL, Ziesche S, Yancy C, Carson P, D’Agostino R Jr, and Functional Genomics and Translational Biology Interdisciplinary Ferdinand K, et al. Combination of isosorbide dinitrate and hydral- Working Groups; and Council on Epidemiology and Prevention. Cir- azine in blacks with heart failure. N Engl J Med 2004;351:2049e57. culation 2006;113:1807e16. 167. Cohn JN, Archibald DG, Ziesche S, Franciosa JA, Harston WE,155. Chin TK, Perloff JK, Williams RG, Jue K, Mohrmann R. Isolated Tristani FE, et al. Effect of vasodilator therapy on mortality in noncompaction of left ventricular myocardium. A study of eight chronic congestive heart failure. Results of a Veterans Administration cases. Circulation 1990;82:507e13. Cooperative Study. N Engl J Med 1986;314:1547e52.
    • Appendix A. Comparison of the 2006 and 2010 HFSA Guideline 2006 Guideline Recommendation 2010 Guideline Recommendation Comments Section 3: Prevention of Ventricular Remodeling, Cardiac Dysfunction, and Heart Failure3.1 A careful and thorough clinical assessment, with appropriate investigation for A careful and thorough clinical assessment, with appropriate investigation for Addition of dietary choices to list known or potential risk factors, is recommended in an effort to prevent known or potential risk factors, is recommended in an effort to prevent of risk factors development of LV remodeling, cardiac dysfunction, and HF. These risk development of LV remodeling, cardiac dysfunction, and HF. These risk factors include, but are not limited to, hypertension, hyperlipidemia, factors include, but are not limited to, hypertension, hyperlipidemia, atherosclerosis, diabetes mellitus, valvular disease, obesity, physical atherosclerosis, diabetes mellitus, valvular disease, obesity, physical inactivity, excessive alcohol intake, and smoking. inactivity, excessive alcohol intake, dietary choices, and smoking. (Strength (Strength of Evidence 5 A) of Evidence 5 A)3.2 No changes3.3 No changes3.4 No changes Section 4: Evaluation of Patients for Ventricular Dysfunction and Heart Failure4.1 Evaluation with a routine history, physical examination, chest x-ray, and Evaluation for clinical manifestations of HF with a routine history and Modification of wording and electrocardiogram (ECG) is recommended in patients with the medical physical examination is recommended in patients with the medical deletion of chest x-ray and conditions or test findings listed in Table 4.1. (Strength of Evidence 5 B) conditions or test findings listed in Table 4.1. (Strength of Evidence 5 B) ECG (retained in Table 4.1)4.2 Assessment of Cardiac Structure and Function. Echocardiography with Assessment of Cardiac Structure and Function. Echocardiography with Modification of wording and Doppler is recommended to determine LV size and function in patients Doppler is recommended to determine cardiac structure and function in terminology without signs or symptoms suggestive of HF who have the risk factors listed asymptomatic patients with the disorders or findings listed in Table 4.2. in Table 4.2. (Strength of Evidence 5 B) (Strength of Evidence 5 B)4.3 Determination of plasma B-type natriuretic peptide (BNP) or N-terminal pro- Routine determination of plasma BNP or NT-proBNP concentration as part of Modification of wording and BNP concentration is not recommended as a routine part of the evaluation a screening evaluation for structural heart disease in asymptomatic patients terminology for structural heart disease in patients at risk but without signs or symptoms is not recommended. (Strength of Evidence 5 B) of HF. (Strength of Evidence 5 B)4.4 Symptoms Consistent with HF. The symptoms listed in Table 4.3 suggest the Symptoms Consistent with HF. The symptoms listed in Table 4.3 suggest the Modification of wording and diagnosis of HF. It is recommended that each of these symptoms be solicited diagnosis of HF. It is recommended that each of these symptoms be elicited addition of depression to Table and graded in all patients in whom the diagnosis of HF is being considered. in all patients in whom the diagnosis of HF is being considered. (Strength of 4.3 (Strength of Evidence 5 B) Evidence 5 B)4.5 Physical Examination. It is recommended that patients suspected of having HF Physical Examination. It is recommended that patients suspected of having HF Modification of wording and undergo careful physical examination with determination of vital signs and undergo careful physical examination with determination of vital signs and change in Strength of Evidence be carefully evaluated for signs and symptoms shown in Table 4.4. (Strength careful evaluation for signs shown in Table 4.4. (Strength of Evidence 5 B) from C to B and addition of of Evidence 5 C) reduced cardiac output and arrhythmia to cardiac abnormalities in Table 4.44.6 It is recommended that BNP or NT-proBNP levels be assessed in all patients It is recommended that BNP or NT-proBNP levels be assessed in all patients Modification of wording and Executive Summary: Heart Failure Practice Guideline suspected of having HF when the diagnosis is not certain. (Strength of suspected of having HF, especially when the diagnosis is not certain. change in Strength of Evidence Evidence 5 B) (Strength of Evidence 5 A) from B to A  (continued on next page) HFSA 511
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments4.7 The differential diagnoses in Table 4.5 should be considered as alternative Differential Diagnosis. The differential diagnoses in Table 4.5 should be Modification of wording and explanations for signs and symptoms consistent with HF. (Strength of considered as alternative explanations for signs and symptoms consistent change in Strength of Evidence Evidence 5 C) with HF. (Strength of Evidence 5 B) from C to B and addition of chronic kidney disease and thyroid abnormalities to Table 4.54.8 No changes4.9 Symptoms. In addition to symptoms characteristic of Symptoms. In addition to symptoms characteristic of HF (dyspnea, fatigue, Clarification of HF symptoms HF, the following symptoms should be considered in the diagnosis of HF: decreased exercise tolerance, fluid retention), evaluation of the following and addition of arrhythmia to symptoms should be considered in the diagnosis of HF: list of symptoms and change in  Angina  Angina Strength of Evidence from C to  Symptoms of possible cerebral hypoperfusion, including syncope, pre-  Symptoms suggestive of embolic events B syncope, or lightheadedness  Symptoms suggestive of sleep-disordered breathing  Symptoms suggestive of embolic events  Symptoms suggestive of arrhythmias, including palpitations  Symptoms suggestive of sleep-disordered breathing  Symptoms of possible cerebral hypoperfusion, including syncope, pre- (Strength of Evidence 5 C) syncope, or lightheadedness (Strength of Evidence 5 B)4.10 No changes 512 Journal of Cardiac Failure Vol. 16 No. 6 June 20104.11 The degree of volume excess is a key consideration during treatment. It is Volume Status. The degree of volume excess is a key consideration during Addition of presence of dyspnea recommended that it be routinely assessed by determining: treatment. It is recommended that it be routinely assessed by determining: on exertion and hepatic  Presence of paroxysmal nocturnal dyspnea or orthopnea  Presence of paroxysmal nocturnal dyspnea or orthopnea enlargement/tenderness to list  Daily weights and vital signs with assessment for orthostatic changes  Presence of dyspnea on exertion of assessments  Presence and degree of rales, S3 gallop, jugular venous pressure elevation,  Daily weights and vital signs with assessment for orthostatic changes positive hepatojugular reflux, edema, and ascites  Presence and degree of rales, S3 gallop, jugular venous pressure elevation, (Strength of Evidence 5 B) hepatic enlargement and tenderness, positive hepatojugular reflux, edema, and ascites (Strength of Evidence 5 B)4.12 It is recommended that the following laboratory tests be obtained routinely in Standard Laboratory Tests. It is recommended that the following laboratory Addition of uric acid to list of patients being evaluated for HF: serum electrolytes, blood urea nitrogen, tests be obtained routinely in patients being evaluated for HF: serum standard laboratory tests creatinine, glucose, calcium, magnesium, lipid profile (low-density electrolytes, blood urea nitrogen, creatinine, glucose, calcium, magnesium, lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides), fasting lipid profile (low-density lipoprotein cholesterol, high-density complete blood count, serum albumin, liver function tests, urinalysis, and lipoprotein cholesterol, triglycerides), complete blood count, serum thyroid function. (Strength of Evidence 5 B) albumin, uric acid, liver function tests, urinalysis, and thyroid function. (Strength of Evidence 5 B)4.13 It is recommended that all patients with HF have an ECG performed to: Electrocardiogram (ECG). It is recommended that all patients with HF have an Addition of electrical  Assess cardiac rhythm and conduction ECG performed to: dyssynchrony and QTc interval  Detect LV hypertrophy  Assess cardiac rhythm and conduction (in some cases, using Holter to list of ECG assessments  Evaluate QRS duration, especially when ejection fraction (EF) !35% monitoring or event monitors)  Detect evidence of myocardial infarction or ischemia  Assess electrical dyssynchrony (wide QRS or bundle branch block), es- (Strength of Evidence 5 B) pecially when left ventricular ejection fraction (LVEF) !35%  Detect LV hypertrophy or other chamber enlargement  Detect evidence of MI or ischemia  Assess QTc interval, especially with drugs that prolong QT intervals (Strength of Evidence 5 B)
    • 4.14 It is recommended that all patients with HF have a posteroanterior and lateral Chest X-Ray. It is recommended that all patients with HF have a postero- Addition of placement of chest X-ray examination for determination of heart size, evidence of fluid anterior and lateral chest X-ray examination for determination of heart size, implanted cardiac devices to overload, and detection of pulmonary and other diseases. (Strength of evidence of fluid overload, detection of pulmonary and other diseases, and list of chest x-rays assessments Evidence 5 B) appropriate placement of implanted cardiac devices. (Strength of Evidence 5 B)4.15 Additional Laboratory Tests. It is recommended that patients with no apparent Additional Laboratory Tests. It is recommended that patients with no apparent Change in Strength of Evidence etiology of HF or no specific clinical features suggesting unusual etiologies etiology of HF or no specific clinical features suggesting unusual etiologies from C to B undergo additional directed blood and laboratory studies to determine the undergo additional directed blood and laboratory studies to determine the cause of HF. cause of HF. (Strength of Evidence 5 B) (Strength of Evidence 5 C)4.16 Evaluation of myocardial ischemia is recommended in those who develop New recommendation new-onset LV systolic dysfunction especially in the setting of suspected myocardial ischemia or worsening symptoms with pre-existing CAD. The choice of testing modality should depend on the clinical suspicion and underlying cardiac risk factors. Coronary angiography should be considered when pre-test probability of underlying ischemic cardiomyopathy is high and an invasive coronary intervention may be considered. (See Section 13 for specific clinical situations and Strength of Evidence)4.17 Exercise testing is not recommended as part of routine evaluation in patients Exercise testing for functional capacity is not recommended as part of routine Modification of wording and (previous with HF. Specific circumstances in which maximal exercise testing with evaluation in patients with HF. Specific circumstances in which maximal deletion of recommendation 4.16) measurement of expired gases should be considered include: exercise testing with measurement of expired gases should be considered for exercise testing for  Assessing disparity between symptomatic limitation and objective indi- include: inducible abnormality in cators of disease severity  Assessing disparity between symptomatic limitation and objective indi- myocardial perfusion or wall  Distinguishing noneHF-related causes of functional limitation, specifi- cators of disease severity motion abnormality cally cardiac versus pulmonary  Distinguishing non HF-related causes of functional limitation, specifically  Considering candidacy for cardiac transplantation or mechanical inter- cardiac versus pulmonary vention  Considering candidacy for cardiac transplantation or mechanical circula-  Determining the prescription for cardiac rehabilitation tory support  Addressing specific employment capabilities  Determining the prescription for cardiac rehabilitation Exercise testing for inducible abnormality in myocardial perfusion or wall  Addressing specific employment capabilities motion abnormality should be considered to screen for the presence of (Strength of Evidence 5 C) coronary artery disease with inducible ischemia. (Strength of Evidence 5 C)4.18 No changes (previous 4.17)4.19 It is recommended that clinical evaluation at each followup visit include the It is recommended that clinical evaluation at each follow-up visit include Change (in second part of (previous assessments listed in Table 4.9. (Strength of Evidence 5 B) determination of the elements listed in Table 4.9. (Strength of recommendation) Strength of 4.18) These assessments should include the same symptoms and signs assessed Evidence 5 B). Evidence from C to B during the initial evaluation. These assessments should include the same symptoms and signs assessed (Strength of Evidence 5 C) during the initial evaluation. (Strength of Evidence 5 B) (continued on next page) Executive Summary: Heart Failure Practice Guideline  HFSA 513
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments4.20 Routine reevaluation of cardiac function by noninvasive or invasive methods is In the absence of deteriorating clinical presentation, repeat measurements of Modifications of (previous not recommended. Repeat measurements of ventricular volume and EF ventricular volume and LVEF should be considered in these limited recommendation throughout 4.19) should be considered under limited circumstances: circumstances:  When a prophylactic implantable  After at least 3 months of medical therapy when prophylactic ICD cardioverter defibrillator (ICD) or CRT device and defibrillator (CRT-D) placement is being considered to confirm that EF criteria are still met. placement is being considered in order to determine that LVEF criteria for (Strength of Evidence 5 B) device placement are still met after medical therapy (Strength of Evidence  In patients who show substantial clinical improvement (for example, in 5 B) response to b-blocker treatment). Such change may denote improved  When patients show substantial clinical prognosis, although it does not in itself mandate alteration or discontin- improvement (for example, in response to beta blocker treatment or uation of specific treatments. (Strength of Evidence 5 C) following pregnancy in patients with peripartum cardiomyopathy). Such Repeat determination of EF is usually unnecessary in patients with previ- change may denote improved prognosis, although it does not in itself ously documented LV dilation and low EF who manifest worsening signs or mandate alteration or discontinuation of specific treatments (see Section 7). symptoms of HF. Repeat measurement should be considered when it is (Strength of Evidence 5 C) likely to prompt a change in patient management, such as cardiac trans-  In alcohol and cardiotoxic substance abusers who have discontinued the plantation. (Strength of Evidence 5 C) abused substance. (Strength of Evidence 5 C)  In patients receiving cardiotoxic chemotherapy. (Strength of Evidence 5 B) Repeat determination of LVEF is usually unnecessary in patients with pre- viously documented LV dilatation and low LVEF who manifest worsening signs or symptoms of HF, unless the information is needed to justify a change in patient management (such as surgery or device implantation). (Strength of Evidence 5 C) 514 Journal of Cardiac Failure Vol. 16 No. 6 June 20104.21 It is recommended that reevaluation of electrolytes and renal function occur at It is recommended that reevaluation of electrolytes and renal function occur at Addition of aldosterone (previous least every 6 months in clinically stable patients and more frequently after least every 6 months in clinically stable patients and more frequently antagonists to list of patients in 4.20) changes in therapy or with evidence of change in volume status. More following changes in therapy or with evidence of change in volume status. whom more frequent frequent assessment of electrolytes and renal function is recommended in More frequent assessment of electrolytes and renal function is assessment of electrolytes and patients with severe HF, those receiving high doses of diuretics, and those recommended in patients with severe HF, those receiving high doses of renal function is who are clinically unstable. (Strength of Evidence 5 C) (See Section 7 for diuretics, those on aldosterone antagonists, and those who are clinically recommended. recommendations regarding patients on angiotensin receptor blockers.) unstable. (Strength of Evidence 5 C) (See Section 7 for recommendations regarding patients on angiotensin receptor blockers.) Section 5: Management of Asymptomatic Patients with Reduced LVEF5.1 It is recommended that all patients with ALVD exercise regularly according to It is recommended that all patients with ALVD exercise regularly according to Minor wording modification a physician-directed prescription to avoid general deconditioning; to a physician-directed prescription to avoid general deconditioning; to improve weight, blood pressure, and diabetes control; and to reduce optimize weight, blood pressure, and diabetes control; and to reduce cardiovascular risk. (Strength of Evidence 5 C) cardiovascular risk. (Strength of Evidence 5 C)5.2 No changes5.3 It is recommended that alcohol consumption be discouraged in patients with Alcohol abstinence is recommended if there is current or previous history of Deleted phrase discouraging ALVD. Abstinence is recommended if there is a current habit or history of excessive alcohol intake. (Strength of Evidence 5 C) alcohol use in ALVD. Other excessive alcohol intake. (Strength of Evidence 5 C) minor wording modifications.5.4 It is recommended that all patients with ALVD with hypertension have It is recommended that all patients with ALVD with hypertension achieve Aggressive blood pressure aggressive blood pressure control. (Strength of Evidence 5 B) optimal blood pressure control. (Strength of Evidence 5 B) control changed to optimal blood pressure control5.5 No changes
    • 5.6 ARBs are recommended for asymptomatic patients with reduced LVEF who ARBs are recommended for asymptomatic patients with reduced LVEF who Minor wording modification are intolerant of ACE inhibitors because of cough or angioedema. (Strength are intolerant of ACE inhibitors from cough or angioedema. (Strength of of Evidence 5 C) Evidence 5 C) Routine use of the combination of ACE inhibitors and ARBs for prevention Routine use of the combination of ACE inhibitors and ARBs for prevention of HF is not recommended in this population. (Strength of Evidence 5 C) of HF is not recommended in this population. (Strength of Evidence 5 C)5.7 It is recommended that beta blocker therapy be administered to asymptomatic Beta blocker therapy should be considered in asymptomatic patients with Changed from ‘‘is patients with reduced LVEF. (Post MI, Strength of Evidence 5 B; nonePost reduced LVEF. (post-MI, Strength of Evidence 5 B; non post-MI, Strength recommended’’ to ‘‘should be MI, Strength of Evidence 5 C) of Evidence 5 C) considered’’ Section 6: Nonpharmacologic Management and Health Care Maintenance in Patients with Chronic Heart Failure6.1 Dietary instruction regarding sodium intake is recommended in all patients Dietary instruction regarding sodium intake is recommended in all patients Minor wording modification with HF. Patients with HF and diabetes, dyslipidemia, or obesity should be with HF. Patients with HF and diabetes, dyslipidemia, or severe obesity given specific instructions regarding carbohydrate or caloric constraints. should be given specific dietary instructions. (Strength of Evidence 5 B) (Strength of Evidence 5 B)6.2 No changes6.3 No changes6.4 It is recommended that specific attention be paid to nutritional management of It is recommended that specific attention be paid to nutritional management of Minor wording modification patients with advanced HF and unintentional weight loss or muscle wasting patients with advanced HF and unintentional weight loss or muscle wasting (cardiac cachexia). Measurement of nitrogen balance, caloric intake, and (cardiac cachexia). Measurement of nitrogen balance, caloric intake, and prealbumin may be useful in determining appropriate nutritional prealbumin may be useful in determining appropriate nutritional supplementation. Caloric supplementation is recommended. Anabolic supplementation. Caloric supplementation is recommended. Anabolic steroids are not recommended for such patients. (Strength of Evidence 5 C) steroids are not recommended for cachexic patients. (Strength of Evidence 5 C)6.5 No changes6.6 Documentation of the type and dose of nutraceutical products used by patients Documentation of the type and dose of naturoceutical products used by Modification of terminology with HF is recommended. (Strength of Evidence 5 C) patients with HF is recommended. (Strength of Evidence 5 C) (nutraceutical to Nutraceutical use is not recommended for relief of symptomatic HF or for Naturoceutical use is not recommended for relief of symptomatic HF or for naturoceutical) the secondary prevention of cardiovascular events. Patients should be the secondary prevention of cardiovascular events. Patients should be instructed to avoid using natural or synthetic products containing ephedra instructed to avoid using natural or synthetic products containing ephedra (ma huang), ephedrine, or its metabolites because of an increase risk of (ma huang), ephedrine, or its metabolites because of an increased risk of mortality and morbidity. Products should be avoided that may have mortality and morbidity. Products should be avoided that may have significant drug interactions with digoxin, vasodilators, beta blockers, significant drug interactions with digoxin, vasodilators, beta blockers, antiarrhythmic drugs, and anticoagulants. (Strength of Evidence 5 B) antiarrhythmic drugs, and anticoagulants. (Strength of Evidence 5 B)6.7 No changes6.8 No changes6.9 No changes6.10 It is recommended that screening for endogenous or prolonged reactive It is recommended that screening for endogenous or prolonged reactive Minor wording modification depression in patients with HF be conducted after diagnosis and at periodic depression in patients with HF be conducted following diagnosis and at Executive Summary: Heart Failure Practice Guideline intervals as clinically indicated. For pharmacologic treatment, selective periodic intervals as clinically indicated. For pharmacologic treatment, serotonin receptor uptake inhibitors are preferred over tricyclic selective serotonin reuptake inhibitors are preferred over tricyclic  antidepressants, because the latter have the potential to cause ventricular antidepressants, because the latter have the potential to cause ventricular arrhythmias, but the potential for drug interactions should be considered. arrhythmias, but the potential for drug interactions should be considered. (Strength of Evidence 5 B) (Strength of Evidence 5 B) HFSA (continued on next page) 515
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments6.11 No changes6.12 No changes6.13 No changes6.14 No changes6.15 Endocarditis prophylaxis is not recommended based on the diagnosis of HF Endocarditis prophylaxis is not recommended based on the diagnosis of HF Addition of criteria for alone. Prophylaxis for dental and other procedures should be given alone. Consistent with the AHA recommendation, ‘prophylaxis should be endocarditis prophylaxis according to standard clinical indications. (Strength of Evidence 5 C) given for only specific cardiac conditions, associated with the highest risk of adverse outcome from endocarditis.’ These conditions include: ‘prosthetic cardiac valves; previous infective endocarditis; congenital heart disease (CHD)’ such as: ‘unrepaired cyanotic CHD, including palliative shunts and conduits; completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first six months after the procedure; repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization); cardiac transplantation recipients who develop cardiac valvulopathy.’ (Strength of Evidence 5 C)6.16 No changes 516 Journal of Cardiac Failure Vol. 16 No. 6 June 20106.17 No changes6.18 No changes6.19 It is recommended that patients with HF undergo exercise testing to determine New recommendation suitability for exercise training (patient does not develop significant ischemia or arrhythmias). (Strength of Evidence = B) If deemed safe, exercise training should be considered for patients with HF in order to facilitate understanding of exercise expectations (heart rate ranges and appropriate levels of exercise training), to increase exercise duration and intensity in a supervised setting, and to promote adherence to a general exercise goal of 30 minutes of moderate activity/exercise, 5 days per week with warm up and cool down exercises. (Strength of Evidence 5 B) Section 7: Heart Failure in Patients with Reduced Ejection Fraction7.1 No changes7.2 It is recommended that other therapy be substituted for ACE inhibitors in the It is recommended that other therapy be substituted for ACE inhibitors in the Minor wording modification following circumstances: following circumstances:  In patients who cannot tolerate ACE inhibitors because of cough, ARBs  In patients who cannot tolerate ACE inhibitors due to cough, ARBs are are recommended. (Strength of Evidence 5 A) recommended. (Strength of Evidence 5 A)  The combination of hydralazine and an oral nitrate may be considered in  The combination of hydralazine and an oral nitrate may be considered in such patients not tolerating ARB therapy. (Strength of Evidence 5 C) such patients not tolerating ARB therapy. (Strength of Evidence 5 C)  Patients intolerant to ACE inhibitors because of hyperkalemia or renal  Patients intolerant to ACE inhibitors from hyperkalemia or renal insuffi- insufficiency are likely to experience the same side effects with ARBs. In ciency are likely to experience the same side effects with ARBs. In these these cases, the combination of hydralazine and an oral nitrate should be cases, the combination of hydralazine and an oral nitrate should be con- considered. (Strength of Evidence 5 C) sidered. (Strength of Evidence 5 C)
    • 7.3 No changes (previous 7.10)7.4 ARBs should be considered in patients experiencing angioedema while on ARBs should be considered in patients experiencing angioedema while on Minor wording modifications (previous ACE inhibitors based on their underlying risk and with recognition that ACE inhibitors based on their underlying risk and with recognition that 7.12) angioedema has been reported infrequently with these agents. (Strength of angioedema has been reported infrequently with ARBs. (Strength of Evidence 5 B) Evidence 5 B) The combination of hydralazine and oral nitrates may be considered in this The combination of hydralazine and oral nitrates may be considered in this setting for patients who do not tolerate ARB therapy. (Strength of setting for patients who do not tolerate ARB therapy. (Strength of Evidence 5 C) Evidence 5 C)7.5 Individual ARBs may be considered as initial therapy rather than ACE Individual ARBs may be considered as initial therapy rather than ACE Terminology modification (previous inhibitors for patients with the following conditions: inhibitors for patients with the following conditions: (changed ‘‘systolic 7.11)  HF post MI (Strength of Evidence 5 A)  HF Post-MI (Strength of Evidence 5 A) dysfunction’’ to ‘‘reduced  Chronic HF and systolic dysfunction (Strength of Evidence 5 B)  Chronic HF and reduced LVEF (Strength of Evidence 5 B) LVEF)7.6 No changes (previous 7.3)7.7 No changes (previous 7.4)7.8 Beta blocker therapy is recommended for patients with a recent Beta blocker therapy is recommended for patients with a recent Minor wording modifications (previous decompensation of HF after optimization of volume status and successful decompensation of HF after optimization of volume status and successful 7.5) discontinuation of intravenous diuretics and vasoactive agents, including discontinuation of intravenous diuretics and vasoactive agents, including inotropic support. Whenever possible, beta blocker therapy should be inotropic support. Whenever possible, beta blocker therapy should be initiated in the hospital setting at a low dose before discharge in stable initiated in the hospital setting at a low dose prior to discharge in stable patients. (Strength of Evidence 5 B) patients. (Strength of Evidence 5 B)7.9 Beta blocker therapy is recommended in the great majority of patients with LV Beta blocker therapy is recommended in the great majority of patients with HF Modification of terminology (previous systolic dysfunction, even if there is concomitant diabetes, chronic and reduced LVEF, even if there is concomitant diabetes, chronic (‘‘LV systolic dysfunction’’ 7.6) obstructive lung disease, or peripheral vascular disease. Beta blocker obstructive lung disease, or peripheral vascular disease. Beta blocker changed to ‘‘reduced LVEF’’) therapy should be used with caution in patients with diabetes with recurrent therapy should be used with caution in patients with diabetes with recurrent hypoglycemia, asthma, or resting limb ischemia. Considerable caution hypoglycemia, with asthma, or with resting limb ischemia. Considerable should be used if beta blockers are initiated in patients with marked caution should be used if beta blockers are initiated in patients with marked bradycardia (!55 beats/min) or marked hypotension (systolic blood bradycardia (!55 beats/min) or marked hypotension (systolic blood pressure !80 mm Hg). Beta blockers are not recommended in patients with pressure !80 mm Hg). Beta blockers are not recommended in patients with asthma with active bronchospasm. (Strength of Evidence 5 C) asthma with active bronchospasm. (Strength of Evidence 5 C)7.10 It is recommended that b-blockade be initiated at low doses and uptitrated It is recommended that beta blockade be initiated at low doses and uptitrated Deleted information related to (previous gradually, typically no sooner than at 2-week intervals. Doses found to be gradually, typically at 2-week intervals in patients with reduced LVEF, and beta blocker management 7.7) effective in HF trials generally are achieved in 8 to 12 weeks. Patients after 3-10 day intervals in patients with reduced LVEF following newly developing worsening HF symptoms or other side effects during titration diagnosed MI. (Strength of Evidence 5 B) may require a dosage adjustment of diuretic or concomitant vasoactive medications. If side effects resolve with medication adjustment, patients can Executive Summary: Heart Failure Practice Guideline subsequently be titrated to target or maximally tolerated doses. Some patients may require a more prolonged interval during uptitration, a  temporary reduction in b-blocker dose, or, in rare cases, withdrawal of therapy. (Strength of Evidence 5 B) HFSA (continued on next page) 517
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments7.11 It is recommended that beta blocker therapy be continued in most patients It is recommended that beta blocker therapy be continued in most patients Addition of criteria for beta (previous experiencing a symptomatic exacerbation of HF during chronic experiencing a symptomatic exacerbation of HF during chronic blocker discontinuation and 7.8) maintenance treatment. (Strength of Evidence 5 C) maintenance treatment, unless they develop cardiogenic shock, refractory reinstitution A temporary reduction of dose in this setting may be considered. Abrupt volume overload, or symptomatic bradycardia (Strength of Evidence 5 C) discontinuation in patients with symptomatic exacerbation should be A temporary reduction of dose (generally by one-half) in this setting may be avoided. (Strength of Evidence 5 C) considered. Abrupt discontinuation in patients with symptomatic If discontinued or reduced, beta blockers should be reinstated or the dose exacerbation should be avoided, unless the situation is life-threatening. should be gradually increased before the patient is discharged. (Strength of Evidence 5 C) If discontinued or reduced, beta blockers should be reinstated before the patient is discharged. In general, doses should be uptitrated to the previous well-tolerated dose as soon as safely possible (Strength of Evidence 5B)7.12 The routine administration of an ARB is not recommended in addition to ACE The routine administration of an ARB is not recommended in addition to ACE Modification of terminology (previous inhibitor and beta blocker therapy in patients with recent acute MI and LV inhibitor and beta blocker therapy in patients with a recent acute MI and (‘‘LV dysfunction’’ changed to 7.13) dysfunction. (Strength of Evidence 5 A) reduced LVEF. (Strength of Evidence 5 A) ‘‘reduced LVEF’’)7.13 The addition of an ARB should be considered in patients with HF due to New recommendation reduced LVEF who have persistent symptoms or progressive worsening despite optimized therapy with an ACE inhibitor and beta blocker. (Strength of Evidence 5 A)7.14 Administration of an aldosterone antagonist is recommended for patients with Administration of an aldosterone antagonist is recommended for patients with Modification of terminology 518 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 NYHA class IV or class III, previously class IV, HF from LV systolic NYHA class IV (or class III, previously class IV) HF from reduced LVEF (‘‘LV systolic dysfunction’’ dysfunction (LVEF #35%) while receiving standard therapy, including (!35%) while receiving standard therapy, including diuretics. (Strength of changed to ‘‘reduced LVEF’’) diuretics. (Strength of Evidence 5 A) Evidence 5 A)7.15 Administration of an aldosterone antagonist should be considered in patients Administration of an aldosterone antagonist should be considered in patients Addition of history of diabetes after an acute MI, with clinical HF signs and symptoms and an LVEF following an acute MI, with clinical HF signs and symptoms or history of mellitus to criteria for therapy !40%. Patients should be on standard therapy, including an ACE inhibitor diabetes mellitus, and an LVEF !40%. Patients should be on standard (or ARB) and a b-blocker. (Strength of Evidence 5 A) therapy, including an ACE inhibitor (or ARB) and a beta blocker. (Strength of Evidence 5 A)7.16 No changes7.17 No changes7.18 No changes7.19 A combination of hydralazine and isosorbide dinitrate is recommended as part A combination of hydralazine and isosorbide dinitrate is recommended as part Modification of terminology of standard therapy in addition to beta blockers and ACE inhibitors for of standard therapy in addition to beta blockers and ACE inhibitors for (‘‘LV systolic dysfunction’’ African Americans with LV systolic dysfunction. African Americans with HF and reduced LVEF. changed to ‘‘reduced LVEF’’)  NYHA III or IV HF (Strength of Evidence 5 A)  NYHA III or IV HF (Strength of Evidence 5 A)  NYHA II HF (Strength of Evidence 5 B)  NYHA II HF (Strength of Evidence 5 B) (See Section 15: Special Pop- (See Section 15 Special Populations) ulations)7.20 A combination of hydralazine and isosorbide dinitrate may be considered in A combination of hydralazine and isosorbide dinitrate may be considered in Modification of terminology noneAfrican American patients with LV systolic dysfunction who remain non-African-American patients with HF and reduced LVEF who remain (‘‘LV systolic dysfunction’’ symptomatic despite optimized standard therapy. (Strength of Evidence 5 symptomatic despite optimized standard therapy. (Strength of Evidence changed to ‘‘reduced LVEF’’) C) 5 C)
    • 7.21 Additional pharmacologic therapy should be considered in patients with HF Additional pharmacologic therapy should be considered in patients with HF Modification of terminology due to systolic dysfunction who have persistent symptoms or progressive and reduced LVEF who have persistent symptoms or progressive worsening (‘‘systolic dysfunction’’ worsening despite optimized therapy with an ACE inhibitor and beta despite optimized therapy with an ACE inhibitor and beta blocker. The changed to ‘‘reduced LVEF’’); blocker. The choice of specific agent will be influenced by clinical choice of specific agent will be influenced by clinical considerations, addition of post-MI HF under considerations, including renal function status, chronic serum potassium including renal function status, chronic serum potassium concentration, aldosterone antagonists concentration, blood pressure, and volume status. The triple combination of blood pressure, and volume status. The triple combination of an ACE an ACE inhibitor, an ARB, and an aldosterone antagonist is not inhibitor, an ARB, and an aldosterone antagonist is not recommended recommended because of the high risk of hyperkalemia. (Strength of because of the high risk of hyperkalemia. (Strength of Evidence 5 C) Evidence 5 C)  Addition of an ARB. (Strength of Evidence 5 A)  Addition of an ARB. (Strength of Evidence 5 A)  Addition of an aldosterone antagonist:  Addition of an aldosterone antagonist: Bfor severe HF (Strength of Evidence 5A) BFor severe HF (Strength of Evidence 5 A) Bfor moderate HF (Strength of Evidence 5 C) B For moderate HF (Strength of Evidence 5 C) B for post-MI HF (Strength of Evidence 5 A)  Addition of the combination of hydralazine/isosorbide dinitrate:  Addition of the combination of hydralazine/isosorbide dinitrate: B For African Americans (Strength of Evidence 5A) B for African Americans (Strength of Evidence 5 A) B For others (Strength of Evidence 5 C) B for others (Strength of Evidence 5 C)7.22 Additional pharmacological therapy should be considered in patients with HF Additional pharmacological therapy should be considered in patients with HF Modification of terminology due to systolic dysfunction who are unable to tolerate a beta blocker and and reduced LVEF who are unable to tolerate a beta blocker and have (‘‘systolic dysfunction’’ have persistent symptoms or progressive worsening despite optimized persistent symptoms or progressive worsening despite optimized therapy changed to ‘‘reduced LVEF’’) therapy with an ACE inhibitor. The choice of specific agent will be with an ACE inhibitor. The choice of specific agent will be influenced by influenced by clinical considerations, including renal function status, clinical considerations, including renal function status, chronic serum chronic serum potassium concentration, blood pressure and volume status. potassium concentration, blood pressure and volume status. The triple The triple combination of an ACE inhibitor, an ARB, and an aldosterone combination of an ACE inhibitor, an ARB, and an aldosterone antagonist is antagonist is not recommended due to the high risk of hyperkalemia. not recommended due to the high risk of hyperkalemia. (Strength of (Strength of Evidence 5 C) Evidence 5 C)  Addition of an ARB. (Strength of Evidence 5 C)  Addition of an ARB. (Strength of Evidence 5 C)  Addition of an aldosterone antagonist:  Addition of an aldosterone antagonist: Bfor severe HF (Strength of Evidence 5 C) Bfor severe HF (Strength of Evidence 5 C) Bfor moderate HF (Strength of Evidence 5 C) Bfor moderate HF (Strength of Evidence 5 C)  Addition of the combination of hydralazine/isosorbide dinitrate:  Addition of the combination of hydralazine/isosorbide dinitrate: B For African-Americans (Strength of Evidence 5 C) B for African Americans (Strength of Evidence 5 C) B for others (Strength of Evidence 5 C) B for others (Strength of Evidence 5 C)7.23 No changes7.24 The initial dose of diuretic may be increased as necessary to relieve The initial dose of diuretic may be increased as necessary to relieve Modification of terminology congestion. Restoration of normal volume status may require multiple congestion. Restoration of normal volume status may require multiple (‘‘noncompliance’’ changed to adjustments over many days and occasionally weeks in patients with severe adjustments over many days and occasionally weeks in patients with severe ‘‘nonadherence’’) fluid overload evidenced by massive edema or ascites. After a diuretic effect fluid overload evidenced by massive edema or ascites. After a diuretic effect is achieved with short acting loop diuretics, increasing administration is achieved with short-acting loop diuretics, increasing administration frequency to twice or even 3 times per day will provide more diuresis with frequency to twice or even 3 times per day will provide more diuresis with less physiologic perturbation than larger single doses. (Strength of Evidence less physiologic perturbation than larger single doses. (Strength of Evidence 5 B) 5 B) Executive Summary: Heart Failure Practice Guideline Oral torsemide may be considered in patients in whom poor absorption of Oral torsemide may be considered in patients in whom poor absorption of oral medication or erratic diuretic effect may be present, particularly those oral medication or erratic diuretic effect may be present, particularly those  with right-sided HF and refractory fluid retention despite high doses of other with right-sided HF and refractory fluid retention despite high doses of other loop diuretics. (Strength of Evidence 5 C) loop diuretics. (Strength of Evidence 5 C) Intravenous administration of diuretics may be necessary to relieve Intravenous administration of diuretics may be necessary to relieve HFSA congestion. (Strength of Evidence 5 A) congestion. (Strength of Evidence 5 A) Diuretic refractoriness may represent patient noncompliance, a direct effect Diuretic refractoriness may represent patient nonadherence, a direct effect of diuretic use on the kidney, or progression of underlying cardiac of diuretic use on the kidney, or progression of underlying cardiac 519 dysfunction. dysfunction. (continued on next page)
