ACC/AHA/ESC Practice Guidelines

      ACC/AHA/ESC 2006 Guidelines for the Management of
      Patients With Atrial Fibril...
Fuster et al        ACC/AHA/ESC Practice Guidelines                              701


                    TABLE OF CONTEN...
702            Circulation                   August 15, 2006


             a. Surgical Ablation . . . . . . . . . . . . ....
TABLE 1.       Applying Classification of Recommendations and Level of Evidence†

                                        ...
704      Circulation       August 15, 2006


often associated with structural heart disease, although a       AF and its p...
Fuster et al     ACC/AHA/ESC Practice Guidelines                 705


  Class IIa                                        ...
706       Circulation       August 15, 2006


           ulation, and patient preferences. (Level of Evi-           5. In ...
Fuster et al      ACC/AHA/ESC Practice Guidelines                 707


       AF and are not recommended. (Level of Evi- ...
708      Circulation       August 15, 2006


              search of thrombus in the left atrium (LA) or left       5. Sot...
Fuster et al      ACC/AHA/ESC Practice Guidelines               709


b. Acute Myocardial Infarction                      ...
710      Circulation      August 15, 2006


             and/or low thromboembolic risk). Therapy                      pul...
Fuster et al     ACC/AHA/ESC Practice Guidelines                   711




                                               ...
712      Circulation       August 15, 2006


A. Prevalence
The estimated prevalence of AF is 0.4% to 1% in the general
pop...
Fibrilación auricular guías
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Fibrilación auricular guías