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments7.25 No changes7.26 Careful observation for the development of side effects, including electrolyte Careful observation for the development of side effects, including electrolyte Addition of worsening renal abnormalities, symptomatic hypotension, and renal dysfunction, is abnormalities, symptomatic hypotension, renal dysfunction, or worsening function to list of potential side recommended in patients treated with diuretics, especially when used at renal function, is recommended in patients treated with diuretics, especially effects high doses and in combination. Patients should undergo routine laboratory when used at high doses and in combination. Patients should undergo studies and clinical examination as dictated by their clinical response. routine laboratory studies and clinical examination as dictated by their (Strength of Evidence 5 B) clinical response. (Strength of Evidence 5 B)7.27 No changes7.28 No changes7.29 Digoxin should be considered for patients with LV systolic dysfunction (LVEF Digoxin may be considered to improve symptoms in patients with reduced Modification from ‘‘should be #40%) who have signs or symptoms of HF while receiving standard LVEF (LVEF #40%) who have signs or symptoms of HF while receiving considered’’ to ‘‘may be therapy, including ACE inhibitors and beta blockers: standard therapy, including ACE inhibitors and beta blockers: considered’’, and change in NYHA class II-III (Strength of Evidence 5 A)  NYHA class II-III (Strength of Evidence 5 B) Strength of Evidence NYHA class IV (Strength of Evidence 5 B)  NYHA class IV (Strength of Evidence 5 C)7.30 It is recommended that the dose of digoxin, which should be based on lean It is recommended that the dose of digoxin, which should be based on lean Addition of a lower serum body mass, renal function and concomitant medications, should be 0.125 body mass, renal function, and concomitant medications, should be 0.125 concentration range (0.7-0.9 mg daily in the majority of patients and the serum digoxin level should be mg daily in the majority of patients and the serum digoxin level should be ng/ml), and change in strength !1.0 ng/mL. (Strength of Evidence 5 C) !1.0 ng/mL, generally 0.7-0.9 ng/mL. (Strength of Evidence 5 B) of evidence from C to B 520 Journal of Cardiac Failure Vol. 16 No. 6 June 20107.31 Adequate control of the ventricular response to atrial fibrillation in patients Digoxin should be considered for achieving adequate control of the ventricular Modification from ‘‘is with HF is recommended. (Level of Evidence 5 B) response to atrial fibrillation in patients with HF. (Strength of Evidence 5 recommended’’ to ‘‘should be B) considered’’7.32 No changes7.33 Treatment with warfarin (goal INR 2.0e3.0) is recommended for all patients Treatment with warfarin (goal international normalized ratio [INR] 2.0-3.0) is Addition of persistent or long- with HF and chronic or documented paroxysmal atrial fibrillation (Strength recommended for all patients with HF and chronic or documented standing atrial fibrillation of Evidence 5 A) or a history of systemic or pulmonary emboli, including paroxysmal, persistent, or long-standing atrial fibrillation (Strength of stroke or transient ischemic attack, (Strength of Evidence 5 C) unless Evidence 5 A) or a history of systemic or pulmonary emboli, including contraindicated. stroke or transient ischemic attack (Strength of Evidence 5 C), unless contraindicated.7.34 No changesPrevious Deleted from current guideline 7.357.35 Long-term treatment with an antithrombotic agent is recommended for Long-term treatment with an antiplatelet agent, generally aspirin in doses of Modification of terminology (previous patients with HF from ischemic cardiomyopathy, whether or not they are 75 to 81 mg, is recommended for patients with HF due to ischemic from ‘‘antithrombotic’’ to 7.36) receiving ACE inhibitors. (Strength of Evidence 5 B) cardiomyopathy, whether or not they are receiving ACE inhibitors. ‘‘antiplatelet’’; addition of Aspirin is recommended in most patients for whom anticoagulation is not (Strength of Evidence 5 B) recommended doses for specifically indicated because of its proven efficacy in non-HF patients with Warfarin (goal INR 2.0-3.0) and clopidogrel (75 mg) also have prevented aspirin. ischemic heart disease, its convenience, and lower cost. Lower doses of vascular events in post-MI patients and may be considered as alternatives to INR range changed to 2.0-3.0 aspirin (75 or 81 mg) may be preferable because data from 2 trials suggest aspirin. (Strength of Evidence 5 B) more frequent worsening of HF at higher doses. (Strength of Evidence 5 C) Warfarin (goal INR 2.0e3.5) and clopidogrel (75 mg) have also prevented vascular events in post MI patients and may be considered as alternatives to aspirin. (Strength of Evidence 5 B)
    • 7.36 Routine use of aspirin is not recommended in patients with HF not from Routine use of aspirin is not recommended in patients with HF without Modification of terminology (previous ischemic cardiomyopathy and without other evidence of atherosclerotic atherosclerotic vascular disease. (Strength of Evidence 5 C) 7.37) vascular disease. (Strength of Evidence 5 C)Previous Deleted from current guideline; 7.38 addressed in recommendation 7.357.37 No changes (previous 7.39)7.38 In patients with HF and an implantable cardioverter defibrillator (ICD), In patients with HF and an ICD, amiodarone may be considered to reduce the Modification of wording (previous amiodarone may be considered to reduce the frequency of repetitive frequency of recurrent symptomatic arrhythmias causing ICD shocks. 7.40) discharges. (Strength of Evidence 5 C) (Strength of Evidence 5 C)7.39 It is recommended that patients taking amiodarone therapy and digoxin or It is recommended that when amiodarone therapy is initiated, the potential for Modification of wording (previous warfarin generally have their maintenance doses of many commonly used interactions with other drugs be reviewed. The maintenance doses of 7.41) agents, such as digoxin, warfarin, and statins, reduced when amiodarone is digoxin, warfarin, and some statins should be reduced when amiodarone is initiated and then carefully monitored for the possibility of adverse drug initiated and then carefully monitored. Adjustment in doses of these drugs interactions. Adjustment in doses of these drugs and laboratory assessment and laboratory assessment of drug activity or serum concentration after of drug activity or serum concentration after initiation of amiodarone is initiation of amiodarone is recommended. (Strength of Evidence 5 A) recommended. (Strength of Evidence 5 A)7.40 Routine use of amiodarone therapy for asymptomatic arrhythmias that are not New recommendation felt to contribute to HF or ventricular dysfunction is not recommended. (Strength of Evidence 5 B)7.41 n-3 polyunsaturated fatty acids (PUFA) may be considered to reduce mortality New recommendation in HF patients with NYHA class II-IV symptoms and reduced LVEF. (Strength of Evidence 5 B) Section 8: Disease Management, Advance Directives, and End-of-Life Care in Heart Failure8.1 It is recommended that patients with HF and their family members or It is recommended that patients with HF and their family members or Deletion of NYHA specific caregivers receive individualized education and counseling that emphasizes caregivers receive individualized education and counseling that emphasizes portion of the self-care. This education and counseling should be delivered by providers self-care. This education and counseling should be delivered by providers recommendation; modification using a team approach in which nurses with expertise in HF management using a team approach in which nurses with expertise in HF management of wording provide the majority of education and counseling, supplemented by provide the majority of education and counseling, supplemented by physician input and, when available and needed, input from dietitians, physician input and, when available and needed, input from dietitians, pharmacists, and other health care providers. All HF patients benefit from pharmacists, and other health care providers. (Strength of Evidence 5 B) education and counseling, but patients in NYHA functional class III or IV Teaching is not sufficient without skill building and specification of critical need the most intensive education, whereas patients in NYHA I or II need target behaviors. It is recommended that essential elements of patient less intensive education. (Strength of Evidence 5 B) education (with associated skills) are utilized to promote self-care as shown Teaching is not sufficient without skill building and specification of critical in Table 8.1. (Strength of Evidence 5 B) target behaviors. Essential elements of patient education to promote self- care with associated skills are shown in Table 8.1. (Strength of Evidence 5 B) Executive Summary: Heart Failure Practice Guideline (continued on next page)  HFSA 521
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments8.2 It is recommended that patients’ literacy, cognitive status, psychologic state, It is recommended that patients’ literacy, cognitive status, psychological state, Deletion of description of culture, and access to social and financial resources be taken into account culture, and access to social and financial resources be taken into account interventions; modification of for optimal education and counseling. Because cognitive impairment and for optimal education and counseling. Because cognitive impairment and Strength of Evidence from C to depression are common in HF and can seriously interfere with learning, depression are common in HF and can seriously interfere with learning, B patients should be screened for these. Appropriate interventions, such as patients should be screened for these. Patients found to be cognitively supportive counseling and pharmacotherapy, are recommended for those impaired need additional support to manage their HF. (Strength of Evidence patients found to be depressed. Patients found to be cognitively impaired 5 B) need additional support to manage their HF. (Strength of Evidence 5 C)8.3 No changes8.4 It is recommended that the frequency and intensity of patient education and It is recommended that the frequency and intensity of patient education and Modification of wording counseling vary according to the stage of illness. Patients in advanced HF counseling vary according to the stage of the illness. Patients in advanced or with persistent difficulty adhering to the recommended regimen require HF or persistent difficulty adhering to the recommended regimen require the the most eduction and counseling. Patients should be offered a variety of most education and counseling. Patients should be offered a variety of options for learning about HF according to their individual preferences: options for learning about HF according to their individual preferences: videotape, one-on-one or group discussion, reading materials, translators, videotape, one-on-one or group discussion, reading materials, translators, telephone calls, mailed information, internet, visits. Repeated exposure to telephone calls, mailed information, internet, visits. Repeated exposure to material is essential because a single session is never sufficient. (Strength of material is recommended because a single session is never sufficient. Evidence 5 B) (Strength of Evidence 5 B)8.5 No changes 522 Journal of Cardiac Failure Vol. 16 No. 6 June 20108.6 No changes8.7 Patients recently hospitalized for HF and other patients at high risk should be Patients recently hospitalized for HF and other patients at high risk for HF Addition of poor health literacy considered for referral to a comprehensive HF disease management program decompensation should be considered for comprehensive HF disease that delivers individualized care. High-risk patients include those with renal management. High-risk patients include those with renal insufficiency, low insufficiency, low output state, diabetes, chronic obstructive pulmonary output state, diabetes, chronic obstructive pulmonary disease, persistent disease, persistent NYHA class III or IV symptoms, frequent hospitalization NYHA class III or IV symptoms, frequent hospitalization for any cause, for any cause, multiple active comorbidities, or a history of depression, multiple active comorbidities, or a history of depression, cognitive cognitive impairment, or persistent nonadherence to therapeutic regimens. impairment, inadequate social support, poor health literacy, or persistent (Strength of Evidence 5 A) nonadherence to therapeutic regimens. (Strength of Evidence 5 A)8.8 No changes8.9 No changes8.10 No changes8.11 Patient and family or caregiver discussions about quality of life and prognosis It is recommended that patient and family or caregiver discussions about Modification of wording are recommended as part of the disease management of HF. (Strength of quality of life and prognosis be included in the disease management of HF. Evidence 5 C) (Strength of Evidence 5 C)
    • 8.12 It is recommended that the patient’s status be optimized medically and It is recommended that Addition of criteria for end of life psychologically before discussing the possibility that end-of-life care is  Seriously ill patients with HF and their families be educated to understand care indicated. The decision to declare a patient as an appropriate candidate for that patients with HF are at high risk of death, even while aggressive ef- end-of-life care should be made by physicians experienced in the care of forts are made to prolong life. patients with HF. End-of-life management should be coordinated with the  Patients with HF be made aware that HF is potentially life-limiting, but patient’s primary care physician. As often as possible, discussions regarding that pharmacologic and device therapies and self-management can end-of-life care should be initiated while the patient is still capable of prolong life. In most cases, chronic HF pharmacologic and device participating in decision making. (Strength of Evidence 5 C) therapies should be optimized as indicated before identifying that patients are near end-of-life.  Identification of end-of-life in a patient should be made in collaboration with clinicians experienced in the care of patients with HF when possible.  End-of-life management should be coordinated with the patient’s primary care physician.  As often as possible, discussions regarding end-of-life care should be initiated while the patient is still capable of participating in decision- making. (Strength of Evidence 5 C)8.13 End-of-life care should be considered in patients who have advanced, End-of-life care should be considered in patients who have advanced, Addition of cardiac device to list persistent HF with symptoms at rest despite repeated attempts to optimize persistent HF with symptoms at rest despite repeated attempts to optimize of optimization therapies; pharmacologic and nonpharmacologic therapy, as evidenced by one or more pharmacologic, cardiac device, and other therapies, as evidenced by 1 or modification of strength of of the following: more of the following: evidence  Frequent hospitalizations (3 or more per year)  HF hospitalization (Strength of Evidence 5 B)  Chronic poor quality of life with inability to accomplish activities of daily  Chronic poor quality of life with minimal or no ability to accomplish living activities of daily living (Strength of Evidence 5 C)  Need for intermittent or continuous intravenous support  Need for continuous intravenous inotropic therapy support (Strength of  Consideration of assist devices as destination therapy Evidence 5 B) (Strength of Evidence 5 C)8.14 It is recommended that end-of-life care strategies be individualized, include It is recommended that end-of-life care strategies be individualized and Addition of information effective symptom management, and avoid unnecessary testing and include core HF pharmacologic therapies, effective symptom management regarding end-of-life care interventions. (Strength of Evidence 5 C) and comfort measures, while avoiding unnecessary testing. New life- strategies prolonging interventions should be discussed with patients and care-givers with careful discussion of whether they are likely to improve symptoms. (Strength of Evidence 5 C)8.15 It is recommended that, as part of end-of life-care, patients and their families/ It is recommended that a specific discussion about resuscitation be held in the Addition of information caregivers be given specific directions concerning their response to clinical context of planning for overall care and for emergencies with all patients regarding resuscitation events if they decide against resuscitation. Inactivation of an implantable with HF. The possibility of SCD for patients with HF should be defibrillation device should be discussed. (Strength of Evidence 5 C) acknowledged. Specific plans to reduce SCD (for example with an ICD) or to allow natural death should be based on the individual patient’s risks and preferences for an attempt at resuscitation with specific discussion of risks and benefits of inactivation the ICD. Preferences for attempts at resuscitation and plans for approach to care should be readdressed at turning points in the patient’s course or if potentially life-prolonging interventions are considered. (Strength of Evidence 5 C)8.16 It is recommended that, as part of end-of-life care, patients and their families/ New recommendation caregivers have a plan to manage a sudden decompensation, death, or Executive Summary: Heart Failure Practice Guideline progressive decline. Inactivation of an implantable defibrillation device  should be discussed in the context of allowing natural death at end of life. A process for deactivating defibrillators should be clarified in all settings in which patients with HF receive care. (Strength of Evidence 5 C) HFSA (continued on next page) 523
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments8.17 Patients with HF undergoing end-of-life care may be considered for hospice Patients with HF receiving end-of-life care should be considered for Modification from ‘‘may be services that can be delivered in the home, a hospital setting, or a special enrollment in hospice that can be delivered in the home, a nursing home, or considered’’ to ‘‘should be hospice unit. (Strength of Evidence 5 C) a special hospice unit. (Strength of Evidence 5 C) considered’’Previous Deleted recommendations; 8.16 and portions of these 8.18 recommendations have been incorporated into recommendations 8.15 and 8.16 Section 9: Electrophysiology Testing and the Use of Devices in Heart Failure9.1 It is recommended that the decision to undertake electrophysiologic It is recommended that the decision to undertake electrophysiologic Modification/clarification of intervention be made in light of functional status and prognosis based on intervention, including ICD implantation, be made in light of functional wording severity of underlying HF and comorbid conditions. If LV dysfunction is status and prognosis based on severity of underlying HF and comorbid a reason for recommending electrophysiologic intervention, LV function conditions. If an ICD is considered due to LV dysfunction which is of recent should be re-assessed, ideally after 3e6 months of optimal medical therapy. onset, LV function should be reassessed, ideally after 3-6 months of optimal (Strength of Evidence 5 C) medical therapy. (Strength of Evidence 5 C)9.2 Immediate evaluation is recommended in patients with HF who present with Immediate evaluation is recommended in patients with HF who present with Modification/clarification of syncope. In the absence of a clear identifiable noncardiac cause, patients syncope. In the absence of a clear identifiable noncardiac cause, wording should be referred for electrophysiologic evaluation. (Strength of consultation with an EP specialist should be obtained. (Strength of Evidence 524 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 Evidence 5 C) 5 C)9.3 No changes9.4 In patients with or without concomitant coronary artery disease (including Revision of LVEF criteria and a prior MI O1 month ago): a. Prophylactic ICD placement should be considered in patients with an strength of evidence based on a) Prophylactic ICD placement should be considered (LVEF #30%) and LVEF #35% and mild to moderate HF symptoms: etiology may be considered (LVEF 31e35%) for those with mild to moderate HF symptoms (NYHA II-III). (Strength of Evidence 5 A) See  Ischemic etiology (Strength of Evidence 5 A) Recommendation 9.1 for additional criteria.  Non-ischemic etiology (Strength of Evidence 5 B) b) Concomitant ICD placement should be considered in patients undergoing See Recommendation 9.1 for additional criteria. implantation of a biventricular pacing device according to the criteria in b. In patients who are undergoing implantation of a biventricular pacing Recommendations 9.7e9.8. (Strength of Evidence 5 B) See Recom- device according to the criteria in recommendations 9.7-9.8, use of a de- mendation 9.1 for additional criteria. vice that provides defibrillation should be considered. (Strength of Evi- dence 5 B) See Recommendation 9.1 for additional criteria.9.5 ICD placement is not recommended in chronic, severe refractory HF when ICD placement is not recommended in chronic, severe refractory HF when Addition of life expectancy there is no reasonable expectation for improvement. (Strength of Evidence there is no reasonable expectation for improvement or in patients with a life criterion to recommendation 5 C) expectancy of less than 1 year. (Strength of Evidence 5 C)9.6 ICD implantation is recommended for survivors of cardiac arrest from ICD implantation is recommended for survivors of cardiac arrest from Revision of MI criteria ventricular fibrillation or hemodynamically unstable sustained ventricular ventricular fibrillation or hemodynamically unstable sustained VT that is not tachycardia without evidence of acute MI or if the event occurs more than due to a transient, potentially reversible cause, such as acute MI. (Strength 48 hours after the onset of infarction in the absence of a recurrent ischemic of Evidence 5 A) event. (Strength of Evidence 5 A)9.7 Biventricular pacing therapy should be considered for patients with sinus Biventricular pacing therapy is recommended for patients in sinus rhythm with Modification from ‘‘should be rhythm, a widened QRS interval ($120 ms) and severe LV systolic a widened QRS interval ($120 ms) and severe LV systolic dysfunction considered’’ to ‘‘is dysfunction (LVEF #35% with LV dilatation O5.5 cm) who have LVEF (# 35%) who have persistent, moderate to severe HF (NYHA III) recommended’’; removal of persistent, moderate to severe HF (NYHA III) despite optimal medical despite optimal medical therapy. (Strength of Evidence 5 A) LV dimension criterion therapy. (Strength of Evidence 5 A)
    • 9.8 Biventricular pacing therapy may be considered for patients with atrial New recommendation fibrillation with a widened QRS interval ($120 ms) and severe LV systolic dysfunction LVEF #35% who have persistent, moderate to severe HF (NYHA III) despite optimal medical therapy. (Strength of Evidence 5 B)9.9 Selected ambulatory NYHA IV patients may be considered for biventricular Selected ambulatory NYHA IV patients in sinus rhythm with QRS $ 120 ms Additional criteria for patient (Previous pacing therapy. (Strength of Evidence 5 B) and LV systolic dysfunction may be considered for biventricular pacing selection 9.8) therapy. (Strength of Evidence 5 B)9.10 Biventricular pacing therapy is not recommended in patients who are Biventricular pacing therapy may be considered in patients with reduced LVEF Modification from ‘‘is not (previous asymptomatic or have mild HF symptoms. (Strength of Evidence 5 C) and QRS R 150 ms who have NYHA I or II HF symptoms. (Strength of recommended’’ to ‘‘may be 9.9) Evidence 5 B) considered’’; modification of strength of evidence from C to B; additional criteria for patient selection9.11 In patients with reduced LVEF who require chronic pacing and in whom New recommendation frequent ventricular pacing is expected, biventricular pacing may be considered. (Strength of Evidence 5 C)9.12 No changes (previous 9.10) Section 10: Surgical Approaches to the Treatment of Heart Failure10.1 No changes10.2 No changes10.3 No changes10.4 No changes10.5 No changes10.6 No changes10.7 Patients with refractory HF and hemodynamic instability, and/or compromised New recommendation end-organ function, with relative contraindications to cardiac transplantation or permanent mechanical circulatory assistance expected to improve with time or restoration of an improved hemodynamic profile should be considered for urgent mechanical circulatory support as a ‘‘bridge to decision.’’ These patients should be referred to a center with expertise in the management of patients with advanced HF. (Strength of Evidence 5 C) Section 11: Evaluation and Management of Patients with Heart Failure and Preserved LVEF11.1 Careful attention to differential diagnosis is recommended in patients with HF Careful attention to differential diagnosis is recommended in patients with HF Addition of cardiac Executive Summary: Heart Failure Practice Guideline and preserved LVEF to distinguish among a variety of cardiac disorders, and preserved LVEF to distinguish among a variety of cardiac disorders, catheterization to list of because treatments may differ. These various entities may be distinguished because treatments may differ. These various entities may be distinguished diagnostic tools, modification  based on echocardiography, electrocardiography, and stress imaging (via based on echocardiography, electrocardiography, and stress imaging (via of Figure 11.3 and addition of exercise or pharmacologic means using myocardial perfusion or exercise or pharmacologic means, using myocardial perfusion or Figures 11.1 and 11.2. echocardiographic imaging). See algorithm in Figure 11.1 for a detailed echocardiographic imaging) and cardiac catheterization. See Figures 11.1, HFSA approach to differential diagnosis. (Strength of Evidence 5 C) 11.2, and 11.3 for guidance to a differential diagnosis. (Strength of Evidence 5 C) 525 (continued on next page)
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments11.2 Evaluation for the possibility of ischemic heart disease and inducible Evaluation for ischemic heart disease and inducible myocardial ischemia is Minor wording modifications myocardial ischemia is recommended in patients with HF and preserved recommended in patients with HF and preserved LVEF (see Section 13). LVEF. (Strength of Evidence 5 C) (Strength of Evidence 5 C)11.3 Aggressive blood pressure management is recommended in patients with HF Blood pressure monitoring is recommended in patients with HF and preserved Modification of terminology and preserved LVEF (Section 14, Recommendation 14.15). (Strength of LVEF (Section 14, Recommendation 14.1). (Strength of Evidence 5 C) (‘‘aggressive blood pressure Evidence 5 C) management’’ changed to ‘‘blood pressure monitoring’’)11.4 No changes11.5 No changes11.6 ARBs or ACE inhibitors should be considered in patients with HF and In the absence of other specific indications for these drugs, ARBs or ACE Modification from ‘‘should be preserved LVEF. (Strength of evidence 5 B) inhibitors may be considered in patients with HF and preserved LVEF. considered’’ to ‘‘may be  ARBs (Strength of Evidence 5 B)  ARBs (Strength of Evidence 5 C) considered’’; modification of  ACE inhibitors (Strength of Evidence 5 C)  ACE inhibitors (Strength of Evidence 5 C) strength of evidence for ARBs from B to C11.7 No changes11.8 No changes 526 Journal of Cardiac Failure Vol. 16 No. 6 June 201011.9 Calcium channel blockers should be considered in patients with: Calcium channel blockers should be considered in patients with HF and Modification of wording  Atrial fibrillation requiring control of ventricular rate in whom b-blockers preserved LVEF and: regarding beta blocker have proven inadequate for this purpose because of intolerance. In these  Atrial fibrillation requiring control of ventricular rate and intolerance to intolerance patients, diltiazem or verapamil should be considered. (Strength of Evi- beta blockers. In these patients, diltiazem or verapamil should be con- dence 5 C) sidered. (Strength of Evidence 5 C)  Symptom-limiting angina. (Strength of Evidence 5 A)  Symptom-limiting angina. (Strength of Evidence 5 A)  Hypertension. Amlodipine should be considered. (Strength of Evidence 5  Hypertension. (Strength of Evidence 5 C) C)11.10 Measures to restore and maintain sinus rhythm should be considered in Measures to restore and maintain sinus rhythm may be considered in patients Modification from ‘‘should be patients who have symptomatic atrial flutter-fibrillation, but this decision who have symptomatic atrial flutter-fibrillation and preserved LVEF, but this considered’’ to ‘‘may be should be individualized. (Strength of Evidence 5 C) decision should be individualized. (Strength of Evidence 5 C) considered’’ Section 12: Evaluation and Management of Patients with Acute Decompensated Heart Failure12.1 The diagnosis of decompensated HF should be based primarily on signs and The diagnosis of ADHF should be based primarily on signs and symptoms. Modification of BNP symptoms. (Strength of Evidence 5 C) (Strength of Evidence 5 C) recommendation from ‘‘should When the diagnosis is uncertain, determination of BNP or NT-proBNP When the diagnosis is uncertain, determination of BNP or NT-proBNP be considered’’ to ‘‘is concentration should be considered in patients being evaluated for dyspnea concentration is recommended in patients being evaluated for dyspnea who recommended’’ who have signs and symptoms compatible with HF. (Strength of Evidence have signs and symptoms compatible with HF. (Strength of Evidence 5 A) 5 A) The natriuretic peptide concentration should not be interpreted in isolation, The natriuretic peptide concentration should not be interpreted in isolation, but in the context of all available clinical data bearing on the diagnosis of but in the context of all available clinical data bearing on the diagnosis of HF, and with the knowledge of cardiac and non-cardiac factors that can raise HF. or lower natriuretic peptide levels.12.2 No changes
    • 12.3 No changes12.4 No changes12.5 No changes12.6 It is recommended that diuretics be administered at doses needed to produce It is recommended that diuretics be administered at doses needed to produce Addition of serum electrolytes a rate of diuresis sufficient to achieve optimal volume status with relief of a rate of diuresis sufficient to achieve optimal volume status with relief of signs and symptoms of congestion (edema, elevated JVP, dyspnea), without signs and symptoms of congestion (edema, elevated JVP, dyspnea), without inducing an excessively rapid reduction in intravascular volume, which may inducing an excessively rapid reduction in 1) intravascular volume, which result in symptomatic hypotension and/or worsening renal function. may result in symptomatic hypotension and/or worsening renal function, or (Strength of Evidence 5 C) 2) serum electrolytes, which may precipitate arrhythmias or muscle cramps. (Strength of Evidence 5 C)12.7 No changes12.8 Monitoring of daily weights, intake, and output is recommended to assess Monitoring of daily weights, intake, and output is recommended to assess Addition of criterion for catheter clinical efficacy of diuretic therapy. Routine use of a Foley catheter is not clinical efficacy of diuretic therapy. Routine use of a Foley catheter is not placement recommended for monitoring volume status. However, placement of recommended for monitoring volume status. However, placement of a catheter is recommended when close monitoring of urine output is needed. a catheter is recommended when close monitoring of urine output is needed (Strength of Evidence 5 C) or if a bladder outlet obstruction is suspected of contributing to worsening renal function. (Strength of Evidence 5 C)12.9 Careful observation for development of a variety of side effects, including Careful observation for development of a variety of side effects, including Addition of gout as side effect renal dysfunction, electrolyte abnormalities and symptomatic hypotension, renal dysfunction, electrolyte abnormalities, symptomatic hypotension, and is recommended in patients treated with diuretics, especially when used at gout is recommended in patients treated with diuretics, especially when high doses and in combination. Patients should undergo routine laboratory used at high doses and in combination. Patients should undergo routine studies and clinical examination as dictated by their clinical response. laboratory studies and clinical examination as dictated by their clinical (Strength of Evidence 5 C) response. (Strength of Evidence 5 C) Serum potassium and magnesium levels should be monitored at least daily It is recommended that serum potassium and magnesium levels should be Wording modified and maintained in the normal range. More frequent monitoring may be monitored at least daily and maintained in the normal range. More frequent necessary when diuresis is rapid. (Strength of Evidence 5 C) monitoring may be necessary when diuresis is rapid. (Strength of Evidence Overly rapid diuresis may be associated with severe muscle cramps, which 5 C) should be treated with potassium replacement if indicated. (Strength of Overly rapid diuresis may be associated with severe muscle cramps. If Evidence 5 C) indicated, treatment with potassium replacement is recommended. (Strength of Evidence 5 C)12.10 No changes12.11 When congestion fails to improve in response to diuretic therapy, the following When congestion fails to improve in response to diuretic therapy, the following Addition of re-evaluation of options should be considered: options should be considered: congestion  Sodium and fluid restriction,  Re-evaluating presence/absence of congestion  Increased doses of loop diuretic,  Sodium and fluid restriction,  Continuous infusion of a loop diuretic, or  Increasing doses of loop diuretic,  Addition of a second type of diuretic orally (metolazone or spironolac-  Continuous infusion of a loop diuretic, or tone) or intravenously (chlorothiazide).  Addition of a second type of diuretic orally (metolazone or spironolac-  A fifth option, ultrafiltration, may be considered. (Strength of Evidence 5 tone) or intravenously (chlorothiazide). C) Another option, ultrafiltration, may be considered. (Strength of Evidence Executive Summary: Heart Failure Practice Guideline 5 C) 12.12 A low-sodium diet (2 g daily) is recommended, as is supplemental oxygen, as A low sodium diet (2 g daily) is recommended for most hospitalized patients. Deletion of supplemental oxygen needed for hypoxemia. (Strength of Evidence 5 C) (Strength of Evidence 5 C) (moved to recommendation In patients with recurrent or refractory volume overload, stricter sodium In patients with recurrent or refractory volume overload, stricter sodium 12.14) restriction may be considered. (Strength of Evidence 5 C) restriction may be considered. (Strength of Evidence 5 C) HFSA (continued on next page) 527
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments12.13 No changes12.14 Routine administration of supplemental oxygen in the absence of hypoxia is Routine administration of supplemental oxygen in the presence of hypoxia is Addition of recommendation for not recommended. (Strength of Evidence 5 C) recommended. (Strength of Evidence 5 C) oxygen in the presence of Routine administration of supplemental oxygen in the absence of hypoxia is hypoxemia not recommended. (Strength of Evidence 5 C)12.15 Use of non-invasive positive pressure ventilation may be considered for New recommendation severely dyspneic patients with clinical evidence of pulmonary edema. (Strength of Evidence 5 A)12.16 Venous thromboembolism prophylaxis with low dose unfractionated heparin, New recommendation low molecular weight heparin, or fondaparinux to prevent proximal deep venous thrombosis and pulmonary embolism is recommended for patients who are admitted to the hospital with ADHF and who are not already anticoagulated and have no contraindication to anticoagulation. (Strength of Evidence 5 B) Venous thromboembolism prophylaxis with a mechanical device (intermittent pneumatic compression devices or graded compression stockings) to prevent proximal deep venous thrombosis and pulmonary embolism should be considered for patients who are admitted to the hospital with ADHF and who are not already anticoagulated and who have a contraindication to anticoagulation. (Strength of Evidence 5 C) 528 Journal of Cardiac Failure Vol. 16 No. 6 June 201012.17 In the absence symptomatic hypotension, intravenous nitroglycerin, In the absence of symptomatic hypotension, intravenous nitroglycerin, Addition of worsening renal (previous nitroprusside, or nesiritide may be considered as an addition to diuretic nitroprusside or nesiritide may be considered as an addition to diuretic function as potential side effect 12.15) therapy for rapid improvement of congestive symptoms in patients admitted therapy for rapid improvement of congestive symptoms in patients admitted with ADHF. Frequent blood pressure monitoring is recommended with with ADHF. (Strength of Evidence 5 B) these agents. (Strength of Evidence 5 B). These agents should be decreased Frequent blood pressure monitoring is recommended with these agents. in dosage on discontinued if symptomatic hypotension develops. (Strength (Strength of Evidence 5 B) of Evidence 5 B) These agents should be decreased in dosage or discontinued if symptomatic Reintroduction in increasing doses may be considered once symptomatic hypotension or worsening renal function develops. (Strength of Evidence hypotension is resolved. (Strength of Evidence 5 C) 5 B) Reintroduction in increasing doses may be considered once symptomatic hypotension is resolved. (Strength of Evidence 5 C)12.18 No changes (previous 12.16)12.19 Intravenous vasodilators (nitroprusside, nitroglycerin, or nesiritide) may be Intravenous vasodilators (nitroprusside, nitroglycerin, or nesiritide) may be Modification of strength of (previous considered in patients with ADHF and advanced HF who have persistent considered in patients with ADHF who have persistent severe HF despite evidence for nitroprusside 12.17) severe HF despite aggressive treatment with diuretics and standard oral aggressive treatment with diuretics and standard oral therapies. from C to B therapies. (Strength of Evidence 5 C)  Nitroprusside (Strength of Evidence 5 B)  Nitroglycerine, Nesiritide (Strength of Evidence 5 C)
    • 12.20 Intravenous inotropes (milrinone or dobutamine) may be considered to relieve Intravenous inotropes (milrinone or dobutamine) may be considered to relieve Modification of strength of (previous symptoms and improve end-organ function in patients with advanced HF symptoms and improve end-organ function in patients with advanced HF evidence from B to C for 12.18) characterized by LV dilation, reduced LVEF, and diminished peripheral characterized by LV dilation, reduced LVEF, and diminished peripheral portions of this perfusion or end-organ dysfunction (low output syndrome), particularly if perfusion or end-organ dysfunction (low output syndrome), particularly if recommendation these patients have marginal systolic blood pressure (!90 mm Hg), have these patients have marginal systolic blood pressure (! 90 mm Hg), have symptomatic hypotension despite adequate filling pressure, or are symptomatic hypotension despite adequate filling pressure, or are unresponsive to, or intolerant of, intravenous vasodilators. (Strength of unresponsive to, or intolerant of, intravenous vasodilators. (Strength of Evidence 5 C) Evidence 5 C) These agents may be considered in similar patients with evidence of fluid These agents may be considered in similar patients with evidence of fluid overload if they respond poorly to intravenous diuretics or manifest overload if they respond poorly to intravenous diuretics or manifest diminished or worsening renal function. (Strength of Evidence 5 C) diminished or worsening renal function. (Strength of Evidence 5 C) When adjunctive therapy is needed in other patients with ADHF, When adjunctive therapy is needed in other patients with ADHF, administration of vasodilators should be considered instead of intravenous administration of vasodilators should be considered instead of intravenous inotropes (milrinone or dobutamine). (Strength of Evidence 5 B) inotropes (milrinone or dobutamine). (Strength of Evidence 5 C) Intravenous inotropes (milrinone or dobutamine) are not recommended Intravenous inotropes (milrinone or dobutamine) are not recommended unless left heart filling pressures are known to be elevated based on direct unless left heart filling pressures are known to be elevated or cardiac index measurement or clear clinical signs. (Strength of Evidence 5 B) is severely impaired based on direct measurement or clear clinical signs. Administration of intravenous inotropes (milrinone or dobutamine) in the (Strength of Evidence 5 C) setting of ADHF should be accompanied by continuous or frequent blood It is recommended that administration of intravenous inotropes (milrinone Wording modified pressure monitoring and continuous monitoring of cardiac rhythm. (Strength or dobutamine) in the setting of ADHF be accompanied by continuous or of Evidence 5 C) frequent blood pressure monitoring and continuous monitoring of cardiac If symptomatic hypotension or worsening tachyarrhythmias develop during rhythm. (Strength of Evidence 5 C) administration of these agents, discontinuation or dose reduction should be If symptomatic hypotension or worsening tachyarrhythmias develop during considered. (Strength of Evidence 5 C) administration of these agents, discontinuation or dose reduction should be considered. (Strength of Evidence 5 C)12.21 No changes (previous 12.19)12.22 Invasive hemodynamic monitoring should be considered in a patient: Invasive hemodynamic monitoring should be considered in a patient: Addition of cardiac transplant as (previous Who is refractory to initial therapy,  who is refractory to initial therapy, criterion for invasive 12.20) Whose volume status and cardiac filling pressures are unclear,  whose volume status and cardiac filling pressures are unclear, hemodynamic monitoring Who has clinically significant hypotension (typically systolic blood pressure  who has clinically significant hypotension (typically SBP ! 80mm Hg) or !80 mm Hg) or worsening renal function during therapy, or worsening renal function during therapy, or In whom documentation of an adequate hemodynamic response to the  who is being considered for cardiac transplant and needs assessment of inotropic agent is necessary when chronic outpatient infusion is being degree and reversibility of pulmonary hypertension, or considered.  in whom documentation of an adequate hemodynamic response to the (Strength of Evidence 5 C) inotropic agent is necessary when chronic outpatient infusion is being considered. (Strength of Evidence 5 C)12.23 No changes (previous 12.21)12.24 It is recommended that every effort be made to use the hospital stay for It is recommended that every effort be made to use the hospital stay for Modification of strength of (previous assessment and improvement of patient compliance via patient and family assessment and improvement of patient adherence via patient and family evidence from C to B; change Executive Summary: Heart Failure Practice Guideline 12.22) education and social support services (Section 8). (Strength education and social support services (see Section 8). (Strength of Evidence in terminology (‘‘compliance’’  of Evidence 5 C) 5 B) to ‘‘adherence’’) (continued on next page) HFSA 529
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments12.25 No changes (previous 12.23)12.26 Discharge planning is recommended as part of the management of patients Discharge planning is recommended as part of the management of patients Addition of alcohol moderation (previous with ADHF. Discharge planning should address the following issues: with ADHF. Discharge planning should address the following issues: and smoking cessation 12.24)  Details regarding medication, dietary sodium restriction, and recommen-  Details regarding medication, dietary sodium restriction, and recommen- ded activity level ded activity level  Follow-up by phone or clinic visit early after discharge to reassess volume  Follow-up by phone or clinic visit early after discharge to reassess volume status status  Medication and dietary compliance  Medication and dietary compliance  Monitoring of body weight, electrolytes, and renal function  Alcohol moderation and smoking cessation  Consideration of referral for formal disease management (Strength of  Monitoring of body weight, electrolytes and renal function Evidence 5 C)  Consideration of referral for formal disease management (Strength of Evidence 5 C) Section 13: Evaluation and Therapy for Heart Failure in the Setting of Ischemic Heart Disease13.1 Assessment for risk factors for CAD is recommended in all patients with Ongoing assessment for risk factors for CAD is recommended in all patients Moved diagnostic portion of chronic HF regardless of EF. (Strength of Evidence 5 A) with chronic HF regardless of LVEF. (Strength of Evidence 5 A) recommendation to 13.2 The diagnostic approach for CAD should be individualized based on patient preference and comorbidities, eligibility and willingness to perform revascularization. (Strength of Evidence 5 C) 530 Journal of Cardiac Failure Vol. 16 No. 6 June 201013.2 It is recommended that the diagnostic approach for CAD be individualized Previously part of 13.1 based on patient preference and comorbidities, eligibility, symptoms suggestive of angina and willingness to undergo revascularization. (Strength of Evidence 5 C)13.3 It is recommended that patients with HF and angina undergo cardiac It is recommended that patients with HF and symptoms suggestive of angina Modification of wording (previous catheterization with coronary angiography to assess for potential undergo cardiac catheterization with coronary angiography to assess for 13.2) revascularization. potential revascularization. (Strength of Evidence 5 B) (Strength of Evidence 5 B)13.4 It is recommended that patients with HF, no angina, and known CAD should It is recommended that, at the initial diagnosis of HF and any time symptoms Clarification of type and timing (previous undergo noninvasive stress imaging and/or coronary angiography to assess worsen without obvious cause, patients with HF, no angina, and known of risk assessments 13.3) severity of coronary disease and the presence of ischemia. (Strength of CAD should undergo risk assessment that may include noninvasive stress Evidence 5 C) imaging and/or coronary angiography to assess severity of coronary disease and the presence of ischemia. (Strength of Evidence 5 C)13.5 No changes (previous 13.4)13.6 No changes (previous 13.5)