  1. 1. ACC/AHA/ESC Practice Guidelines ACC/AHA/ESC 2006 Guidelines for the Management of Patients With Atrial Fibrillation—Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the European Heart Rhythm Association and the Heart Rhythm Society WRITING COMMITTEE MEMBERS Valentin Fuster, MD, PhD, FACC, FAHA, FESC, Co-Chair; Lars E. Rydén, MD, PhD, FACC, FESC, FAHA, Co-Chair; David S. Cannom, MD, FACC; Harry J. Crijns, MD, FACC, FESC*; Anne B. Curtis, MD, FACC, FAHA; Kenneth A. Ellenbogen, MD, FACC†; Jonathan L. Halperin, MD, FACC, FAHA; Jean-Yves Le Heuzey, MD, FESC; G. Neal Kay, MD, FACC; James E. Lowe, MD, FACC; S. Bertil Olsson, MD, PhD, FESC; Eric N. Prystowsky, MD, FACC; Juan Luis Tamargo, MD, FESC; Samuel Wann, MD, FACC, FESC ACC/AHA TASK FORCE MEMBERS Sidney C. Smith, Jr, MD, FACC, FAHA, FESC, Chair; Alice K. Jacobs, MD, FACC, FAHA, Vice-Chair; Cynthia D. Adams, MSN, APRN-BC, FAHA; Jeffery L. Anderson, MD, FACC, FAHA; Elliott M. Antman, MD, FACC, FAHA‡; Jonathan L. Halperin, MD, FACC, FAHA; Sharon Ann Hunt, MD, FACC, FAHA; Rick Nishimura, MD, FACC, FAHA; Joseph P. Ornato, MD, FACC, FAHA; Richard L. Page, MD, FACC, FAHA; Barbara Riegel, DNSc, RN, FAHA ESC COMMITTEE FOR PRACTICE GUIDELINES Silvia G. Priori, MD, PhD, FESC, Chair; Jean-Jacques Blanc, MD, FESC, France; Andrzej Budaj, MD, FESC, Poland; A. John Camm, MD, FESC, FACC, FAHA, United Kingdom; Veronica Dean, France; Jaap W. Deckers, MD, FESC, The Netherlands; Catherine Despres, France; Kenneth Dickstein, MD, PhD, FESC, Norway; John Lekakis, MD, FESC, Greece; Keith McGregor, PhD, France; Marco Metra, MD, Italy; Joao Morais, MD, FESC, Portugal; Ady Osterspey, MD, Germany; Juan Luis Tamargo, MD, FESC, Spain; José Luis Zamorano, MD, FESC, Spain *European Heart Rhythm Association Official Representative. †Heart Rhythm Society Official Representative. ‡Immediate Past Chair. This document was approved by the American College of Cardiology Foundation Board of Trustees in June 2006; by the American Heart Association Science Advisory and Coordinating Committee in June 2006; and by the European Society of Cardiology Committee for Practice Guidelines in June 2006. When this document is cited, the American College of Cardiology Foundation, the American Heart Association, and the European Society of Cardiology request that the following citation format be used: Fuster V, Rydén LE, Cannom DS, Crijns HJ, Curtis AB, Ellenbogen KA, Halperin JL, Le Heuzey J-Y, Kay GN, Lowe JE, Olsson SB, Prystowsky EN, Tamargo JL, Wann S, Smith SC Jr, Jacobs AK, Adams CD, Anderson JL, Antman EM, Hunt SA, Nishimura R, Ornato JP, Page RL, Riegel B, Priori SG, Blanc J-J, Budaj A, Camm AJ, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Zamorano JL. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation— executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation). Circulation. 2006;114:700-752. Published online before print August 2, 2006. DOI: 10/1161/CIRCULATIONAHA.106.177031. This article has been copublished in the August 15, 2006, issues of Circulation and the Journal of the American College of Cardiology and the August 16, 2006, issue of the European Heart Journal. Copies: This document is available on the World Wide Web sites of the American College of Cardiology (www.acc.org), the American Heart Association (www.americanheart.org), and the European Society of Cardiology (www.escardio.org). Single and bulk reprints of both the online full-text guidelines and the published executive summary (published in the August 15, 2006, issues of Circulation and the Journal of the American College of Cardiology and the August 16, 2006, issue of the European Heart Journal) are available from Oxford University Press by contacting Special Sales (special.sales@oxfordjournals.org), Journals Division, Oxford University Press, Great Clarendon Street, Oxford, OX2 6DP, UK. Phone 44 (0) 1865 353827, Fax 44 (0) 1865 353774, Work Mobile 44 07841322925. Single copies of the executive summary and the full-text guidelines are also available by calling 800-253-4636 or writing the American College of Cardiology Foundation, Resource Center, at 9111 Old Georgetown Road, Bethesda, MD 20814-1699. To purchase bulk reprints, fax 212-633-3820 or e-mail reprints@elsevier.com. To purchase Circulation reprints: Up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 410-528-4121, fax 410-528-4264, or e-mail kelle.ramsay@wolterskluwer.com. Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association or the European Society of Cardiology. Please direct requests to copyright.permissions@heart.org or journals.permissions@oxfordjournals.org. (Circulation. 2006;114:700-752.) © 2006 by the American College of Cardiology Foundation, the American Heart Association, Inc, and the European Society of Cardiology. Circulation is available at http://www.circulationaha.org DOI: 10.1161/CIRCULATIONAHA.106.177031 700
  2. 2. Fuster et al ACC/AHA/ESC Practice Guidelines 701 TABLE OF CONTENTS VI. Causes, Associated Conditions, Clinical Preamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .702 Manifestations, and Quality of Life . . . . . . . . . . . .715 A. Causes and Associated Conditions . . . . . . . . . .715 I. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .702 1. Reversible Causes of Atrial Fibrillation . . . . . . .715 A. Organization of Committee and 2. Atrial Fibrillation Without Associated Evidence Review . . . . . . . . . . . . . . . . . . . . . . . .702 Heart Disease . . . . . . . . . . . . . . . . . . . . . . . .715 Classification of Recommendations . . . . . . . . .704 3. Medical Conditions Associated With Level of Evidence . . . . . . . . . . . . . . . . . . . . . . .704 Atrial Fibrillation . . . . . . . . . . . . . . . . . . . . .715 B. Changes Since the Initial Publication of 4. Atrial Fibrillation With Associated These Guidelines in 2001 . . . . . . . . . . . . . . . . .704 Heart Disease . . . . . . . . . . . . . . . . . . . . . . . .715 C. Recommendations for Management of 5. Familial Atrial Fibrillation . . . . . . . . . . . . . .716 Patients With Atrial Fibrillation . . . . . . . . . . . .704 6. Autonomic Influences in Atrial Fibrillation . . . .716 Recommendations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .704 B. Clinical Manifestations . . . . . . . . . . . . . . . . . . .716 1. Pharmacological Rate Control During C. Quality of Life . . . . . . . . . . . . . . . . . . . . . . . . . .716 Atrial Fibrillation . . . . . . . . . . . . . . . . . . . . .704 VII. Clinical Evaluation. . . . . . . . . . . . . . . . . . . . . . . . . .716 2. Preventing Thromboembolism . . . . . . . . . . .705 A. Basic Evaluation of the Patient With 3. Cardioversion of Atrial Fibrillation . . . . . . .706 Atrial Fibrillation . . . . . . . . . . . . . . . . . . . . . . . .716 a. Pharmacological Cardioversion . . . . . . . .706 1. Clinical History and Physical Examination. . .716 b. Direct-Current Cardioversion . . . . . . . . .707 2. Investigations. . . . . . . . . . . . . . . . . . . . . . . . .716 c. Pharmacological Enhancement of VIII. Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .718 Direct-Current Cardioversion . . . . . . . . .707 A. Strategic Objectives . . . . . . . . . . . . . . . . . . . . . .718 d. Prevention of Thromboembolism in B. Pharmacological and Nonpharmacological Patients With Atrial Fibrillation Treatment Options . . . . . . . . . . . . . . . . . . . . . . .718 Undergoing Cardioversion. . . . . . . . . . . .707 1. Heart Rate Control Versus Rhythm Control . . .718 4. Maintenance of Sinus Rhythm . . . . . . . . . . .708 a. Pharmacological Rate Control During 5. Special Considerations . . . . . . . . . . . . . . . . .708 Atrial Fibrillation . . . . . . . . . . . . . . . . . . .720 a. Postoperative Atrial Fibrillation . . . . . . .708 b. Regulation of Atrioventricular Nodal b. Acute Myocardial Infarction . . . . . . . . . .709 Conduction by Pacing . . . . . . . . . . . . . . .720 c. Management of Atrial Fibrillation c. Atrioventricular Nodal Ablation . . . . . . .720 Associated With the Wolff-Parkinson-White 2. Preventing Thromboembolism . . . . . . . . . . .722 (WPW) Preexcitation Syndrome . . . . . . . .709 a. Risk Stratification . . . . . . . . . . . . . . . . . .722 d. Hyperthyroidism. . . . . . . . . . . . . . . . . . . .709 b. Antithrombotic Strategies for Prevention e. Management of Atrial Fibrillation of Ischemic Stroke and Systemic During Pregnancy . . . . . . . . . . . . . . . . . .709 Embolism . . . . . . . . . . . . . . . . . . . . . . . . . .723 f. Management of Atrial Fibrillation in Patients c. Nonpharmacological Approaches to With Hypertrophic Cardiomyopathy Prevention of Thromboembolism . . . . . .725 (HCM) . . . . . . . . . . . . . . . . . . . . . . . . . . .710 3. Cardioversion of Atrial Fibrillation . . . . . . .726 g. Management of Atrial Fibrillation in Patients a. Pharmacological Cardioversion . . . . . . . .727 With Pulmonary Disease . . . . . . . . . . . . .710 4. Pharmacological Agents to Maintain II. Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .710 Sinus Rhythm . . . . . . . . . . . . . . . . . . . . . . . .727 A. Atrial Fibrillation . . . . . . . . . . . . . . . . . . . . . . . .710 a. Agents With Proven Efficacy to B. Related Arrhythmias . . . . . . . . . . . . . . . . . . . . .710 Maintain Sinus Rhythm . . . . . . . . . . . . . .727 III. Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .711 b. Out-of-Hospital Initiation of IV. Epidemiology and Prognosis . . . . . . . . . . . . . . . . . .711 Antiarrhythmic Drugs in Patients A. Prevalence. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .712 With Atrial Fibrillation . . . . . . . . . . . . . .728 B. Incidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .712 5. Direct-Current Cardioversion of Atrial C. Prognosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .712 Fibrillation and Atrial Flutter . . . . . . . . . . . .731 V. Pathophysiological Mechanisms . . . . . . . . . . . . . . .712 a. Technical and Procedural Aspects . . . . .731 A. Atrial Factors . . . . . . . . . . . . . . . . . . . . . . . . . . .712 b. Risks and Complications of Direct-Current 1. Atrial Pathology as a Cause of Atrial Cardioversion of Atrial Fibrillation. . . . .732 Fibrillation . . . . . . . . . . . . . . . . . . . . . . . . . .712 c. Pharmacological Enhancement of 2. Mechanisms of Atrial Fibrillation . . . . . . . .712 Direct-Current Cardioversion . . . . . . . . .732 3. Atrial Electrical Remodeling . . . . . . . . . . . .713 d. Prevention of Thromboembolism in 4. Other Factors Contributing to Atrial Patients With Atrial Fibrillation Fibrillation . . . . . . . . . . . . . . . . . . . . . . . . . . .713 Undergoing Conversion . . . . . . . . . . . . . .732 B. Atrioventricular Conduction . . . . . . . . . . . . . . .713 6. Maintenance of Sinus Rhythm . . . . . . . . . . .734 1. General Aspects . . . . . . . . . . . . . . . . . . . . . .713 a. Pharmacological Therapy . . . . . . . . . . . .734 2. Atrioventricular Conduction in Preexcitation b. Predictors of Recurrent Atrial Fibrillation . . .734 Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . .714 c. General Approach to Antiarrhythmic C. Myocardial and Hemodynamic Consequences Drug Therapy . . . . . . . . . . . . . . . . . . . . . .734 of Atrial Fibrillation. . . . . . . . . . . . . . . . . . . . . .714 d. Selection of Antiarrhythmic Agents in D. Thromboembolism . . . . . . . . . . . . . . . . . . . . . . .714 Patients With Cardiac Diseases. . . . . . . .735 1. Pathophysiology of Thrombus Formation . . . . .714 7. Nonpharmacological Therapy for 2. Clinical Implications . . . . . . . . . . . . . . . . . . .715 Atrial Fibrillation . . . . . . . . . . . . . . . . . . . . .735
  3. 3. 702 Circulation August 15, 2006 a. Surgical Ablation . . . . . . . . . . . . . . . . . . .735 statements of all such relationships that might be perceived as real b. Catheter Ablation . . . . . . . . . . . . . . . . . . .736 or potential conflicts of interest. Writing Committee members are c. Suppression of Atrial Fibrillation also strongly encouraged to declare a previous relationship with Through Pacing . . . . . . . . . . . . . . . . . . . .737 industry that might be perceived as relevant to guideline develop- d. Internal Atrial Defibrillators . . . . . . . . . .737 ment. If a Writing Committee member develops a new relationship C. Primary Prevention. . . . . . . . . . . . . . . . . . . . . . .737 with industry during his or her tenure, he or she is required to notify IX. Proposed Management Strategies . . . . . . . . . . . . . .737 guideline staff in writing. The continued participation of the Writing A. Overview of Algorithms for Management of Patients With Atrial Fibrillation . . . . . . . . . .738 Committee member will be reviewed. These statements are re- 1. Newly Discovered Atrial Fibrillation. . . . . .738 viewed by the parent Task Force, reported orally to all members of 2. Recurrent Paroxysmal Atrial Fibrillation . . . .738 the Writing Committee at each meeting, and updated and reviewed 3. Recurrent Persistent Atrial Fibrillation . . . .739 by the Writing Committee as changes occur. Please refer to the 4. Permanent Atrial Fibrillation . . . . . . . . . . . .739 methodology manuals for further description of the policies used in Appendix I . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .740 guideline development, including relationships with industry, avail- Appendix II . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .741 able on the ACC, AHA, and ESC World Wide Web sites (http:// Appendix III . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .743 www.acc.org/clinical/manual/manual_introltr.htm, http://circ.aha- References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .745 journals.org/manual/ and http://www.escardio.org/knowledge/ Preamble guidelines/Rules/). Please see Appendix I for author relationships It is important that the medical profession play a significant role with industry and Appendix II for peer reviewer relationships with in critically evaluating the use of diagnostic procedures and industry that are pertinent to these guidelines. therapies as they are introduced and tested in the detection, These practice guidelines are intended to assist healthcare management, or prevention of disease states. Rigorous and providers in clinical decision making by describing a range of expert analysis of the available data documenting absolute and generally acceptable approaches for the diagnosis, manage- relative benefits and risks of those procedures and therapies can ment, and prevention of specific diseases and conditions. produce helpful guidelines that improve the effectiveness of These guidelines attempt to define practices that meet the care, optimize patient outcomes, and favorably affect the overall needs of most patients in most circumstances. These guide- cost of care by focusing resources on the most effective strategies. line recommendations reflect a consensus of expert opinion The American College of Cardiology Foundation (ACCF) after a thorough review of the available, current scientific and the American Heart Association (AHA) have jointly en- evidence and are intended to improve patient care. If these gaged in the production of such guidelines in the area of guidelines are used as the basis for regulatory/payer deci- cardiovascular disease since 1980. The ACC/AHA Task Force sions, the ultimate goal is quality of care and serving the on Practice Guidelines, whose charge is to develop, update, or patient’s best interests. The ultimate judgment regarding care revise practice guidelines for important cardiovascular diseases of a particular patient must be made by the healthcare and procedures, directs this effort. The Task Force is pleased to provider and the patient in light of all of the circumstances have this guideline developed in conjunction with the European presented by that patient. There are circumstances in which Society of Cardiology (ESC). Writing committees are charged deviations from these guidelines are appropriate. with the task of performing an assessment of the evidence and The guidelines will be reviewed annually by the ACC/AHA acting as an independent group of authors to develop or update Task Force on Practice Guidelines and the ESC Committee for written recommendations for clinical practice. Practice Guidelines and will be considered current unless they are Experts in the subject under consideration have been selected updated, revised, or sunsetted and withdrawn from distribution. The from all 3 organizations to examine subject-specific data and to executive summary and recommendations are published in the write guidelines. The process includes additional representatives August 15, 2006, issue of the Journal of the American College of from other medical practitioner and specialty groups when appro- Cardiology, August 15, 2006, issue of Circulation, and August 16, priate. Writing committees are specifically charged to perform a 2006, issue of the European Heart Journal. The full-text guidelines formal literature review, weigh the strength of evidence for or are e-published in the same issues of the Journal of the American against a particular treatment or procedure, and include estimates of College of Cardiology and Circulation and published in September expected health outcomes where data exist. Patient-specific modi- 9, 2006, issue of Europace, as well as posted on the ACC fiers, comorbidities, and issues of patient preference that might (www.acc.org), AHA (www.americanheart.org), and ESC (www. influence the choice of particular tests or therapies are considered as escardio.org) World Wide Web sites. Copies of the full text and the well as frequency of follow-up and cost-effectiveness. When executive summary are available from all 3 organizations. available, information from studies on cost will be considered; Sidney C. Smith, Jr, MD, FACC, FAHA, FESC, Chair, however, review of data on efficacy and clinical outcomes will ACC/AHA Task Force on Practice Guidelines constitute the primary basis for preparing recommendations in Silvia G. Priori, MD, PhD, FESC, Chair, ESC Committee these guidelines. for Practice Guidelines The ACC/AHA Task Force on Practice Guidelines and the ESC Committee for Practice Guidelines make every effort to avoid any I. Introduction actual, potential, or perceived conflict of interest that might arise as A. Organization of Committee and Evidence a result of an outside relationship or personal interest of the Writing Review Committee. Specifically, all members of the Writing Committee Atrial fibrillation (AF) is the most common sustained cardiac and peer reviewers of the document are asked to provide disclosure rhythm disturbance, increasing in prevalence with age. AF is