    • 13.7 Any of the following imaging tests may be used to identify inducible ischemia Any of the following imaging tests should be considered to identify inducible Modification of wording (previous or viable but nocontractile myocardium: ischemia or viable myocardium: 13.6)  Exercise or pharmacologic stress myocardial perfusion imaging  Exercise or pharmacologic stress myocardial perfusion imaging  Exercise or pharmacologic stress echocardiography  Exercise or pharmacologic stress echocardiography  Cardiac magnetic resonance imaging  Cardiac magnetic resonance imaging  Positron emission tomography scanning (Strength of Evidence 5 B)  Positron emission tomography scanning (Strength of Evidence 5 B)13.8 No changes (previous 13.7)13.9 Antiplatelet therapy is recommended in patients with HF and CAD unless Antiplatelet therapy is recommended to reduce vascular events in patients with Addition of indication for (previous contraindicated. (Aspirin, Strength of Evidence 5 B; Clopidogrel, Strength HF and CAD unless contraindicated. (aspirin, Strength of Evidence 5 A; antiplatelet therapy, and 13.8) of Evidence 5 C) clopidogrel, Strength of Evidence 5 B) modification of strength of evidence13.10 ACE inhibitors are recommended in all patients with systolic dysfunction or ACE inhibitors are recommended in all patients with either reduced or Modification of terminology (previous preserved systolic function after an MI. (Strength of Evidence 5 A) preserved LVEF after an MI. (Strength of Evidence 5 A) (‘‘systolic dysfunction’’ 13.9) changed to ‘‘reduced LVEF’’)13.11 No changes (previous 13.10)13.12 It is recommended that ACE-inhibitor and beta blocker therapy be initiated It is recommended that ACE-inhibitor and beta blocker therapy be initiated Modification of terminology (previous early (!48 hours) during hospitalization in hemodynamically stable post early (!48 hours) during hospitalization in hemodynamically stable post- (‘‘LV dysfunction’’ changed to 13.11) MI patients with LV dysfunction or HF. (Strength of Evidence 5 A) MI patients with reduced LVEF or HF. (Strength of Evidence 5 A) ‘‘reduced LVEF’’)13.13 No changes (previous 13.12)13.14 Calcium channel blockers should be considered in patients with HF who have Calcium channel blockers may be considered in patients with HF who have Addition of calcium channel (previous angina despite the optimal use of beta blockers and nitrates. Amlodipine and angina despite the optimal use of beta blockers and nitrates. Amlodipine and blockers that should be 13.13) felodipine are the preferred calcium channel blockers in patients with felodipine are the preferred calcium channel blockers in patients with avoided angina and decreased systolic function. (Strength of Evidence 5 C) angina and decreased systolic function. Based on available data, first generation calcium channel blockers (i.e. diltiazem, verapamil) should be avoided in patients with CAD, HF, and LVEF !40, unless necessary for heart rate control or other indications. (Strength of Evidence 5 C)13.15 No changes (previous 13.14)13.16 No changes (previous 13.15) Executive Summary: Heart Failure Practice Guideline Section 14: Managing Patients with Hypertension and Heart Failure 14.1 It is recommended that blood pressure be aggressively treated to lower systolic It is recommended that blood pressure be optimally treated to lower systolic Modification of wording and and usually diastolic levels. Target resting levels should be !130/!80 mm and usually diastolic levels. More than 1 drug may be required. Target change in strength of evidence Hg, if tolerated. (Strength of Evidence 5 C) resting levels should be !130/!80 mm Hg, if tolerated. (Strength of from C to A HFSA Evidence 5 A) (continued on next page) 531
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation CommentsPrevious Deleted 14.214.2 No changes (previous 14.3)14.3 No changes (previous 14.4)14.4 If BP remains O130/80 mm Hg then the addition of a diuretic is If blood pressure remains O130/80 mm Hg then the addition of a thiazide Modified to specify thiazide (previous recommended, followed by a calcium antagonist or other antihypertensive diuretic is recommended, followed by a dihydropyridine calcium antagonist diuretic or dihydropyridine 14.5) drugs. (Strength of Evidence 5 C) (eg, amlodipine or felodipine) or other antihypertensive drugs. (Strength of calcium channel antagonist Evidence 5 C)14.5 No changes (previous 14.6)14.6 If blood pressure remains O130/80 mm Hg, a noncardiac-depressing calcium If blood pressure remains O130/80 mm Hg, a dihydropyridine calcium Modified to specify (previous antagonist (eg, amlodipine) may be considered or other antihypertensive antagonist (eg, amlodipine or felodipine) may be considered or other dihydropyridine 14.7) medication doses increased. (Strength of Evidence 5 C) antihypertensive medication doses increased. (Strength of Evidence 5 C) 532 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 Section 15: Management of Heart Failure in Special Populations15.1 No changes15.2 No changes15.3 No changes15.4 No changes15.5 No changes15.6 ARBs are recommended for administration to symptomatic and asymptomatic New recommendation women with an LVEF # 40% who are intolerant to ACE inhibitors for reasons other than hyperkalemia or renal insufficiency. (Strength of Evidence 5 A)15.7 The combination of hydralazine/isosorbide dinitrate is recommended as New recommendation standard therapy for African American women with moderate to severe HF symptoms who are on background neurohormonal inhibition. (Strength of Evidence 5 B)15.8 No changes (previous 15.6)
    • 15.9 No changes (previous 15.7)15.10 No changes (previous 15.8)15.11 No changes (previous 15.9) Section 16: Myocarditis: Current Treatment16.1 No changes16.2 No changes Section 17: Genetic Evaluation of Cardiomyopathy New section Executive Summary: Heart Failure Practice Guideline  HFSA 533
    • 534 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 Appendix B. Acronyms Appendix B. (continued) PPAR-a peroxisome proliferator-activated receptor-alphaAcronym Meaning PUFA polyunsaturated fatty acidsACE angiotensin converting enzyme PVC premature ventricular contractionADA American Diabetes Association QTc QT interval corrected for heart rateADHF acute decompensated heart failure RAAS renin-angiotensin-aldosterone systemAF atrial fibrillation RCM restrictive cardiomyopathyAHA/ACC American Heart Association/American College of RV right ventricular Cardiology SAECG signal-averaged electrocardiogramALVD asymptomatic left ventricular dysfunction SAVER surgical anterior ventricular endocardial restorationARB angiotensin receptor blocker SBP systolic blood pressureARVD/C arrhythmogenic right ventricular dysplasia/ SCD sudden cardiac death cardiomyopathy SDC serum digoxin concentrationAV arteriovenous SPECT single-photon emission computed tomographyBMI body mass index SSRI selective serotonin reuptake inhibitorsBNP B-type natriuretic peptide STEMI ST-elevation myocardial infarctionBUN blood urea nitrogen TNF-a tumor necrosis factor-alphaCABG coronary artery bypass graft UFH unfractionated heparinCAD coronary artery disease USDA United States Department of AgricultureCHD congenital heart disease VE/VCO2 ventilation equivalent of carbon dioxide (productionCI confidence interval slope)CK-MM creatinine kinase MM isoenzyme VF ventricular fibrillationCOPD chronic obstructive pulmonary disease VT ventricular tachycardiaCOX-2 cyclooxygenase-2 Clinical TrialsCPAP continuous positive airway pressure Acronym Full Trial NameCPR cardiopulmonary resuscitation ACCOMPLISH Avoiding Cardiovascular Events Through CombinationCR/XL controlled release/extended release Therapy in Patients Living with SystolicCREST a limited cutaneous form of scleroderma defined by Hypertension calsinosis, Raynaud’s syndrome, esophageal ADHERE Acute Decompensated Heart Failure National Registry dysmotility, sclerodactyly, and telangiectasia (Registry)CRT cardiac resynchronization therapy AFFIRM Atrial Fibrillation Follow-Up Investigation of RhythmCRT-D cardiac resynchronization therapy device and Management defibrillator A-HeFT African-American Heart Failure TrialCTR cardiothoracic ratio ALLHAT Antihypertensive and Lipid-Lowering Treatment toDASH Dietary Approaches to Stop Hypertension Prevent Heart Attack TrialDBP diastolic blood pressure ALOFT Aliskiren Observation of Heart Failure TreatmentDCM dilated cardiomyopathy B-CONVINCED Beta Blocker Continuation Versus Interruption onDNR do not resuscitate Patients with Congestive Heart Failure HospitalizedDVT deep venous thrombosis for a Decompensation EpisodeECG electrocardiogram CANPAP Canadian Continuous Positive Airway Pressure forED emergency department Patients with Central Sleep Apnea and Heart FailureEP, EPS electrophysiology, electrophysiology study CAPRICORN Carvedilol Post-Infarct Survival Control in LeftEVCPP endoventricular circular patch plasty Ventricular DysfunctionFDC familial dilated cardiomyopathy CARE-HF Cardiac Resynchronization-Heart FailureGFR, eGFR glomerular filtration rate, estimated glomerular filtration CHARM Candesartan in Heart Failure Assessment of Reduction rate in Mortality and Morbidity (Also CHARM-Added,HCM hypertrophic cardiomyopathy CHARM-Alternative, CHARM-Preserved)HF heart failure CIBIS Cardiac Insufficiency Bisoprolol StudyHFSA Heart Failure Society of America COACH Coordinating Study Evaluating Outcomes of AdvisingHR hazard ratio and Counseling in Heart FailureICD implantable cardioverter defibrillator COMET Carvedilol or Metoprolol European TrialINR international normalized ratio COMPANION Comparison of Medical Therapy, Pacing, andJVP jugular venous pressure Defibrillation in Chronic Heart FailureLA left atrial CONSENSUS Cooperative New Scandinavian Enalapril SurvivalLMWH low molecular weight heparin II Study IILV left ventricular COPERNICUS Carvedilol Prospective Randomized CumulativeLVAD left ventricular assist device Survival StudyLVEF left ventricular ejection fraction DIG Digitalis Investigation GroupLVH left ventricular hypertrophy EFFECT Enhanced Feedback for Effective Cardiac TreatmentLVNC left ventricular noncompaction (Evaluation Tool)MI myocardial infarction EPHESUS Epleronone Post-Acute Myocardial Infarction HeartMRI magnetic resonance imaging Failure Efficacy and Survival StudyNCEP National Cholesterol Education Program ESCAPE Evaluation Study of Congestive Heart Failure andNIV non-invasive ventilation Pulmonary Artery Catheterization EffectivenessNSAID non-steroidal anti-inflammatory drug EUROPA European Trial on Reduction of Cardiac Events withNT-proBNP N-terminal pro-B-type natriuretic peptide Perindopril in Stable Coronary Artery DiseaseNYHA New York Heart Association FAIR-HF Ferinject Assessment in Patients with Iron DeficiencyOMIM Online Mendelian Inheritance in Man (online resource) and Chronic Heart FailureOU observation unit GISSI Gruppo Italiano Per Lo Studio Della SopravvivenzaPCI percutaneous coronary intervention Nell’infarto Miocardico (GISSI-Prevenzione, GISSI-PCWP pulmonary capillary wedge pressure HF)PE pulmonary embolism GUSTO-1 Global Utilization of Streptokinase and TissuePET-CT positron emission tomography e computed tomography Plasminogen Activator for Occluded CoronaryPMI point of maximal impulse ArteriesPND paroxysmal nocturnal dyspnea (continued on next page) (continued)
    • Executive Summary: Heart Failure Practice Guideline  HFSA 535 Appendix B. (continued)HEART Heart Failure Revascularization TrialHELP Hospitalized Elderly Longitudinal ProjectHERS Heart and Estrogen/Progestin Replacement StudyHF-ACTION A Controlled Trial Investigating Outcomes of Exercise TrainingHOBIPACE Homburg Biventricular Pacing EvaluationHOPE Heart Outcomes Prevention EvaluationHOT Hypertension Optimal TreatmentINTERMACS Interagency Registry for Mechanically Assisted Circulatory Support (Registry)I-PRESERVE Irbesartan in Heart Failure with Preserved Ejection FractionIRON-HF Iron Supplementation in Heart Failure Patients with AnemiaISIS-4 Fourth International Study of Infarct SurvivalMADIT-CRT Multi-Center Automatic Defibrillator Implantation Trial with Cardiac Resynchronization TherapyMERIT-HF Metoprolol CR?XL Randomized Intervention Trial in Congestive Heart FailureMIRACLE Multicenter Insync Clinical StudyMTT Myocarditis Treatment TrialMUSTT Multicenter Unsustained Tachycardia TrialNHANES National Health and Nutrition Examination Survey Epidemiologic Follow-Up StudyOAT Occluded Artery TrialOPTIMAAL Optimal Trial in Myocardial Infarction with the Angiotensin II Antagonist LosartanOPTIME-HF Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart FailureOPTIMIZE-HF Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (Registry)PRIDE N-Terminal Pro-BNP Investigation of Dyspnea in the Emergency DepartmentPRIMA Can Pro-Brain-Natriuretic-Peptide Guided Therapy of Chronic Heart Failure Improve Heart Failure Morbidity and Mortality?PROVED Prospective Randomized Study of Ventricular Function and Efficacy of DigoxinRADIANCE Randomized Assessment of Digoxin on Inhibitors of the Angiotensin Converting SystemRALES Randomized Aldactone Evaluation StudyRED-HF Reduction of Events with Darbepoetin Alfa in Heart FailureREMATCH Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart FailureREVERSE Resynchronization Reverses Remodeling in Systolic Left Ventricular DysfunctionREVERT Reversal of Ventricular Remodeling with Toprol-XLSCD-HeFT Sudden Cardiac Death in Heart Failure TrialSENIORS Study of the Effects of Nebivolol Intervention on Outcomes and Rehospitalization in Seniors with Heart FailureSOLVD Studies of Left Ventricular DysfunctionSTARS-BNP Systolic Heart Failure Treatment Supported By BNPSTICH Surgical Treatment for Ischemic Heart FailureSUPPORT Study to Understand Prognoses and Preferences for Outcomes and Risks of TreatmentTIME-CHF Trial of Intensified Vs Standard Medical Therapy in Elderly Patients with Congestive Heart FailureUKPDS United Kingdom Prospective Diabetes StudyVal-HeFT Valsartan Heart Failure TrialVALIANT The Valsartan in Acute Myocardial Infarction TrialV-HeFT Vasodilator Heart Failure TrialVMAC Vasodilator in the Management of Acute Heart FailureWASH Warfarin/Aspirin Study in Heart FailureWATCH Warfarin and Antiplatelet Therapy in Chronic Heart Failure
    • Appendix C. Financial Disclosure Equity Interests/ Other Intellectual Consulting Speaker’s Research Stock/Stock Equity Royalty Non-Royalty Financial Property FellowshipName Fees/Honoraria Bureau Grants Options Interests Income Payments Benefit Salary Rights SupportNancy M. Albert, Medtronic R.N., Ph.DInder S. Anand, Amgen Novartis CVRx, Novartis VA Medical M.D., Ph.D. Pharmaceuticals, Pharma- Pharmaceuticals, Center Boston Scientific, ceuticals Paracor Corventis, CVRx, Merck, Medtronic, N30, ParacorJ. Malcolm O. Arnold, Abbott, Boehringer M.D. Ingelheim, GlaxoSmithKline, Merck-Frosst, Novartis, PfizerJohn P. Boehmer, M.D. Boston, Scientific, Boston Scientific, Medtronic, CardioMEMS, St. Jude Medtronic, Novartis, 536 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 ParacorJohn C. Burnett, M.D. Anexon, Nile Anexon, Bayer, BioRad, Anexon, Nile Therapeutics, Merck, Nile Therapeutics Otsuka Therapeutics, TrevenaJohn Chin, M.D. Gilead, Otsuka Boston Scientific, Eli Lilly, Gilead, NovartisJay N. Cohn, M.D. GlaxoSmithKline CPC, LLC HDT, Inc. MLHFQ, NitroMedSean P. Collins, Abbott Point-of-Care, Abbott Point-of-Care, M.D., MSc Astellas, Bayer, BRAHMS Diagnostics, Corthera, The National Institutes of Medicines Health/NHLBI Company, OtsukaJustin A. Ezekowitz, Amgen, Bristol-Myers Amgen, Bristol-Myers MBBCh Squibb, Pfizer Squibb, Merck, Ortho-Biotech/Johnson & JohnsonThomas Force, M.D. Merck Schering GlaxoSmithKline Plough/MerckBart Galle, Ph.D. disclosures: none
    • Michael M. Givertz, Cardioxyl Asahi Kasei M.D.Sarah J. Goodlin, M.D. Servier Boston Scientific CARE, St. Jude Medical FoundationBarry H. Greenberg, Biogen Idec, Gilead, Merck, M.D. CardioMEMS, Novartis, sanofi- Corthera, aventis Cytokinetics, GlaxoSmithKline, Otsuka, Paracor, St. Jude, ZensunRay E. Hershberger, disclosures: none M.D.Steven R. Houser, disclosures: none Ph.D.Jonathan G. Howlett, AstraZeneca, AstraZeneca, AstraZeneca, Medtronic, M.D. Merck, Novartis, Merck, Novartis, Merck, Novartis, Schering, Servier Schering, Servier Schering, ServierSharon A. Hunt, M.D. disclosures: noneMariell Jessup, M.D. Medtronic Boston ScientificStuart D. Katz, M.D. Amgen, Dura Heart Terumo, Merck, ParacorMarc Klapholz, M.D. GlaxoSmithKline, GlaxoSmithKline Medtronic, Paracor, St. Jude, ScheringMarvin W. Kronenberg, Cardiovascular M.D. Services of AmericaJoAnn Lindenfeld, M.D. Astellas, Boston Merck Scientific, Forest, Medtronic, N30Douglas L. Mann, M.D. ARMGO Miragen Pharmaceuticals, Medtronic, Miragen, Executive Summary: Heart Failure Practice Guideline Nile Therapeutics, PeriCor  Therapeutics (continued on next page) HFSA 537
    • Appendix C. (continued) Equity Interests/ Other Intellectual Consulting Speaker’s Research Stock/Stock Equity Royalty Non-Royalty Financial Property FellowshipName Fees/Honoraria Bureau Grants Options Interests Income Payments Benefit Salary Rights SupportBarry M. Massie, M.D. ARCA, Boehringer, Merck Bristol-Myers Squibb, Corthera, Cytokinetics, Duke Clinical Research Institute, Merck, Nile Therapeutics, Novartis, sanofi- aventis, St. Jude, Takeda, TrevenaMandeep R. Mehra, Geron, Johnson & National Institutes M.D. Johnson, of Health Medtronic, Pericor, Solvay, St. JudeLuisa Mestroni, M.D. M01 RR00051- University of 1575 Colorado (employee) 538 Journal of Cardiac Failure Vol. 16 No. 6 June 2010Alan B. Miller, M.D. disclosures: noneDebra K. Moser, disclosures: none R.N., DNSc.Mariann R. Piano, disclosures: none R.N., Ph.D.Richard J. Rodeheffer, disclosures: none M.D.Joseph G. Rogers, M.D. Forrest Boston Scientific, Pharmaceuticals, Medtronic ThoratecChristine E. Seidman, HHMI & NIH M.D.Randall C. Starling, BioControl, Biotronik, Medtronic, CardioMEMS Medtronic M.D., MPH Medtronic, Novartis, Thoratec NovartisWilliam G. Stevenson, disclosures: none M.D.
    • Wendy Gattis Stough, ARCA Discovery, Inc., Pharm.D. Gilead Sciences, Inc., GlaxoSmithKlline, Heart Failure Society of America, Medtronic, Otsuka, SciosW.H. Wilson Tang, Medtronic, Merck & Abbott Laboratories M.D. CompanyMatthew R.G. Taylor, Genzyme Muscular Dystrophy M.D., Ph.D. Therapeutics Association/March of Dimes/Genzyme TherapeuticsJohn R. Teerlink, M.D. Abbott Laboratories, Abbott Laboratories, Cytokinetics BAS Medical/ BAS Medical/Corthera, Corthera, Biogen Bristol-Myers Squibb, Idec, Bristol-Myers Cytokinetics, Squibb, GlaxoSmithKline, CardioDynamics, Merck, National CardioMEMS, Institutes of Health, CoGeneSys, Novartis, sanofi-aventis Cytokinetics, Geron, GlaxoSmithKline, Icon Medical Imaging, Indigo Pharma, Kowa Pharma, Luitpold Pharma, Merck, Momentum Research, Nile Therapeutics, Novartis, sanofi- aventis, Scios/ Johnson & JohnsonJeffery A. Towbin, disclosure: none M.D.Mary N. Walsh, M.D. ARCA, Boston Scientific, EMERGE, Medtronic, United Health CareClyde W. Yancy, M.D. disclosures: noneCheryl Yano disclosures: noneMichael R. Zile, M.D. ABIM, BMS, CorAssist, BMS, Boston, Scientific, Department MUSC, OCD/ Executive Summary: Heart Failure Practice Guideline CVRx, DC Devices, CVRx, Department of of VA, J&J Gilead, Medtronic, VA, Gilead, Medtronic, MUSC,  Merck, N30, Novartis, Merck, National Heart, National OCD/J&J, sanofi- Lung and Blood Heart, Lung aventis, Up-To-Date Institute, Novartis, and Blood OCD/J&J, Pfizer, Institute HFSA sanofi-aventis 539
    • Journal of Cardiac Failure Vol. 16 No. 6 2010 HFSA 2010 Comprehensive Heart Failure Practice Guideline HFSA 2010 Comprehensive Heart Failure Practice Guideline HEART FAILURE SOCIETY OF AMERICA St. Paul, Minnesota Guideline Committee Members JoAnn Lindenfeld, MD1 (Chair) Nancy M. Albert, RN, PhD Debra K. Moser, RN, DNSc John P. Boehmer, MD Joseph G. Rogers, MD Sean P. Collins, MD, MSc Randall C. Starling, MD, MPH Justin A. Ezekowitz, MBBCh William G. Stevenson, MD Michael M. Givertz, MD W. H. Wilson Tang, MD Stuart D. Katz, MD John R. Teerlink, M Marc Klapholz, MD Mary N. Walsh, MD Executive Council Douglas L. Mann, MD, President Inder S. Anand, MD Steven R. Houser, PhD J. Malcolm O. Arnold, MD Mariell L. Jessup, MD John C. Burnett, Jr., MD Barry M. Massie, MD John Chin, MD Mandeep R. Mehra, MD Jay N. Cohn, MD Mariann R. Piano RN, PhD Thomas Force, MD Clyde W. Yancy, MD Barry H. Greenberg, MD Michael R. Zile, MD ABSTRACT Heart failure (HF) is a syndrome characterized by high mortality, frequent hospitalization, reduced quality of life, and a complex therapeutic regimen. Knowledge about HF is accumulating so rapidly that individ- ual clinicians may be unable to readily and adequately synthesize new information into effective strategies of care for patients with this syndrome. Trial data, though valuable, often do not give direction for indi- vidual patient management. These characteristics make HF an ideal candidate for practice guidelines. The 2010 Heart Failure Society of America comprehensive practice guideline addresses the full range of eval- uation, care, and management of patients with HF. Key Words: Heart failure, practice guidelines. From the 1Department of Cardiology, University of Colorado Health Multiple copies, modification, alteration, enhancement, and/or distribution ofSciences Center, Denver, CO. this document are not permitted without the express written permission of the Heart The document should be cited as follows: Lindenfeld, J, Albert NM, Failure Society of America. Please direct requests to info@hfsa.org.Boehmer JP, Collins SP, Ezekowitz JA, Givertz MM, Klapholz M, Moser Acknowledgment of Support: Administrative support provided by the HeartDK, Rogers JG, Starling RC, Stevenson WG, Tang WHW, Teerlink JR, Walsh Failure Society of America.MN. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail See page e34 for disclosure information.2010;16:e1-e194. 1071-9164/$ - see front matter A copy of the HFSA Comprehensive Heart Failure Practice Guideline can Ó 2010 Elsevier Inc. All rights reserved.be found at www.onlinejcf.com doi:10.1016/j.cardfail.2010.04.004 e1
    • e2 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 Table of Contents HFSA 2010 Comprehensive Heart Failure Practice Guideline Section 1: Development and Implementation of a Comprehensive Heart Failure Practice Guideline......... e3 Section 2: Conceptualization and Working Definition of Heart Failure ...................................................... e34 Section 3: Prevention of Ventricular Remodeling, Cardiac Dysfunction, and Heart Failure...................... e38 Section 4. Evaluation of Patients for Ventricular Dysfunction and Heart Failure....................................... e44 Section 5: Management of Asymptomatic Patients With Reduced Left Ventricular Ejection Fraction ..... e57 Section 6: Nonpharmacologic Management and Health Care Maintenance in Patients With Chronic Heart Failure.......................................................................................................... e61 Section 7: Heart Failure in Patients With Reduced Ejection Fraction......................................................... e73 Section 8: Disease Management, Advance Directives, and End-of-Life Care in Heart Failure ................. e98 Section 9: Electrophysiology Testing and the Use of Devices in Heart Failure ....................................... e115 Section 10: Surgical Approaches to the Treatment of Heart Failure........................................................... e122 Section 11: Evaluation and Management of Patients With Heart Failure and Preserved Left Ventricular Ejection Fraction ............................................................................................. e126 Section 12: Evaluation and Management of Patients With Acute Decompensated Heart Failure............................................................................................................................... e134 Section 13: Evaluation and Therapy for Heart Failure in the Setting of Ischemic Heart Disease.............................................................................................................................. e157 Section 14: Managing Patients With Hypertension and Heart Failure ........................................................ e166 Section 15: Management of Heart Failure in Special Populations .............................................................. e169 Section 16: Myocarditis: Current Treatment ................................................................................................ e176 Section 17: Genetic Evaluation of Cardiomyopathy .................................................................................... e180
    • Journal of Cardiac Failure Vol. 16 No. 6 2010 Section 1: Development and Implementation of determining strength of recommendation. Strength of evi-a Comprehensive Heart Failure Practice Guideline dence is determined both by the type of evidence available and the assessment of validity, applicability, and certainty Introduction of a specific type of evidence. Following the lead of previ- ous guidelines, strength of evidence in this guideline is Heart failure (HF) is a syndrome characterized by high heavily dependent on the source or type of evidence used.mortality, frequent hospitalization, poor quality of life, and The HFSA guideline process has used three grades (A, B,multiple comorbidities. As a result, heart failure manage- or C) to characterize the type of evidence available to sup-ment inevitably involves both a multidimensional assess- port specific recommendations (Table 1.2).ment process and a complex therapeutic regimen. It must be recognized, however, that the evidence sup-Knowledge about the pathophysiology and treatment of HF porting recommendations is based largely on population re-continues to accumulate very rapidly so that individual clini- sponses that may not always apply to individuals within thecians may be unable to readily and adequately synthesize population. Therefore, the totality of data may supportnew information into effective principles of care for patients overall benefit of one treatment over another but cannot as-with this syndrome. Trial data, though valuable, often do not sure that all patients will respond similarly. Thus, guide-give adequate direction for individual patient management. lines can best serve as evidence-based recommendations Given the complex and changing picture of HF and the for management, not as mandates for management in everyaccumulation of evidence-based HF therapy, it is not possi- patient. Furthermore, it must be recognized that trial datable for the clinician to rely solely on personal experience on which recommendations are based have often been car-and observation to guide therapeutic decisions. This situa- ried out with background therapy not comparable to ther-tion is exacerbated because HF is now a chronic condition apy in current use. Therefore, physician decisionsin most patients, meaning that the outcome of therapeutic regarding the management of individual patients may notdecisions might not be apparent for several years. The nat- always precisely match the recommendations. A knowl-ural history and prognosis of individual patients differs con- edgeable physician who integrates the guidelines with phar-siderably, making it difficult to generalize. Treatments macologic and physiologic insight and knowledge of themight not dramatically improve symptoms of the disease individual being treated should provide the best patientprocess, yet might prevent of delay its progression and management.the occurrence of morbid events and deaths. The assess-ment of specific therapeutic outcomes is complicated by Strength of Evidence A. Randomized controlled clinicalthe potential differential impact of various cotherapies. trials provide what is considered the most valid form of The complexity of HF, its high prevalence, and the avail- guideline evidence. Some guidelines require at least 2 pos-ability of many therapeutic options make it an ideal area for itive randomized clinical trials before the evidence forpractice guidelines. Additional assumptions driving the de- a recommendation can be designated level A. The HFSAvelopment of HF guidelines are presented in Table 1.1. guideline committee has occasionally accepted a single ran- The first HF guideline developed by the Heart Failure So- domized, controlled, outcome-based clinical trial as suffi-ciety of America (HFSA) had a narrow scope, concentrating cient for level A evidence when the single trial is largeon the pharmacologic treatment of chronic, symptomatic left with a substantial number of endpoints and has consistentventricular dysfunction.1 It did not consider subsets of the and robust outcomes. However, randomized clinical trialclinical syndrome of HF, such as acute decompensated HF data, whether derived from one or multiple trials, haveand ‘‘diastolic dysfunction,’’ or issues such as prevention. not been taken simply at face value. They have been eval-The subsequent comprehensive clinical practice guideline uated for: (1) endpoints studied, (2) level of significance,published in 2006 addressed a full range of topics including (3) reproducibility of findings, (4) generalizability of studyprevention, evaluation, disease management, and pharmaco-logic and device therapy for patients with HF.2 The 2010guideline updates and expands each of these areas and adds Table 1.1. Assumptions Underlying HFSA Practice Guidelinea section on the Genetic Evaluation of Cardiomyopathy pub-lished separately in 2009.3 The discussion of end of life man- Clinical decisions must be made.agement has also been considerably expanded. Correct course of action may not be readily apparent. Multiple non-pharmacologic, pharmacologic, and device therapies are available. HFSA Guideline Approach to Medical Evidence Reasonably valid methods exist to address knowledge base and evaluate medical evidence. Data beyond randomized clinical trials exist that enhance medical decision Two considerations are critical in the development of making.practice guidelines: assessing strength of evidence and Uncertainties remain concerning approaches to treatment after review of totality of medical evidence. Expert opinion has a role in management decisions when Strength of Evidence A data are not available to guide management. 1071-9164/$ - see front matter A consensus of experts remains the best method of management Ó 2010 Elsevier Inc. All rights reserved. recommendations when Strength of Evidence A data are not available. doi:10.1016/j.cardfail.2010.05.010 e3
    • e4 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 Table 1.2. Relative Weight of Evidence Used to Develop them, experts are exposed to rare safety issues and gain HFSA Practice Guideline insight into the perceptions of practitioners concerningHierarchy of Types of Evidence the efficacy of particular treatments across a wide spectrumLevel A Randomized, Controlled, Clinical Trials of HF. May be assigned based on results of a single Despite the case that can be made for its value, recom- methodologically rigorous trialLevel B Cohort and Case-Control Studies mendations based on expert opinion alone have been lim- Post hoc, subgroup analysis, and meta-analysis ited to those circumstances when a definite consensus Prospective observational studies or registries could be reached across the guideline panel and reviewers.Level C Expert Opinion Observational studies-epidemiologic findings Safety reporting from large-scale use in practice HFSA Guideline Approach to Strength of Recommendationresults, and (5) sample size and number of events on which Determining Strength. Although level of evidence isoutcome results are based. important, the strength given to specific recommendations is critical. The process used to determine the strength of in- Strength of Evidence B. The HFSA guideline process dividual recommendations is complex. The goal of guide-also considers evidence arising from cohort studies or line development is to achieve the best recommendationssmaller clinical trials with physiologic or surrogate end- for evaluation and management, considering not only effi-points. This level B evidence is derived from studies that cacy, but the cost, convenience, side effect profile, andare diverse in design and may be prospective or retrospec- safety of various therapeutic approaches. The HFSA guide-tive in nature. They may involve subgroup analyses of clin- line committee often determined the strength of a recom-ical trials or have a case control or propensity adjusted mendation by the ‘‘totality of evidence,’’ which isdesign using a matched subset of trial populations. Dose- a synthesis of all types of available data, pro and con, aboutresponse studies, when available, may involve all or a por- a particular therapeutic option.tion of the clinical trial population. Evidence generatedfrom these studies has well-recognized, inherent limita- Totality of Evidence. Totality of evidence includes nottions. Nevertheless, their value is enhanced through atten- only results of clinical trials, but also expert opinion andtion to factors such as pre-specification of hypotheses, findings from epidemiologic and basic science studies.biologic rationale, and consistency of findings between Agreement among various types of evidence, especiallystudies and across different populations. from different methodologies, increases the likelihood that a particular therapy is valuable. Although many equate Strength of Evidence C. The present HFSA guideline evidence-based medicine with the results of a few individ-makes extensive use of expert opinion, or C-level evidence. ual clinical trials, the best judgment seems to be derivedThe need to formulate recommendations based on expert from a careful analysis of all available trial data combinedopinion is driven primarily by a paucity of evidence in areas with integration of results from the basic laboratory and thecritical to a comprehensive guideline or by evidence de- findings of epidemiologic studies.rived from a study population not fully representative ofthe broad spectrum of HF patients. For example, the diag- Scale of Strength. The HFSA guideline employs the cat-nostic process and the steps used to evaluate and monitor egorization for strength of recommendation outlined inpatients with established HF have not been the subject of Table 1.3. There are several degrees of favorable recom-clinical studies that formally test the accuracy of one ap- mendations and a single category for therapies felt to beproach versus another. In addition, trials often enroll pa- not effective. The phrase ‘‘is recommended’’ should betients that differ from the general HF population in age or taken to mean that the recommended therapy or manage-gender distribution and in background therapies. In situa- ment process should be followed as often as possible in in-tions such as these, recommendations must be based on ex- dividual patients. Exceptions are carefully delineated.pert opinion or go unaddressed. ‘‘Should be considered’’ means that a majority of patients The value of expert opinion as a form of evidence re- should receive the intervention, with some discretionmains disputed. Many contend that expert opinion isa weak form of observational evidence, based on practice Table 1.3. HFSA System for Classifying the Strength ofexperience and subject to biases and limitations. Advocates Recommendationsbelieve expert opinion represents a complex synthesis of ‘‘Is recommended’’ Part of routine careobservational insights into disease pathophysiology and Exceptions to therapy should be minimized ‘‘Should be considered’’ Majority of patients should receive thethe benefits of therapy in broad populations of patients. interventionThey stress the value of the interchange of experience Some discretion in application to individualand ideas among colleagues, who collectively treat thou- patients should be allowed ‘‘May be considered’’ Individualization of therapy is indicatedsands of patients. Through contact with numerous individ- ‘‘Is not recommended’’ Therapeutic intervention should not be usedual health care providers who may discuss patients with
    • Heart Failure Practice Guideline  HFSA e5involving individual patients. ‘‘May be considered’’ means influenced by their own experiences with particular thera-that individualization of therapy is indicated (Table 1.3). pies, but still generally agree on the clinical value of trialWhen the available evidence is considered to be insufficient data. Discomfort with the results of trials reported as posi-or too premature, or consensus fails, issues are labeled un- tive or negative generally focus on factors that potentiallyresolved and included as appropriate at the end of the rele- compromise the evidence. Unfortunately, there are no abso-vant section. lute rules for downgrading or upgrading trial results or for deciding whether the limitations of the trial are sufficient to negate what has been regarded as a traditionally positive or Process of Guideline Development negative statistical result. The HFSA guideline committee sought resolution of Key steps in the development of this guideline are listed difficult cases through consensus building. An open, dy-in Table 1.4. Having determined the broad scope of the cur- namic discussion meant that no single voice was allowedrent guideline, subcommittees of the guideline committee to dominate. Written documents were essential to this pro-were formed for each section of the guideline. Literature cess, because they provided the opportunity for feedbacksearches with relevant key words and phrases for each from all members of the group. On occasion, consensusguideline section were provided to members of the subcom- of opinion was sufficient to override positive or negativemittees and the full Guideline Committee. Members of each results of almost any form of evidence. The HFSA processsubcommittee were asked to review the search and identify had a strong commitment to recommendations basedany additional relevant medical evidence for each assigned on objective evidence rigorously reviewed by a panel ofsection. Changes in recommendation and background were experts.carried out by each subcommittee with conference calls di- Issues that caused particular difficulty for the HFSArected by the Guideline Committee chair. Each section was guideline process usually were some of the more importantpresented for comments and consensus approval to the ones faced by the committee, because they mirrored thoseGuideline Committee. Once subsections were complete, that are often most challenging to clinicians in day-to-daythe Executive Council reviewed and commented on each practice. The foundation of the HFSA guideline processsection and these comments were returned to the Guideline was the belief that the careful judgment of recognized opin-Committee for changes and once complete, for final ap- ion leaders in these controversial areas is more likely to beproval by the Executive Council. Appendix A provides correct than ad hoc decisions made ‘‘on the spot’’ by phy-a grid showing changes to the 2006 guideline. sicians in practice. The involvement of many groups in the development of Consensus. The development of a guideline involves the this guideline helped avoid the introduction of real or per-selection of individuals with expertise and experience to ceived bias, which can be personal, practice-based, or baseddrive the process of formulating specific recommendations on financial interest. Committee members and reviewersand producing a written document. The role of these ex- from the Executive Council received no direct financialperts goes well beyond the formulation of recommenda- support from the HFSA or any other source for the develop-tions supported by expert opinion. ment of the guideline. Support was provided by the HFSA Experts involved in the guideline process must function administrative staff, but the writing of the document wasas a collective, not as isolated individuals. Expert opinion performed on a volunteer basis primarily by the Committee.is not always unanimous. Interpretations of data vary. Dis- Information concerning financial relationships that mightagreements arise over the generalizability and applicability represent conflicts of interest was collected annually fromof trial results to various patient subgroups. Experts are all members of the Guideline Committee and the Executive Council. Current relationships are shown in Appendix C. Table 1.4. Steps in the Development of the 2010 HFSA Practice Guideline Dissemination and Continuity. The value of a practiceDetermine the scope of the practice guideline guideline is significantly influenced by the scope of its dis-Form subcommittees with expertise for each guideline section semination. The first and second HFSA guidelines werePerform literature search relevant to each guideline section and distribute to subcommittee and committee members available on the Internet, and thousands of copies wereSolicit additional relevant information from subcommittee and committee downloaded. The current document will be accessible on members for each subsection the Internet both for file transfer and as a hypertext sourceFormulate new recommendations and revise previous recommendations assigning Strength of Recommendation and Strength of Evidence of detailed knowledge concerning HF.Form consensus of subcommittee for each section by conference call An important final consideration is the continuity of theAssign writing of additional or revised background by subcommittee guideline development process. The intent is to createFull committee review of each section with revisions by subcommitteeReview of each completed section by Executive Council with revisions a ‘‘living document’’ that will be updated and amended made by full committee and returned to Executive Council for final as necessary to ensure continuing relevance. The rapid de- approval. velopment of new knowledge in HF from basic and clinicalDisseminate documentUpdate document as changes are necessary research and the continuing evolution of pharmacologic and device therapy for this condition provides a strong mandate
    • e6 Journal of Cardiac Failure Vol. 16 No. 6 June 2010for timely updates. The HFSA intends to undertake targeted has emerged as an alternative strategy. The methodologyreviews and updates in areas where new research has impli- of guideline development needs improvement, but whencations for practice. Section 17: The Genetic Evaluation of these documents are properly conceived and formulated,Cardiomyopathy is an example of this policy. their importance to patient care seems evident. This HFSA guideline on HF is designed as a ‘‘living document,’’ Summary which will continue to serve as a resource for helping patients with HF. Practice guidelines have become a major part of the clin-ical landscape and seem likely to become more rather thanless pervasive. Some may perceive guidelines as anothermechanism for process management or as another instru-ment for cost control. But there is a more patient- Referencescentered rationale for their development, especially for 1. Adams K, Baughman K, Dec W, Elkayam U, Forker A, Gheorghiade M,a common, potentially debilitating, and often fatal syn- et al. Heart Failure Society of America (HFSA) practice guidelines.drome such as HF. Despite advances in clinical trial meth- HFSA guidelines for management of patients with heart failure causedodology and the extensive use of studies to evaluate by left ventricular systolic dysfunctionepharmacological approaches.therapeutics and the care process, essential elements of J Card Fail 1999;5:357e82.the management process remain undefined for many clini- 2. Adams K, Lindenfeld J, Arnold J, Baker D, Barnard D, Baughman K,cal problems. HF is no exception. Traditionally, manage- et al. HFSA 2006 Comprehensive Heart Failure Practice Guideline. J Card Fail 2006;12:e1ee122.ment guidelines were determined on an ad hoc basis by 3. Hershberger RE, Lindenfeld J, Mestroni L, Seidman CE, Taylor MR,physicians and other health care providers in the field. Towbin JA. Genetic evaluation of cardiomyopathyea Heart FailureThe development and utilization of practice guidelines Society of America practice guideline. J Card Fail 2009;15:83e97.