  4. 4. TABLE 1. Applying Classification of Recommendations and Level of Evidence† Size of Treatment Effect Class I Class IIa Class IIb Class III Benefit Risk Benefit Risk Benefit Risk Risk Benefit Additional studies with focused objectives Additional studies with broad objectives needed; No additional studies needed needed additional registry data would be helpful Procedure/treatment SHOULD be IT IS REASONABLE to perform Procedure/treatment MAY BE CONSIDERED Procedure/treatment should NOT be performed/administered procedure/administer treatment performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL Level A • Recommendation that procedure or • Recommendation in favor of treatment or • Recommendation’s usefulness/efficacy less well • Recommendation that procedure or treatment is Multiple (3 to 5) population treatment is useful/effective procedure being useful/effective established not useful/effective and may be harmful risk strata evaluated* • Sufficient evidence from multiple • Some conflicting evidence from multiple • Greater conflicting evidence from multiple • Sufficient evidence from multiple randomized trials General consistency of randomized trials or meta-analyses randomized trials or meta-analyses randomized trials or meta-analyses or meta-analyses direction and magnitude of effect Level B • Recommendation that procedure or • Recommendation in favor of treatment or • Recommendation’s usefulness/efficacy less well • Recommendation that procedure or treatment is Fuster et al Limited (2 to 3) population risk treatment is useful/effective procedure being useful/effective established not useful/effective and may be harmful strata evaluated* • Limited evidence from single randomized • Some conflicting evidence from single • Greater conflicting evidence from single • Limited evidence from single randomized trial or trial or nonrandomized studies randomized trial or nonrandomized studies randomized trial or nonrandomized studies nonrandomized studies Level C • Recommendation that procedure or • Recommendation in favor of treatment or • Recommendation’s usefulness/efficacy less well • Recommendation that procedure or treatment is Very limited (1 to 2) population treatment is useful/effective procedure being useful/effective established not useful/effective and may be harmful risk strata evaluated* • Only expert opinion, case studies, or • Only diverging expert opinion, case studies, or • Only diverging expert opinion, case studies, or • Only expert opinion, case studies, or standard-of-care standard-of-care standard-of-care standard-of-care Estimate of Certainty (Precision) of Treatment Effect *Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective. †In 2003, the ACC/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when writing recommendations. All guideline recommendations have been written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document (including headings above sets of recommendations), would still convey the full intent of the recommendation. It is hoped that this will increase readers’ comprehension of the guidelines and will allow queries at the individual recommendation level. ACC/AHA/ESC Practice Guidelines 703
  5. 5. 704 Circulation August 15, 2006 often associated with structural heart disease, although a AF and its pathogenesis and the general priorities of rate substantial proportion of patients with AF have no detect- control, prevention of thromboembolism, and methods avail- able heart disease. Hemodynamic impairment and throm- able for use in selected patients to correct the arrhythmia and boembolic events related to AF result in significant mor- maintain normal sinus rhythm. Advances in catheter-based bidity, mortality, and cost. Accordingly, the American ablation technologies are incorporated in expanded sections College of Cardiology (ACC), the American Heart Asso- and recommendations, with the recognition that such vital ciation (AHA), and the European Society of Cardiology details as patient selection, optimum catheter positioning, (ESC) created a committee to establish guidelines for absolute rates of treatment success, and the frequency of optimum management of this frequent and complex complications remain incompletely defined. Sections on drug arrhythmia. therapy have been confined to human studies with com- The committee was composed of representatives of the pounds approved for clinical use in North America and/or ACC, AHA, ESC, the European Heart Rhythm Association Europe. As data on the management of patients prone to AF (EHRA), and the Heart Rhythm Society (HRS). The docu- in special circumstances are more robust, recommendations ment was reviewed by reviewers nominated by these organi- are based on a higher level of evidence than in the first edition zations and will be reviewed annually by the Task Force and of these guidelines. Every effort was made to maintain considered current unless the Task Force revises or with- consistency with other ACC/AHA and ESC practice draws it from distribution. guidelines. The ACC/AHA/ESC Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial C. Recommendations for Management of Patients Fibrillation conducted a comprehensive review of the rele- With Atrial Fibrillation vant literature from 2001 to 2006 using the PubMed/MED- Classification of Recommendations and Level of Evidence LINE and Cochrane Library databases. Searches focused on are expressed in the ACC/AHA/ESC format as follows and English-language sources and studies in human subjects. described in Table 1. Recommendations are evidence Articles related to animal experimentation were cited when based and derived primarily from published data. The important to understanding concepts pertinent to patient reader is referred to the full-text guidelines for a complete management. description of the rationale and evidence supporting these recommendations. Classification of Recommendations Recommendations • Class I: Conditions for which there is evidence and/or general agreement that a given procedure/therapy is bene- 1. Pharmacological Rate Control During Atrial ficial, useful, and effective. Fibrillation • Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/ Class I efficacy of performing the procedure/therapy. 1. Measurement of the heart rate at rest and control Class IIa: Weight of evidence/opinion is in favor of of the rate using pharmacological agents (either a usefulness/efficacy. beta blocker or nondihydropyridine calcium Class IIb: Usefulness/efficacy is less well established by channel antagonist, in most cases) are recom- evidence/opinion. mended for patients with persistent or permanent • Class III: Conditions for which there is evidence and/or AF. (Level of Evidence: B) general agreement that a procedure/therapy is not useful or 2. In the absence of preexcitation, intravenous ad- effective and in some cases may be harmful. ministration of beta blockers (esmolol, metopro- Level of Evidence lol, or propranolol) or nondihydropyridine cal- The weight of evidence was ranked from highest (A) to cium channel antagonists (verapamil, diltiazem) is lowest (C), as follows: recommended to slow the ventricular response to AF in the acute setting, exercising caution in patients with hypotension or heart failure (HF). • Level of Evidence A: Data derived from multiple random- (Level of Evidence: B) ized clinical trials or meta-analyses. 3. Intravenous administration of digoxin or amiod- • Level of Evidence B: Data derived from a single random- arone is recommended to control the heart rate in ized trial, or nonrandomized studies. patients with AF and HF who do not have an • Level of Evidence C: Only consensus opinion of experts, accessory pathway. (Level of Evidence: B) case studies, or standard-of-care. 4. In patients who experience symptoms related to AF B. Changes Since the Initial Publication of These during activity, the adequacy of heart rate control should be assessed during exercise, adjusting phar- Guidelines in 2001 macological treatment as necessary to keep the rate The Writing Committee considered evidence published since in the physiological range. (Level of Evidence: C) 2001 and drafted revised recommendations to incorporate 5. Digoxin is effective following oral administration results from major clinical trials such as those that compared to control the heart rate at rest in patients with AF rhythm control and rate control approaches to long-term and is indicated for patients with HF, left ventric- management. The text has been reorganized to reflect the ular (LV) dysfunction, or for sedentary individu- implications for patient care, beginning with recognition of als. (Level of Evidence: C)
  6. 6. Fuster et al ACC/AHA/ESC Practice Guidelines 705 Class IIa Class I 1. A combination of digoxin and either a beta 1. Antithrombotic therapy to prevent thromboem- blocker or nondihydropyridine calcium channel bolism is recommended for all patients with AF, antagonist is reasonable to control the heart rate except those with lone AF or contraindications. both at rest and during exercise in patients with (Level of Evidence: A) AF. The choice of medication should be individu- 2. The selection of the antithrombotic agent should be alized and the dose modulated to avoid bradycar- based upon the absolute risks of stroke and bleeding dia. (Level of Evidence: B) and the relative risk and benefit for a given patient. 2. It is reasonable to use ablation of the AV node or (Level of Evidence: A) accessory pathway to control heart rate when phar- 3. For patients without mechanical heart valves at macological therapy is insufficient or associated with high risk of stroke, chronic oral anticoagulant side effects. (Level of Evidence: B) therapy with a vitamin K antagonist is recom- 3. Intravenous amiodarone can be useful to con- mended in a dose adjusted to achieve the target trol the heart rate in patients with AF when intensity international normalized ratio (INR) other measures are unsuccessful or contraindi- of 2.0 to 3.0, unless contraindicated. Factors cated. (Level of Evidence: C) associated with highest risk for stroke in pa- 4. When electrical cardioversion is not necessary tients with AF are prior thromboembolism in patients with AF and an accessory pathway, (stroke, transient ischemic attack [TIA], or sys- intravenous procainamide or ibutilide is a rea- temic embolism) and rheumatic mitral stenosis. sonable alternative. (Level of Evidence: C) (Level of Evidence: A) 4. Anticoagulation with a vitamin K antagonist is Class IIb recommended for patients with more than 1 mod- 1. When the ventricular rate cannot be adequately erate risk factor. Such factors include age 75 y or controlled both at rest and during exercise in greater, hypertension, HF, impaired LV systolic patients with AF using a beta blocker, nondihy- function (ejection fraction 35% or less or frac- dropyridine calcium channel antagonist, or tional shortening less than 25%), and diabetes digoxin, alone or in combination, oral amiodarone mellitus. (Level of Evidence: A) may be administered to control the heart rate. 5. INR should be determined at least weekly during (Level of Evidence: C) initiation of therapy and monthly when anticoagu- 2. Intravenous procainamide, disopyramide, ibuti- lation is stable. (Level of Evidence: A) lide, or amiodarone may be considered for 6. Aspirin, 81–325 mg daily, is recommended as an hemodynamically stable patients with AF in- alternative to vitamin K antagonists in low-risk volving conduction over an accessory pathway. patients or in those with contraindications to oral (Level of Evidence: B) anticoagulation. (Level of Evidence: A) 3. When the rate cannot be controlled with pharma- 7. For patients with AF who have mechanical cological agents or tachycardia-mediated cardio- heart valves, the target intensity of anticoagu- myopathy is suspected, catheter-directed ablation lation should be based on the type of prosthesis, of the AV node may be considered in patients with maintaining an INR of at least 2.5. (Level of AF to control the heart rate. (Level of Evidence: C) Evidence: B) 8. Antithrombotic therapy is recommended for Class III patients with atrial flutter as for those with AF. 1. Digitalis should not be used as the sole agent to (Level of Evidence: C) control the rate of ventricular response in patients with paroxysmal AF. (Level of Evidence: B) Class IIa 2. Catheter ablation of the AV node should not be 1. For primary prevention of thromboembolism attempted without a prior trial of medication to in patients with nonvalvular AF who have control the ventricular rate in patients with AF. just 1 of the following validated risk factors, (Level of Evidence: C) antithrombotic therapy with either aspirin or 3. In patients with decompensated HF and AF, a vitamin K antagonist is reasonable, based intravenous administration of a nondihydro- upon an assessment of the risk of bleeding pyridine calcium channel antagonist may exac- complications, ability to safely sustain ad- erbate hemodynamic compromise and is not justed chronic anticoagulation, and patient recommended. (Level of Evidence: C) preferences: age greater than or equal to 75 y 4. Intravenous administration of digitalis glyco- (especially in female patients), hypertension, sides or nondihydropyridine calcium channel HF, impaired LV function, or diabetes melli- antagonists to patients with AF and a preexci- tus. (Level of Evidence: A) tation syndrome may paradoxically accelerate 2. For patients with nonvalvular AF who have 1 or the ventricular response and is not recom- more of the following less well-validated risk fac- mended. (Level of Evidence: C) tors, antithrombotic therapy with either aspirin or a vitamin K antagonist is reasonable for preven- 2. Preventing Thromboembolism tion of thromboembolism: age 65 to 74 y, fe- (For recommendations regarding antithrombotic male gender, or CAD. The choice of agent should therapy in patients with AF undergoing cardiover- be based upon the risk of bleeding complications, sion, see Section I.C.3.d.) ability to safely sustain adjusted chronic anticoag-
  7. 7. 706 Circulation August 15, 2006 ulation, and patient preferences. (Level of Evi- 5. In patients with AF younger than 60 y without dence: B) heart disease or risk factors for thromboembolism 3. It is reasonable to select antithrombotic therapy (lone AF), the risk of thromboembolism is low using the same criteria irrespective of the pat- without treatment and the effectiveness of aspirin tern (i.e., paroxysmal, persistent, or permanent) for primary prevention of stroke relative to the of AF. (Level of Evidence: B) risk of bleeding has not been established. (Level of 4. In patients with AF who do not have mechanical Evidence: C) prosthetic heart valves, it is reasonable to inter- 6. In patients with AF who sustain ischemic stroke rupt anticoagulation for up to 1 wk without or systemic embolism during treatment with low- substituting heparin for surgical or diagnostic intensity anticoagulation (INR 2.0 to 3.0), rather procedures that carry a risk of bleeding. (Level than add an antiplatelet agent, it may be reason- of Evidence: C) able to raise the intensity of the anticoagulation to 5. It is reasonable to reevaluate the need for a maximum target INR of 3.0 to 3.5. (Level of anticoagulation at regular intervals. (Level of Evidence: C) Evidence: C) Class III Class IIb Long-term anticoagulation with a vitamin K an- 1. In patients 75 y of age and older at increased risk tagonist is not recommended for primary preven- of bleeding but without frank contraindications to tion of stroke in patients below the age of 60 y oral anticoagulant therapy, and in other patients without heart disease (lone AF) or any risk factors with moderate risk factors for thromboembolism for thromboembolism. (Level of Evidence: C) who are unable to safely tolerate anticoagulation at the standard intensity of INR 2.0 to 3.0, a lower 3. Cardioversion of Atrial Fibrillation INR target of 2.0 (range 1.6 to 2.5) may be considered for primary prevention of ischemic a. Pharmacological Cardioversion stroke and systemic embolism. (Level of Evidence: C) Class I 2. When surgical procedures require interruption Administration of flecainide, dofetilide, of oral anticoagulant therapy for longer than 1 propafenone, or ibutilide is recommended for wk in high-risk patients, unfractionated hepa- pharmacological cardioversion of AF. (Level of rin may be administered or low-molecular- Evidence: A) weight heparin given by subcutaneous injection, although the efficacy of these alternatives in this Class IIa situation is uncertain. (Level of Evidence: C) 1. Administration of amiodarone is a reasonable 3. Following percutaneous coronary intervention or option for pharmacological cardioversion of revascularization surgery in patients with AF, AF. (Level of Evidence: A) low-dose aspirin (less than 100 mg per d) and/or 2. A single oral bolus dose of propafenone or clopidogrel (75 mg per d) may be given concur- flecainide (“pill-in-the-pocket”) can be ad- rently with anticoagulation to prevent myocardial ministered to terminate persistent AF outside ischemic events, but these strategies have not been the hospital once treatment has proved safe in thoroughly evaluated and are associated with an hospital for selected patients without sinus or increased risk of bleeding. (Level of Evidence: C) AV node dysfunction, bundle-branch block, 4. In patients undergoing percutaneous coronary QT-interval prolongation, the Brugada syn- intervention, anticoagulation may be inter- drome, or structural heart disease. Before rupted to prevent bleeding at the site of periph- antiarrhythmic medication is initiated, a beta eral arterial puncture, but the vitamin K antag- blocker or nondihydropyridine calcium chan- onist should be resumed as soon as possible nel antagonist should be given to prevent after the procedure and the dose adjusted to rapid AV conduction in the event atrial flut- achieve an INR in the therapeutic range. Aspi- ter occurs. (Level of Evidence: C) rin may be given temporarily during the hiatus, 3. Administration of amiodarone can be benefi- but the maintenance regimen should then con- cial on an outpatient basis in patients with sist of the combination of clopidogrel, 75 mg paroxysmal or persistent AF when rapid res- daily, plus warfarin (INR 2.0 to 3.0). Clopi- toration of sinus rhythm is not deemed nec- dogrel should be given for a minimum of 1 mo essary. (Level of Evidence: C) after implantation of a bare metal stent, at least 3 mo for a sirolimus-eluting stent, at least 6 mo Class IIb for a paclitaxel-eluting stent, and 12 mo or Administration of quinidine or procainamide might longer in selected patients, following which war- be considered for pharmacological cardioversion of farin may be continued as monotherapy in the AF, but the usefulness of these agents is not well absence of a subsequent coronary event. When established. (Level of Evidence: C) warfarin is given in combination with clopi- dogrel or low-dose aspirin, the dose intensity Class III must be carefully regulated. (Level of Evidence: 1. Digoxin and sotalol may be harmful when C) used for pharmacological cardioversion of