    • Appendix A. Comparison of the 2006 and 2010 HFSA Guideline 2006 Guideline Recommendation 2010 Guideline Recommendation Comments Section 3: Prevention of Ventricular Remodeling, Cardiac Dysfunction, and Heart Failure3.1 A careful and thorough clinical assessment, with appropriate investigation for A careful and thorough clinical assessment, with appropriate investigation for Addition of dietary choices to list known or potential risk factors, is recommended in an effort to prevent known or potential risk factors, is recommended in an effort to prevent of risk factors development of LV remodeling, cardiac dysfunction, and HF. These risk development of LV remodeling, cardiac dysfunction, and HF. These risk factors include, but are not limited to, hypertension, hyperlipidemia, factors include, but are not limited to, hypertension, hyperlipidemia, atherosclerosis, diabetes mellitus, valvular disease, obesity, physical atherosclerosis, diabetes mellitus, valvular disease, obesity, physical inactivity, excessive alcohol intake, and smoking. inactivity, excessive alcohol intake, dietary choices, and smoking. (Strength (Strength of Evidence 5 A) of Evidence 5 A)3.2 No changes3.3 No changes3.4 No changes Section 4: Evaluation of Patients for Ventricular Dysfunction and Heart Failure4.1 Evaluation with a routine history, physical examination, chest x-ray, and Evaluation for clinical manifestations of HF with a routine history and Modification of wording and electrocardiogram (ECG) is recommended in patients with the medical physical examination is recommended in patients with the medical deletion of chest x-ray and conditions or test findings listed in Table 4.1. (Strength of Evidence 5 B) conditions or test findings listed in Table 4.1. (Strength of Evidence 5 B) ECG (retained in Table 4.1)4.2 Assessment of Cardiac Structure and Function. Echocardiography with Assessment of Cardiac Structure and Function. Echocardiography with Modification of wording and Doppler is recommended to determine LV size and function in patients Doppler is recommended to determine cardiac structure and function in terminology without signs or symptoms suggestive of HF who have the risk factors listed asymptomatic patients with the disorders or findings listed in Table 4.2. in Table 4.2. (Strength of Evidence 5 B) (Strength of Evidence 5 B)4.3 Determination of plasma B-type natriuretic peptide (BNP) or N-terminal pro- Routine determination of plasma BNP or NT-proBNP concentration as part of Modification of wording and BNP concentration is not recommended as a routine part of the evaluation a screening evaluation for structural heart disease in asymptomatic patients terminology for structural heart disease in patients at risk but without signs or symptoms is not recommended. (Strength of Evidence 5 B) of HF. (Strength of Evidence 5 B)4.4 Symptoms Consistent with HF. The symptoms listed in Table 4.3 suggest the Symptoms Consistent with HF. The symptoms listed in Table 4.3 suggest the Modification of wording and diagnosis of HF. It is recommended that each of these symptoms be solicited diagnosis of HF. It is recommended that each of these symptoms be elicited addition of depression to Table and graded in all patients in whom the diagnosis of HF is being considered. in all patients in whom the diagnosis of HF is being considered. (Strength of 4.3 (Strength of Evidence 5 B) Evidence 5 B)4.5 Physical Examination. It is recommended that patients suspected of having HF Physical Examination. It is recommended that patients suspected of having HF Modification of wording and undergo careful physical examination with determination of vital signs and undergo careful physical examination with determination of vital signs and change in Strength of Evidence be carefully evaluated for signs and symptoms shown in Table 4.4. (Strength careful evaluation for signs shown in Table 4.4. (Strength of Evidence 5 B) from C to B and addition of of Evidence 5 C) reduced cardiac output and arrhythmia to cardiac abnormalities in Table 4.4 Heart Failure Practice Guideline4.6 It is recommended that BNP or NT-proBNP levels be assessed in all patients It is recommended that BNP or NT-proBNP levels be assessed in all patients Modification of wording and suspected of having HF when the diagnosis is not certain. (Strength of suspected of having HF, especially when the diagnosis is not certain. change in Strength of Evidence  Evidence 5 B) (Strength of Evidence 5 A) from B to A (continued on next page) HFSA e7
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments4.7 The differential diagnoses in Table 4.5 should be considered as alternative Differential Diagnosis. The differential diagnoses in Table 4.5 should be Modification of wording and explanations for signs and symptoms consistent with HF. (Strength of considered as alternative explanations for signs and symptoms consistent change in Strength of Evidence Evidence 5 C) with HF. (Strength of Evidence 5 B) from C to B and addition of chronic kidney disease and thyroid abnormalities to Table 4.54.8 No changes4.9 Symptoms. In addition to symptoms characteristic of Symptoms. In addition to symptoms characteristic of HF (dyspnea, fatigue, Clarification of HF symptoms HF, the following symptoms should be considered in the diagnosis of HF: decreased exercise tolerance, fluid retention), evaluation of the following and addition of arrhythmia to symptoms should be considered in the diagnosis of HF: list of symptoms and change in  Angina  Angina Strength of Evidence from C to  Symptoms of possible cerebral hypoperfusion, including syncope, pre-  Symptoms suggestive of embolic events B syncope, or lightheadedness  Symptoms suggestive of sleep-disordered breathing  Symptoms suggestive of embolic events  Symptoms suggestive of arrhythmias, including palpitations  Symptoms suggestive of sleep-disordered breathing  Symptoms of possible cerebral hypoperfusion, including syncope, (Strength of Evidence 5 C) presyncope, or lightheadedness (Strength of Evidence 5 B)4.10 No changes e8 Journal of Cardiac Failure Vol. 16 No. 6 June 20104.11 The degree of volume excess is a key consideration during treatment. It is Volume Status. The degree of volume excess is a key consideration during Addition of presence of dyspnea recommended that it be routinely assessed by determining: treatment. It is recommended that it be routinely assessed by determining: on exertion and hepatic  Presence of paroxysmal nocturnal dyspnea or orthopnea  Presence of paroxysmal nocturnal dyspnea or orthopnea enlargement/tenderness to list  Daily weights and vital signs with assessment for orthostatic changes  Presence of dyspnea on exertion of assessments  Presence and degree of rales, S3 gallop, jugular venous pressure elevation,  Daily weights and vital signs with assessment for orthostatic changes positive hepatojugular reflux, edema, and ascites  Presence and degree of rales, S3 gallop, jugular venous pressure elevation, (Strength of Evidence 5 B) hepatic enlargement and tenderness, positive hepatojugular reflux, edema, and ascites (Strength of Evidence 5 B)4.12 It is recommended that the following laboratory tests be obtained routinely in Standard Laboratory Tests. It is recommended that the following laboratory Addition of uric acid to list of patients being evaluated for HF: serum electrolytes, blood urea nitrogen, tests be obtained routinely in patients being evaluated for HF: serum standard laboratory tests creatinine, glucose, calcium, magnesium, lipid profile (low-density electrolytes, blood urea nitrogen, creatinine, glucose, calcium, magnesium, lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides), fasting lipid profile (low-density lipoprotein cholesterol, high-density complete blood count, serum albumin, liver function tests, urinalysis, and lipoprotein cholesterol, triglycerides), complete blood count, serum thyroid function. (Strength of Evidence 5 B) albumin, uric acid, liver function tests, urinalysis, and thyroid function. (Strength of Evidence 5 B)4.13 It is recommended that all patients with HF have an ECG performed to: Electrocardiogram (ECG). It is recommended that all patients with HF have an Addition of electrical  Assess cardiac rhythm and conduction ECG performed to: dyssynchrony and QTc interval  Detect LV hypertrophy  Assess cardiac rhythm and conduction (in some cases, using Holter to list of ECG assessments  Evaluate QRS duration, especially when ejection fraction (EF) !35% monitoring or event monitors)  Detect evidence of myocardial infarction or ischemia  Assess electrical dyssynchrony (wide QRS or bundle branch block), es- (Strength of Evidence 5 B) pecially when left ventricular ejection fraction (LVEF) !35%  Detect LV hypertrophy or other chamber enlargement  Detect evidence of MI or ischemia  Assess QTc interval, especially with drugs that prolong QT intervals (Strength of Evidence 5 B)
    • 4.14 It is recommended that all patients with HF have a posteroanterior and lateral Chest X-Ray. It is recommended that all patients with HF have a postero- Addition of placement of chest X-ray examination for determination of heart size, evidence of fluid anterior and lateral chest X-ray examination for determination of heart size, implanted cardiac devices to overload, and detection of pulmonary and other diseases. (Strength of evidence of fluid overload, detection of pulmonary and other diseases, and list of chest x-rays assessments Evidence 5 B) appropriate placement of implanted cardiac devices. (Strength of Evidence 5 B)4.15 Additional Laboratory Tests. It is recommended that patients with no apparent Additional Laboratory Tests. It is recommended that patients with no apparent Change in Strength of Evidence etiology of HF or no specific clinical features suggesting unusual etiologies etiology of HF or no specific clinical features suggesting unusual etiologies from C to B undergo additional directed blood and laboratory studies to determine the undergo additional directed blood and laboratory studies to determine the cause of HF. cause of HF. (Strength of Evidence 5 B) (Strength of Evidence 5 C)4.16 Evaluation of myocardial ischemia is recommended in those who develop New recommendation new-onset LV systolic dysfunction especially in the setting of suspected myocardial ischemia or worsening symptoms with pre-existing CAD. The choice of testing modality should depend on the clinical suspicion and underlying cardiac risk factors. Coronary angiography should be considered when pre-test probability of underlying ischemic cardiomyopathy is high and an invasive coronary intervention may be considered. (See Section 13 for specific clinical situations and Strength of Evidence)4.17 Exercise testing is not recommended as part of routine evaluation in patients Exercise testing for functional capacity is not recommended as part of routine Modification of wording and (previous with HF. Specific circumstances in which maximal exercise testing with evaluation in patients with HF. Specific circumstances in which maximal deletion of recommendation 4.16) measurement of expired gases should be considered include: exercise testing with measurement of expired gases should be considered for exercise testing for  Assessing disparity between symptomatic limitation and objective indi- include: inducible abnormality in cators of disease severity  Assessing disparity between symptomatic limitation and objective indi- myocardial perfusion or wall  Distinguishing noneHF-related causes of functional limitation, specifi- cators of disease severity motion abnormality cally cardiac versus pulmonary  Distinguishing non HF-related causes of functional limitation, specifically  Considering candidacy for cardiac transplantation or mechanical inter- cardiac versus pulmonary vention  Considering candidacy for cardiac transplantation or mechanical circula-  Determining the prescription for cardiac rehabilitation tory support  Addressing specific employment capabilities  Determining the prescription for cardiac rehabilitation Exercise testing for inducible abnormality in myocardial perfusion or wall  Addressing specific employment capabilities motion abnormality should be considered to screen for the presence of (Strength of Evidence 5 C) coronary artery disease with inducible ischemia. (Strength of Evidence 5 C)4.18 No changes (previous 4.17)4.19 It is recommended that clinical evaluation at each followup visit include the It is recommended that clinical evaluation at each follow-up visit include Change (in second part of (previous assessments listed in Table 4.9. (Strength of Evidence 5 B) determination of the elements listed in Table 4.9. (Strength of recommendation) Strength of 4.18) These assessments should include the same symptoms and signs assessed Evidence 5 B). Evidence from C to B during the initial evaluation. These assessments should include the same symptoms and signs assessed (Strength of Evidence 5 C) during the initial evaluation. (Strength of Evidence 5 B) (continued on next page) Heart Failure Practice Guideline  HFSA e9
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments4.20 Routine reevaluation of cardiac function by noninvasive or invasive methods is In the absence of deteriorating clinical presentation, repeat measurements of Modifications of (previous not recommended. Repeat measurements of ventricular volume and EF ventricular volume and LVEF should be considered in these limited recommendation throughout 4.19) should be considered under limited circumstances: circumstances:  When a prophylactic implantable  After at least 3 months of medical therapy when prophylactic ICD cardioverter defibrillator (ICD) or CRT device and defibrillator (CRT-D) placement is being considered to confirm that EF criteria are still met. placement is being considered in order to determine that LVEF criteria for (Strength of Evidence 5 B) device placement are still met after medical therapy (Strength of Evidence  In patients who show substantial clinical improvement (for example, in 5 B) response to b-blocker treatment). Such change may denote improved  When patients show substantial clinical prognosis, although it does not in itself mandate alteration or discontin- improvement (for example, in response to beta blocker treatment or uation of specific treatments. (Strength of Evidence 5 C) following pregnancy in patients with peripartum cardiomyopathy). Such Repeat determination of EF is usually unnecessary in patients with previ- change may denote improved prognosis, although it does not in itself ously documented LV dilation and low EF who manifest worsening signs or mandate alteration or discontinuation of specific treatments (see Section 7). symptoms of HF. Repeat measurement should be considered when it is (Strength of Evidence 5 C) likely to prompt a change in patient management, such as cardiac trans-  In alcohol and cardiotoxic substance abusers who have discontinued the plantation. (Strength of Evidence 5 C) abused substance. (Strength of Evidence 5 C)  In patients receiving cardiotoxic chemotherapy. (Strength of Evidence 5 B) Repeat determination of LVEF is usually unnecessary in patients with pre- viously documented LV dilatation and low LVEF who manifest worsening signs or symptoms of HF, unless the information is needed to justify a change in patient management (such as surgery or device implantation). (Strength of Evidence 5 C) e10 Journal of Cardiac Failure Vol. 16 No. 6 June 20104.21 It is recommended that reevaluation of electrolytes and renal function occur at It is recommended that reevaluation of electrolytes and renal function occur at Addition of aldosterone (previous least every 6 months in clinically stable patients and more frequently after least every 6 months in clinically stable patients and more frequently antagonists to list of patients in 4.20) changes in therapy or with evidence of change in volume status. More following changes in therapy or with evidence of change in volume status. whom more frequent frequent assessment of electrolytes and renal function is recommended in More frequent assessment of electrolytes and renal function is assessment of electrolytes and patients with severe HF, those receiving high doses of diuretics, and those recommended in patients with severe HF, those receiving high doses of renal function is who are clinically unstable. (Strength of Evidence 5 C) (See Section 7 for diuretics, those on aldosterone antagonists, and those who are clinically recommended. recommendations regarding patients on angiotensin receptor blockers.) unstable. (Strength of Evidence 5 C) (See Section 7 for recommendations regarding patients on angiotensin receptor blockers.) Section 5: Management of Asymptomatic Patients with Reduced LVEF5.1 It is recommended that all patients with ALVD exercise regularly according to It is recommended that all patients with ALVD exercise regularly according to Minor wording modification a physician-directed prescription to avoid general deconditioning; to a physician-directed prescription to avoid general deconditioning; to improve weight, blood pressure, and diabetes control; and to reduce optimize weight, blood pressure, and diabetes control; and to reduce cardiovascular risk. (Strength of Evidence 5 C) cardiovascular risk. (Strength of Evidence 5 C)5.2 No changes5.3 It is recommended that alcohol consumption be discouraged in patients with Alcohol abstinence is recommended if there is current or previous history of Deleted phrase discouraging ALVD. Abstinence is recommended if there is a current habit or history of excessive alcohol intake. (Strength of Evidence 5 C) alcohol use in ALVD. Other excessive alcohol intake. (Strength of Evidence 5 C) minor wording modifications.5.4 It is recommended that all patients with ALVD with hypertension have It is recommended that all patients with ALVD with hypertension achieve Aggressive blood pressure aggressive blood pressure control. (Strength of Evidence 5 B) optimal blood pressure control. (Strength of Evidence 5 B) control changed to optimal blood pressure control5.5 No changes
    • 5.6 ARBs are recommended for asymptomatic patients with reduced LVEF who ARBs are recommended for asymptomatic patients with reduced LVEF who Minor wording modification are intolerant of ACE inhibitors because of cough or angioedema. (Strength are intolerant of ACE inhibitors from cough or angioedema. (Strength of of Evidence 5 C) Evidence 5 C) Routine use of the combination of ACE inhibitors and ARBs for prevention Routine use of the combination of ACE inhibitors and ARBs for prevention of HF is not recommended in this population. (Strength of Evidence 5 C) of HF is not recommended in this population. (Strength of Evidence 5 C)5.7 It is recommended that beta blocker therapy be administered to asymptomatic Beta blocker therapy should be considered in asymptomatic patients with Changed from ‘‘is patients with reduced LVEF. (Post MI, Strength of Evidence 5 B; nonePost reduced LVEF. (post-MI, Strength of Evidence 5 B; non post-MI, Strength recommended’’ to ‘‘should be MI, Strength of Evidence 5 C) of Evidence 5 C) considered’’ Section 6: Nonpharmacologic Management and Health Care Maintenance in Patients with Chronic Heart Failure6.1 Dietary instruction regarding sodium intake is recommended in all patients Dietary instruction regarding sodium intake is recommended in all patients Minor wording modification with HF. Patients with HF and diabetes, dyslipidemia, or obesity should be with HF. Patients with HF and diabetes, dyslipidemia, or severe obesity given specific instructions regarding carbohydrate or caloric constraints. should be given specific dietary instructions. (Strength of Evidence 5 B) (Strength of Evidence 5 B)6.2 No changes6.3 No changes6.4 It is recommended that specific attention be paid to nutritional management of It is recommended that specific attention be paid to nutritional management of Minor wording modification patients with advanced HF and unintentional weight loss or muscle wasting patients with advanced HF and unintentional weight loss or muscle wasting (cardiac cachexia). Measurement of nitrogen balance, caloric intake, and (cardiac cachexia). Measurement of nitrogen balance, caloric intake, and prealbumin may be useful in determining appropriate nutritional prealbumin may be useful in determining appropriate nutritional supplementation. Caloric supplementation is recommended. Anabolic supplementation. Caloric supplementation is recommended. Anabolic steroids are not recommended for such patients. (Strength of Evidence 5 C) steroids are not recommended for cachexic patients. (Strength of Evidence 5 C)6.5 No changes6.6 Documentation of the type and dose of nutraceutical products used by patients Documentation of the type and dose of naturoceutical products used by Modification of terminology with HF is recommended. (Strength of Evidence 5 C) patients with HF is recommended. (Strength of Evidence 5 C) (nutraceutical to Nutraceutical use is not recommended for relief of symptomatic HF or for Naturoceutical use is not recommended for relief of symptomatic HF or for naturoceutical) the secondary prevention of cardiovascular events. Patients should be the secondary prevention of cardiovascular events. Patients should be instructed to avoid using natural or synthetic products containing ephedra instructed to avoid using natural or synthetic products containing ephedra (ma huang), ephedrine, or its metabolites because of an increase risk of (ma huang), ephedrine, or its metabolites because of an increased risk of mortality and morbidity. Products should be avoided that may have mortality and morbidity. Products should be avoided that may have significant drug interactions with digoxin, vasodilators, beta blockers, significant drug interactions with digoxin, vasodilators, beta blockers, antiarrhythmic drugs, and anticoagulants. (Strength of Evidence 5 B) antiarrhythmic drugs, and anticoagulants. (Strength of Evidence 5 B)6.7 No changes6.8 No changes6.9 No changes Heart Failure Practice Guideline6.10 It is recommended that screening for endogenous or prolonged reactive It is recommended that screening for endogenous or prolonged reactive Minor wording modification depression in patients with HF be conducted after diagnosis and at periodic depression in patients with HF be conducted following diagnosis and at  intervals as clinically indicated. For pharmacologic treatment, selective periodic intervals as clinically indicated. For pharmacologic treatment, serotonin receptor uptake inhibitors are preferred over tricyclic selective serotonin reuptake inhibitors are preferred over tricyclic antidepressants, because the latter have the potential to cause ventricular antidepressants, because the latter have the potential to cause ventricular arrhythmias, but the potential for drug interactions should be considered. arrhythmias, but the potential for drug interactions should be considered. HFSA (Strength of Evidence 5 B) (Strength of Evidence 5 B) e11 (continued on next page)
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments6.11 No changes6.12 No changes6.13 No changes6.14 No changes6.15 Endocarditis prophylaxis is not recommended based on the diagnosis of HF Endocarditis prophylaxis is not recommended based on the diagnosis of HF Addition of criteria for alone. Prophylaxis for dental and other procedures should be given alone. Consistent with the AHA recommendation, ‘prophylaxis should be endocarditis prophylaxis according to standard clinical indications. (Strength of Evidence 5 C) given for only specific cardiac conditions, associated with the highest risk of adverse outcome from endocarditis.’ These conditions include: ‘prosthetic cardiac valves; previous infective endocarditis; congenital heart disease (CHD)’ such as: ‘unrepaired cyanotic CHD, including palliative shunts and conduits; completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first six months after the procedure; repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization); cardiac transplantation recipients who develop cardiac valvulopathy.’ (Strength of Evidence 5 C)6.16 No changes e12 Journal of Cardiac Failure Vol. 16 No. 6 June 20106.17 No changes6.18 No changes6.19 It is recommended that patients with HF undergo exercise testing to determine New recommendation suitability for exercise training (patient does not develop significant ischemia or arrhythmias). (Strength of Evidence = B) If deemed safe, exercise training should be considered for patients with HF in order to facilitate understanding of exercise expectations (heart rate ranges and appropriate levels of exercise training), to increase exercise duration and intensity in a supervised setting, and to promote adherence to a general exercise goal of 30 minutes of moderate activity/exercise, 5 days per week with warm up and cool down exercises. (Strength of Evidence 5 B) Section 7: Heart Failure in Patients with Reduced Ejection Fraction7.1 No changes7.2 It is recommended that other therapy be substituted for ACE inhibitors in the It is recommended that other therapy be substituted for ACE inhibitors in the Minor wording modification following circumstances: following circumstances:  In patients who cannot tolerate ACE inhibitors because of cough, ARBs  In patients who cannot tolerate ACE inhibitors due to cough, ARBs are are recommended. (Strength of Evidence 5 A) recommended. (Strength of Evidence 5 A)  The combination of hydralazine and an oral nitrate may be considered in  The combination of hydralazine and an oral nitrate may be considered in such patients not tolerating ARB therapy. (Strength of Evidence 5 C) such patients not tolerating ARB therapy. (Strength of Evidence 5 C)  Patients intolerant to ACE inhibitors because of hyperkalemia or renal  Patients intolerant to ACE inhibitors from hyperkalemia or renal insuffi- insufficiency are likely to experience the same side effects with ARBs. In ciency are likely to experience the same side effects with ARBs. In these these cases, the combination of hydralazine and an oral nitrate should be cases, the combination of hydralazine and an oral nitrate should be con- considered. (Strength of Evidence 5 C) sidered. (Strength of Evidence 5 C)
    • 7.3 No changes (previous 7.10)7.4 ARBs should be considered in patients experiencing angioedema while on ARBs should be considered in patients experiencing angioedema while on Minor wording modifications (previous ACE inhibitors based on their underlying risk and with recognition that ACE inhibitors based on their underlying risk and with recognition that 7.12) angioedema has been reported infrequently with these agents. (Strength of angioedema has been reported infrequently with ARBs. (Strength of Evidence 5 B) Evidence 5 B) The combination of hydralazine and oral nitrates may be considered in this The combination of hydralazine and oral nitrates may be considered in this setting for patients who do not tolerate ARB therapy. (Strength of setting for patients who do not tolerate ARB therapy. (Strength of Evidence 5 C) Evidence 5 C)7.5 Individual ARBs may be considered as initial therapy rather than ACE Individual ARBs may be considered as initial therapy rather than ACE Terminology modification (previous inhibitors for patients with the following conditions: inhibitors for patients with the following conditions: (changed ‘‘systolic 7.11)  HF post MI (Strength of Evidence 5 A)  HF Post-MI (Strength of Evidence 5 A) dysfunction’’ to ‘‘reduced  Chronic HF and systolic dysfunction (Strength of Evidence 5 B)  Chronic HF and reduced LVEF (Strength of Evidence 5 B) LVEF)7.6 No changes (previous 7.3)7.7 No changes (previous 7.4)7.8 Beta blocker therapy is recommended for patients with a recent Beta blocker therapy is recommended for patients with a recent Minor wording modifications (previous decompensation of HF after optimization of volume status and successful decompensation of HF after optimization of volume status and successful 7.5) discontinuation of intravenous diuretics and vasoactive agents, including discontinuation of intravenous diuretics and vasoactive agents, including inotropic support. Whenever possible, beta blocker therapy should be inotropic support. Whenever possible, beta blocker therapy should be initiated in the hospital setting at a low dose before discharge in stable initiated in the hospital setting at a low dose prior to discharge in stable patients. (Strength of Evidence 5 B) patients. (Strength of Evidence 5 B)7.9 Beta blocker therapy is recommended in the great majority of patients with LV Beta blocker therapy is recommended in the great majority of patients with HF Modification of terminology (previous systolic dysfunction, even if there is concomitant diabetes, chronic and reduced LVEF, even if there is concomitant diabetes, chronic (‘‘LV systolic dysfunction’’ 7.6) obstructive lung disease, or peripheral vascular disease. Beta blocker obstructive lung disease, or peripheral vascular disease. Beta blocker changed to ‘‘reduced LVEF’’) therapy should be used with caution in patients with diabetes with recurrent therapy should be used with caution in patients with diabetes with recurrent hypoglycemia, asthma, or resting limb ischemia. Considerable caution hypoglycemia, with asthma, or with resting limb ischemia. Considerable should be used if beta blockers are initiated in patients with marked caution should be used if beta blockers are initiated in patients with marked bradycardia (!55 beats/min) or marked hypotension (systolic blood bradycardia (!55 beats/min) or marked hypotension (systolic blood pressure !80 mm Hg). Beta blockers are not recommended in patients with pressure !80 mm Hg). Beta blockers are not recommended in patients with asthma with active bronchospasm. (Strength of Evidence 5 C) asthma with active bronchospasm. (Strength of Evidence 5 C)7.10 It is recommended that b-blockade be initiated at low doses and uptitrated It is recommended that beta blockade be initiated at low doses and uptitrated Deleted information related to (previous gradually, typically no sooner than at 2-week intervals. Doses found to be gradually, typically at 2-week intervals in patients with reduced LVEF, and beta blocker management 7.7) effective in HF trials generally are achieved in 8 to 12 weeks. Patients after 3-10 day intervals in patients with reduced LVEF following newly developing worsening HF symptoms or other side effects during titration diagnosed MI. (Strength of Evidence 5 B) may require a dosage adjustment of diuretic or concomitant vasoactive Heart Failure Practice Guideline medications. If side effects resolve with medication adjustment, patients can subsequently be titrated to target or maximally tolerated doses. Some  patients may require a more prolonged interval during uptitration, a temporary reduction in b-blocker dose, or, in rare cases, withdrawal of therapy. (Strength of Evidence 5 B) HFSA (continued on next page) e13
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments7.11 It is recommended that beta blocker therapy be continued in most patients It is recommended that beta blocker therapy be continued in most patients Addition of criteria for beta (previous experiencing a symptomatic exacerbation of HF during chronic experiencing a symptomatic exacerbation of HF during chronic blocker discontinuation and 7.8) maintenance treatment. (Strength of Evidence 5 C) maintenance treatment, unless they develop cardiogenic shock, refractory reinstitution A temporary reduction of dose in this setting may be considered. Abrupt volume overload, or symptomatic bradycardia (Strength of Evidence 5 C) discontinuation in patients with symptomatic exacerbation should be A temporary reduction of dose (generally by one-half) in this setting may be avoided. (Strength of Evidence 5 C) considered. Abrupt discontinuation in patients with symptomatic If discontinued or reduced, beta blockers should be reinstated or the dose exacerbation should be avoided, unless the situation is life-threatening. should be gradually increased before the patient is discharged. (Strength of Evidence 5 C) If discontinued or reduced, beta blockers should be reinstated before the patient is discharged. In general, doses should be uptitrated to the previous well-tolerated dose as soon as safely possible (Strength of Evidence 5B)7.12 The routine administration of an ARB is not recommended in addition to ACE The routine administration of an ARB is not recommended in addition to ACE Modification of terminology (previous inhibitor and beta blocker therapy in patients with recent acute MI and LV inhibitor and beta blocker therapy in patients with a recent acute MI and (‘‘LV dysfunction’’ changed to 7.13) dysfunction. (Strength of Evidence 5 A) reduced LVEF. (Strength of Evidence 5 A) ‘‘reduced LVEF’’)7.13 The addition of an ARB should be considered in patients with HF due to New recommendation reduced LVEF who have persistent symptoms or progressive worsening despite optimized therapy with an ACE inhibitor and beta blocker. (Strength of Evidence 5 A)7.14 Administration of an aldosterone antagonist is recommended for patients with Administration of an aldosterone antagonist is recommended for patients with Modification of terminology e14 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 NYHA class IV or class III, previously class IV, HF from LV systolic NYHA class IV (or class III, previously class IV) HF from reduced LVEF (‘‘LV systolic dysfunction’’ dysfunction (LVEF #35%) while receiving standard therapy, including (!35%) while receiving standard therapy, including diuretics. (Strength of changed to ‘‘reduced LVEF’’) diuretics. (Strength of Evidence 5 A) Evidence 5 A)7.15 Administration of an aldosterone antagonist should be considered in patients Administration of an aldosterone antagonist should be considered in patients Addition of history of diabetes after an acute MI, with clinical HF signs and symptoms and an LVEF following an acute MI, with clinical HF signs and symptoms or history of mellitus to criteria for therapy !40%. Patients should be on standard therapy, including an ACE inhibitor diabetes mellitus, and an LVEF !40%. Patients should be on standard (or ARB) and a b-blocker. (Strength of Evidence 5 A) therapy, including an ACE inhibitor (or ARB) and a beta blocker. (Strength of Evidence 5 A)7.16 No changes7.17 No changes7.18 No changes7.19 A combination of hydralazine and isosorbide dinitrate is recommended as part A combination of hydralazine and isosorbide dinitrate is recommended as part Modification of terminology of standard therapy in addition to beta blockers and ACE inhibitors for of standard therapy in addition to beta blockers and ACE inhibitors for (‘‘LV systolic dysfunction’’ African Americans with LV systolic dysfunction. African Americans with HF and reduced LVEF. changed to ‘‘reduced LVEF’’)  NYHA III or IV HF (Strength of Evidence 5 A)  NYHA III or IV HF (Strength of Evidence 5 A)  NYHA II HF (Strength of Evidence 5 B)  NYHA II HF (Strength of Evidence 5 B) (See Section 15: Special (See Section 15 Special Populations) Populations)7.20 A combination of hydralazine and isosorbide dinitrate may be considered in A combination of hydralazine and isosorbide dinitrate may be considered in Modification of terminology noneAfrican American patients with LV systolic dysfunction who remain non-African-American patients with HF and reduced LVEF who remain (‘‘LV systolic dysfunction’’ symptomatic despite optimized standard therapy. (Strength of Evidence 5 symptomatic despite optimized standard therapy. (Strength of Evidence changed to ‘‘reduced LVEF’’) C) 5 C)