  8. 8. Fuster et al ACC/AHA/ESC Practice Guidelines 707 AF and are not recommended. (Level of Evi- tion of antiarrhythmic medication. (Level of dence: A) Evidence: C) 2. Quinidine, procainamide, disopyramide, and dofetilide should not be started out of hospital Class IIb for conversion of AF to sinus rhythm. (Level 1. For patients with persistent AF, administration of Evidence: B) of beta blockers, disopyramide, diltiazem, dofetilide, procainamide, or verapamil may be b. Direct-Current Cardioversion considered, although the efficacy of these agents to enhance the success of direct-current cardio- Class I version or to prevent early recurrence of AF is 1. When a rapid ventricular response does not uncertain. (Level of Evidence: C) respond promptly to pharmacological mea- 2. Out-of-hospital initiation of antiarrhythmic sures for patients with AF with ongoing myo- medications may be considered in patients cardial ischemia, symptomatic hypotension, without heart disease to enhance the success angina, or HF, immediate R-wave synchro- of cardioversion of AF. (Level of Evidence: C) nized direct-current cardioversion is recom- 3. Out-of-hospital administration of antiar- mended. (Level of Evidence: C) rhythmic medications may be considered to 2. Immediate direct-current cardioversion is enhance the success of cardioversion of AF in recommended for patients with AF involving patients with certain forms of heart disease preexcitation when very rapid tachycardia or once the safety of the drug has been verified hemodynamic instability occurs. (Level of Ev- for the patient. (Level of Evidence: C) idence: B) 3. Cardioversion is recommended in patients d. Prevention of Thromboembolism in Patients With without hemodynamic instability when symp- Atrial Fibrillation Undergoing Cardioversion toms of AF are unacceptable to the patient. In case of early relapse of AF after cardiover- Class I sion, repeated direct-current cardioversion 1. For patients with AF of 48-h duration or attempts may be made following administra- longer, or when the duration of AF is unknown, tion of antiarrhythmic medication. (Level of anticoagulation (INR 2.0 to 3.0) is recom- Evidence: C) mended for at least 3 wk prior to and 4 wk after cardioversion, regardless of the method (elec- Class IIa trical or pharmacological) used to restore sinus 1. Direct-current cardioversion can be useful to rhythm. (Level of Evidence: B) restore sinus rhythm as part of a long-term 2. For patients with AF of more than 48-h management strategy for patients with AF. duration requiring immediate cardioversion (Level of Evidence: B) because of hemodynamic instability, heparin 2. Patient preference is a reasonable consideration should be administered concurrently (unless in the selection of infrequently repeated cardio- contraindicated) by an initial intravenous bo- versions for the management of symptomatic or lus injection followed by a continuous infu- recurrent AF. (Level of Evidence: C) sion in a dose adjusted to prolong the acti- vated partial thromboplastin time to 1.5 to 2 Class III times the reference control value. Thereafter, 1. Frequent repetition of direct-current cardio- oral anticoagulation (INR 2.0 to 3.0) should version is not recommended for patients who be provided for at least 4 wk, as for patients have relatively short periods of sinus rhythm undergoing elective cardioversion. Limited between relapses of AF after multiple cardio- data support subcutaneous administration of version procedures despite prophylactic antiar- low-molecular-weight heparin in this indica- rhythmic drug therapy. (Level of Evidence: C) tion. (Level of Evidence: C) 2. Electrical cardioversion is contraindicated in 3. For patients with AF of less than 48-h duration patients with digitalis toxicity or hypokale- associated with hemodynamic instability (an- mia. (Level of Evidence: C) gina pectoris, myocardial infarction [MI], shock, or pulmonary edema), cardioversion c. Pharmacological Enhancement of Direct-Current should be performed immediately without de- Cardioversion lay for prior initiation of anticoagulation. (Level of Evidence: C) Class IIa 1. Pretreatment with amiodarone, flecainide, Class IIa ibutilide, propafenone, or sotalol can be use- 1. During the 48 h after onset of AF, the need ful to enhance the success of direct-current for anticoagulation before and after cardio- cardioversion and prevent recurrent AF. version may be based on the patient’s risk of (Level of Evidence: B) thromboembolism. (Level of Evidence: C) 2. In patients who relapse to AF after successful 2. As an alternative to anticoagulation prior to car- cardioversion, it can be useful to repeat the dioversion of AF, it is reasonable to perform procedure following prophylactic administra- transesophageal echocardiography (TEE) in
  9. 9. 708 Circulation August 15, 2006 search of thrombus in the left atrium (LA) or left 5. Sotalol can be beneficial in outpatients in sinus atrial appendage (LAA). (Level of Evidence: B) rhythm with little or no heart disease, prone to 2a. For patients with no identifiable throm- paroxysmal AF, if the baseline uncorrected QT bus, cardioversion is reasonable imme- interval is less than 460 ms, serum electrolytes diately after anticoagulation with un- are normal, and risk factors associated with fractionated heparin (e.g., initiated by class III drug–related proarrhythmia are not intravenous bolus injection and an infu- present. (Level of Evidence: C) sion continued at a dose adjusted to 6. Catheter ablation is a reasonable alternative to prolong the activated partial thrombo- pharmacological therapy to prevent recurrent plastin time to 1.5 to 2 times the control AF in symptomatic patients with little or no LA value until oral anticoagulation has enlargement. (Level of Evidence: C) been established with an oral vitamin K antagonist (e.g., warfarin) as evidenced Class III by an INR equal to or greater than 2.0). 1. Antiarrhythmic therapy with a particular drug (Level of Evidence: B) Thereafter, con- is not recommended for maintenance of sinus tinuation of oral anticoagulation (INR rhythm in patients with AF who have well- 2.0 to 3.0) is reasonable for a total defined risk factors for proarrhythmia with anticoagulation period of at least 4 wk, that agent. (Level of Evidence: A) as for patients undergoing elective car- 2. Pharmacological therapy is not recommended for dioversion. (Level of Evidence: B) Lim- maintenance of sinus rhythm in patients with ited data are available to support the advanced sinus node disease or atrioventricular subcutaneous administration of a low- (AV) node dysfunction unless they have a func- molecular-weight heparin in this indica- tioning electronic cardiac pacemaker. (Level of tion. (Level of Evidence: C) Evidence: C) 2b. For patients in whom thrombus is identi- fied by TEE, oral anticoagulation (INR 5. Special Considerations 2.0 to 3.0) is reasonable for at least 3 wk prior to and 4 wk after restoration of a. Postoperative Atrial Fibrillation sinus rhythm, and a longer period of anticoagulation may be appropriate even Class I after apparently successful cardioversion, 1. Unless contraindicated, treatment with an because the risk of thromboembolism of- oral beta blocker to prevent postoperative AF ten remains elevated in such cases. (Level is recommended for patients undergoing car- of Evidence: C) diac surgery. (Level of Evidence: A) 3. For patients with atrial flutter undergoing 2. Administration of AV nodal blocking agents cardioversion, anticoagulation can be benefi- is recommended to achieve rate control in cial according to the recommendations as for patients who develop postoperative AF. patients with AF. (Level of Evidence: C) (Level of Evidence: B) 4. Maintenance of Sinus Rhythm Class IIa 1. Preoperative administration of amiodarone re- Class I duces the incidence of AF in patients undergo- Before initiating antiarrhythmic drug therapy, ing cardiac surgery and represents appropriate treatment of precipitating or reversible causes of prophylactic therapy for patients at high risk AF is recommended. (Level of Evidence: C) for postoperative AF. (Level of Evidence: A) 2. It is reasonable to restore sinus rhythm by Class IIa pharmacological cardioversion with ibutilide 1. Pharmacological therapy can be useful in pa- or direct-current cardioversion in patients tients with AF to maintain sinus rhythm and who develop postoperative AF as advised for prevent tachycardia-induced cardiomyopathy. nonsurgical patients. (Level of Evidence: B) (Level of Evidence: C) 3. It is reasonable to administer antiarrhythmic 2. Infrequent, well-tolerated recurrence of AF is medications in an attempt to maintain sinus reasonable as a successful outcome of antiar- rhythm in patients with recurrent or refractory rhythmic drug therapy. (Level of Evidence: C) postoperative AF, as recommended for other 3. Outpatient initiation of antiarrhythmic drug patients who develop AF. (Level of Evidence: B) therapy is reasonable in patients with AF who 4. It is reasonable to administer antithrombotic have no associated heart disease when the agent medication in patients who develop postoper- is well tolerated. (Level of Evidence: C) ative AF, as recommended for nonsurgical 4. In patients with lone AF without structural patients. (Level of Evidence: B) heart disease, initiation of propafenone or fle- cainide can be beneficial on an outpatient basis Class IIb in patients with paroxysmal AF who are in sinus Prophylactic administration of sotalol may be rhythm at the time of drug initiation. (Level of considered for patients at risk of developing AF Evidence: B) following cardiac surgery. (Level of Evidence: B)