    • 7.21 Additional pharmacologic therapy should be considered in patients with HF Additional pharmacologic therapy should be considered in patients with HF Modification of terminology due to systolic dysfunction who have persistent symptoms or progressive and reduced LVEF who have persistent symptoms or progressive worsening (‘‘systolic dysfunction’’ worsening despite optimized therapy with an ACE inhibitor and beta despite optimized therapy with an ACE inhibitor and beta blocker. The changed to ‘‘reduced LVEF’’); blocker. The choice of specific agent will be influenced by clinical choice of specific agent will be influenced by clinical considerations, addition of post-MI HF under considerations, including renal function status, chronic serum potassium including renal function status, chronic serum potassium concentration, aldosterone antagonists concentration, blood pressure, and volume status. The triple combination of blood pressure, and volume status. The triple combination of an ACE an ACE inhibitor, an ARB, and an aldosterone antagonist is not inhibitor, an ARB, and an aldosterone antagonist is not recommended recommended because of the high risk of hyperkalemia. (Strength of because of the high risk of hyperkalemia. (Strength of Evidence 5 C) Evidence 5 C)  Addition of an ARB. (Strength of Evidence 5 A)  Addition of an ARB. (Strength of Evidence 5 A)  Addition of an aldosterone antagonist:  Addition of an aldosterone antagonist: Bfor severe HF (Strength of Evidence 5A) BFor severe HF (Strength of Evidence 5 A) Bfor moderate HF (Strength of Evidence 5 C) B For moderate HF (Strength of Evidence 5 C) B for post-MI HF (Strength of Evidence 5 A)  Addition of the combination of hydralazine/isosorbide dinitrate:  Addition of the combination of hydralazine/isosorbide dinitrate: B For African Americans (Strength of Evidence 5A) B for African Americans (Strength of Evidence 5 A) B For others (Strength of Evidence 5 C) B for others (Strength of Evidence 5 C)7.22 Additional pharmacological therapy should be considered in patients with HF Additional pharmacological therapy should be considered in patients with HF Modification of terminology due to systolic dysfunction who are unable to tolerate a beta blocker and and reduced LVEF who are unable to tolerate a beta blocker and have (‘‘systolic dysfunction’’ have persistent symptoms or progressive worsening despite optimized persistent symptoms or progressive worsening despite optimized therapy changed to ‘‘reduced LVEF’’) therapy with an ACE inhibitor. The choice of specific agent will be with an ACE inhibitor. The choice of specific agent will be influenced by influenced by clinical considerations, including renal function status, clinical considerations, including renal function status, chronic serum chronic serum potassium concentration, blood pressure and volume status. potassium concentration, blood pressure and volume status. The triple The triple combination of an ACE inhibitor, an ARB, and an aldosterone combination of an ACE inhibitor, an ARB, and an aldosterone antagonist is antagonist is not recommended due to the high risk of hyperkalemia. not recommended due to the high risk of hyperkalemia. (Strength of (Strength of Evidence 5 C) Evidence 5 C)  Addition of an ARB. (Strength of Evidence 5 C)  Addition of an ARB. (Strength of Evidence 5 C)  Addition of an aldosterone antagonist:  Addition of an aldosterone antagonist: Bfor severe HF (Strength of Evidence 5 C) Bfor severe HF (Strength of Evidence 5 C) Bfor moderate HF (Strength of Evidence 5 C) Bfor moderate HF (Strength of Evidence 5 C)  Addition of the combination of hydralazine/isosorbide dinitrate:  Addition of the combination of hydralazine/isosorbide dinitrate: B For African-Americans (Strength of Evidence 5 C) B for African Americans (Strength of Evidence 5 C) B for others (Strength of Evidence 5 C) B for others (Strength of Evidence 5 C)7.23 No changes7.24 The initial dose of diuretic may be increased as necessary to relieve The initial dose of diuretic may be increased as necessary to relieve Modification of terminology congestion. Restoration of normal volume status may require multiple congestion. Restoration of normal volume status may require multiple (‘‘noncompliance’’ changed to adjustments over many days and occasionally weeks in patients with severe adjustments over many days and occasionally weeks in patients with severe ‘‘nonadherence’’) fluid overload evidenced by massive edema or ascites. After a diuretic effect fluid overload evidenced by massive edema or ascites. After a diuretic effect is achieved with short acting loop diuretics, increasing administration is achieved with short-acting loop diuretics, increasing administration frequency to twice or even 3 times per day will provide more diuresis with frequency to twice or even 3 times per day will provide more diuresis with less physiologic perturbation than larger single doses. (Strength of Evidence less physiologic perturbation than larger single doses. (Strength of Evidence Heart Failure Practice Guideline 5 B) 5 B) Oral torsemide may be considered in patients in whom poor absorption of Oral torsemide may be considered in patients in whom poor absorption of  oral medication or erratic diuretic effect may be present, particularly those oral medication or erratic diuretic effect may be present, particularly those with right-sided HF and refractory fluid retention despite high doses of other with right-sided HF and refractory fluid retention despite high doses of other loop diuretics. (Strength of Evidence 5 C) loop diuretics. (Strength of Evidence 5 C) HFSA Intravenous administration of diuretics may be necessary to relieve Intravenous administration of diuretics may be necessary to relieve congestion. (Strength of Evidence 5 A) congestion. (Strength of Evidence 5 A) Diuretic refractoriness may represent patient noncompliance, a direct effect Diuretic refractoriness may represent patient nonadherence, a direct effect e15 of diuretic use on the kidney, or progression of underlying cardiac of diuretic use on the kidney, or progression of underlying cardiac dysfunction. dysfunction. (continued on next page)
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments7.25 No changes7.26 Careful observation for the development of side effects, including electrolyte Careful observation for the development of side effects, including electrolyte Addition of worsening renal abnormalities, symptomatic hypotension, and renal dysfunction, is abnormalities, symptomatic hypotension, renal dysfunction, or worsening function to list of potential side recommended in patients treated with diuretics, especially when used at renal function, is recommended in patients treated with diuretics, especially effects high doses and in combination. Patients should undergo routine laboratory when used at high doses and in combination. Patients should undergo studies and clinical examination as dictated by their clinical response. routine laboratory studies and clinical examination as dictated by their (Strength of Evidence 5 B) clinical response. (Strength of Evidence 5 B)7.27 No changes7.28 No changes7.29 Digoxin should be considered for patients with LV systolic dysfunction (LVEF Digoxin may be considered to improve symptoms in patients with reduced Modification from ‘‘should be #40%) who have signs or symptoms of HF while receiving standard LVEF (LVEF #40%) who have signs or symptoms of HF while receiving considered’’ to ‘‘may be therapy, including ACE inhibitors and beta blockers: standard therapy, including ACE inhibitors and beta blockers: considered’’, and change in NYHA class II-III (Strength of Evidence 5 A)  NYHA class II-III (Strength of Evidence 5 B) Strength of Evidence NYHA class IV (Strength of Evidence 5 B)  NYHA class IV (Strength of Evidence 5 C)7.30 It is recommended that the dose of digoxin, which should be based on lean It is recommended that the dose of digoxin, which should be based on lean Addition of a lower serum body mass, renal function and concomitant medications, should be 0.125 body mass, renal function, and concomitant medications, should be 0.125 concentration range (0.7-0.9 mg daily in the majority of patients and the serum digoxin level should be mg daily in the majority of patients and the serum digoxin level should be ng/ml), and change in strength e16 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 !1.0 ng/mL. (Strength of Evidence 5 C) !1.0 ng/mL, generally 0.7-0.9 ng/mL. (Strength of Evidence 5 B) of evidence from C to B7.31 Adequate control of the ventricular response to atrial fibrillation in patients Digoxin should be considered for achieving adequate control of the ventricular Modification from ‘‘is with HF is recommended. (Level of Evidence 5 B) response to atrial fibrillation in patients with HF. (Strength of Evidence 5 recommended’’ to ‘‘should be B) considered’’7.32 No changes7.33 Treatment with warfarin (goal INR 2.0e3.0) is recommended for all patients Treatment with warfarin (goal international normalized ratio [INR] 2.0-3.0) is Addition of persistent or long- with HF and chronic or documented paroxysmal atrial fibrillation (Strength recommended for all patients with HF and chronic or documented standing atrial fibrillation of Evidence 5 A) or a history of systemic or pulmonary emboli, including paroxysmal, persistent, or long-standing atrial fibrillation (Strength of stroke or transient ischemic attack, (Strength of Evidence 5 C) unless Evidence 5 A) or a history of systemic or pulmonary emboli, including contraindicated. stroke or transient ischemic attack (Strength of Evidence 5 C), unless contraindicated.7.34 No changesPrevious Deleted from current guideline 7.357.35 Long-term treatment with an antithrombotic agent is recommended for Long-term treatment with an antiplatelet agent, generally aspirin in doses of Modification of terminology (previous patients with HF from ischemic cardiomyopathy, whether or not they are 75 to 81 mg, is recommended for patients with HF due to ischemic from ‘‘antithrombotic’’ to 7.36) receiving ACE inhibitors. (Strength of Evidence 5 B) cardiomyopathy, whether or not they are receiving ACE inhibitors. ‘‘antiplatelet’’; addition of Aspirin is recommended in most patients for whom anticoagulation is not (Strength of Evidence 5 B) recommended doses for specifically indicated because of its proven efficacy in non-HF patients with Warfarin (goal INR 2.0-3.0) and clopidogrel (75 mg) also have prevented aspirin. ischemic heart disease, its convenience, and lower cost. Lower doses of vascular events in post-MI patients and may be considered as alternatives to INR range changed to 2.0-3.0 aspirin (75 or 81 mg) may be preferable because data from 2 trials suggest aspirin. (Strength of Evidence 5 B) more frequent worsening of HF at higher doses. (Strength of Evidence 5 C) Warfarin (goal INR 2.0e3.5) and clopidogrel (75 mg) have also prevented vascular events in post MI patients and may be considered as alternatives to aspirin. (Strength of Evidence 5 B)
    • 7.36 Routine use of aspirin is not recommended in patients with HF not from Routine use of aspirin is not recommended in patients with HF without Modification of terminology (previous ischemic cardiomyopathy and without other evidence of atherosclerotic atherosclerotic vascular disease. (Strength of Evidence 5 C) 7.37) vascular disease. (Strength of Evidence 5 C)Previous Deleted from current guideline; 7.38 addressed in recommendation 7.357.37 No changes (previous 7.39)7.38 In patients with HF and an implantable cardioverter defibrillator (ICD), In patients with HF and an ICD, amiodarone may be considered to reduce the Modification of wording (previous amiodarone may be considered to reduce the frequency of repetitive frequency of recurrent symptomatic arrhythmias causing ICD shocks. 7.40) discharges. (Strength of Evidence 5 C) (Strength of Evidence 5 C)7.39 It is recommended that patients taking amiodarone therapy and digoxin or It is recommended that when amiodarone therapy is initiated, the potential for Modification of wording (previous warfarin generally have their maintenance doses of many commonly used interactions with other drugs be reviewed. The maintenance doses of 7.41) agents, such as digoxin, warfarin, and statins, reduced when amiodarone is digoxin, warfarin, and some statins should be reduced when amiodarone is initiated and then carefully monitored for the possibility of adverse drug initiated and then carefully monitored. Adjustment in doses of these drugs interactions. Adjustment in doses of these drugs and laboratory assessment and laboratory assessment of drug activity or serum concentration after of drug activity or serum concentration after initiation of amiodarone is initiation of amiodarone is recommended. (Strength of Evidence 5 A) recommended. (Strength of Evidence 5 A)7.40 Routine use of amiodarone therapy for asymptomatic arrhythmias that are not New recommendation felt to contribute to HF or ventricular dysfunction is not recommended. (Strength of Evidence 5 B)7.41 n-3 polyunsaturated fatty acids (PUFA) may be considered to reduce mortality New recommendation in HF patients with NYHA class II-IV symptoms and reduced LVEF. (Strength of Evidence 5 B) Section 8: Disease Management, Advance Directives, and End-of-Life Care in Heart Failure8.1 It is recommended that patients with HF and their family members or It is recommended that patients with HF and their family members or Deletion of NYHA specific caregivers receive individualized education and counseling that emphasizes caregivers receive individualized education and counseling that emphasizes portion of the self-care. This education and counseling should be delivered by providers self-care. This education and counseling should be delivered by providers recommendation; modification using a team approach in which nurses with expertise in HF management using a team approach in which nurses with expertise in HF management of wording provide the majority of education and counseling, supplemented by provide the majority of education and counseling, supplemented by physician input and, when available and needed, input from dietitians, physician input and, when available and needed, input from dietitians, pharmacists, and other health care providers. All HF patients benefit from pharmacists, and other health care providers. (Strength of Evidence 5 B) education and counseling, but patients in NYHA functional class III or IV Teaching is not sufficient without skill building and specification of critical need the most intensive education, whereas patients in NYHA I or II need target behaviors. It is recommended that essential elements of patient less intensive education. (Strength of Evidence 5 B) education (with associated skills) are utilized to promote self-care as shown Teaching is not sufficient without skill building and specification of critical in Table 8.1. (Strength of Evidence 5 B) target behaviors. Essential elements of patient education to promote self- care with associated skills are shown in Table 8.1. (Strength of Evidence 5 Heart Failure Practice Guideline B)  (continued on next page) HFSA e17
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments8.2 It is recommended that patients’ literacy, cognitive status, psychologic state, It is recommended that patients’ literacy, cognitive status, psychological state, Deletion of description of culture, and access to social and financial resources be taken into account culture, and access to social and financial resources be taken into account interventions; modification of for optimal education and counseling. Because cognitive impairment and for optimal education and counseling. Because cognitive impairment and Strength of Evidence from C to depression are common in HF and can seriously interfere with learning, depression are common in HF and can seriously interfere with learning, B patients should be screened for these. Appropriate interventions, such as patients should be screened for these. Patients found to be cognitively supportive counseling and pharmacotherapy, are recommended for those impaired need additional support to manage their HF. (Strength of Evidence patients found to be depressed. Patients found to be cognitively impaired 5 B) need additional support to manage their HF. (Strength of Evidence 5 C)8.3 No changes8.4 It is recommended that the frequency and intensity of patient education and It is recommended that the frequency and intensity of patient education and Modification of wording counseling vary according to the stage of illness. Patients in advanced HF counseling vary according to the stage of the illness. Patients in advanced or with persistent difficulty adhering to the recommended regimen require HF or persistent difficulty adhering to the recommended regimen require the the most eduction and counseling. Patients should be offered a variety of most education and counseling. Patients should be offered a variety of options for learning about HF according to their individual preferences: options for learning about HF according to their individual preferences: videotape, one-on-one or group discussion, reading materials, translators, videotape, one-on-one or group discussion, reading materials, translators, telephone calls, mailed information, internet, visits. Repeated exposure to telephone calls, mailed information, internet, visits. Repeated exposure to material is essential because a single session is never sufficient. (Strength of material is recommended because a single session is never sufficient. Evidence 5 B) (Strength of Evidence 5 B)8.5 No changes e18 Journal of Cardiac Failure Vol. 16 No. 6 June 20108.6 No changes8.7 Patients recently hospitalized for HF and other patients at high risk should be Patients recently hospitalized for HF and other patients at high risk for HF Addition of poor health literacy considered for referral to a comprehensive HF disease management program decompensation should be considered for comprehensive HF disease that delivers individualized care. High-risk patients include those with renal management. High-risk patients include those with renal insufficiency, low insufficiency, low output state, diabetes, chronic obstructive pulmonary output state, diabetes, chronic obstructive pulmonary disease, persistent disease, persistent NYHA class III or IV symptoms, frequent hospitalization NYHA class III or IV symptoms, frequent hospitalization for any cause, for any cause, multiple active comorbidities, or a history of depression, multiple active comorbidities, or a history of depression, cognitive cognitive impairment, or persistent nonadherence to therapeutic regimens. impairment, inadequate social support, poor health literacy, or persistent (Strength of Evidence 5 A) nonadherence to therapeutic regimens. (Strength of Evidence 5 A)8.8 No changes8.9 No changes8.10 No changes8.11 Patient and family or caregiver discussions about quality of life and prognosis It is recommended that patient and family or caregiver discussions about Modification of wording are recommended as part of the disease management of HF. (Strength of quality of life and prognosis be included in the disease management of HF. Evidence 5 C) (Strength of Evidence 5 C)
    • 8.12 It is recommended that the patient’s status be optimized medically and It is recommended that Addition of criteria for end of life psychologically before discussing the possibility that end-of-life care is  Seriously ill patients with HF and their families be educated to understand care indicated. The decision to declare a patient as an appropriate candidate for that patients with HF are at high risk of death, even while aggressive ef- end-of-life care should be made by physicians experienced in the care of forts are made to prolong life. patients with HF. End-of-life management should be coordinated with the  Patients with HF be made aware that HF is potentially life-limiting, but patient’s primary care physician. As often as possible, discussions regarding that pharmacologic and device therapies and self-management can end-of-life care should be initiated while the patient is still capable of prolong life. In most cases, chronic HF pharmacologic and device participating in decision making. (Strength of Evidence 5 C) therapies should be optimized as indicated before identifying that patients are near end-of-life.  Identification of end-of-life in a patient should be made in collaboration with clinicians experienced in the care of patients with HF when possible.  End-of-life management should be coordinated with the patient’s primary care physician.  As often as possible, discussions regarding end-of-life care should be initiated while the patient is still capable of participating in decision- making. (Strength of Evidence 5 C)8.13 End-of-life care should be considered in patients who have advanced, End-of-life care should be considered in patients who have advanced, Addition of cardiac device to list persistent HF with symptoms at rest despite repeated attempts to optimize persistent HF with symptoms at rest despite repeated attempts to optimize of optimization therapies; pharmacologic and nonpharmacologic therapy, as evidenced by one or more pharmacologic, cardiac device, and other therapies, as evidenced by 1 or modification of strength of of the following: more of the following: evidence  Frequent hospitalizations (3 or more per year)  HF hospitalization (Strength of Evidence 5 B)  Chronic poor quality of life with inability to accomplish activities of daily  Chronic poor quality of life with minimal or no ability to accomplish living activities of daily living (Strength of Evidence 5 C)  Need for intermittent or continuous intravenous support  Need for continuous intravenous inotropic therapy support (Strength of  Consideration of assist devices as destination therapy Evidence 5 B) (Strength of Evidence 5 C)8.14 It is recommended that end-of-life care strategies be individualized, include It is recommended that end-of-life care strategies be individualized and Addition of information effective symptom management, and avoid unnecessary testing and include core HF pharmacologic therapies, effective symptom management regarding end-of-life care interventions. (Strength of Evidence 5 C) and comfort measures, while avoiding unnecessary testing. New life- strategies prolonging interventions should be discussed with patients and care-givers with careful discussion of whether they are likely to improve symptoms. (Strength of Evidence 5 C)8.15 It is recommended that, as part of end-of life-care, patients and their families/ It is recommended that a specific discussion about resuscitation be held in the Addition of information caregivers be given specific directions concerning their response to clinical context of planning for overall care and for emergencies with all patients regarding resuscitation events if they decide against resuscitation. Inactivation of an implantable with HF. The possibility of SCD for patients with HF should be defibrillation device should be discussed. (Strength of Evidence 5 C) acknowledged. Specific plans to reduce SCD (for example with an ICD) or to allow natural death should be based on the individual patient’s risks and preferences for an attempt at resuscitation with specific discussion of risks and benefits of inactivation the ICD. Preferences for attempts at resuscitation and plans for approach to care should be readdressed at turning points in the patient’s course or if potentially life-prolonging interventions are considered. (Strength of Evidence 5 C)8.16 It is recommended that, as part of end-of-life care, patients and their families/ New recommendation Heart Failure Practice Guideline caregivers have a plan to manage a sudden decompensation, death, or progressive decline. Inactivation of an implantable defibrillation device  should be discussed in the context of allowing natural death at end of life. A process for deactivating defibrillators should be clarified in all settings in which patients with HF receive care. (Strength of Evidence 5 C) HFSA (continued on next page) e19
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments8.17 Patients with HF undergoing end-of-life care may be considered for hospice Patients with HF receiving end-of-life care should be considered for Modification from ‘‘may be services that can be delivered in the home, a hospital setting, or a special enrollment in hospice that can be delivered in the home, a nursing home, or considered’’ to ‘‘should be hospice unit. (Strength of Evidence 5 C) a special hospice unit. (Strength of Evidence 5 C) considered’’Previous Deleted recommendations; 8.16 and portions of these 8.18 recommendations have been incorporated into recommendations 8.15 and 8.16 Section 9: Electrophysiology Testing and the Use of Devices in Heart Failure9.1 It is recommended that the decision to undertake electrophysiologic It is recommended that the decision to undertake electrophysiologic Modification/clarification of intervention be made in light of functional status and prognosis based on intervention, including ICD implantation, be made in light of functional wording severity of underlying HF and comorbid conditions. If LV dysfunction is status and prognosis based on severity of underlying HF and comorbid a reason for recommending electrophysiologic intervention, LV function conditions. If an ICD is considered due to LV dysfunction which is of recent should be re-assessed, ideally after 3e6 months of optimal medical therapy. onset, LV function should be reassessed, ideally after 3-6 months of optimal (Strength of Evidence 5 C) medical therapy. (Strength of Evidence 5 C)9.2 Immediate evaluation is recommended in patients with HF who present with Immediate evaluation is recommended in patients with HF who present with Modification/clarification of syncope. In the absence of a clear identifiable noncardiac cause, patients syncope. In the absence of a clear identifiable noncardiac cause, wording e20 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 should be referred for electrophysiologic evaluation. (Strength of consultation with an EP specialist should be obtained. (Strength of Evidence Evidence 5 C) 5 C)9.3 No changes9.4 In patients with or without concomitant coronary artery disease (including Revision of LVEF criteria and a prior MI O1 month ago): a. Prophylactic ICD placement should be considered in patients with an strength of evidence based on a) Prophylactic ICD placement should be considered (LVEF #30%) and LVEF #35% and mild to moderate HF symptoms: etiology may be considered (LVEF 31e35%) for those with mild to moderate HF symptoms (NYHA II-III). (Strength of Evidence 5 A) See  Ischemic etiology (Strength of Evidence 5 A) Recommendation 9.1 for additional criteria.  Non-ischemic etiology (Strength of Evidence 5 B) b) Concomitant ICD placement should be considered in patients undergoing See Recommendation 9.1 for additional criteria. implantation of a biventricular pacing device according to the criteria in b. In patients who are undergoing implantation of a biventricular pacing Recommendations 9.7e9.8. (Strength of Evidence 5 B) See Recom- device according to the criteria in recommendations 9.7-9.8, use of a de- mendation 9.1 for additional criteria. vice that provides defibrillation should be considered. (Strength of Evi- dence 5 B) See Recommendation 9.1 for additional criteria.9.5 ICD placement is not recommended in chronic, severe refractory HF when ICD placement is not recommended in chronic, severe refractory HF when Addition of life expectancy there is no reasonable expectation for improvement. (Strength of Evidence there is no reasonable expectation for improvement or in patients with a life criterion to recommendation 5 C) expectancy of less than 1 year. (Strength of Evidence 5 C)9.6 ICD implantation is recommended for survivors of cardiac arrest from ICD implantation is recommended for survivors of cardiac arrest from Revision of MI criteria ventricular fibrillation or hemodynamically unstable sustained ventricular ventricular fibrillation or hemodynamically unstable sustained VT that is not tachycardia without evidence of acute MI or if the event occurs more than due to a transient, potentially reversible cause, such as acute MI. (Strength 48 hours after the onset of infarction in the absence of a recurrent ischemic of Evidence 5 A) event. (Strength of Evidence 5 A)9.7 Biventricular pacing therapy should be considered for patients with sinus Biventricular pacing therapy is recommended for patients in sinus rhythm with Modification from ‘‘should be rhythm, a widened QRS interval ($120 ms) and severe LV systolic a widened QRS interval ($120 ms) and severe LV systolic dysfunction considered’’ to ‘‘is dysfunction (LVEF #35% with LV dilatation O5.5 cm) who have LVEF (# 35%) who have persistent, moderate to severe HF (NYHA III) recommended’’; removal of persistent, moderate to severe HF (NYHA III) despite optimal medical despite optimal medical therapy. (Strength of Evidence 5 A) LV dimension criterion therapy. (Strength of Evidence 5 A)
    • 9.8 Biventricular pacing therapy may be considered for patients with atrial New recommendation fibrillation with a widened QRS interval ($120 ms) and severe LV systolic dysfunction LVEF #35% who have persistent, moderate to severe HF (NYHA III) despite optimal medical therapy. (Strength of Evidence 5 B)9.9 Selected ambulatory NYHA IV patients may be considered for biventricular Selected ambulatory NYHA IV patients in sinus rhythm with QRS $ 120 ms Additional criteria for patient (Previous pacing therapy. (Strength of Evidence 5 B) and LV systolic dysfunction may be considered for biventricular pacing selection 9.8) therapy. (Strength of Evidence 5 B)9.10 Biventricular pacing therapy is not recommended in patients who are Biventricular pacing therapy may be considered in patients with reduced LVEF Modification from ‘‘is not (previous asymptomatic or have mild HF symptoms. (Strength of Evidence 5 C) and QRS R 150 ms who have NYHA I or II HF symptoms. (Strength of recommended’’ to ‘‘may be 9.9) Evidence 5 B) considered’’; modification of strength of evidence from C to B; additional criteria for patient selection9.11 In patients with reduced LVEF who require chronic pacing and in whom New recommendation frequent ventricular pacing is expected, biventricular pacing may be considered. (Strength of Evidence 5 C)9.12 No changes (previous 9.10) Section 10: Surgical Approaches to the Treatment of Heart Failure10.1 No changes10.2 No changes10.3 No changes10.4 No changes10.5 No changes10.6 No changes10.7 Patients with refractory HF and hemodynamic instability, and/or compromised New recommendation end-organ function, with relative contraindications to cardiac transplantation or permanent mechanical circulatory assistance expected to improve with time or restoration of an improved hemodynamic profile should be considered for urgent mechanical circulatory support as a ‘‘bridge to decision.’’ These patients should be referred to a center with expertise in the management of patients with advanced HF. (Strength of Evidence 5 C) Section 11: Evaluation and Management of Patients with Heart Failure and Preserved LVEF Heart Failure Practice Guideline11.1 Careful attention to differential diagnosis is recommended in patients with HF Careful attention to differential diagnosis is recommended in patients with HF Addition of cardiac  and preserved LVEF to distinguish among a variety of cardiac disorders, and preserved LVEF to distinguish among a variety of cardiac disorders, catheterization to list of because treatments may differ. These various entities may be distinguished because treatments may differ. These various entities may be distinguished diagnostic tools, modification based on echocardiography, electrocardiography, and stress imaging (via based on echocardiography, electrocardiography, and stress imaging (via of Figure 11.3 and addition of exercise or pharmacologic means using myocardial perfusion or exercise or pharmacologic means, using myocardial perfusion or Figures 11.1 and 11.2. HFSA echocardiographic imaging). See algorithm in Figure 11.1 for a detailed echocardiographic imaging) and cardiac catheterization. See Figures 11.1, approach to differential diagnosis. (Strength of Evidence 5 C) 11.2, and 11.3 for guidance to a differential diagnosis. (Strength of Evidence 5 C) e21 (continued on next page)
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments11.2 Evaluation for the possibility of ischemic heart disease and inducible Evaluation for ischemic heart disease and inducible myocardial ischemia is Minor wording modifications myocardial ischemia is recommended in patients with HF and preserved recommended in patients with HF and preserved LVEF (see Section 13). LVEF. (Strength of Evidence 5 C) (Strength of Evidence 5 C)11.3 Aggressive blood pressure management is recommended in patients with HF Blood pressure monitoring is recommended in patients with HF and preserved Modification of terminology and preserved LVEF (Section 14, Recommendation 14.15). (Strength of LVEF (Section 14, Recommendation 14.1). (Strength of Evidence 5 C) (‘‘aggressive blood pressure Evidence 5 C) management’’ changed to ‘‘blood pressure monitoring’’)11.4 No changes11.5 No changes11.6 ARBs or ACE inhibitors should be considered in patients with HF and In the absence of other specific indications for these drugs, ARBs or ACE Modification from ‘‘should be preserved LVEF. (Strength of evidence 5 B) inhibitors may be considered in patients with HF and preserved LVEF. considered’’ to ‘‘may be  ARBs (Strength of Evidence 5 B)  ARBs (Strength of Evidence 5 C) considered’’; modification of  ACE inhibitors (Strength of Evidence 5 C)  ACE inhibitors (Strength of Evidence 5 C) strength of evidence for ARBs from B to C11.7 No changes11.8 No changes e22 Journal of Cardiac Failure Vol. 16 No. 6 June 201011.9 Calcium channel blockers should be considered in patients with: Calcium channel blockers should be considered in patients with HF and Modification of wording  Atrial fibrillation requiring control of ventricular rate in whom b-blockers preserved LVEF and: regarding beta blocker have proven inadequate for this purpose because of intolerance. In these  Atrial fibrillation requiring control of ventricular rate and intolerance to intolerance patients, diltiazem or verapamil should be considered. (Strength of beta blockers. In these patients, diltiazem or verapamil should be Evidence 5 C) considered. (Strength of Evidence 5 C)  Symptom-limiting angina. (Strength of Evidence 5 A)  Symptom-limiting angina. (Strength of Evidence 5 A)  Hypertension. Amlodipine should be considered. (Strength of  Hypertension. (Strength of Evidence 5 C) Evidence 5 C)11.10 Measures to restore and maintain sinus rhythm should be considered in Measures to restore and maintain sinus rhythm may be considered in patients Modification from ‘‘should be patients who have symptomatic atrial flutter-fibrillation, but this decision who have symptomatic atrial flutter-fibrillation and preserved LVEF, but this considered’’ to ‘‘may be should be individualized. (Strength of Evidence 5 C) decision should be individualized. (Strength of Evidence 5 C) considered’’ Section 12: Evaluation and Management of Patients with Acute Decompensated Heart Failure12.1 The diagnosis of decompensated HF should be based primarily on signs and The diagnosis of ADHF should be based primarily on signs and symptoms. Modification of BNP symptoms. (Strength of Evidence 5 C) (Strength of Evidence 5 C) recommendation from ‘‘should When the diagnosis is uncertain, determination of BNP or NT-proBNP When the diagnosis is uncertain, determination of BNP or NT-proBNP be considered’’ to ‘‘is concentration should be considered in patients being evaluated for dyspnea concentration is recommended in patients being evaluated for dyspnea who recommended’’ who have signs and symptoms compatible with HF. (Strength of Evidence have signs and symptoms compatible with HF. (Strength of Evidence 5 A) 5 A) The natriuretic peptide concentration should not be interpreted in isolation, The natriuretic peptide concentration should not be interpreted in isolation, but in the context of all available clinical data bearing on the diagnosis of but in the context of all available clinical data bearing on the diagnosis of HF, and with the knowledge of cardiac and non-cardiac factors that can raise HF. or lower natriuretic peptide levels.12.2 No changes
    • 12.3 No changes12.4 No changes12.5 No changes12.6 It is recommended that diuretics be administered at doses needed to produce It is recommended that diuretics be administered at doses needed to produce Addition of serum electrolytes a rate of diuresis sufficient to achieve optimal volume status with relief of a rate of diuresis sufficient to achieve optimal volume status with relief of signs and symptoms of congestion (edema, elevated JVP, dyspnea), without signs and symptoms of congestion (edema, elevated JVP, dyspnea), without inducing an excessively rapid reduction in intravascular volume, which may inducing an excessively rapid reduction in 1) intravascular volume, which result in symptomatic hypotension and/or worsening renal function. may result in symptomatic hypotension and/or worsening renal function, or (Strength of Evidence 5 C) 2) serum electrolytes, which may precipitate arrhythmias or muscle cramps. (Strength of Evidence 5 C)12.7 No changes12.8 Monitoring of daily weights, intake, and output is recommended to assess Monitoring of daily weights, intake, and output is recommended to assess Addition of criterion for catheter clinical efficacy of diuretic therapy. Routine use of a Foley catheter is not clinical efficacy of diuretic therapy. Routine use of a Foley catheter is not placement recommended for monitoring volume status. However, placement of recommended for monitoring volume status. However, placement of a catheter is recommended when close monitoring of urine output is needed. a catheter is recommended when close monitoring of urine output is needed (Strength of Evidence 5 C) or if a bladder outlet obstruction is suspected of contributing to worsening renal function. (Strength of Evidence 5 C)12.9 Careful observation for development of a variety of side effects, including Careful observation for development of a variety of side effects, including Addition of gout as side effect renal dysfunction, electrolyte abnormalities and symptomatic hypotension, renal dysfunction, electrolyte abnormalities, symptomatic hypotension, and is recommended in patients treated with diuretics, especially when used at gout is recommended in patients treated with diuretics, especially when high doses and in combination. Patients should undergo routine laboratory used at high doses and in combination. Patients should undergo routine studies and clinical examination as dictated by their clinical response. laboratory studies and clinical examination as dictated by their clinical (Strength of Evidence 5 C) response. (Strength of Evidence 5 C) Serum potassium and magnesium levels should be monitored at least daily It is recommended that serum potassium and magnesium levels should be Wording modified and maintained in the normal range. More frequent monitoring may be monitored at least daily and maintained in the normal range. More frequent necessary when diuresis is rapid. (Strength of Evidence 5 C) monitoring may be necessary when diuresis is rapid. (Strength of Evidence Overly rapid diuresis may be associated with severe muscle cramps, which 5 C) should be treated with potassium replacement if indicated. (Strength of Overly rapid diuresis may be associated with severe muscle cramps. If Evidence 5 C) indicated, treatment with potassium replacement is recommended. (Strength of Evidence 5 C)12.10 No changes12.11 When congestion fails to improve in response to diuretic therapy, the following When congestion fails to improve in response to diuretic therapy, the following Addition of re-evaluation of options should be considered: options should be considered: congestion  Sodium and fluid restriction,  Re-evaluating presence/absence of congestion  Increased doses of loop diuretic,  Sodium and fluid restriction,  Continuous infusion of a loop diuretic, or  Increasing doses of loop diuretic,  Addition of a second type of diuretic orally (metolazone or spironolac-  Continuous infusion of a loop diuretic, or tone) or intravenously (chlorothiazide).  Addition of a second type of diuretic orally (metolazone or spironolac-  A fifth option, ultrafiltration, may be considered. (Strength of Evidence 5 tone) or intravenously (chlorothiazide). Heart Failure Practice Guideline C) Another option, ultrafiltration, may be considered. (Strength of Evidence 5 C) 12.12 A low-sodium diet (2 g daily) is recommended, as is supplemental oxygen, as A low sodium diet (2 g daily) is recommended for most hospitalized patients. Deletion of supplemental oxygen needed for hypoxemia. (Strength of Evidence 5 C) (Strength of Evidence 5 C) (moved to recommendation In patients with recurrent or refractory volume overload, stricter sodium In patients with recurrent or refractory volume overload, stricter sodium 12.14) HFSA restriction may be considered. (Strength of Evidence 5 C) restriction may be considered. (Strength of Evidence 5 C) e23 (continued on next page)