  10. 10. Fuster et al ACC/AHA/ESC Practice Guidelines 709 b. Acute Myocardial Infarction (ECG) (greater than or equal to 120-ms du- ration) or with a rapid preexcited ventricular Class I response. (Level of Evidence: C) 1. Direct-current cardioversion is recom- mended for patients with severe hemodynam- Class IIa ic compromise or intractable ischemia, or Intravenous flecainide or direct-current cardio- when adequate rate control cannot be version is reasonable when very rapid ventricu- achieved with pharmacological agents in pa- lar rates occur in patients with AF involving tients with acute MI and AF. (Level of Evi- conduction over an accessory pathway. (Level of dence: C) Evidence: B) 2. Intravenous administration of amiodarone is recommended to slow a rapid ventricular Class IIb response to AF and improve LV function in It may be reasonable to administer intravenous patients with acute MI. (Level of Evidence: C) quinidine, procainamide, disopyramide, ibutil- 3. Intravenous beta blockers and nondihydro- ide, or amiodarone to hemodynamically stable pyridine calcium antagonists are recom- patients with AF involving conduction over an mended to slow a rapid ventricular response accessory pathway. (Level of Evidence: B) to AF in patients with acute MI who do not display clinical LV dysfunction, bronchos- Class III pasm, or AV block. (Level of Evidence: C) Intravenous administration of digitalis glyco- 4. For patients with AF and acute MI, adminis- sides or nondihydropyridine calcium channel tration of unfractionated heparin by either con- antagonists is not recommended in patients with tinuous intravenous infusion or intermittent WPW syndrome who have preexcited ventricu- subcutaneous injection is recommended in a lar activation during AF. (Level of Evidence: B) dose sufficient to prolong the activated partial thromboplastin time to 1.5 to 2 times the con- d. Hyperthyroidism trol value, unless contraindications to anticoag- ulation exist. (Level of Evidence: C) Class I 1. Administration of a beta blocker is recom- Class IIa mended to control the rate of ventricular Intravenous administration of digitalis is rea- response in patients with AF complicating sonable to slow a rapid ventricular response and thyrotoxicosis, unless contraindicated. (Level improve LV function in patients with acute MI of Evidence: B) and AF associated with severe LV dysfunction 2. In circumstances when a beta blocker cannot and HF. (Level of Evidence: C) be used, administration of a nondihydropyr- idine calcium channel antagonist (diltiazem Class III or verapamil) is recommended to control the The administration of class IC antiarrhythmic ventricular rate in patients with AF and drugs is not recommended in patients with AF in thyrotoxicosis. (Level of Evidence: B) the setting of acute MI. (Level of Evidence: C) 3. In patients with AF associated with thyrotox- icosis, oral anticoagulation (INR 2.0 to 3.0) is c. Management of Atrial Fibrillation Associated With recommended to prevent thromboembolism, the Wolff-Parkinson-White (WPW) Preexcitation as recommended for AF patients with other Syndrome risk factors for stroke. (Level of Evidence: C) 4. Once a euthyroid state is restored, recom- Class I mendations for antithrombotic prophylaxis 1. Catheter ablation of the accessory pathway is are the same as for patients without hyper- recommended in symptomatic patients with thyroidism. (Level of Evidence: C) AF who have WPW syndrome, particularly those with syncope due to rapid heart rate or e. Management of Atrial Fibrillation During Pregnancy those with a short bypass tract refractory period. (Level of Evidence: B) Class I 2. Immediate direct-current cardioversion is 1. Digoxin, a beta blocker, or a nondihydropyr- recommended to prevent ventricular fibrilla- idine calcium channel antagonist is recom- tion in patients with a short anterograde mended to control the rate of ventricular bypass tract refractory period in whom AF response in pregnant patients with AF. (Level occurs with a rapid ventricular response as- of Evidence: C) sociated with hemodynamic instability. (Level 2. Direct-current cardioversion is recom- of Evidence: B) mended in pregnant patients who become 3. Intravenous procainamide or ibutilide is rec- hemodynamically unstable due to AF. (Level ommended to restore sinus rhythm in pa- of Evidence: C) tients with WPW in whom AF occurs without 3. Protection against thromboembolism is rec- hemodynamic instability in association with a ommended throughout pregnancy for all pa- wide QRS complex on the electrocardiogram tients with AF (except those with lone AF
  11. 11. 710 Circulation August 15, 2006 and/or low thromboembolic risk). Therapy pulmonary illness or exacerbation of chronic (anticoagulant or aspirin) should be chosen pulmonary disease. (Level of Evidence: C) according to the stage of pregnancy. (Level of 2. A nondihydropyridine calcium channel an- Evidence: C) tagonist (diltiazem or verapamil) is recom- mended to control the ventricular rate in Class IIb patients with obstructive pulmonary dis- 1. Administration of heparin may be consid- ease who develop AF. (Level of Evidence: C) ered during the first trimester and last 3. Direct-current cardioversion should be at- month of pregnancy for patients with AF tempted in patients with pulmonary disease and risk factors for thromboembolism. Un- who become hemodynamically unstable as fractionated heparin may be administered a consequence of AF. (Level of Evidence: C) either by continuous intravenous infusion in a dose sufficient to prolong the activated Class III partial thromboplastin time to 1.5 to 2 1. Theophylline and beta-adrenergic agonist times the control value or by intermittent agents are not recommended in patients with subcutaneous injection in a dose of 10 000 bronchospastic lung disease who develop AF. to 20 000 units every 12 h, adjusted to (Level of Evidence: C) prolong the mid-interval (6 h after injec- 2. Beta blockers, sotalol, propafenone, and tion) activated partial thromboplastin time adenosine are not recommended in patients to 1.5 times control. (Level of Evidence: B) with obstructive lung disease who develop 2. Despite the limited data available, subcuta- AF. (Level of Evidence: C) neous administration of low-molecular- weight heparin may be considered during the first trimester and last month of preg- nancy for patients with AF and risk factors for thromboembolism. (Level of Evidence: II. Definition C) 3. Administration of an oral anticoagulant may A. Atrial Fibrillation be considered during the second trimester for AF is a supraventricular tachyarrhythmia characterized by pregnant patients with AF at high thrombo- uncoordinated atrial activation with consequent deteriora- embolic risk. (Level of Evidence: C) tion of mechanical function. On the ECG, rapid oscilla- 4. Administration of quinidine or procainamide tions, or fibrillatory waves that vary in amplitude, shape, may be considered to achieve pharmacologi- and timing, replace consistent P waves, and there is an cal cardioversion in hemodynamically stable irregular ventricular response that is rapid when conduc- patients who develop AF during pregnancy. tion is intact.1 The ventricular response depends on elec- (Level of Evidence: C) trophysiological properties of the AV node and other f. Management of Atrial Fibrillation in Patients With conducting tissues, vagal and sympathetic tone, the pres- Hypertrophic Cardiomyopathy (HCM) ence or absence of accessory pathways, and the action of drugs.2 When AV block or ventricular or AV junctional Class I tachycardia is present, the cardiac cycles (R-R intervals) Oral anticoagulation (INR 2.0 to 3.0) is recom- may be regular. In patients with pacemakers, diagnosis of mended in patients with HCM who develop AF, AF may require pacemaker inhibition to expose fibrillatory as for other patients at high risk of thromboem- activity. An irregular, sustained, wide-QRS-complex bolism. (Level of Evidence: B) tachycardia suggests AF with conduction over an acces- Class IIa sory pathway or AF with bundle-branch block. Atrial Antiarrhythmic medications can be useful to flutter is usually readily distinguished from AF. Extremely prevent recurrent AF in patients with HCM. rapid rates (greater than 200 beats per minute) suggest an Available data are insufficient to recommend accessory pathway or ventricular tachycardia. one agent over another in this situation, but (a) disopyramide combined with a beta blocker or nondihydropyridine calcium channel antagonist B. Related Arrhythmias or (b) amiodarone alone is generally preferred. AF may occur in association with atrial flutter or atrial (Level of Evidence: C) tachycardia. The typical form of atrial flutter is characterized by a saw-tooth pattern of regular atrial activation called g. Management of Atrial Fibrillation in Patients With flutter (ƒ) waves on the ECG, particularly visible in leads II, Pulmonary Disease III, aVF, and V1. If untreated, the atrial rate typically ranges Class I from 240 to 320 beats per minute, with ƒ waves inverted in 1. Correction of hypoxemia and acidosis is the ECG leads II, III, and aVF and upright in lead V1. The recommended primary therapeutic measure direction of activation in the right atrium (RA) may be for patients who develop AF during an acute reversed, resulting in upright ƒ waves in leads II, III, and aVF