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments12.13 No changes12.14 Routine administration of supplemental oxygen in the absence of hypoxia is Routine administration of supplemental oxygen in the presence of hypoxia is Addition of recommendation for not recommended. (Strength of Evidence 5 C) recommended. (Strength of Evidence 5 C) oxygen in the presence of Routine administration of supplemental oxygen in the absence of hypoxia is hypoxemia not recommended. (Strength of Evidence 5 C)12.15 Use of non-invasive positive pressure ventilation may be considered for New recommendation severely dyspneic patients with clinical evidence of pulmonary edema. (Strength of Evidence 5 A)12.16 Venous thromboembolism prophylaxis with low dose unfractionated heparin, New recommendation low molecular weight heparin, or fondaparinux to prevent proximal deep venous thrombosis and pulmonary embolism is recommended for patients who are admitted to the hospital with ADHF and who are not already anticoagulated and have no contraindication to anticoagulation. (Strength of Evidence 5 B) Venous thromboembolism prophylaxis with a mechanical device (intermittent pneumatic compression devices or graded compression stockings) to prevent proximal deep venous thrombosis and pulmonary embolism should be considered for patients who are admitted to the hospital with ADHF and who are not already anticoagulated and who have e24 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 a contraindication to anticoagulation. (Strength of Evidence 5 C)12.17 In the absence symptomatic hypotension, intravenous nitroglycerin, In the absence of symptomatic hypotension, intravenous nitroglycerin, Addition of worsening renal (previous nitroprusside, or nesiritide may be considered as an addition to diuretic nitroprusside or nesiritide may be considered as an addition to diuretic function as potential side effect 12.15) therapy for rapid improvement of congestive symptoms in patients admitted therapy for rapid improvement of congestive symptoms in patients admitted with ADHF. Frequent blood pressure monitoring is recommended with with ADHF. (Strength of Evidence 5 B) these agents. (Strength of Evidence 5 B). These agents should be decreased Frequent blood pressure monitoring is recommended with these agents. in dosage on discontinued if symptomatic hypotension develops. (Strength (Strength of Evidence 5 B) of Evidence 5 B) These agents should be decreased in dosage or discontinued if symptomatic Reintroduction in increasing doses may be considered once symptomatic hypotension or worsening renal function develops. (Strength of Evidence hypotension is resolved. (Strength of Evidence 5 C) 5 B) Reintroduction in increasing doses may be considered once symptomatic hypotension is resolved. (Strength of Evidence 5 C)12.18 No changes (previous 12.16)12.19 Intravenous vasodilators (nitroprusside, nitroglycerin, or nesiritide) may be Intravenous vasodilators (nitroprusside, nitroglycerin, or nesiritide) may be Modification of strength of (previous considered in patients with ADHF and advanced HF who have persistent considered in patients with ADHF who have persistent severe HF despite evidence for nitroprusside 12.17) severe HF despite aggressive treatment with diuretics and standard oral aggressive treatment with diuretics and standard oral therapies. from C to B therapies. (Strength of Evidence 5 C)  Nitroprusside (Strength of Evidence 5 B)  Nitroglycerine, Nesiritide (Strength of Evidence 5 C)
    • 12.20 Intravenous inotropes (milrinone or dobutamine) may be considered to relieve Intravenous inotropes (milrinone or dobutamine) may be considered to relieve Modification of strength of (previous symptoms and improve end-organ function in patients with advanced HF symptoms and improve end-organ function in patients with advanced HF evidence from B to C for 12.18) characterized by LV dilation, reduced LVEF, and diminished peripheral characterized by LV dilation, reduced LVEF, and diminished peripheral portions of this perfusion or end-organ dysfunction (low output syndrome), particularly if perfusion or end-organ dysfunction (low output syndrome), particularly if recommendation these patients have marginal systolic blood pressure (!90 mm Hg), have these patients have marginal systolic blood pressure (! 90 mm Hg), have symptomatic hypotension despite adequate filling pressure, or are symptomatic hypotension despite adequate filling pressure, or are unresponsive to, or intolerant of, intravenous vasodilators. (Strength of unresponsive to, or intolerant of, intravenous vasodilators. (Strength of Evidence 5 C) Evidence 5 C) These agents may be considered in similar patients with evidence of fluid These agents may be considered in similar patients with evidence of fluid overload if they respond poorly to intravenous diuretics or manifest overload if they respond poorly to intravenous diuretics or manifest diminished or worsening renal function. (Strength of Evidence 5 C) diminished or worsening renal function. (Strength of Evidence 5 C) When adjunctive therapy is needed in other patients with ADHF, When adjunctive therapy is needed in other patients with ADHF, administration of vasodilators should be considered instead of intravenous administration of vasodilators should be considered instead of intravenous inotropes (milrinone or dobutamine). (Strength of Evidence 5 B) inotropes (milrinone or dobutamine). (Strength of Evidence 5 C) Intravenous inotropes (milrinone or dobutamine) are not recommended Intravenous inotropes (milrinone or dobutamine) are not recommended unless left heart filling pressures are known to be elevated based on direct unless left heart filling pressures are known to be elevated or cardiac index measurement or clear clinical signs. (Strength of Evidence 5 B) is severely impaired based on direct measurement or clear clinical signs. Administration of intravenous inotropes (milrinone or dobutamine) in the (Strength of Evidence 5 C) setting of ADHF should be accompanied by continuous or frequent blood It is recommended that administration of intravenous inotropes (milrinone Wording modified pressure monitoring and continuous monitoring of cardiac rhythm. (Strength or dobutamine) in the setting of ADHF be accompanied by continuous or of Evidence 5 C) frequent blood pressure monitoring and continuous monitoring of cardiac If symptomatic hypotension or worsening tachyarrhythmias develop during rhythm. (Strength of Evidence 5 C) administration of these agents, discontinuation or dose reduction should be If symptomatic hypotension or worsening tachyarrhythmias develop during considered. (Strength of Evidence 5 C) administration of these agents, discontinuation or dose reduction should be considered. (Strength of Evidence 5 C)12.21 No changes (previous 12.19)12.22 Invasive hemodynamic monitoring should be considered in a patient: Invasive hemodynamic monitoring should be considered in a patient: Addition of cardiac transplant as (previous Who is refractory to initial therapy,  who is refractory to initial therapy, criterion for invasive 12.20) Whose volume status and cardiac filling pressures are unclear,  whose volume status and cardiac filling pressures are unclear, hemodynamic monitoring Who has clinically significant hypotension (typically systolic blood pressure  who has clinically significant hypotension (typically SBP ! 80mm Hg) or !80 mm Hg) or worsening renal function during therapy, or worsening renal function during therapy, or In whom documentation of an adequate hemodynamic response to the  who is being considered for cardiac transplant and needs assessment of inotropic agent is necessary when chronic outpatient infusion is being degree and reversibility of pulmonary hypertension, or considered.  in whom documentation of an adequate hemodynamic response to the (Strength of Evidence 5 C) inotropic agent is necessary when chronic outpatient infusion is being considered. (Strength of Evidence 5 C)12.23 No changes (previous 12.21)12.24 It is recommended that every effort be made to use the hospital stay for It is recommended that every effort be made to use the hospital stay for Modification of strength of Heart Failure Practice Guideline (previous assessment and improvement of patient compliance via patient and family assessment and improvement of patient adherence via patient and family evidence from C to B; change 12.22) education and social support services (Section 8). (Strength education and social support services (see Section 8). (Strength of Evidence in terminology (‘‘compliance’’  of Evidence 5 C) 5 B) to ‘‘adherence’’) (continued on next page) HFSA e25
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation Comments12.25 No changes (previous 12.23)12.26 Discharge planning is recommended as part of the management of patients Discharge planning is recommended as part of the management of patients Addition of alcohol moderation (previous with ADHF. Discharge planning should address the following issues: with ADHF. Discharge planning should address the following issues: and smoking cessation 12.24)  Details regarding medication, dietary sodium restriction, and recommen-  Details regarding medication, dietary sodium restriction, and recommen- ded activity level ded activity level  Follow-up by phone or clinic visit early after discharge to reassess volume  Follow-up by phone or clinic visit early after discharge to reassess volume status status  Medication and dietary compliance  Medication and dietary compliance  Monitoring of body weight, electrolytes, and renal function  Alcohol moderation and smoking cessation  Consideration of referral for formal disease management (Strength of  Monitoring of body weight, electrolytes and renal function Evidence 5 C)  Consideration of referral for formal disease management (Strength of Evidence 5 C) Section 13: Evaluation and Therapy for Heart Failure in the Setting of Ischemic Heart Disease13.1 Assessment for risk factors for CAD is recommended in all patients with Ongoing assessment for risk factors for CAD is recommended in all patients Moved diagnostic portion of chronic HF regardless of EF. (Strength of Evidence 5 A) with chronic HF regardless of LVEF. (Strength of Evidence 5 A) recommendation to 13.2 The diagnostic approach for CAD should be individualized based on patient preference and comorbidities, eligibility and willingness to perform e26 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 revascularization. (Strength of Evidence 5 C)13.2 It is recommended that the diagnostic approach for CAD be individualized Previously part of 13.1 based on patient preference and comorbidities, eligibility, symptoms suggestive of angina and willingness to undergo revascularization. (Strength of Evidence 5 C)13.3 It is recommended that patients with HF and angina undergo cardiac It is recommended that patients with HF and symptoms suggestive of angina Modification of wording (previous catheterization with coronary angiography to assess for potential undergo cardiac catheterization with coronary angiography to assess for 13.2) revascularization. potential revascularization. (Strength of Evidence 5 B) (Strength of Evidence 5 B)13.4 It is recommended that patients with HF, no angina, and known CAD should It is recommended that, at the initial diagnosis of HF and any time symptoms Clarification of type and timing (previous undergo noninvasive stress imaging and/or coronary angiography to assess worsen without obvious cause, patients with HF, no angina, and known of risk assessments 13.3) severity of coronary disease and the presence of ischemia. (Strength of CAD should undergo risk assessment that may include noninvasive stress Evidence 5 C) imaging and/or coronary angiography to assess severity of coronary disease and the presence of ischemia. (Strength of Evidence 5 C)13.5 No changes (previous 13.4)13.6 No changes (previous 13.5)
    • 13.7 Any of the following imaging tests may be used to identify inducible ischemia Any of the following imaging tests should be considered to identify inducible Modification of wording (previous or viable but nocontractile myocardium: ischemia or viable myocardium: 13.6)  Exercise or pharmacologic stress myocardial perfusion imaging  Exercise or pharmacologic stress myocardial perfusion imaging  Exercise or pharmacologic stress echocardiography  Exercise or pharmacologic stress echocardiography  Cardiac magnetic resonance imaging  Cardiac magnetic resonance imaging  Positron emission tomography scanning (Strength of Evidence 5 B)  Positron emission tomography scanning (Strength of Evidence 5 B)13.8 No changes (previous 13.7)13.9 Antiplatelet therapy is recommended in patients with HF and CAD unless Antiplatelet therapy is recommended to reduce vascular events in patients with Addition of indication for (previous contraindicated. (Aspirin, Strength of Evidence 5 B; Clopidogrel, Strength HF and CAD unless contraindicated. (aspirin, Strength of Evidence 5 A; antiplatelet therapy, and 13.8) of Evidence 5 C) clopidogrel, Strength of Evidence 5 B) modification of strength of evidence13.10 ACE inhibitors are recommended in all patients with systolic dysfunction or ACE inhibitors are recommended in all patients with either reduced or Modification of terminology (previous preserved systolic function after an MI. (Strength of Evidence 5 A) preserved LVEF after an MI. (Strength of Evidence 5 A) (‘‘systolic dysfunction’’ 13.9) changed to ‘‘reduced LVEF’’)13.11 No changes (previous 13.10)13.12 It is recommended that ACE-inhibitor and beta blocker therapy be initiated It is recommended that ACE-inhibitor and beta blocker therapy be initiated Modification of terminology (previous early (!48 hours) during hospitalization in hemodynamically stable post early (!48 hours) during hospitalization in hemodynamically stable post- (‘‘LV dysfunction’’ changed to 13.11) MI patients with LV dysfunction or HF. (Strength of Evidence 5 A) MI patients with reduced LVEF or HF. (Strength of Evidence 5 A) ‘‘reduced LVEF’’)13.13 No changes (previous 13.12)13.14 Calcium channel blockers should be considered in patients with HF who have Calcium channel blockers may be considered in patients with HF who have Addition of calcium channel (previous angina despite the optimal use of beta blockers and nitrates. Amlodipine and angina despite the optimal use of beta blockers and nitrates. Amlodipine and blockers that should be 13.13) felodipine are the preferred calcium channel blockers in patients with felodipine are the preferred calcium channel blockers in patients with avoided angina and decreased systolic function. (Strength of Evidence 5 C) angina and decreased systolic function. Based on available data, first generation calcium channel blockers (i.e. diltiazem, verapamil) should be avoided in patients with CAD, HF, and LVEF !40, unless necessary for heart rate control or other indications. (Strength of Evidence 5 C)13.15 No changes (previous 13.14)13.16 No changes (previous Heart Failure Practice Guideline 13.15)  Section 14: Managing Patients with Hypertension and Heart Failure14.1 It is recommended that blood pressure be aggressively treated to lower systolic It is recommended that blood pressure be optimally treated to lower systolic Modification of wording and and usually diastolic levels. Target resting levels should be !130/!80 mm and usually diastolic levels. More than 1 drug may be required. Target change in strength of evidence HFSA Hg, if tolerated. (Strength of Evidence 5 C) resting levels should be !130/!80 mm Hg, if tolerated. (Strength of from C to A Evidence 5 A) e27 (continued on next page)
    • Appendix A. (continued) 2006 Guideline Recommendation 2010 Guideline Recommendation CommentsPrevious Deleted 14.214.2 No changes (previous 14.3)14.3 No changes (previous 14.4)14.4 If BP remains O130/80 mm Hg then the addition of a diuretic is If blood pressure remains O130/80 mm Hg then the addition of a thiazide Modified to specify thiazide (previous recommended, followed by a calcium antagonist or other antihypertensive diuretic is recommended, followed by a dihydropyridine calcium antagonist diuretic or dihydropyridine 14.5) drugs. (Strength of Evidence 5 C) (eg, amlodipine or felodipine) or other antihypertensive drugs. (Strength of calcium channel antagonist Evidence 5 C)14.5 No changes (previous 14.6)14.6 If blood pressure remains O130/80 mm Hg, a noncardiac-depressing calcium If blood pressure remains O130/80 mm Hg, a dihydropyridine calcium Modified to specify (previous antagonist (eg, amlodipine) may be considered or other antihypertensive antagonist (eg, amlodipine or felodipine) may be considered or other dihydropyridine e28 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 14.7) medication doses increased. (Strength of Evidence 5 C) antihypertensive medication doses increased. (Strength of Evidence 5 C) Section 15: Management of Heart Failure in Special Populations15.1 No changes15.2 No changes15.3 No changes15.4 No changes15.5 No changes15.6 ARBs are recommended for administration to symptomatic and asymptomatic New recommendation women with an LVEF # 40% who are intolerant to ACE inhibitors for reasons other than hyperkalemia or renal insufficiency. (Strength of Evidence 5 A)15.7 The combination of hydralazine/isosorbide dinitrate is recommended as New recommendation standard therapy for African American women with moderate to severe HF symptoms who are on background neurohormonal inhibition. (Strength of Evidence 5 B)15.8 No changes (previous 15.6)
    • 15.9 No changes (previous 15.7)15.10 No changes (previous 15.8)15.11 No changes (previous 15.9) Section 16: Myocarditis: Current Treatment16.1 No changes16.2 No changes Section 17: Genetic Evaluation of Cardiomyopathy New section Heart Failure Practice Guideline  HFSA e29
    • Appendix C. Financial Disclosure Equity Interests/ Other Intellectual Consulting Speaker’s Research Stock/Stock Equity Royalty Non-Royalty Financial Property FellowshipName Fees/Honoraria Bureau Grants Options Interests Income Payments Benefit Salary Rights SupportNancy M. Albert, Medtronic R.N., Ph.DInder S. Anand, Amgen Novartis CVRx, Novartis VA Medical M.D., Ph.D. Pharmaceuticals, Pharma- Pharmaceuticals, Center Boston Scientific, ceuticals Paracor Corventis, CVRx, Merck, Medtronic, N30, ParacorJ. Malcolm O. Arnold, Abbott, Boehringer M.D. Ingelheim, GlaxoSmithKline, Merck-Frosst, Novartis, PfizerJohn P. Boehmer, M.D. Boston, Scientific, Boston Scientific, Medtronic, CardioMEMS, St. Jude Medtronic, Novartis, e30 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 ParacorJohn C. Burnett, M.D. Anexon, Nile Anexon, Bayer, BioRad, Anexon, Nile Therapeutics, Merck, Nile Therapeutics Otsuka Therapeutics, TrevenaJohn Chin, M.D. Gilead, Otsuka Boston Scientific, Eli Lilly, Gilead, NovartisJay N. Cohn, M.D. GlaxoSmithKline CPC, LLC HDT, Inc. MLHFQ, NitroMedSean P. Collins, Abbott Point-of-Care, Abbott Point-of-Care, M.D., MSc Astellas, Bayer, BRAHMS Diagnostics, Corthera, The National Institutes of Medicines Health/NHLBI Company, OtsukaJustin A. Ezekowitz, Amgen, Bristol-Myers Amgen, Bristol-Myers MBBCh Squibb, Pfizer Squibb, Merck, Ortho-Biotech/Johnson & JohnsonThomas Force, M.D. Merck Schering GlaxoSmithKline Plough/MerckBart Galle, Ph.D. disclosures: none
    • Michael M. Givertz, Cardioxyl Asahi Kasei M.D.Sarah J. Goodlin, M.D. Servier Boston Scientific CARE, St. Jude Medical FoundationBarry H. Greenberg, Biogen Idec, Gilead, Merck, M.D. CardioMEMS, Novartis, sanofi- Corthera, aventis Cytokinetics, GlaxoSmithKline, Otsuka, Paracor, St. Jude, ZensunRay E. Hershberger, disclosures: none M.D.Steven R. Houser, disclosures: none Ph.D.Jonathan G. Howlett, AstraZeneca, AstraZeneca, AstraZeneca, Medtronic, M.D. Merck, Novartis, Merck, Novartis, Merck, Novartis, Schering, Servier Schering, Servier Schering, ServierSharon A. Hunt, M.D. disclosures: noneMariell Jessup, M.D. Medtronic Boston ScientificStuart D. Katz, M.D. Amgen, Dura Heart Terumo, Merck, ParacorMarc Klapholz, M.D. GlaxoSmithKline, GlaxoSmithKline Medtronic, Paracor, St. Jude, ScheringMarvin W. Kronenberg, Cardiovascular M.D. Services of AmericaJoAnn Lindenfeld, M.D. Astellas, Boston Merck Scientific, Forest, Medtronic, N30Douglas L. Mann, M.D. ARMGO Miragen Pharmaceuticals, Heart Failure Practice Guideline Medtronic, Miragen, Nile Therapeutics,  PeriCor Therapeutics (continued on next page) HFSA e31
    • Appendix C. (continued) Equity Interests/ Other Intellectual Consulting Speaker’s Research Stock/Stock Equity Royalty Non-Royalty Financial Property FellowshipName Fees/Honoraria Bureau Grants Options Interests Income Payments Benefit Salary Rights SupportBarry M. Massie, M.D. ARCA, Boehringer, Merck Bristol-Myers Squibb, Corthera, Cytokinetics, Duke Clinical Research Institute, Merck, Nile Therapeutics, Novartis, sanofi- aventis, St. Jude, Takeda, TrevenaMandeep R. Mehra, Geron, Johnson & National Institutes M.D. Johnson, of Health Medtronic, Pericor, Solvay, St. JudeLuisa Mestroni, M.D. M01 RR00051- University of 1575 Colorado e32 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 (employee)Alan B. Miller, M.D. disclosures: noneDebra K. Moser, disclosures: none R.N., DNSc.Mariann R. Piano, disclosures: none R.N., Ph.D.Richard J. Rodeheffer, disclosures: none M.D.Joseph G. Rogers, M.D. Forrest Boston Scientific, Pharmaceuticals, Medtronic ThoratecChristine E. Seidman, HHMI & NIH M.D.Randall C. Starling, BioControl, Biotronik, Medtronic, CardioMEMS Medtronic M.D., MPH Medtronic, Novartis, Thoratec NovartisWilliam G. Stevenson, disclosures: none M.D.
    • Wendy Gattis Stough, ARCA Discovery, Inc., Pharm.D. Gilead Sciences, Inc., GlaxoSmithKlline, Heart Failure Society of America, Medtronic, Otsuka, SciosW.H. Wilson Tang, Medtronic, Merck & Abbott Laboratories M.D. CompanyMatthew R.G. Taylor, Genzyme Muscular Dystrophy M.D., Ph.D. Therapeutics Association/March of Dimes/Genzyme TherapeuticsJohn R. Teerlink, M.D. Abbott Laboratories, Abbott Laboratories, Cytokinetics BAS Medical/ BAS Medical/Corthera, Corthera, Biogen Bristol-Myers Squibb, Idec, Bristol-Myers Cytokinetics, Squibb, GlaxoSmithKline, CardioDynamics, Merck, National CardioMEMS, Institutes of Health, CoGeneSys, Novartis, sanofi-aventis Cytokinetics, Geron, GlaxoSmithKline, Icon Medical Imaging, Indigo Pharma, Kowa Pharma, Luitpold Pharma, Merck, Momentum Research, Nile Therapeutics, Novartis, sanofi- aventis, Scios/ Johnson & JohnsonJeffery A. Towbin, disclosure: none M.D.Mary N. Walsh, M.D. ARCA, Boston Scientific, EMERGE, Medtronic, United Health CareClyde W. Yancy, M.D. disclosures: noneCheryl Yano disclosures: none Heart Failure Practice GuidelineMichael R. Zile, M.D. ABIM, BMS, BMS, Boston, Scientific, Department MUSC, OCD/ CorAssist, CVRx, CVRx, Department of of VA, J&J  DC Devices, Gilead, VA, Gilead, MUSC, Medtronic, Merck, Medtronic, Merck, National N30, Novartis, National Heart, Lung Heart, Lung OCD/J&J, sanofi- and Blood Institute, and Blood HFSA aventis, Up-To-Date Novartis, OCD/J&J, Institute Pfizer, sanofi-aventis e33
    • Journal of Cardiac Failure Vol. 16 No. 6 2010 Section 2: Conceptualization and Working Table 2.1. Additional HF Definitions Definition of Heart Failure ‘‘HF With Reduced Left A clinical syndrome characterized by Ventricular Ejection Fraction signs and symptoms of HF and Heart failure (HF) remains a major and growing societal (LVEF)’’ Sometimes: reduced LVEF. Most commonlyproblem despite advances in detection and therapy.1-4 How- ‘‘HF With a Dilated Left associated with LV chamberever, there is no widely accepted characterization and def- Ventricle’’ dilation. ‘‘HF With Preserved LVEF’’ A clinical syndrome characterized byinition of HF, probably because of the complexity of the Sometimes: ‘‘HF With signs and symptoms of HF withsyndrome. The conceptualization and working definition Nondilated LV’’ preserved LVEF. Most commonlyof HF presented here emerged as these guidelines were de- associated with a nondilated LV chamber. May be the result ofveloped. They are critical to understanding HF and ap- valvular disease or other causesproaching its treatment appropriately. (Section 11). ‘‘Myocardial Remodeling’’ Pathologic myocardial hypertrophy or dilation in response to increased Conceptual Background. HF is a syndrome rather than myocardial stress. These changesa primary diagnosis. It has many potential etiologies, di- are generally accompanied byverse clinical features, and numerous clinical subsets. Pa- pathologic changes in the cardiac interstitium. Myocardialtients may have a variety of primary cardiovascular remodeling is generally adiseases and never develop cardiac dysfunction, and those progressive disorder.in whom cardiac dysfunction is identified through testingmay never develop clinical HF. In addition to cardiac dys- from the loss or dysfunction of myocardial muscle or inter-function, other factors, such as vascular stiffness, dyssyn- stitium.chrony, and renal sodium handling, play major roles in HF is a syndrome caused by cardiac dysfunction, gen-the manifestation of the syndrome of HF. erally resulting from myocardial muscle dysfunction Patients at risk for many cardiovascular diseases are at or loss and characterized by either LV dilation orrisk for HF. Early identification and treatment of risk fac- hypertrophy or both. Whether the dysfunction is pri-tors is perhaps the most significant step in limiting the pub- marily systolic or diastolic or mixed, it leads to neuro-lic health impact of HF.5-7 Emphasis on primary and hormonal and circulatory abnormalities, usuallysecondary prevention is particularly critical because of resulting in characteristic symptoms such as fluidthe difficulty of successfully treating left ventricular (LV) retention, shortness of breath, and fatigue, especiallydysfunction, especially when severe.5 Current therapeutic on exertion. In the absence of appropriate therapeuticadvances in the treatment of HF do not make prevention intervention, HF is usually progressive at the level ofany less important. both cardiac function and clinical symptoms. The Although HF is progressive, current therapy may provide severity of clinical symptoms may vary substantiallystability and even reversibility. The inexorable progression during the course of the disease process and may notof HF from LV remodeling and dysfunction is no longer in- correlate with changes in underlying cardiac func-evitable. Prolonged survival with mild to moderate LV dys- tion. Although HF is progressive and often fatal,function is now possible. Therapy with angiotensin- patients can be stabilized and myocardial dysfunctionconverting enzyme inhibitors (or angiotensin receptor and remodeling may improve, either spontaneously orblockers), beta blockers, and cardiac resynchronization as a consequence of therapy. In physiologic terms, HFtherapy can lead to slowing or to partial reversal of remod- is a syndrome characterized by either or both pulmo-eling. nary and systemic venous congestion and/or inade- Because of this prolonged survival, comorbid conditions, quate peripheral oxygen delivery, at rest or duringsuch as coronary artery disease or renal failure, can prog- stress, caused by cardiac dysfunction.ress, complicating treatment. Given this prolonged survival,considerable attention is devoted in this guideline to diseasemanagement, the use of multidrug therapy, and the manage-ment of patients with HF at the end of life. Additional Definitions Working Definition. Although HF may be caused by HF is often classified as HF with reduced systolic func-a variety of disorders, including valvular abnormalities tion versus HF with preserved systolic function. Myocardialand dysrhythmias, the following comprehensive guideline remodeling often precedes the clinical syndrome of HF.and this working definition focus on HF primarily Additional definitions are provided in Table 2.1. A table of acronyms and their meaning is provided in Appendix B. Disclosures 1071-9164/$ - see front matter Ó 2010 Elsevier Inc. All rights reserved. doi:10.1016/j.cardfail.2010.05.011 See Appendix C. e34
    • Heart Failure Practice Guideline  HFSA e35 References 4. McCullough PA, Philbin EF, Spertus JA, Kaatz S, Sandberg KR, Weaver WD. Confirmation of a heart failure epidemic: findings from the Resource Utilization Among Congestive Heart Failure (REACH)1. Fang J, Mensah GA, Croft JB, Keenan NL. Heart failure-related hospi- study. J Am Coll Cardiol 2002;39:60e9. talization in the U.S., 1979 to 2004. J Am Coll Cardiol 2008;52: 5. Baker DW. Prevention of heart failure. J Card Fail 2002;8:333e46. 428e34. 6. Dunlay SM, Weston SA, Jacobsen SJ, Roger VL. Risk factors for heart fail-2. Koelling TM, Chen RS, Lubwama RN, L’Italien GJ, Eagle KA. ure: a population-based case-control study. Am J Med 2009;122:1023e8. The expanding national burden of heart failure in the United States: 7. Lee DS, Gona P, Vasan RS, Larson MG, Benjamin EJ, Wang TJ, et al. the influence of heart failure in women. Am Heart J 2004;147: Relation of disease pathogenesis and risk factors to heart failure with 74e8. preserved or reduced ejection fraction: insights from the framingham3. Loehr LR, Rosamond WD, Chang PP, Folsom AR, Chambless LE. heart study of the national heart, lung, and blood institute. Circulation Heart failure incidence and survival (from the Atherosclerosis Risk in 2009;119:3070e7. Communities study). Am J Cardiol 2008;101:1016e22.
    • e36 Journal of Cardiac Failure Vol. 16 No. 6 June 2010 Appendix B. Acronyms Appendix B. (continued) PPAR-a peroxisome proliferator-activated receptor-alphaAcronym Meaning PUFA polyunsaturated fatty acidsACE angiotensin converting enzyme PVC premature ventricular contractionADA American Diabetes Association QTc QT interval corrected for heart rateADHF acute decompensated heart failure RAAS renin-angiotensin-aldosterone systemAF atrial fibrillation RCM restrictive cardiomyopathyAHA/ACC American Heart Association/American College of RV right ventricular Cardiology SAECG signal-averaged electrocardiogramALVD asymptomatic left ventricular dysfunction SAVER surgical anterior ventricular endocardial restorationARB angiotensin receptor blocker SBP systolic blood pressureARVD/C arrhythmogenic right ventricular dysplasia/ SCD sudden cardiac death cardiomyopathy SDC serum digoxin concentrationAV arteriovenous SPECT single-photon emission computed tomographyBMI body mass index SSRI selective serotonin reuptake inhibitorsBNP B-type natriuretic peptide STEMI ST-elevation myocardial infarctionBUN blood urea nitrogen TNF-a tumor necrosis factor-alphaCABG coronary artery bypass graft UFH unfractionated heparinCAD coronary artery disease USDA United States Department of AgricultureCHD congenital heart disease VE/VCO2 ventilation equivalent of carbon dioxide (productionCI confidence interval slope)CK-MM creatinine kinase MM isoenzyme VF ventricular fibrillationCOPD chronic obstructive pulmonary disease VT ventricular tachycardiaCOX-2 cyclooxygenase-2 Clinical TrialsCPAP continuous positive airway pressure Acronym Full Trial NameCPR cardiopulmonary resuscitation ACCOMPLISH Avoiding Cardiovascular Events Through CombinationCR/XL controlled release/extended release Therapy in Patients Living with SystolicCREST a limited cutaneous form of scleroderma defined by Hypertension calsinosis, Raynaud’s syndrome, esophageal ADHERE Acute Decompensated Heart Failure National Registry dysmotility, sclerodactyly, and telangiectasia (Registry)CRT cardiac resynchronization therapy AFFIRM Atrial Fibrillation Follow-Up Investigation of RhythmCRT-D cardiac resynchronization therapy device and Management defibrillator A-HeFT African-American Heart Failure TrialCTR cardiothoracic ratio ALLHAT Antihypertensive and Lipid-Lowering Treatment toDASH Dietary Approaches to Stop Hypertension Prevent Heart Attack TrialDBP diastolic blood pressure ALOFT Aliskiren Observation of Heart Failure TreatmentDCM dilated cardiomyopathy B-CONVINCED Beta Blocker Continuation Versus Interruption onDNR do not resuscitate Patients with Congestive Heart Failure HospitalizedDVT deep venous thrombosis for a Decompensation EpisodeECG electrocardiogram CANPAP Canadian Continuous Positive Airway Pressure forED emergency department Patients with Central Sleep Apnea and Heart FailureEP, EPS electrophysiology, electrophysiology study CAPRICORN Carvedilol Post-Infarct Survival Control in LeftEVCPP endoventricular circular patch plasty Ventricular DysfunctionFDC familial dilated cardiomyopathy CARE-HF Cardiac Resynchronization-Heart FailureGFR, eGFR glomerular filtration rate, estimated glomerular filtration CHARM Candesartan in Heart Failure Assessment of Reduction rate in Mortality and Morbidity (Also CHARM-Added,HCM hypertrophic cardiomyopathy CHARM-Alternative, CHARM-Preserved)HF heart failure CIBIS Cardiac Insufficiency Bisoprolol StudyHFSA Heart Failure Society of America COACH Coordinating Study Evaluating Outcomes of AdvisingHR hazard ratio and Counseling in Heart FailureICD implantable cardioverter defibrillator COMET Carvedilol or Metoprolol European TrialINR international normalized ratio COMPANION Comparison of Medical Therapy, Pacing, andJVP jugular venous pressure Defibrillation in Chronic Heart FailureLA left atrial CONSENSUS Cooperative New Scandinavian Enalapril SurvivalLMWH low molecular weight heparin II Study IILV left ventricular COPERNICUS Carvedilol Prospective Randomized CumulativeLVAD left ventricular assist device Survival StudyLVEF left ventricular ejection fraction DIG Digitalis Investigation GroupLVH left ventricular hypertrophy EFFECT Enhanced Feedback for Effective Cardiac TreatmentLVNC left ventricular noncompaction (Evaluation Tool)MI myocardial infarction EPHESUS Epleronone Post-Acute Myocardial Infarction HeartMRI magnetic resonance imaging Failure Efficacy and Survival StudyNCEP National Cholesterol Education Program ESCAPE Evaluation Study of Congestive Heart Failure andNIV non-invasive ventilation Pulmonary Artery Catheterization EffectivenessNSAID non-steroidal anti-inflammatory drug EUROPA European Trial on Reduction of Cardiac Events withNT-proBNP N-terminal pro-B-type natriuretic peptide Perindopril in Stable Coronary Artery DiseaseNYHA New York Heart Association FAIR-HF Ferinject Assessment in Patients with Iron DeficiencyOMIM Online Mendelian Inheritance in Man (online resource) and Chronic Heart FailureOU observation unit GISSI Gruppo Italiano Per Lo Studio Della SopravvivenzaPCI percutaneous coronary intervention Nell’infarto Miocardico (GISSI-Prevenzione, GISSI-PCWP pulmonary capillary wedge pressure HF)PE pulmonary embolism GUSTO-1 Global Utilization of Streptokinase and TissuePET-CT positron emission tomography e computed tomography Plasminogen Activator for Occluded CoronaryPMI point of maximal impulse ArteriesPND paroxysmal nocturnal dyspnea (continued on next page) (continued)
    • Heart Failure Practice Guideline  HFSA e37 Appendix B. (continued)HEART Heart Failure Revascularization TrialHELP Hospitalized Elderly Longitudinal ProjectHERS Heart and Estrogen/Progestin Replacement StudyHF-ACTION A Controlled Trial Investigating Outcomes of Exercise TrainingHOBIPACE Homburg Biventricular Pacing EvaluationHOPE Heart Outcomes Prevention EvaluationHOT Hypertension Optimal TreatmentINTERMACS Interagency Registry for Mechanically Assisted Circulatory Support (Registry)I-PRESERVE Irbesartan in Heart Failure with Preserved Ejection FractionIRON-HF Iron Supplementation in Heart Failure Patients with AnemiaISIS-4 Fourth International Study of Infarct SurvivalMADIT-CRT Multi-Center Automatic Defibrillator Implantation Trial with Cardiac Resynchronization TherapyMERIT-HF Metoprolol CR?XL Randomized Intervention Trial in Congestive Heart FailureMIRACLE Multicenter Insync Clinical StudyMTT Myocarditis Treatment TrialMUSTT Multicenter Unsustained Tachycardia TrialNHANES National Health and Nutrition Examination Survey Epidemiologic Follow-Up StudyOAT Occluded Artery TrialOPTIMAAL Optimal Trial in Myocardial Infarction with the Angiotensin II Antagonist LosartanOPTIME-HF Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart FailureOPTIMIZE-HF Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (Registry)PRIDE N-Terminal Pro-BNP Investigation of Dyspnea in the Emergency DepartmentPRIMA Can Pro-Brain-Natriuretic-Peptide Guided Therapy of Chronic Heart Failure Improve Heart Failure Morbidity and Mortality?PROVED Prospective Randomized Study of Ventricular Function and Efficacy of DigoxinRADIANCE Randomized Assessment of Digoxin on Inhibitors of the Angiotensin Converting SystemRALES Randomized Aldactone Evaluation StudyRED-HF Reduction of Events with Darbepoetin Alfa in Heart FailureREMATCH Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart FailureREVERSE Resynchronization Reverses Remodeling in Systolic Left Ventricular DysfunctionREVERT Reversal of Ventricular Remodeling with Toprol-XLSCD-HeFT Sudden Cardiac Death in Heart Failure TrialSENIORS Study of the Effects of Nebivolol Intervention on Outcomes and Rehospitalization in Seniors with Heart FailureSOLVD Studies of Left Ventricular DysfunctionSTARS-BNP Systolic Heart Failure Treatment Supported By BNPSTICH Surgical Treatment for Ischemic Heart FailureSUPPORT Study to Understand Prognoses and Preferences for Outcomes and Risks of TreatmentTIME-CHF Trial of Intensified Vs Standard Medical Therapy in Elderly Patients with Congestive Heart FailureUKPDS United Kingdom Prospective Diabetes StudyVal-HeFT Valsartan Heart Failure TrialVALIANT The Valsartan in Acute Myocardial Infarction TrialV-HeFT Vasodilator Heart Failure TrialVMAC Vasodilator in the Management of Acute Heart FailureWASH Warfarin/Aspirin Study in Heart FailureWATCH Warfarin and Antiplatelet Therapy in Chronic Heart Failure