  12. 12. Fuster et al ACC/AHA/ESC Practice Guidelines 711 Figure 1. Patterns of atrial fibrillation (AF). 1, Episodes that generally last 7 d or less (most less than 24 h); 2, episodes that usually last more than 7 d; 3, cardioversion failed or not attempted; and 4, both paroxysmal and persis- tent AF may be recurrent. and inversion in lead V1. Atrial flutter may degenerate into to how long the diagnosis has been present in a given patient. AF, and AF may convert to atrial flutter. Atrial flutter is Thus, in a patient with paroxysmal AF, episodes lasting usually readily distinguished from AF, but misdiagnosis may seconds to hours may occur repeatedly for years. occur when fibrillatory atrial activity is prominent in more This terminology applies to episodes lasting longer than than 1 ECG lead.3 30 s without a reversible cause. Secondary AF in the setting Focal atrial tachycardias, AV reentrant tachycardias, and of acute MI, cardiac surgery, pericarditis, myocarditis, hyper- AV nodal reentrant tachycardias may also trigger AF. In these thyroidism, or acute pulmonary disease is considered sepa- tachycardias, distinct P waves are typically separated by an rately. In these situations, AF is not the primary problem, and isoelectric baseline, and their morphology may localize the concurrent treatment of the underlying disorder usually ter- origin of the arrhythmia. minates the arrhythmia. Conversely, when AF occurs in the course of a concurrent disorder like well-controlled hypothy- III. Classification roidism, the general principles for management of the ar- Various classification systems have been proposed for AF rhythmia apply. based on the ECG pattern,1 epicardial4 or endocavitary The term lone AF applies to individuals younger than 60 y recordings, mapping of atrial electrical activity, or clinical without clinical or echocardiographic evidence of cardiopul- features. Although the pattern of AF can change over time, it monary disease, including hypertension.5 These patients have may be helpful to characterize the arrhythmia at a given a favorable prognosis with respect to thromboembolism and moment. The classification scheme recommended here rep- mortality. Over time, patients move out of the lone AF resents a consensus driven by a desire for simplicity and category due to aging or development of cardiac abnormali- clinical relevance. ties such as enlargement of the LA, and the risks of throm- The clinician should distinguish a first-detected episode of boembolism and mortality rise. The term nonvalvular AF AF, whether or not symptomatic or self-limited, recognizing refers to cases without rheumatic mitral valve disease, pros- the uncertainty about the actual duration of the episode and about previous undetected episodes (Fig. 1). After 2 or more thetic heart valve, or valve repair. episodes, AF is considered recurrent. If the arrhythmia terminates spontaneously, recurrent AF is designated parox- IV. Epidemiology and Prognosis ysmal; when sustained beyond 7 d, it is termed persistent. AF is the most common arrhythmia in clinical practice, Termination with pharmacological therapy or direct-current accounting for approximately one third of hospitalizations for cardioversion does not alter the designation. First-detected cardiac rhythm disturbances. An estimated 2.3 million people AF may be either paroxysmal or persistent. The category of in North America and 4.5 million people in the European persistent AF also includes cases of long-standing AF (e.g., Union have paroxysmal or persistent AF.9 During the past longer than 1 y), usually leading to permanent AF, in which 20 y, hospital admissions for AF have increased by 66%7 due cardioversion has failed or has been foregone. to the aging of the population, a rising prevalence of chronic These categories are not mutually exclusive, and a partic- heart disease, more frequent diagnosis through use of ambu- ular patient may have several episodes of paroxysmal AF and latory monitoring devices, and other factors. AF is an occasional persistent AF, or the reverse, but it is practical to extremely expensive public health problem (approximately categorize a given patient by his or her most frequent €3000 [approximately U.S. $3600] annually per patient)8; the presentation. The definition of permanent AF is often arbi- total cost burden approaches €13.5 billion (approximately trary, and the duration refers both to individual episodes and U.S. $15.7 billion) in the European Union.
  13. 13. 712 Circulation August 15, 2006 A. Prevalence The estimated prevalence of AF is 0.4% to 1% in the general population,9 increasing with age to 8% in those older than 80 y.10 Among men, the age-adjusted prevalence has more than doubled over a generation,10 while the prevalence in women has remained constant.11 The median age of patients with AF is about 75 y. The number of men and women with AF is about equal, but approximately 60% of those over 75 y old are female. Based on limited data, the age-adjusted risk of developing AF in blacks seems less than half that in whites. In population-based studies, patients with no history of Figure 2. Posterior view of principal electrophysiological mecha- cardiopulmonary disease account for fewer than 12% of all nisms of atrial fibrillation. A, Focal activation. The initiating focus (indicated by the star) often lies within the region of the pulmo- cases of AF.10 In case series, however, the observed propor- nary veins. The resulting wavelets represent fibrillatory conduc- tion of lone AF was sometimes greater than 30%.12 tion, as in multiple-wavelet reentry. B, Multiple-wavelet reentry. Wavelets (indicated by arrows) randomly re-enter tissue previ- B. Incidence ously activated by the same or another wavelet. The routes the In prospective studies, the incidence of AF increases from wavelets travel vary. Reproduced with permission from Konings KT, Kirchhof CJ, Smeets JR, et al. High-density mapping of less than 0.1% per year in people younger than 40 y to over electrically induced atrial fibrillation in humans. Circulation 1.5% per year among women and 2% among men older than 1994;89:1665–1680.45 LA indicates left atrium; PV, pulmonary 80 y.13 In patients treated for HF, the 3-y incidence of AF was vein; ICV, inferior vena cava; SCV, superior vena cava; and RA, almost 10%.14 Angiotensin inhibition may be associated with right atrium. a reduced incidence of AF in patients with HF15 and hypertension.16 distinguish changes due to AF from those due to associated heart disease. Atrial fibrosis may precede the onset of AF,26 and C. Prognosis juxtaposition of patchy fibrosis with normal atrial fibers may AF is associated with an increased long-term risk of stroke,17 account for nonhomogeneity of conduction.27 Interstitial fibrosis HF, and all-cause mortality, especially among women.18 The may result from apoptosis leading to replacement of atrial mortality rate of patients with AF is about double that of myocytes,28 loss of myofibrils, accumulation of glycogen gran- patients in normal sinus rhythm and is linked to the severity ules, disruption of cell coupling at gap junctions,29 and organelle of underlying heart disease.19 In the Etude en Activité aggregates30 and may be triggered by atrial dilation in any type Libérale sur la Fibrillation Auriculaire Study (ALFA), about of heart disease associated with AF. two thirds of the 5% annualized mortality was attributed to Patients with valvular heart disease who have mild fibrosis cardiovascular causes.12 In large HF trials (COMET [Carve- respond more successfully to cardioversion than those with dilol Or Metoprolol European Trial], Val-HeFT [Valsartan severe fibrosis, and fibrosis is thought to contribute to Heart Failure Trial]), AF was a strong independent risk factor persistent AF.31 The concentration of membrane-bound gly- for mortality and morbidity.20,21 HF promotes AF, AF aggra- coproteins that regulate cell– cell and cell–matrix interactions vates HF, and individuals with either condition who develop (disintegrin and metalloproteinases) in human atrial myocar- the alternate condition share a poor prognosis.22 Thus, man- dium has been reported to double during AF, and these aging patients with the associated conditions is a major changes may contribute to atrial dilation in patients with challenge, and randomized trials are needed to investigate the longstanding AF. Dilation of the atria activates several impact of AF on prognosis in HF. molecular pathways, including the renin-angiotensin-aldoste- The rate of ischemic stroke among patients with nonval- rone system (RAAS). Angiotensin II is upregulated in re- vular AF averages 5% per year, 2 to 7 times that of people sponse to stretch,32 and atrial tissue from patients with without AF.23 One of every 6 strokes occurs in a patient with AF, and when TIAs and clinically “silent” strokes detected by persistent AF demonstrates increased expression of angioten- brain imaging are considered, the rate of brain ischemia sin-converting enzyme (ACE).33 Angiotensin inhibition may accompanying nonvalvular AF exceeds 7% per year.24 In prevent AF by reducing fibrosis.34 Atrial dilation and inter- patients with rheumatic heart disease and AF in the Framing- stitial fibrosis in HF facilitate sustained AF.35 The regional ham Heart Study, stroke risk was increased 17-fold compared electrical silence (suggesting scar), voltage reduction, and with age-matched controls,25 and attributable risk was 5 times conduction slowing described in patients with HF are similar greater than in those with nonrheumatic AF.23 The risk of to changes in the atria that occur as a consequence of aging.36 stroke increased with age; the annual risk of stroke attribut- 2. Mechanisms of Atrial Fibrillation able to AF was 1.5% in participants aged 50 to 59 y and Available data support a “focal” triggering mechanism involving 23.5% in those aged 80 to 89 y.23 automaticity or multiple reentrant wavelets, but these mecha- nisms are not mutually exclusive and may coexist (Fig. 2). V. Pathophysiological Mechanisms The important observation that a focal source for AF could A. Atrial Factors be identified and ablation of this source could extinguish 1. Atrial Pathology as a Cause of Atrial Fibrillation AF37 supported a focal origin. While pulmonary veins (PVs) The most frequent histopathological changes in AF are atrial are the most frequent source of these rapidly atrial impulses, fibrosis and loss of atrial muscle mass, but it is difficult to foci have also been found in the superior vena cava, ligament

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