    • Journal of Cardiac Failure Vol. 16 No. 6 2010Section 3: Prevention of Ventricular Remodeling, 3.2 The recommended goals for the management of Cardiac Dysfunction, and Heart Failure specific risk factors for the development of cardiac dysfunction and HF are shown in Table 3.1. Overview These recommendations are based are well-documented data.17,20,30e39 Heart failure (HF) is an all-too-frequent outcome of hy-pertension and arterial vascular disease, making it a major Backgroundpublic health concern.1,2 Epidemiologic, clinical, and basicresearch have identified a number of antecedent conditions Hypertension. It is estimated that 74% of patients withthat predispose individuals to HF and its predecessors, left HF have a history of blood pressure O140/90 mmHg.40ventricular (LV) remodeling and dysfunction.3e11 Recogni- A history of hypertension has been associated with a highertion that many of these risk factors can be modified and that risk of HF hospitalization among post-MI patients withouttreating HF is difficult and costly has focused attention on a prior HF history enrolled in the EPHESUS study.41preventive strategies for HF. Hypertension is a particularly significant risk factor for Development of both systolic and diastolic dysfunction the development of HF in women.9 Results from numerousrelated to adverse ventricular remodeling may take years randomized controlled clinical trials have proven antihyper-to produce significant ill effects.12e18 Although the precise tensive therapy can reduce the incidence of symptomaticmechanisms for the transition to symptomatic HF are not HF by 50% to 80%. The risk reduction (both absoluteclear, many modifiable factors have been identified that pre- and relative) is greatest in severe hypertension (O160/dispose or aggravate the remodeling process and the devel- 110 mm Hg) and least in those with mild hypertensionopment of cardiac dysfunction. Treatment of systemic (O145/95 mm Hg). Optimal blood pressure for the preven-hypertension, with or without LV hypertrophy, reduces tion of HF is not known. Data from recent trials suggest thatthe development of HF.19e27 Prevention of myocardial in- 130/80 mm Hg or lower is the optimal blood pressure forfarction (MI) in patients with atherosclerotic cardiovascular patients with documented end-organ disease (diabetesdisease is a critical intervention, since occurrence of MI with nephropathy, patients with proteinuria).31 The Worldconfers an 8- to 10-fold increased risk for subsequent Health Organization has suggested an optimal blood pres-HF.20 Other modifiable risk factors include anemia, diabe- sure of 115/75 mm Hg for individuals with no documentedtes, hyperlipidemia, obesity, valvular abnormalities, alco- end-organ disease. It is uncertain whether additional ther-hol, certain illicit drugs, some cardiotoxic medications, apy to lower blood pressure further will confer additionaland diet.28,29 Consumption of one or more breakfast cereals benefit.per week and four or more servings of fruits and vegetables Reducing blood pressure is a critical component of HFper day, as well as frequent exercise and moderate alcohol prevention. The choice of antihypertensive agent shoulduse have been individually and jointly associated with be made in the context of the patient’s cardiovascular riskslower lifetime risk of HF in men.29 and comorbidities or other compelling indications.31 In general, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta blockers, and diuretics when used as anti-hypertensives all decrease thePatients with Risk Factors for Ventricular Remod- risk of developing HF, while amlodipine is associated eling, Cardiac Dysfunction, and HF with increased risk.42e50 However, in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart AttackRecommendations Trial (ALLHAT), amlodipine was associated with a lower overall risk of cardiovascular events as compared to lisino-3.1 A careful and thorough clinical assessment, with pril or chlorthalidone.48e50 Meta- analyses have confirmed appropriate investigation for known or potential these findings.51,52 In the Avoiding Cardiovascular Events risk factors, is recommended in an effort to prevent through Combination Therapy in Patients Living with Sys- development of LV remodeling, cardiac dysfunc- tolic Hypertension (ACCOMPLISH) trial, a combination of tion, and HF. These risk factors include, but are benazepril and amlodipine decreased time to cardiovascular not limited to, hypertension, hyperlipidemia, ath- death or cardiovascular events by 20% compared to the erosclerosis, diabetes mellitus, valvular disease, combination of benazepril-hydrochlorthiazide without an obesity, physical inactivity, excessive alcohol intake, increase in HF hospitalizations.53 dietary choices, and smoking. (Strength of Evi- Restriction of dietary sodium intake has been associated dence 5 A) with blood pressure reduction similar to single drug ther- apy. The Dietary Approaches to Stop Hypertension (ie, DASH) diet, rich in potassium and calcium, has been 1071-9164/$ - see front matter Ó 2010 Elsevier Inc. All rights reserved. associated with a reduced incidence of hypertension requir- doi:10.1016/j.cardfail.2010.05.012 ing drug therapy.54 Lower rates of HF have been observed e38
    • Heart Failure Practice Guideline  HFSA e39 Table 3.1. Goals for the Management of Risk Factors for the Development of Heart FailureRisk Factor Population Treatment Goal Strength of EvidenceHypertension No diabetes or renal disease !140/90 mmHg A Diabetes !130/80 mmHg A Renal insufficiency and 127/75 A O1g/day of proteinuria Renal insufficiency and 130/85 A #1 g/day of proteinuria Everyone with hypertension Limit sodium to #1500 mg/day ADiabetes See American Diabetes Association (ADA) GuidelineHyperlipidemia See National Cholesterol Education Program (NCEP) GuidelinePhysical Inactivity Everyone Sustained aerobic activity 20-30 B minutes, 3-5 times weeklyObesity BMI O30 Weight reduction to achieve BMI !30 CExcessive alcohol intake Men Limit alcohol intake to 1-2 drink C equivalents per day Women 1 drink equivalent per day Those with propensity to abuse Abstention alcohol or with alcoholic cardiomyopathySmoking Everyone Cessation AVitamin/mineral deficiency Everyone Diet high in Kþ/calcium BPoor diet Everyone 4 or more servings of fruit and B vegetables per day; One or more servings of breakfast cereal per weekin both men and women consuming diets consistent with incident HF is less clear. Data from the Physicians’ HealthDASH.55 See Table 3.2 for sodium equivalents. Study did not find an association between high total choles- terol or low HDL cholesterol and incident HF after adjust- Hyperlipidemia. In a large randomized study of a statin ment for traditional cardiovascular risk factors.59 There isversus placebo in patients with MI and elevated low-density no indication to use statins specifically for the treatmentlipoprotein, treatment with a statin was associated with of HF, but statins are indicated to treat hyperlipidemia ina highly significant reduction in all-cause mortality and re- HF patients.current MI.8,37 A 20% reduction in the incidence of HF wasnoted in patients treated with statin therapy. Recurrent MI Obesity. The American Heart Association and the Euro-during this study was associated with a large relative pean Society of Cardiology recommend an ideal body massincrease in mortality and HF; thus, it is possible that the index (BMI) of 25e27 kg/m2. BMI is calculated by dividingreduction in the risk of incident HF may have been related the patient’s weight in kilograms by his or her height into the reduction in recurrent MI rather than to a direct effect meters squared. Obesity is defined as a BMI $30, overweightof the statin. as a BMI $25. Waist-to-hip ratio may be a more powerful Similarly, in the Heart Protection Study, randomization predictor than BMI of the risk of MI and subsequent HF.60to simvastatin was associated with a 14% reduction in the Adults with BMI of 25 or 30 kg/m2 who had a higher waistrisk of hospitalization or death due to HF.56 Whether the re- circumference had higher rates of HF incidence than thoseduction was due to a direct effect on HF or an indirect effect with lower waist circumference.61 Obesity is associatedthrough a reduction in vascular events could not be deter- with metabolic syndrome, increasingly accepted as a majormined from the analysis. In large randomized, controlled risk factor for the development of cardiovascular disease.trials, statins have not been shown to improve clinical out- Excessive body fat results in increased metabolic demand,come among patients with existing New York Heart Asso- ventricular hypertrophy, and sleep-disordered breathing, allciation (NYHA) class II-IV HF.57,58 of which promote the development of HF. The relationship Although dyslipidemia is clearly associated with the between obesity and the risk of HF is well established,7 al-development of coronary heart disease, its contribution to though some data suggest that other pathophysiologic pro- cesses associated with obesity such as inflammation may Table 3.2. Sodium Equivalents have a greater influence on the development of HF than obesity itself.62 There is an increasing body of opinion thatSalt Sodium Chloride Sodium obesity is associated with a distinct form of cardiomyopathy.1 ⁄4 teaspoon 1550 mg 600 mg A retrospective analysis of echocardiograms for 13,382½ teaspoon 3100 mg 1200 mg subjects with BMI data revealed no association between3 ⁄4 teaspoon 4650 mg 1800 mg LV systolic function and BMI, suggesting that other mecha-1 teaspoon 6100 mg 2400 mg nisms may play a role in the development of HF in obese
    • e40 Journal of Cardiac Failure Vol. 16 No. 6 June 2010persons.63 However, in a study of 2,042 adults in Olmsted reduces adverse outcomes in patients with establishedCounty, Minnesota, LV diastolic dysfunction was strongly vascular disease and those with established ventricularassociated with waist-to-hip ratio, even after adjustment for remodeling or dysfunction.standard cardiovascular risk factors.64 Weight reduction has been shown to improve most of the Diabetes. Diabetes is a known predictor of HF in patientsadverse effects of obesity. It is likely that weight reduction with and without established cardiovascular disease.72e75in obese individuals reduces the likelihood of subsequent Women with diabetes are at particular risk. In the HeartHF, although no data exist to confirm this hypothesis. and Estrogen/Progestin Replacement Study (HERS), post- menopausal women with diabetes had a 3.0% annual inci- Physical Inactivity. The benefits of exercise are well dence of developing HF even in the absence of other riskdocumented and include reduction of recurrent MI in survi- factors.72 Leung et al reported the adjusted rate of incidentvors of MI, improved exercise capacity, improved affect HF among patients with type-2 diabetes as 794 cases perand quality of life, and better control of hypertension. 100,000 person years, compared with 275 per 100,000These results are achieved with a minimum of 20e30 min- person-years in the general population, even after adjustmentutes of sustained submaximal exercise 3e5 times per week for demographic differences.76 In the diabetic heart, myocyte(see Section 6).65 In one population-based study of men, free fatty acid uptake and oxidation is increased. This leads toexercising 5 or more times per week reduced the lifetime free fatty acid induced insulin resistance and intracellularrisk of HF at age 40 years.29 accumulation of triglyceride and free fatty acids, which may contribute to the development of cardiomyopathy. Alcohol Intake. Alcoholic cardiomyopathy is associated Downregulation of PPAR-a also appears to play an importantwith a substantial intake of alcohol (70 g or greater per role.77 Additionally, many patients with diabetes have otherday of chronic ingestion). Avoiding substantial ingestion comorbidities that are also associated with the developmentof alcohol is clearly advisable, but the safe level of mod- of HF, including ischemic heart disease, hypertension, anderate ingestion has been difficult to define. Other factors LV hypertrophy.77 More research is needed to evaluate thesuch as drinking patterns, beverage type, and genetic var- effect of glycemic control on HF risk. In the United Kingdomiations affecting alcohol metabolism may also influence Prospective Diabetes Study (UKPDS), the absolute risk ofthe relationship between alcohol and incident HF.66 There a HF event was significantly lower for patients randomizedare conflicting reports regarding the effects of alcohol in- to tight glycemic control as compared to less tight controlgestion upon left ventricular ejection fraction (LVEF) in (RR 0.44, 99% CI 0.2e0.94, P5.0043).78those with and without HF. At present, 2 drinks per dayfor men and 1 drink per day for women is considered ac- Recommendationceptable, even in individuals with other cardiovascular risk 3.3 ACE inhibitors are recommended for prevention offactors. One drink is equivalent to 12e14 g of alcohol, the HF in patients at high risk of this syndrome, in-amount in 1.5 ounces of 80 proof spirits, 12 ounces of cluding those with coronary artery disease, periph-beer, or 5 ounces of wine. Those with for a propensity eral vascular disease, or stroke. Patients withto abuse alcohol should be counseled to abstain. diabetes and another major risk factor or patientsPopulation-based studies have established an association with diabetes who smoke or have microalbuminu-between moderate alcohol intake (up to 2 drinks per day ria are also at high risk and should receive ACEfor men or 1 drink per day for women) and a reduction inhibitors. (Strength of Evidence 5 A)in incident HF.29,67,68 One study also suggests that lightto moderate alcohol consumption is not associated with Backgroundan adverse prognosis in patients with LV systolic dysfunc-tion.68 While some data suggest that low risk drinking Findings from at least three randomized, controlled tri-decreases the risk of HF in patients with antecedent coro- als support the use of ACE inhibitors in patients at highnary artery disease, it seems prudent to follow the national risk for the development of HF. In one study of patientsrecommendations referred to above. older than age 55 with documented vascular disease or multiple cardiac risk factors, including diabetes, treatment Smoking Cessation. There is a substantial body of data with an ACE inhibitor reduced the annual risk of develop-concerning the adverse effects of smoking in patients with ing HF by 23%.20 A study of patients older than age 18vascular disease or reduced LVEF. Smoking cessation is with documented coronary artery disease showed thatassociated with a 50% reduction in 5-year mortality in sur- treatment with an ACE inhibitor reduced total mortalityvivors of acute MI.69 In the Studies of Left Ventricular Dys- by 14% over 4.2 years, even though patients were alreadyfunction (SOLVD) study of patients with either receiving aggressive treatment for vascular disease.44 Insymptomatic or asymptomatic LV dysfunction, nonsmokers a third study, patients with previous stroke and mild hy-or former smokers showed improved mortality when pertension treated with an ACE inhibitor-based antihyper-compared with current smokers.70,71 These and other obser- tensive regimen showed a 26% reduction in subsequentvational data suggest smoking cessation dramatically HF.33
    • Heart Failure Practice Guideline  HFSA e41 Several trials studied the use of an ARB in patients at 4. Grundy SM, Balady GJ, Criqui MH, Fletcher G, Greenland P,high risk for developing HF.79,80 In one the composite car- Hiratzka LF, et al. Primary prevention of coronary heart disease: guid- ance from Framingham: a statement for healthcare professionals fromdiovascular event rate did not differ in patients with diabe- the AHA Task Force on Risk Reduction. American Heart Association.tes treated with an ARB, amlodipine, or placebo.79 In Circulation 1998;97:1876e87.another, patients at risk for or with cardiovascular disease, 5. Hellermann JP, Jacobsen SJ, Reeder GS, Lopez-Jimenez F,including HF, did better when treated with an ARB on top Weston SA, Roger VL. Heart failure after myocardial infarction: prev-of conventional antihypertensive therapy as compared sup- alence of preserved left ventricular systolic function in the community. Am Heart J 2003;145:742e8.plementary conventional treatment.80 A recent trial com- 6. Howard BV. Blood pressure in 13 American Indian communities: theparing the use of an ACE inhibitor versus an ARB in Strong Heart Study. Public Health Rep 1996;111(Suppl. 2):47e8.a population with vascular disease or high-risk diabetes, 7. Kenchaiah S, Evans JC, Levy D, Wilson PW, Benjamin EJ,but no HF, found that the ARB was non-inferior to the Larson MG, et al. Obesity and the risk of heart failure. N Engl JACE inhibitor in preventing the primary end point of car- Med 2002;347:305e13. 8. Kjekshus J, Pedersen TR, Olsson AG, Faergeman O, Pyorala K. Thediovascular death, MI, stroke, or HF hospitalization.81 effects of simvastatin on the incidence of heart failure in patientsBased on these results, it is reasonable to say that, at least with coronary heart disease. J Card Fail 1997;3:249e54.in those high risk patients who do not tolerate an ACE in- 9. Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progressionhibitor, an ARB should be used. from hypertension to congestive heart failure. JAMA 1996;275: 1557e62. 10. Lopes AA, Andrade J, Noblat AC, Silveira MA. Reduction in diastolicRecommendation blood pressure and cardiovascular mortality in nondiabetic hyperten-3.4 Beta blockers are recommended for patients with sive patients. A reanalysis of the HOT study. Arq Bras Cardiol 2001;77:132e7. prior MI to reduce mortality, recurrent MI, and 11. Stratton IM, Adler AI, Neil HA, Matthews DR, Manley SE, Cull CA, the development of HF. (Strength of Evidence 5 A) et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observa-Background tional study. BMJ 2000;321:405e12. 12. Kostis JB, Davis BR, Cutler J, Grimm RH Jr, Berge KG, Cohen JD, Beta blockers are known to reduce cardiac ischemia, et al. Prevention of heart failure by antihypertensive drug treatmentreinfarction, and myocardial remodeling after acute MI. in older persons with isolated systolic hypertension. SHEP Coopera- tive Research Group. JAMA 1997;278:212e6.Studies in patients with recent MI (most published in the pre- 13. McDonagh TA, Morrison CE, Lawrence A, Ford I, Tunstall-Pedoe H,thrombolytic era) have shown that beta blockers are McMurray JJ, et al. Symptomatic and asymptomatic left-ventricularassociated with a large reduction in HF and recurrent all- systolic dysfunction in an urban population. Lancet 1997;350:829e33.cause hospitalizations, HF hospitalizations, and recurrent 14. McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural his-MI.46,82e90 More recent data confirm this finding, showing tory of congestive heart failure: the Framingham study. N Engl J Med 1971;285:1441e6.risk reduction for the development of HF in the 25% to 15. Mitchell GF, Pfeffer JM, Pfeffer MA. The transition to failure in the45% range 1 year after MI.91 Data from the Carvedilol spontaneously hypertensive rat. Am J Hypertens 1997;10:120Se6S.Post-Infarct Survival Control in Left Ventricular Dysfunction 16. Moser M, Hebert PR. Prevention of disease progression, left ventric-(CAPRICORN) Echo Substudy demonstrated a significant ular hypertrophy and congestive heart failure in hypertension treat-decrease in LV end systolic volume and a significant increase ment trials. J Am Coll Cardiol 1996;27:1214e8. 17. Pearson TA, Blair SN, Daniels SR, Eckel RH, Fair JM, Fortmann SP,in LVEF at 6 months post-MI for patients randomized to car- et al. AHA Guidelines for Primary Prevention of Cardiovascular Diseasevedilol as compared to placebo.92 Patients most at risk for HF and Stroke: 2002 Update: Consensus Panel Guide to Comprehensiveand death after MI - women and patients with advanced age, Risk Reduction for Adult Patients Without Coronary or Other Athero-diabetes, renal disease, or previous revascularization - appear sclerotic Vascular Diseases. American Heart Association Science Advi-to derive the most benefit, but unfortunately are less likely to sory and Coordinating Committee. Circulation 2002;106:388e91. 18. Pfeffer JM, Pfeffer MA, Fletcher P, Fishbein MC, Braunwald E. Fa-receive beta blockade post MI.93,94 Even among patients with vorable effects of therapy on cardiac performance in spontaneouslyasymptomatic LV dysfunction without a recent MI, beta hypertensive rats. Am J Physiol 1982;242:H776e84.blocker therapy has been shown to decrease LV end systolic 19. Adler AI, Stratton IM, Neil HA, Yudkin JS, Matthews DR, Cull CA,and end diastolic volume and increase LVEF at 6 and 12 et al. Association of systolic blood pressure with macrovascular andmonths as compared to placebo.95 microvascular complications of type 2 diabetes (UKPDS 36): prospec- tive observational study. BMJ 2000;321:412e9. 20. Arnold JM, Yusuf S, Young J, Mathew J, Johnstone D, Avezum A, et al. Prevention of Heart Failure in Patients in the Heart Outcomes References Prevention Evaluation (HOPE) Study. Circulation 2003;107: 1284e90. 1. Centers for Disease Control and Prevention. Mortality from congestive 21. Baker DW. Prevention of heart failure. J Card Fail 2002;8:333e46. heart failureeUnited States, 1980-1990. JAMA 1994;271:813e4. 22. Fagard RH, Staessen JA. Treatment of isolated systolic hypertension 2. Centers for Disease Control and Prevention. Changes in mortality in the elderly: the Syst-Eur trial. Systolic Hypertension in Europe from heart failureeUnited States, 1980-1995. JAMA 1998;280: (Syst-Eur) Trial Investigators. Clin Exp Hypertens 1999;21:491e7. 874e5. 23. Hansson L. Recent intervention trials in hypertension initiated in 3. Fox KF, Cowie MR, Wood DA, Coats AJ, Gibbs JS, Underwood SR, SwedeneHOT, CAPPP and others. Hypertension Optimal Treatment et al. Coronary artery disease as the cause of incident heart failure in Study. Captopril Prevention Project. Clin Exp Hypertens 1999;21: the population. Eur Heart J 2001;22:228e36. 507e15.
    • e42 Journal of Cardiac Failure Vol. 16 No. 6 June 201024. Hawkins CM. Isolated Systolic Hypertension, Morbidity, and Mortal- infarction and left ventricular systolic dysfunction. Am J Cardiol ity: The SHEP Experience. Am J Geriatr Cardiol 1993;2:25e7. 2009;103:1374e80.25. Lauer MS, Anderson KM, Levy D. Influence of contemporary versus 42. Berl T, Hunsicker LG, Lewis JB, Pfeffer MA, Porush JG, Rouleau JL, 30-year blood pressure levels on left ventricular mass and geometry: et al. Cardiovascular outcomes in the Irbesartan Diabetic Nephropathy the Framingham Heart Study. J Am Coll Cardiol 1991;18:1287e94. Trial of patients with type 2 diabetes and overt nephropathy. Ann In-26. UK Prospective Diabetes Study Group. Efficacy of atenolol and cap- tern Med 2003;138:542e9. topril in reducing risk of macrovascular and microvascular complica- 43. Brenner BM, Cooper ME, de ZD, Keane WF, Mitch WE, Parving HH, tions in type 2 diabetes: UKPDS 39. BMJ 1998;317:713e20. et al. Effects of losartan on renal and cardiovascular outcomes in pa-27. United Kingdom Prospective Diabetes Study Group. United Kingdom tients with type 2 diabetes and nephropathy. N Engl J Med 2001;345: Prospective Diabetes Study (UKPDS). 13: Relative efficacy of ran- 861e9. domly allocated diet, sulphonylurea, insulin, or metformin in patients 44. Fox KM. Efficacy of perindopril in reduction of cardiovascular events with newly diagnosed non-insulin dependent diabetes followed for among patients with stable coronary artery disease: randomised, three years. BMJ 1995;310:83e8. double-blind, placebo-controlled, multicentre trial (the EUROPA28. He J, Ogden LG, Bazzano LA, Vupputuri S, Loria C, Whelton PK. study). Lancet 2003;362:782e8. Risk factors for congestive heart failure in US men and women: 45. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of NHANES I epidemiologic follow-up study. Arch Intern Med an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascu- 2001161:996e1002. lar events in high-risk patients. The Heart Outcomes Prevention Eval-29. Djousse L, Driver JA, Gaziano JM. Relation between modifiable life- uation Study Investigators. N Engl J Med 2000;342:145e53. style factors and lifetime risk of heart failure. JAMA 2009;302: 46. Beta-Blocker Heart Attack Study Group. The beta-blocker heart attack 394e400. trial. beta-Blocker Heart Attack Study Group. JAMA 1981;246:30. Antman EM, Hand M, Armstrong PW, Bates ER, Green LA, 2073e4. Halasyamani LK, et al. 2007 focused update of the ACC/AHA 2004 47. Pfeffer MA, Braunwald E, Moye LA, Basta L, Brown EJ Jr, guidelines for the management of patients with ST-elevation myocar- Cuddy TE, et al. Effect of captopril on mortality and morbidity in dial infarction: a report of the American College of Cardiology/Amer- patients with left ventricular dysfunction after myocardial infarction. ican Heart Association Task Force on Practice Guidelines. J Am Coll Results of the survival and ventricular enlargement trial. The SAVE Cardiol 2008;51:210e47. Investigators. N Engl J Med 1992;327:669e77.31. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, 48. ALLHAT Investigators. Major outcomes in high-risk hypertensive Izzo JL Jr, et al. Seventh report of the Joint National Committee on patients randomized to angiotensin-converting enzyme inhibitor or Prevention, Detection, Evaluation, and Treatment of High Blood Pres- calcium channel blocker vs diuretic: The Antihypertensive and sure. Hypertension 2003;42:1206e52. Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).32. National Cholesterol Education Program (NCEP) Expert Panel on JAMA 2002;288:2981e97. Detection for Evaluation and Treatment of High Blood Cholesterol 49. Leenen FH, Nwachuku CE, Black HR, Cushman WC, Davis BR, in Adults (Adult Treatment Panel III). Third Report of the National Simpson LM, et al. Clinical events in high-risk hypertensive patients Cholesterol Education Program (NCEP) Expert Panel on Detection, randomly assigned to calcium channel blocker versus angiotensin- Evaluation, and Treatment of High Blood Cholesterol in Adults converting enzyme inhibitor in the antihypertensive and lipid- (Adult Treatment Panel III) final report. Circulation 2002;106: lowering treatment to prevent heart attack trial. Hypertension 2006; 3143e421. 48:374e84.33. Randomised trial of a perindopril-based blood-pressure-lowering reg- 50. Nissen SE, Tuzcu EM, Libby P, Thompson PD, Ghali M, Garza D, imen among 6,105 individuals with previous stroke or transient ischae- et al. Effect of antihypertensive agents on cardiovascular events in mic attack. Lancet 2001;358:1033e41. patients with coronary disease and normal blood pressure: the34. Bakris GL, Weir MR, Shanifar S, Zhang Z, Douglas J, van Dijk DJ, CAMELOT study: a randomized controlled trial. JAMA 2004;292: et al. Effects of blood pressure level on progression of diabetic ne- 2217e25. phropathy: results from the RENAAL study. Arch Intern Med 2003; 51. Verdecchia P, Angeli F, Cavallini C, Gattobigio R, Gentile G, 163:1555e65. Staessen JA, et al. Blood pressure reduction and renin-angiotensin sys-35. De BG, Ambrosioni E, Borch-Johnsen K, Brotons C, Cifkova R, tem inhibition for prevention of congestive heart failure: a meta-anal- Dallongeville J, et al. European guidelines on cardiovascular disease ysis. Eur Heart J 2009;30:679e88. prevention in clinical practice. Third Joint Task Force of European 52. Bangalore S, Wild D, Parkar S, Kukin M, Messerli FH. Beta-blockers and Other Societies on Cardiovascular Disease Prevention in Clinical for primary prevention of heart failure in patients with hypertension Practice. Eur Heart J 2003;24:1601e10. insights from a meta-analysis. J Am Coll Cardiol 2008;52:1062e72.36. Krauss RM, Eckel RH, Howard B, Appel LJ, Daniels SR, 53. Jamerson K, Weber MA, Bakris GL, Dahlof B, Pitt B, Shi V, et al. Deckelbaum RJ, et al. AHA Dietary Guidelines: revision 2000: A Benazepril plus amlodipine or hydrochlorothiazide for hypertension statement for healthcare professionals from the Nutrition Committee in high-risk patients. N Engl J Med 2008;359:2417e28. of the American Heart Association. Circulation 2000;102:2284e99. 54. Craddick SR, Elmer PJ, Obarzanek E, Vollmer WM, Svetkey LP,37. Krum H, McMurray JJ. Statins and chronic heart failure: do we need Swain MC. The DASH diet and blood pressure. Curr Atheroscler a large-scale outcome trial? J Am Coll Cardiol 2002;39:1567e73. Rep 2003;5:484e91.38. Wood D. European and American recommendations for coronary 55. Levitan EB, Wolk A, Mittleman MA. Consistency with the DASH diet heart disease prevention. Eur Heart J 1998;19(Suppl A):A12e9. and incidence of heart failure. Arch Intern Med 2009;169:851e7.39. Zanchetti A, Hansson L, Menard J, Leonetti G, Rahn KH, Warnold I, 56. Emberson JR, Ng LL, Armitage J, Bowman L, Parish S, Collins R. et al. Risk assessment and treatment benefit in intensively treated hy- N-terminal Pro-B-type natriuretic peptide, vascular disease risk, and pertensive patients of the hypertension Optimal Treatment (HOT) cholesterol reduction among 20,536 patients in the MRC/BHF heart study. J Hypertens 2001;19:819e25. protection study. J Am Coll Cardiol 2007;49:311e9.40. Lloyd-Jones D, Adams R, Carnethon M, De SG, Ferguson TB, 57. Kjekshus J, Apetrei E, Barrios V, Bohm M, Cleland JG, Cornel JH, Flegal K, et al. Heart Disease and Stroke Statisticse2009 Update: et al. Rosuvastatin in older patients with systolic heart failure. N A Report From the American Heart Association Statistics Commit- Engl J Med 2007;357:2248e61. tee and Stroke Statistics Subcommittee. Circulation 2009;119: 58. Tavazzi L, Maggioni AP, Marchioli R, Barlera S, Franzosi MG, e21e181. Latini R, et al. Effect of rosuvastatin in patients with chronic heart41. Ahmed A, Pitt B. A history of systemic hypertension and incident failure (the GISSI-HF trial): a randomised, double-blind, placebo- heart failure hospitalization in patients with acute myocardial controlled trial. Lancet 2008;372:1231e9.
    • Heart Failure Practice Guideline  HFSA e4359. Dhingra R, Sesso HD, Kenchaiah S, Gaziano JM. Differential effects Trial of patients with type 2 diabetes and overt nephropathy. Ann In- of lipids on the risk of heart failure and coronary heart disease: the tern Med 2003;138:542e9. Physicians’ Health Study. Am Heart J 2008;155:869e75. 80. Mochizuki S, Dahlof B, Shimizu M, Ikewaki K, Yoshikawa M,60. Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG, Taniguchi I, et al. Valsartan in a Japanese population with hyperten- Commerford P, et al. Obesity and the risk of myocardial infarction sion and other cardiovascular disease (Jikei Heart Study): a rando- in 27,000 participants from 52 countries: a case-control study. Lancet mised, open-label, blinded endpoint morbidity-mortality study. 2005;366:1640e9. Lancet 2007;369:1431e9.61. Levitan EB, Yang AZ, Wolk A, Mittleman MA. Adiposity and inci- 81. Yusuf S, Teo KK, Pogue J, Dyal L, Copland I, Schumacher H, et al. dence of heart failure hospitalization and mortality: a population- Telmisartan, ramipril, or both in patients at high risk for vascular based prospective study. Circ Heart Fail 2009;2:202e8. events. N Engl J Med 2008;358:1547e59.62. Bahrami H, Bluemke DA, Kronmal R, Bertoni AG, Lloyd-Jones DM, 82. A randomized trial of propranolol in patients with acute myocardial Shahar E, et al. Novel metabolic risk factors for incident heart failure infarction. II. Morbidity results. JAMA 1983;250:2814e9. and their relationship with obesity: the MESA (Multi-Ethnic Study of 83. International Collaborative Study Group. Reduction of infarct size by Atherosclerosis) study. J Am Coll Cardiol 2008;51:1775e83. the early use of intravenous timolol in acute myocardial infarction.63. Movahed MR, Saito Y. Lack of association between obesity and left Am J Cardiol 1984;54:14Ee5E. ventricular systolic dysfunction. Echocardiography 2009;26:128e32. 84. Exner DV, Dries DL, Waclawiw MA, Shelton B, Domanski MJ. Beta-64. Ammar KA, Redfield MM, Mahoney DW, Johnson M, Jacobsen SJ, adrenergic blocking agent use and mortality in patients with asymp- Rodeheffer RJ. Central obesity: association with left ventricular dys- tomatic and symptomatic left ventricular systolic dysfunction: a post function and mortality in the community. Am Heart J 2008;156: hoc analysis of the Studies of Left Ventricular Dysfunction. J Am 975e81. Coll Cardiol 1999;33:916e23. ˜65. Pina IL, Apstein CS, Balady GJ, Belardinelli R, Chaitman BR, 85. Lund-Johansen P. The Norwegian Multicenter Study on timolol after Duscha BD, et al. Exercise and heart failure: A statement from the myocardial infarction. Part II. Effect in different risk groups, causes American Heart Association Committee on exercise, rehabilitation, of death, heart arrest, reinfarctions, rehospitalizations and adverse ex- and prevention. Circulation 2003;107:1210e25. periences. Acta Med Scand Suppl 1981;651:243e52.66. Djousse L, Gaziano JM. Alcohol consumption and heart failure: a sys- 86. Pratt CM, Roberts R. Chronic beta blockade therapy in patients after tematic review. Curr Atheroscler Rep 2008;10:117e20. myocardial infarction. Am J Cardiol 1983;52:661e4.67. Djousse L, Gaziano JM. Alcohol consumption and risk of heart failure 87. Rodda BE. The Timolol Myocardial Infarction Study: an evaluation of in the Physicians’ Health Study I. Circulation 2007;115:34e9. selected variables. Circulation 1983;67. I101eI1I6.68. Cooper HA, Exner DV, Domanski MJ. Light-to-moderate alcohol con- 88. Roque F, Amuchastegui LM, Lopez Morillos MA, Mon GA, sumption and prognosis in patients with left ventricular systolic dys- Girotti AL, Drajer S, et al. Beneficial effects of timolol on infarct function. J Am Coll Cardiol 2000;35:1753e9. size and late ventricular tachycardia in patients with acute myocardial69. Burt A, Thornley P, Illingworth D, White P, Shaw TR, Turner R. Stop- infarction. Circulation 1987;76:610e7. ping smoking after myocardial infarction. Lancet 1974;1:304e6. 89. Simon T, Mary-Krause M, Funck-Brentano C, Lechat P, Jaillon P.70. Jay SJ. Smoking is an important component in the analysis of heart Bisoprolol dose-response relationship in patients with congestive heart failure. Arch Intern Med 1999;159:2225e6. failure: a subgroup analysis in the cardiac insufficiency bisoprolol71. Nicolozakes AW, Binkley PF, Leier CV. Hemodynamic effects of study(CIBIS II). Eur Heart J 2003;24:552e9. smoking in congestive heart failure. Am J Med Sci 1988;296:377e80. 90. Vantrimpont P, Rouleau JL, Wun CC, Ciampi A, Klein M, Sussex B, et al.72. Bibbins-Domingo K, Lin F, Vittinghoff E, Barrett-Connor E, Additive beneficial effects of beta-blockers to angiotensin-converting Hulley SB, Grady D, et al. Predictors of heart failure among women enzyme inhibitors in the Survival and Ventricular Enlargement (SAVE) with coronary disease. Circulation 2004;110:1424e30. Study. SAVE Investigators. J Am Coll Cardiol 1997;29:229e36.73. Bertoni AG, Hundley WG, Massing MW, Bonds DE, Burke GL, 91. Dargie HJ. Effect of carvedilol on outcome after myocardial infarction Goff DC Jr. Heart failure prevalence, incidence, and mortality in the in patients with left-ventricular dysfunction: the CAPRICORN rando- elderly with diabetes. Diabetes Care 2004;27:699e703. mised trial. Lancet 2001;357:1385e90.74. Kannel WB, Hjortland M, Castelli WP. Role of diabetes in congestive 92. Doughty RN, Whalley GA, Walsh HA, Gamble GD, Lopez-Sendon J, heart failure: the Framingham study. Am J Cardiol 1974;34:29e34. Sharpe N. Effects of carvedilol on left ventricular remodeling after75. Nichols GA, Hillier TA, Erbey JR, Brown JB. Congestive heart failure acute myocardial infarction: the CAPRICORN Echo Substudy. Circu- in type 2 diabetes: prevalence, incidence, and risk factors. Diabetes lation 2004;109:201e6. Care 2001;24:1614e9. 93. Krumholz HM, Radford MJ, Wang Y, Chen J, Heiat A, Marciniak TA.76. Leung AA, Eurich DT, Lamb DA, Majumdar SR, Johnson JA, National use and effectiveness of beta-blockers for the treatment of el- Blackburn DF, et al. Risk of heart failure in patients with recent- derly patients after acute myocardial infarction: National Cooperative onset type 2 diabetes: population-based cohort study. J Card Fail Cardiovascular Project. JAMA 1998;280:623e9. 2009;15:152e7. 94. Soumerai SB, McLaughlin TJ, Spiegelman D, Hertzmark E,77. Saunders J, Mathewkutty S, Drazner MH, McGuire DK. Cardiomyop- Thibault G, Goldman L. Adverse outcomes of underuse of beta- athy in type 2 diabetes: update on pathophysiological mechanisms. blockers in elderly survivors of acute myocardial infarction. JAMA Herz 2008;33:184e90. 1997;277:115e21.78. UK Prospective Diabetes Study Group. Tight blood pressure control 95. Colucci WS, Kolias TJ, Adams KF, Armstrong WF, Ghali JK, and risk of macrovascular and microvascular complications in type Gottlieb SS, et al. Metoprolol reverses left ventricular remodeling in 2 diabetes: UKPDS 38. BMJ 1998;317:703e13. patients with asymptomatic systolic dysfunction: the REversal of79. Berl T, Hunsicker LG, Lewis JB, Pfeffer MA, Porush JG, Rouleau JL, VEntricular Remodeling with Toprol-XL (REVERT) trial. Circulation et al. Cardiovascular outcomes in the Irbesartan Diabetic Nephropathy 2007;116:49e56.
    • Journal of Cardiac Failure Vol. 16 No. 6 2010 Section 4: Evaluation of Patients for Ventricular Table 4.1. Indications for Evaluation of Clinical Dysfunction and Heart Failure Manifestations of HF Conditions Hypertension Overview Diabetes Obesity CAD (eg, after MI, revascularization) Patients undergoing evaluation for ventricular dysfunc- Peripheral arterial disease or cerebrovascular diseasetion and heart failure (HF) fall into 3 general groups: (1) Valvular heart diseasepatients at risk of developing HF, (2) patients suspected Family history of cardiomyopathy in a first-degree relativeof having HF based on signs and symptoms or incidental History of exposure to cardiac toxinsevidence of abnormal cardiac structure or function, and Sleep-disordered breathing(3) patients with established symptomatic HF. Test Findings Sustained arrhythmias Abnormal ECG (eg, LVH, left bundle branch block, pathologic Q waves) Patients at Risk for HF. Patients identified to be at risk Cardiomegaly on chest X-rayfor HF require aggressive management of modifiable riskfactors as outlined in Section 3 of this guideline. Patients Table 4.2. Assess Cardiac Structure and Function inwith risk factors may have undetected abnormalities of Patients with the Following Disorders or Findingscardiac structure or function. In addition to risk factor re-duction, these patients require careful assessment for the Coronary artery disease (eg, after MI, revascularization) Valvular heart diseasepresence of symptoms of HF and, depending on their under- Family history of cardiomyopathy in a first-degree relativelying risk, may warrant noninvasive evaluation of cardiac Atrial fibrillation or flutterstructure and function. Electrocardiographic evidence of LVH, left bundle branch block, or pathologic Q waves Complex ventricular arrhythmia Patients Suspected of Having HF. The evaluation of pa- Cardiomegalytients suspected of having HF focuses on interpretation ofsigns and symptoms that have led to the consideration of Backgroundthis diagnosis. Careful history and physical examination,combined with evaluation of cardiac structure and function, Identification of Risk Factors. Identification of riskshould be undertaken to determine the cause of symptoms factors, predisposing conditions, and markers that conferand to evaluate the degree of underlying cardiac pathology. increased risk for developing HF is an important part of the routine medical evaluation.1 A number of conditions Patients With Established HF. The evaluation of pa- predispose to the development of HF,2e12 and persuasivetients with an established diagnosis of HF is undertaken evidence exists that treatment of these risk factors decreasesto identify the etiology, assess symptom nature and severity, the likelihood of subsequent HF (see Guideline Section 3determine functional impairment, and establish a prognosis. for more details on risk factor modification and HF preven-Follow-up of patients with HF or cardiac dysfunction in- tion). Although risk factors vary in the degree to which theyvolves continuing reassessment of symptoms, functional are modifiable, detection of any risk factor identifies a pa-capacity, prognosis, and therapeutic effectiveness. tient in whom aggressive risk factor modification and more careful follow-up are warranted. Evaluation of Patients at Risk Method of Evaluation. Patients at risk for developing cardiac dysfunction should undergo careful history andRecommendations physical examination to detect evidence of clinical HF4.1 Evaluation for clinical manifestations of HF with and to uncover other conditions that predispose to HF. a routine history and physical examination is rec- Appropriate therapies should be introduced to reduce the ommended in patients with the medical conditions likelihood that left ventricular (LV) dysfunction will de- or test findings listed in Table 4.1. (Strength of velop. Selected groups of high-risk patients and patients Evidence 5 B) with signs and symptoms of HF should undergo echocar- diographic examination to assess cardiac structure and4.2 Assessment of Cardiac Structure and Function. function.13 This initial examination may identify patients Echocardiography with Doppler is recommended with cardiac dysfunction with or without symptomatic to determine cardiac structure and function in HF. These patients should undergo evaluation and treatment asymptomatic patients with the disorders or find- as defined in this guideline. ings listed in Table 4.2. (Strength of Evidence 5 B) Echocardiography. The presence of certain risk factors makes the likelihood of underlying ventricular remodeling 1071-9164/$ - see front matter Ó 2010 Elsevier Inc. All rights reserved. and dysfunction sufficiently likely to warrant diagnostic doi:10.1016/j.cardfail.2010.05.013 echocardiography (Table 4.2). e44
    • Heart Failure Practice Guideline  HFSA e45 Characterization of cardiac structure and function is criti- patients in whom the diagnosis of HF is being consid-cal for proper diagnosis, estimation of prognosis, and ered. (Strength of Evidence 5 B)therapeutic decision-making. Contributions of cardiac dys-function to the HF syndrome extend beyond the traditional Backgroundview of simply quantifying LV systolic function (or left ven-tricular ejection fraction, LVEF), since the capacity and the Symptoms. Thorough detection and evaluation of symp-efficiency of the LV also dictates the adequacy of stroke toms is critical in the assessment of patients suspected ofvolume. This may explain why approximately 50% of having HF. The most common symptoms are dyspnea andpatients with symptoms and signs of HF have a preserved fatigue from fluid retention, the inability to adequately aug-LVEF.14e17 Therefore, echocardiographic and Doppler ment cardiac output and oxygen delivery during exertion, orassessment should include analysis of chamber sizes, valve peripheral factors such as abnormal respiratory and skeletalfunction, LV mass and wall thickness, parameters of LV sys- muscle structure and function. These often manifest astolic and diastolic function, right ventricular (RV) systolic exercise intolerance or a reduction in the intensity of usualfunction, the presence of pulmonary hypertension, and the activities. Signs of HF relate to manifestations of fluidpresence of pericardial disease. In patients whose echocardio- retention. Dyspnea is typically noted during activity butgraphic imaging is unsatisfactory or when the degree of LVEF may be severe enough to be present at rest. Dyspnea mayinfluences therapeutic decision making, other techniques be intermittent even when present at rest or manifest assuch as radionuclide ventriculography, cardiac magnetic periodic breathing (e.g., Cheynes-Stokes respiration).26 Pa-resonance imaging, or computed tomography may be used. tients whose cardiac dysfunction evolves chronically may reduce their activity to minimize symptoms.27 ComparingRecommendation current activity level with exercise tolerance in the past may be helpful in detecting a decline in functional capacity.4.3 Routine determination of plasma B-type natri- A patient’s functional capacity should be judged with allow- uretic peptide (BNP) or N-terminal pro-BNP ance for age and level of conditioning. Congestion may take (NT-proBNP) concentration as part of a screening many forms. Orthopnea and paroxysmal nocturnal dyspnea evaluation for structural heart disease in asymp- are symptoms of elevated left heart filling pressures that tomatic patients is not recommended. (Strength of are more specific to underlying central congestion. These pa- Evidence 5 B) tients may or may not have visible edema. Peripheral edema occurs in the presence of elevated right-sided filling pres-Background sures, together with impaired renal handling of sodium and Interest is high in developing markers of cardiac dysfunc- water. Significant volume overload typically is associatedtion that can be used to screen patients at risk for HF. Although with substantial functional incapacity, yet patients may pres-initial data suggest that determination of BNP or NT-proBNP ent with fatigue or exercise intolerance and manifest no signslevels may be useful in this regard, data are insufficient to make of fluid retention. Symptoms may occur in isolation or not bea specific recommendation concerning their use for screening classically related to physical signs. Nocturnal symptomsin a routine manner. The positive predictive value for these may predominate, whereas daytime symptoms, such as dysp-tests in a low-prevalence and asymptomatic population for nea on exertion, may be absent.the purpose of detecting cardiac dysfunction varies amongstudies, and the possibility of false positive results has signifi- Less Common Presenting Symptoms. Patients may re-cant cost-effectiveness implications.18e23 port nocturnal wheezing or cough, which can reflect fluid BNP is released by the heart in response to increased ven- overload. In patients receiving angiotensin-converting en-tricular filling pressures, but may also be increased in the zyme (ACE) inhibitors, worsening cough should not be as-plasma as a result of ongoing myocardial dysfunction or hy- sumed to be drug-related, because it may be a manifestationpertrophy. A low plasma BNP or NT-proBNP concentration of increasing left heart filling pressures (Section 7). Patientshas a high negative predictive value for cardiac dysfunctionin patients presenting to the emergency room with dyspnea, Table 4.3. Symptoms Suggesting the Diagnosis of HFand it may therefore be used to exclude HF as a cause of dysp- Symptoms Dyspnea at rest or on exertionnea with a relatively high degree of certainty.24,25 Reduction in exercise capacity Orthopnea Paroxysmal nocturnal dyspnea (PND) or Evaluation of Patients Suspected of Having nocturnal cough Heart Failure Edema Ascites or scrotal edema Less specific Early satiety, nausea and vomiting, abdominalRecommendation presentations of HF discomfort Wheezing or cough4.4 Symptoms Consistent with HF. The symptoms listed Unexplained fatigue Confusion/delirium in Table 4.3 suggest the diagnosis of HF. It is recom- Depression/weakness (especially in the elderly) mended that each of these symptoms be elicited in all
    • e46 Journal of Cardiac Failure Vol. 16 No. 6 June 2010with severely decompensated cardiac failure may present diagnosis, estimate prognosis, and monitor the responsewith gastrointestinal symptoms representative of hepatic to therapy of patients with acute HF.23,24,32,33congestion or visceral edema, including early satiety, nau- Measurement of these peptides has been proposed in casessea, vomiting, and right upper quadrant pain. of acute dyspnea where the diagnosis of HF is uncertain, as evident from large, multicenter investigations.23,24,33 The di-Recommendation agnostic accuracy of BNP, using a cutoff value of 100 pg/mL, was 83% relative to the assessment made by the independent4.5 Physical Examination. It is recommended that pa- cardiologists, whereas the negative predictive value of BNP tients suspected of having HF undergo careful for HF when levels were !50 pg/mL was 96%. As expected, physical examination with determination of vital measurement of BNP/NT-proBNP appeared to be most use- signs and careful evaluation for signs shown in ful in patients with an intermediate probability of HF. Plasma Table 4.4. (Strength of Evidence 5 B) NT-Pro BNP cut points of O450 pg/mL for patients younger than 50 years of age, O900 pg/mL for patients age 50-74 Table 4.4. Signs to Evaluate in Patients Suspected of years of age, and O1800 pg/mL for patients 75 years or older Having HF were equally sensitive and specific for diagnosing HF; with !300 pg/mL providing 98% negative predictive value forCardiac Abnormality Sign ruling out HF.23,33Elevated cardiac filling pressures Elevated jugular venous pressure BNP was found to be predictive of HF when LV function and fluid overload S3 gallop was depressed or preserved, but cannot reliably distinguish Rales Hepatojugular reflux between the two.34 In patients with HF associated with pre- Ascites served LVEF, the BNP cutoff value of 100 pg/mL still had Edema a sensitivity of 86% and a negative predictive value of 96%.Cardiac enlargement Laterally displaced or prominent apical impulse BNP and NT-proBNP levels increase with age, more so in Murmurs suggesting valvular older women or in those with underlying renal insufficiency, dysfunction in which case the same cutoff ranges may not provide theReduced cardiac output Narrow pulse pressure Cool extremities same degree of specificity for the diagnosis of HF, especially Tachycardia with pulsus alternans in elderly women with dyspnea.35 However, BNP and NT-Arrhythmia Irregular pulse suggestive of atrial proBNP levels should be interpreted with some caution in fibrillation or frequent ectopy patients with morbid obesity as they may have lower than expected plasma BNP/NT-proBNP levels.36e38Background Recommendation 4.7 Differential Diagnosis. The differential diagnoses in Elevation of the jugular venous pressure, hepatic enlarge- Table 4.5 should be considered as alternative expla-ment or tenderness or pulsatility, and lower extremity edema nations for signs and symptoms consistent with HF.are manifestations of elevated right heart filling pressures, as- (Strength of Evidence 5 B)sociated with impaired renal sodium and water clearance.28e31They also can be due to hepatic or renal dysfunction, varioushypo-oncotic states, as well as venous thromboembolism. If Table 4.5. Differential Diagnosis for HFdue to cardiac disorders, these findings may be accompanied Symptoms and Signsby a loud pulmonic closure sound, RV heave, and a RV S3 Myocardial ischemia(lower left sternal border) consistent with pulmonary hyper- Pulmonary disease (pneumonia, asthma, chronic obstructive pulmonarytension. A prominent laterally displaced apical impulse is disease, pulmonary embolus, primary pulmonary hypertension) Sleep-disordered breathingindicative of LV enlargement. Increased left heart filling pres- Obesitysure is suggested by rales, diminished breath sounds, wheez- Deconditioninging, and an apical S3 gallop.29 Malnutrition Anemia Hepatic failureRecommendation Chronic kidney disease Hypoalbuminemia4.6 It is recommended that BNP or NT-proBNP levels be Venous stasis assessed in all patients suspected of having HF, espe- Depression Anxiety and hyperventilation syndromes cially when the diagnosis is not certain. (Strength of Hyper or hypo-thyroidism Evidence 5 A)Background Background Two forms of natriuretic peptide, BNP and NT-proBNP, A number of signs and symptoms of HF are nonspecific,have been studied extensively as aids to establish the particularly shortness of breath, which may reflect
    • Heart Failure Practice Guideline  HFSA e47underlying pulmonary disease or physical deconditioning.26 Table 4.7. Criteria for NYHA Functional Classification inRecognizing this lack of specificity is particularly important Patients With HFin a general practice setting where patients often present with Class I No limitation of physical activity. Ordinary physicalnoncardiac causes of shortness of breath or edema. In patients activity does not cause undue fatigue, palpitation, orwith dyspnea who do not present with clear signs of HF, the dyspnea. Class II Slight limitation of physical activity. Comfortable at rest,possibility of a pulmonary pathology, including pulmonary but ordinary physical activity results in fatigue,embolism, should be considered and evaluated. Spirometry, palpitations, or dyspnea.chest computed tomography, ventilation-perfusion lung Class III IIIA: Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue,scan, or pulmonary angiography should be performed as clin- palpitation, or dyspnea. IIIB: Marked limitation ofically indicated. It is important to recognize that sleep apnea physical activity. Comfortable at rest, but minimaland HF frequently coexist.39e42 In patients with fatigue who exertion causes fatigue, palpitation, or dyspnea. Class IV Unable to carry on any physical activity without discomfort.are without clear signs of HF, physical deconditioning, sleep Symptoms of cardiac insufficiency present at rest. If anyapnea, hypothyroidism, and depression should be considered physical activity is undertaken, discomfort is increased.as potential causes. Edema may be due to calcium channelblockers, other drugs (e.g. thiazolidinediones, non steroidal 4.11 Volume Status. The degree of volume excess is a keyanti-inflammatory drugs [NSAIDs], pregabalin), hypoalbu- consideration during treatment. It is recommendedminemia, or venous stasis. that it be routinely assessed by determining:  Presence of paroxysmal nocturnal dyspnea orRecommendations orthopnea4.8 It is recommended that patients with a diagnosis of  Presence of dyspnea on exertion HF undergo evaluation as outlined in Table 4.6.  Daily weights and vital signs with assessment (Strength of Evidence 5 C) for orthostatic changes  Presence and degree of rales, S3 gallop, jugular Table 4.6. Initial Evaluation of Patients venous pressure elevation, hepatic enlargement With a Diagnosis of HF and tenderness, positive hepatojugular reflux,Assess clinical severity of HF by history and physical examination edema, and ascites (Strength of Evidence 5 B)Assess cardiac structure and functionDetermine the etiology of HF, with particular attention to reversible causesEvaluate for coronary disease and myocardial ischemia BackgroundEvaluate the risk of life-threatening arrhythmiaIdentify any exacerbating factors for HF Characteristic Symptoms. The presence or absence andIdentify comorbidities which influence therapy severity of characteristic symptoms of HF, including thoseIdentify barriers to adherence related to exercise tolerance and fluid overload, should be documented in all patients undergoing initial evaluation.4.9 Symptoms. In addition to symptoms characteristic Comorbidities. Symptoms of comorbidities commonly of HF (dyspnea, fatigue, decreased exercise toler- associated with HF should be sought. These include an- ance, fluid retention), evaluation of the following gina,43 symptoms of sleep-disordered breathing, presyn- symptoms should be considered in the diagnosis cope, or syncope. of HF:  Angina Physical Examination. The physical examination should  Symptoms suggestive of embolic events focus on the detection and etiology of structural heart dis-  Symptoms suggestive of sleep-disordered breath- ease, current volume status, and the severity of HF, as a guide ing to initiating therapy and a baseline to gauge the effect of that  Symptoms suggestive of arrhythmias, including therapy. Height and weight should be recorded. Supine and palpitations upright vital signs should be taken to assess for orthostasis.  Symptoms of possible cerebral hypoperfusion, Presence of an S3 gallop and elevation of jugular venous including syncope, presyncope, or lightheaded- pressure are invaluable specific markers of elevated cardiac ness (Strength of Evidence 5 B) filling pressures. A positive Kussmaul can be a flag for4.10 Functional Capacity/Activity Level. It is recommen- restrictive disease or significant HF. ded that the severity of clinical disease and func- Murmurs such as those of aortic stenosis or mitral regurgi- tional limitation be evaluated and recorded and the tation may provide clues to the etiology of LV dysfunction. ability to perform typical daily activities be deter- Murmurs of tricuspid regurgitation and mitral regurgitation mined. This evaluation may be graded by metrics vary depending on the degree of pulmonary or systemic pres- such as New York Heart Association (NYHA) func- sure, respectively, volume overload, ventricular dilatation, and tional class (Table 4.7) (Strength of Evidence 5 A) failure of leaflet coaptation or elevated pulmonary pressures. or by the 6-minute walk test. (Strength of Evidence The physical examination has limitations. Pulmonary 5 C) rales are an insensitive indicator of elevation in pulmonary
    • e48 Journal of Cardiac Failure Vol. 16 No. 6 June 2010venous pressure, unless they occur abruptly.27 Overt pulmo- X-ray examination for determination of heartnary edema rarely occurs where left heart filling pressure is size, evidence of fluid overload, detection of pul-chronically elevated, as the pulmonary vasculature adapts monary and other diseases, and appropriatewith increased lymphatic drainage. Ascites is common in placement of implanted cardiac devices. (Strengthpatients with advanced HF (with contributing right HF), of Evidence 5 B)but it may be difficult to appreciate on physical examina- 4.15 Additional Laboratory Tests. It is recommendedtion. Although abdominal complaints can be misleading, that patients with no apparent etiology of HF orhistory often is a better indicator of excess abdominal fluid no specific clinical features suggesting unusual eti-than physical examination. Hepatojugular reflux is a sensi- ologies undergo additional directed blood and lab-tive indicator of volume expansion and may be demon- oratory studies to determine the cause of HF.strated in states of RV dysfunction.31 (Strength of Evidence 5 B) Functional Assessment. Determination of baseline exer- Background: Initial Diagnostic Testingcise and functional limitation is important during the initialevaluation of patients with established HF. Decisions re- Electrocardiogram and Chest X-Ray. The electrocar-garding hospitalization and response to medications and diogram (ECG) provides important information on acute is-other interventions are aided by estimation of the degree chemia, prior MI, conduction abnormalities, arrhythmias,of limitation present at the first evaluation. and ventricular hypertrophy.50 A chest radiograph may A number of strategies can be employed to assist in these show evidence for cardiac chamber enlargement, increasedestimates, including 6-minute walk test distance.44 One pulmonary venous pressure, interstitial or alveolar edema,common, time-tested, and simple metric is the NYHA func- pleural effusions, valvular or pericardial calcification, ortional classification, which is shown in Table 4.7. 45 Al- coexisting lung disease.though NYHA class is subjective, numerous longitudinalstudies have shown the prognostic power of this determina- Laboratory Evaluation. The complete blood count maytion, and serial evaluation is helpful to gauge response to show anemia.51,52 Hyponatremia, from free water retention,therapy. Therapeutic recommendations often are directed may reflect elevated serum vasopressin levels and activationtoward patients within particular NYHA classes, based on of the renin-angiotensin system.53,54 Hyponatremia, whichuse of this indicator as an entry criterion for clinical trials. has been associated with poor prognosis,55,56 may also re-Success of therapy may be indicated by improvement of at sult from excessive diuresis, but more often indicates severeleast 1 functional class.46e49 HF with excess total body salt and water. Elevated serum creatinine may not only reflect important underlying renal impairment but may also represent a prerenal state from re-Recommendations duced cardiac output, venous congestion, intraabdominal4.12 Standard Laboratory Tests. It is recommended that hypertension or excessive diuresis.57e59 Renal dysfunction the following laboratory tests be obtained routinely is associated with a worse prognosis.60e63 Prerenal azote- in patients being evaluated for HF: serum electro- mia is usually associated with a disproportionate increase lytes, blood urea nitrogen, creatinine, glucose, cal- in blood urea nitrogen. If creatinine is disproportionately el- cium, magnesium, fasting lipid profile (low-density evated, it generally indicates intrinsic renal disease. Hypo- lipoprotein cholesterol, high-density lipoprotein albuminemia contributes to low plasma oncotic pressure cholesterol, triglycerides), complete blood count, se- and edema formation. An abnormal urinary sediment may rum albumin, uric acid, liver function tests, urinaly- suggest glomerular disease or infection, and proteinuria sis, and thyroid function. (Strength of Evidence 5 B) may play a role in low oncotic pressure and edema forma- tion. Hyper- or hypothyroidism can precipitate or aggravate4.13 Electrocardiogram (ECG). It is recommended that ventricular dysfunction and clinical HF and may be clini- all patients with HF have an ECG performed to: cally occult in the elderly. A lipid profile is valuable in pa-  assess cardiac rhythm and conduction (in some tients with significant risk factors for or a documented cases, using Holter monitoring or event monitors) history of coronary artery disease.  assess electrical dyssynchrony (wide QRS or bun- dle branch block), especially when LVEF !35% Determination of Etiology. Initial assignment of HF eti-  detect LV hypertrophy or other chamber ology should be as specific as possible. Significant differ- enlargement ences in prognosis are commonly noted among the various  detect evidence of myocardial infarction (MI) etiologies of HF, and identification of specific etiologies, or ischemia such as ischemic heart disease, may trigger specific direc-  assess QTc interval, especially with drugs that tions for evaluation and treatment (Section 13). A number prolong QT intervals (Strength of Evidence 5 B) of common etiologies dominate the causes of HF in most4.14 Chest X-Ray. It is recommended that all patients practice settings. Ischemic heart disease remains a common with HF have a postero-anterior and lateral chest cause, especially among patients with reduced LVEF.43
    • Heart Failure Practice Guideline  HFSA e49Background: Common Etiologic Factors common causes should be sought as indicated below. A family history of cardiomyopathy should be solicited, espe- Coronary Artery Disease. Patients with evidence of cially if non-ischemic cardiomyopathy is associated witha MI, coronary artery bypass graft surgery, or percutaneous conduction system disease and arrhythmias. A finding ofangioplasty or patients who have coronary artery narrowing idiopathic cardiomyopathy might warrant cardiovascularof greater than 70% in at least 1 artery are most likely to testing in first- and second-degree relatives.66e68 Apicalhave an ischemic cardiomyopathy.64 On the other hand, ballooning (‘‘tako-tsubo’’) cardiomyopathy is a transientthe mere presence of atherosclerotic coronary artery disease syndrome with profound anteroapical dysfunction of un-may not necessarily explain the underlying etiology if clear etiology and associated with emotional stress orcardiac dysfunction is out of proportion to the degree of high catecholamines surge. Table 4.8 lists physical and lab-coronary artery disease. Patients with initially established oratory findings that can point to less common etiologies.non-ischemic cardiomyopathy can also develop progressivecoronary artery disease, leading to adverse clinical out- Table 4.8. Physical Examination Findingscomes, such as sudden cardiac death. Related to Etiology Physical Examination Findings and Implications Hypertension. Population-based analyses have shownhypertension to be the most important population- Skin Pigmentation: iron overload Lipid deposits: hyperlipidemiaattributable risk for HF.5,65 Hypertensive or previously Spider angiomata: liver diseasehypertensive patients with a non-dilated left ventricle, Easy bruisability, nail pitting, amyloidosispreserved LVEF, left atrial enlargement, and concentric Cushingoid features: glucocorticoid excess Skin laxity: pseudoxanthoma elasticumLV hypertrophy are most likely to have hypertension as Rash: pellagrathe principal etiology for HF. Among all hypertensive pa- Malar rash of discoid: lupustients with HF, elevated blood pressure should be presumed Sclerodactyly or skin tightening: CREST or sclerodermato contribute to both the cardiovascular pathology and Lymph nodes Adenopathy: sarcoidosis; lymphomaongoing clinical manifestations of the disease. Thyroid Modularity enlargement: hyper- or The assignment of hypertension as an etiology, particu- hypothyroidism Jugular veins Kussmaul sign: constriction or restrictionlarly of LV systolic dysfunction, has been challenged of Heart rate Resting tachycardia: a very rapid ventricularlate. Clearly, hypertension often is associated with ischemic response to atrial fibrillation or persistentheart disease and typically is not considered primary in tachyarrhythmia may suggest a tachycardia- induced cardiomyopathythese cases. Documentation of the presence of hypertension Carotids Delayed upstroke: aortic stenosismay be difficult in many cases of apparently idiopathic car- Bifid carotid contour: may suggest hypertrophicdiomyopathy unless the medical history is carefully re- cardiomyopathy Carotid bruits may suggest associatedviewed. Many patients with a history of hypertension will atherosclerotic diseasenot be hypertensive when presenting with systolic dysfunc- Cardiac palpation Hyperdynamic, laterally displaced apicaltion. Likewise, hypertension may emerge as ventricular impulse: LV volume overload (aortic or mitral regurgitation),an adynamic point of maximalfunction improves with institution of proper medical ther- impulse suggests a dilated cardiomyopathy.apy. In any event, close observation for the development These displaced PMI findings are usuallyof hypertension is warranted during follow-up. accompanied by an S3 gallop Cardiac auscultation Murmurs: specific valvular pathologies of aortic stenosis, aortic regurgitation, mitral stenosis Alcoholic Cardiomyopathy. Careful history should be and mitral regurgitation may be presentdirected to determining the quantity of alcohol consump- indicating the potential etiology. Elevation of diastolic pressures may lessen traditionaltion. In the absence of a clear alternative, an alcoholic eti- murmurs of regurgitation and low cardiacology is likely among patients with a dilated left ventricle output may lessen traditional murmurs of stenosisand history of consuming excessive amounts of alcohol. Diastolic knock: pericardial disease Diastolic plop: thrombus or atrial myxoma Valvular Disease. In patients with chronic valvular dis- Extremities Cyanosis: may be a manifestation of extreme low output state or right to left shuntingease, physical findings may not be characteristic because of through a congenital defectlow cardiac output. This is especially true of patients with Bounding peripheral pulse and a Quincke’s sign:‘‘low gradient aortic stenosis.’’ A history of known valvular suggest wide pulse pressure and may be clues to hyperthyroidism, aortic regurgitation, AVor rheumatic heart disease should be sought. Detection of fistulaoccult valvular disease is one reason for the importance of Warm extremities and high cardiac output:routine echocardiography as part of the evaluation process. beriberi, hyperthyroidism Idiopathic and Familial Dilated Cardiomyopathy. A Familial Hypertrophic Cardiomyopathy. Hypertrophicnumber of patients have no apparent cause for their HF de- cardiomyopathy is an autosomal dominant condition withspite careful clinical evaluation. The label idiopathic car- both genotypic and phenotypic variability, and patientsdiomyopathy represents a diagnosis of exclusion, and less with this condition may present with dyspnea or syncope.
    • e50 Journal of Cardiac Failure Vol. 16 No. 6 June 2010Echocardiography is an effective diagnostic approach. Drugs Associated With HF Exacerbation. Some phar-Genetic testing is often indicated.68 macologic agents, including selected calcium channel blockers and antiarrhythmics, may depress cardiac function Peripartum Cardiomyopathy. HF occurring 1 month and increase the likelihood of HF or exacerbation of preex-before or within 5 months of delivery, with no prior patient istent or subclinical heart dysfunction.78,79 NSAIDs havehistory of heart disease or other etiology of cardiomyopa- been associated with an increased risk of HF hospitaliza-thy, is generally labeled peripartum cardiomyopathy. tion, and they should be recognized as a causative factor for HF exacerbation and avoided in these patients.80 Thia- Chagas Cardiomyopathy. In patients from Latin Amer- zelinediones and pregabalin are also associated with fluidica presenting with electrocardiographic and echocardio- retention in patients with HF, and they are not recommen-graphic manifestations of ‘‘ischemic’’ cardiomyopathy, ded in patients with symptomatic HF.81,82 Tumor necrosisbut who are found to have no significant coronary artery factor antagonists have also been associated with new onsetdisease on angiography, the diagnosis of Chagas cardiomy- and/or exacerbation of existing HF.83opathy should be considered, and Trypanosoma Cruzi titerschecked, if they come from an endemic region (e.g., Connective Tissue Disorders. Systemic lupus erythemato-Central or South America). sus, scleroderma, and other connective tissue disorders may represent a cause of HF. Vasculitis, hypertension, systemic lu- Endocrine Abnormalities. Pheochromocytoma should pus erythematosus, pericardial involvement, and renal impair-be considered in patients with hypertension that is particu- ment all may contribute to the syndrome of HF. Sclerodermalarly difficult to manage or is characterized by severe fluctu- may be associated with myocardial fibrosis with restrictiveations in blood pressure. Because hypo- or hyperthyroidism physiology. In the presence of characteristic skin changes, ar-can exacerbate HF and, on rare occasion, can represent the thritis, or other organ system involvement, serum antinuclearprincipal cause of HF, thyroid-stimulating hormone should antibody and rheumatoid factor should be measured.be measured. Acromegaly is a rare, but well-recognized,finding in cardiomyopathy and may be uncovered by obtain- Toxin Exposure. Lead, arsenic, and cobalt are threeing a history of increase in jaw, hand, or foot size, or by toxins that may cause progressive myocardial dysfunction.comparison of the patient’s current features with dated pho- A history of consumption of lead paint or drinking of welltographs. Diabetes mellitus is commonly associated with the water may provide clues to this unusual cause.development of HF, especially in those with microvasculardiseases such as retinopathy or microalbuminuria.69 Diabetes Myocarditis (see also section 16). Rapidly progressivemellitus can contribute directly to the development of HF, via cardiomyopathy, including a rapidly deteriorating clinicalits role as a risk factor for coronary artery disease, or second- condition, should raise suspicion of active myocarditis, in-ary to diabetic agents such as thiazolidinediones that cause cluding giant cell myocarditis, and represents an indicationfluid retention (see Section 3 for a full discussion of the for consideration of endomyocardial biopsy.84 Myocarditiscontribution of diabetes to the development of HF). may be characterized with a subclinical onset or gradual de- terioration. Hepatitis C or HIV infection may be a cause of Cardiotoxin Exposure. Anthracyclines and occasionally myocarditis, and there should be a low threshold for mea-other anti-cancer agents may result in cardiomyopathy, de- surement of viral serology.85e88pending on the dose received.70,71 In rare cases, sulphurcontaining drugs and a number of other agents, including Nutritional Deficiencies. Beriberi (thiamine deficiency)some antibiotics, may initiate an allergic inflammatory re- may appear in individuals on fad diets or those hospitalizedaction leading to eosinophilic myocarditis and decline in in intensive care units receiving inadequate nutrition.heart function.72 Dating the onset of HF to the initiation Patients with protein-losing enteropathy due to right HFof these agents will be helpful. may develop thiamine deficiency. Selenium deficiency has been recognized as a potential etiology. Radiation Therapy. Chest radiation can affect all cardiacstructures, including the pericardium, myocardium, coronary Amyloidosis. HF with preserved LVEF and minimal or noarteries and heart valves, and result in a constrictive/restrictive LV dilatation, coupled with increased LV and RV wall thick-cardiomyopathy, valvular heart disease and/or ischemic heart ness by echocardiogram, despite normal or diminished QRSdisease. Ideally, evaluation and management of radiation- voltage on ECG, should raise suspicion of amyloidosis.89induced heart disease should involve a HF specialist and/or Serum and urine immunoelectrophoresis should be per-cardiac surgeon with expertise in cardio-oncology.73 formed, along with measurement of serum free light chains, and confirmation with endomyocardial biopsy (and in some Exposure to Illicit Drugs. The use of stimulant drugs cases genotyping) may be warranted to determine the pres-such as cocaine and methamphetamine may lead to the de- ence and subtype of amyloidosis involved as they mayvelopment of HF.74e77 Patients should be educated on the have different prognosis and management strategies. In par-cardiovascular risks of using these agents. ticular, specific testing for the presence of transthyretin
    • Heart Failure Practice Guideline  HFSA e51deposition (familial or wild-type) may identify subtypes that Cardiac MRI may provide reliable accuracy in determiningare amenable to transplantation considerations. Cardiac cardiac involvement of iron deposition.magnetic resonance imaging (MRI) can also aid with thediagnosis and prognosis of cardiac amyloidosis. Recommendations Hemoglobinopathies. Repeated transfusions from chronic 4.16 Evaluation of myocardial ischemia is recommen-hemolytic anemia may result in iatrogenic iron overload. ded in those who develop new-onset LV systolic dys- function especially in the setting of suspected High Output States. Hyperthyroidism, arteriovenous myocardial ischemia or worsening symptoms with(AV) malformations (rarely), large AV fistulas used for di- pre-existing CAD. The choice of testing modalityalysis, or sepsis may result in severe volume overload and should depend on the clinical suspicion and under-high output failure, characterized by preserved LVEF lying cardiac risk factors. Coronary angiographywith increased ventricular volumes. HF related to sepsis should be considered when pre-test probability ofand other critical acute illnesses is usually a result of tran- underlying ischemic cardiomyopathy is high andsient LV dysfunction that is often self-resolving. an invasive coronary intervention may be consid- ered. (See Section 13 for specific clinical situations Tachycardia Mediated Cardiomyopathy. Several types and Strength of Evidence)of tachycardias including ectopic atrial tachycardia, perma- 4.17 Exercise testing for functional capacity is notnent junctional reciprocating tachycardia (PJRT) using an ac- recommended as part of routine evaluation in pa-cessory pathway, atrial fibrillation with a rapid ventricular tients with HF. Specific circumstances in whichresponse, incessant idiopathic ventricular tachycardias, and maximal exercise testing with measurement offrequent premature ventricular beats have been associated expired gases should be considered include:with the development of a reversible dilated cardiomyopathy.  Assessing disparity between symptomatic limita-Although conclusive studies are lacking to determine the up- tion and objective indicators of disease severityper limit of heart rate that may be associated with the devel-  Distinguishing non HF-related causes of func-opment of a cardiomyopathy, a general consensus is that tional limitation, specifically cardiac versuspersistent tachycardia O110 beats per minute is required to pulmonaryinduced cardiomyopathy. In addition, frequent premature  Considering candidacy for cardiac transplan-ventricular contractions (PVCs) (20-30% of all beats or tation or mechanical circulatory supportO10,000 per 24 hour)90,91 may also be associated with the  Determining the prescription for cardiac reha-development of cardiomyopathy.92,93 The optimal level of bilitationrate control to prevent the development of cardiomyopathy  Addressing specific employment capabilitiesin patients with atrial fibrillation is not known. In general, (Strength of Evidence 5 C)a resting ventricular response of 60 to 80 beats per minuteand a ventricular response between 90-115 beats per minute Backgroundduring moderate exercise have been suggested.94 TheAFFIRM (Atrial Fibrillation Follow-up Investigation of Treadmill exercise testing, with or without measurementRhythm Management) trial targeted heart rates of #80 of oxygen uptake, to assess functional capacity is not rou-bpm at rest, #110 bpm during a 6 minute walk test, or an av- tinely required in the evaluation of patients with a knownerage heart rate of 100 beats per minute over at least 18 hours diagnosis of HF. Nevertheless, there are a number of clini-of continuous ambulatory monitoring.95 cal circumstances in which such testing is beneficial.96 Exertional dyspnea and exercise intolerance may be due Sarcoidosis. Sarcoid can mimic many things; it commonly to noncardiac causes, especially pulmonary. When thereis associated with conduction abnormalities and ventricular is a disparity between symptoms and objective findings oftachyarrhythmias. Hilar lymphadenopathy may be a clue to HF, exercise testing with measurement of expired gases tothe diagnosis of sarcoidosis. It can be confirmed by endo- determine peak oxygen consumption may be useful.myocardial biopsy, although false negatives are frequent Measurement of peak oxygen uptake may be of assistanceand a negative biopsy does not exclude a diagnosis of sarcoid- in determining candidacy for cardiac transplantation byosis. Cardiac MRI or specialized positron emission tomogra- quantifying functional limitation and adding prognostic in-phy e computed tomography (PET-CT) protocols may help formation.97 There is no uniform agreement on a cutoff into determine the presence of inflammation. peak oxygen uptake that constitutes an absolute criterion for candidacy for transplantation. A value of !10 mL O2 Hemochromatosis. In the setting of dilated cardiomyop- kg/min denotes severe functional incapacity and poor prog-athy, darkened skin, and diabetes, hemochromatosis should nosis, whereas a value of !14 mL O2 kg/min indicates a pa-be excluded using ferritin. In acute inflammatory states, tient with underlying advanced HF in whom advancedwhen ferritin is elevated, other tests, such as iron, iron sat- therapeutic options such as transplantation or ventricular as-uration, and total iron-binding capacity, may be considered. sist devices may be considered.98 The test should be
    • e52 Journal of Cardiac Failure Vol. 16 No. 6 June 2010performed after optimizing medical therapy. Several studies associated with a dilated left ventricle and new ventricularsuggest that measuring peak oxygen uptake may be less use- arrhythmias or conduction abnormalities) and are poorly re-ful in predicting prognosis in patients on beta blockers.99,100 sponsive to appropriate medical therapy, the diagnosis ofIt is commonly recognized that women have lower peak ox- giant cell myocarditis should be considered. Retrospectiveygen uptake than men. In younger individuals (!50 years of data suggest that this disease is associated with high mortal-age) and women, percent of predicted peak VO2 #50%, or ity rates and that it may respond to immunosuppres-a minute ventilation equivalent of carbon dioxide production sion.84,101 Clinical trials performed in patients with moreslope (VE/VCO2) of O35 are also indicators of poor progno- common forms of lymphocytic myocarditis have failed tosis and can be considerations for transplant candidacy.98 In demonstrate a clinical benefit from immunosuppressiveobese subjects a calculation of VO2 by lean body mass may therapy, and these patients have a high rate of spontaneousalso be helpful.98 recovery.102,103 Other clinical scenarios that may warrant considerations for endomyocardial biopsy including Common Errors in Initial Assessment suspicion for eosinophilic/hypersensitivity myocarditis or drug-induced cardiomyopathy, and the confirmation of in- General History. Historical information should be well- filtrative cardiomyopathies, such as amyloidosis (systemicdocumented wherever possible. For example, electrocardio- or transyretin) or sarcoidosis, or suspected forms of cardio-graphic or enzyme evidence of prior MI should be reviewed, myopathies, such as glycogen storage disease. 104rather than relying on the patient’s description of the event.Early symptoms of HF, such as cough and rales, often are in- Follow-Up Evaluationcorrectly attributed to respiratory infection. Specific evi-dence should be sought to confirm or refute the diagnosis. Recommendation 4.19 It is recommended that clinical evaluation at each Physical Examination. There are a number of ways in follow-up visit include determination of the elementswhich the patient’s volume status may be misjudged. Rales listed in Table 4.9. (Strength of Evidence 5 B).may be due to pulmonary disease, rather than pulmonaryedema. Conversely, severe chronic volume overload may oc- These assessments should include the same symp-cur in the absence of pulmonary rales. Edema may be due to toms and signs assessed during the initial evalua-venous stasis disease or medications such as calcium channel tion. (Strength of Evidence 5 B)blockers, rather than volume overload. Assessment of jugular Table 4.9. Elements to Determine at Follow-Upvenous pressure and its wave form is invaluable in the accu- Visits of HF Patientsrate assessment of volume status. However, the absence of Functional capacity and activity levelevidence of volume overload on examination does not ex- Changes in body weightclude the possibility of severe functional impairment related Patient understanding of and adherence with dietary sodium restrictionto HF. In addition, patients may have volume expansion and Patient understanding of and adherence with medical regimen History of arrhythmia, syncope, presyncope, palpitation or ICD dischargeyet not manifest rales on chest examination. Cardiac mur- Adherence and response to therapeutic interventionsmurs may vary significantly depending upon the patient’s The presence or absence of exacerbating factors for HF, includingvolume status. Decreased murmur intensity may be due to worsening ischemic heart disease, hypertension, and new or worsening valvular diseaseelevated filling pressures or low cardiac output. BackgroundRecommendation Volume Assessment. Determination of serial changes in4.18 Routine endomyocardial biopsy is not recommen- volume status is a critical part of the follow-up of the pa- ded in cases of new-onset HF. Endomyocardial bi- tient with HF. Ongoing efforts to achieve diuresis may be opsy should be considered in patients with rapidly underway as part of the management plan. Diuretic therapy progressive clinical HF or ventricular dysfunc- can be difficult to adjust, and identifying the optimal main- tion, despite appropriate medical therapy. Endo- tenance dose can be challenging. States of persistent fluid myocardial biopsy also should be considered in overload or excessive weight loss are common. Restriction patients suspected of having myocardial infiltra- of dietary sodium intake is a key factor in optimizing fluid tive processes, such as sarcoidosis or amyloidosis, balance. Improved adherence to dietary sodium restriction or in patients with malignant arrhythmias out of may result in significant negative fluid balance, mandating proportion to LV dysfunction, where sarcoidosis adjustment of diuretic therapy. and giant cell myocarditis are considerations. (Strength of Evidence 5 C) Pharmacologic Therapy. The difficulty associated with maintaining an appropriate pharmacologic regimen inBackground patients with HF is well known, even when the patient In patients who present with rapidly progressive signs has experienced clinical benefit from specific medications.and symptoms of HF and ventricular dysfunction (often Economic factors, polypharmacy, side effects, and
    • Heart Failure Practice Guideline  HFSA e53misperceptions concerning the relationship of medications considered if the finding of further reduction in LVEF isto specific somatic feelings all limit adherence with chronic likely to prompt additional treatment. A good example ismedical regimens. Careful review of current medications the patient manifesting progressive signs and symptomsmay uncover lack of adherence and also detect use of of HF who might be listed for cardiac transplantation ifover-the-counter medications that may be detrimental. further worsening of LVEF is not prevented.Recommendation Recommendation4.20 In the absence of deteriorating clinical presenta- 4.21 It is recommended that reevaluation of electro- tion, repeat measurements of ventricular volume lytes and renal function occur at least every 6 and LVEF should be considered in these limited months in clinically stable patients and more fre- circumstances: quently following changes in therapy or with ev-  When a prophylactic implantable cardioverter idence of change in volume status. More frequent defibrillator (ICD) or cardiac resynchronization assessment of electrolytes and renal function is therapy device and defibrillator (CRT-D) place- recommended in patients with severe HF, those ment is being considered in order to determine receiving high doses of diuretics, those on aldo- that LVEF criteria for device placement are still sterone antagonists, and those who are clinically met after medical therapy (Strength of Evidence unstable. (Strength of Evidence 5 C) 5 B)  When patients show substantial clinical im- See Section 7 for recommendations for patients on provement (for example, in response to beta an aldosterone receptor antagonist. blocker treatment or following pregnancy in patients with peripartum cardiomyopathy). Background Such change may denote improved prognosis, The approach to laboratory assessment during follow-up although it does not in itself mandate alteration must be individualized. Circumstances requiring more fre- or discontinuation of specific treatments (see quent monitoring of renal function and electrolytes include Section 7). (Strength of Evidence 5 C) severe HF, changes in volume status or worsening signs and  In alcohol and cardiotoxic substance abusers symptoms of HF, diabetes, prescription of an aldosterone who have discontinued the abused substance. antagonist, and initiation or active adjustment of ACE in- (Strength of Evidence 5 C) hibitors or diuretics. Moderate to severe renal dysfunction  In patients receiving cardiotoxic chemother- is common in patients with HF and reduced LVEF and in apy. (Strength of Evidence 5 B) patients with HF and preserved LVEF, and it may be asso- ciated with hyperkalemia. Diabetics, elderly and patients Repeat determination of LVEF is usually unneces- with chronic renal insufficiency are at particular risk for hy- sary in patients with previously documented LV perkalemia and require more frequent laboratory monitor- dilatation and low LVEF who manifest worsening ing during follow-up. signs or symptoms of HF, unless the information is The role of serial measurements of cardiac biomarkers needed to justify a change in patient management remains controversial, although some studies have sug- (such as surgery or device implantation). gested that sequential monitoring may provide useful risk (Strength of Evidence 5 C) prediction,105 even though the precise test ranges and fre- quencies have not yet been established.106 The role ofBackground BNP and NT-proBNP in risk stratification has been very Follow-Up Assessment of Ventricular Function. There consistent, although the majority of studies have demon-generally is no reason for repeat echocardiography unless it strated the value of a single-point measurement as it relatesis anticipated that findings will prompt a change in therapy. to long-term outcomes. The STARS-BNP (Systolic HeartThere is no evidence that changes in LV volume or LVEF Failure Treatment Supported by BNP) study demonstratedwarrant modifications in therapy with drugs such as ACE a significant reduction in HF death or HF hospitalizationinhibitors or beta blockers. However, the substantial im- for patients randomized to BNP-guided therapy.107 Otherprovement or normalization in LV volumes and LVEF often studies of biomarker-guided therapeutic management ofseen with beta blocker treatment is associated with im- HF have not demonstrated improved clinical outcomes as-proved prognosis, and patients deserve this information. It sociated with this approach as compared to standard clini-is reasonable to consider repeat echocardiography for this cal management, although some benefits have been foundpurpose at least 3 or more months after initiation of beta in specific subgroups such as those !75 years of age andblockade, particularly if the patient has manifested im- in patients whose NT-proBNP were consistently below tar-provement in signs and symptoms of HF. get levels during follow-up.108,109 The incremental value of In patients with previously documented ventricular dila- serial BNP testing solely for the purpose of risk stratifica-tation and reduced LVEF, repeat measurement should be tion has not been established.
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