Heart failure

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Heart failure

  1. 1. Heart Failure http://emedicine.medscape.com/article/163062-overview Author: Ioana Dumitru, MD; Chief Editor: Henry H Ooi, MBBCh more... Updated: Aug 30, 2011 Background Signs and symptoms of heart failure include tachycardia and manifestations of venous congestion (eg, edema) and low cardiac output (eg, fatigue). Breathlessness, a cardinal symptom of left ventricular (LV) failure, may manifest with progressively increasing severity. (See Clinical Presentation.) Heart failure can be classified according to a variety of factors. The New York Heart Association (NYHA) classification for heart failure is based on the relation between symptoms and the amount of effort required to provoke them, and The American College of Cardiology/American Heart Association (ACC/AHA) heart failure guidelines complement the NYHA classification to reflect the progression of disease. (See Clinical Presentation.) Laboratory studies should include a complete blood count (CBC), electrolytes, and renal and liver function studies, and 2-dimensional echocardiography is recommended in the initial evaluation of patients with known or suspected heart failure. Two principal features of the chest radiograph are the size and shape of the cardiac silhouette and edema at the lung bases, and pulse oximetry is highly accurate for assessing the presence of hypoxemia and, therefore, the severity of heart failure. (See Workup.) In acute heart failure, patient care consists of stabilizing the patients’ clinical condition; establishing the diagnosis, etiology, and precipitating factors; and initiating therapies to provide rapid symptom relief. Surgical options for heart failure include heart transplantation, coronary artery bypass grafting (CABG), valve replacement or repair, ventricular restoration, cardiac resynchronization therapy (CRT, implantable cardioverter-defibrillators (ICDs), and ventricular assist devices (VADs). (See Treatment and Management.) The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Along with oxygen, medications assisting with symptom relief include diuretics, digoxin, inotropes, oxygen, and morphine. Drugs that can exacerbate heart failure should be avoided (NSAIDs, calcium channel blockers, most antiarrhythmic drugs). (See Medications.) Pathophysiology The common pathophysiologic state that perpetuates the progression of heart failure is extremely complex, regardless of the precipitating event. Compensatory mechanisms exist on every level of organization, from subcellular all the way through organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does heart failure ensue. Most important among the adaptations are the Frank-Starling mechanism, in which an increased preload helps to sustain cardiac performance; alterations in myocyte regeneration and death; myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented; and activation of neurohumoral systems. The release of norepinephrine by adrenergic cardiac nerves augments myocardial contractility and includes activation of the renin-angiotensin-aldosterone system [RAAS], the sympathetic nervous system [SNS], and other neurohumoral adjustments that act to maintain arterial pressure and perfusion of vital organs. In acute heart failure, the finite adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance. The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration.[1] This process eventually leads to remodeling, usually the eccentric type. Eccentric remodeling further worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle. The idea of lowering wall stress to slow the process of remodeling has long been exploited in treating heart failure patients.[2]1 of 30 9/3/2011 8:27 AM
  2. 2. Heart Failure http://emedicine.medscape.com/article/163062-overview The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendocrine systems, most notably the above-mentioned adrenergic systems and RAAS. The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytosolic calcium entry. The increased calcium entry into the myocytes augments myocardial contractility and impairs myocardial relaxation (lusitropy). The calcium overload may induce arrhythmias and lead to sudden death. The increase in afterload and myocardial contractility (known as inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy expenditure and a further decrease in cardiac output. The increase in myocardial energy expenditure leads to myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses. In addition, the activation of the RAAS leads to salt and water retention, resulting in increased preload and further increases in myocardial energy expenditure. Increases in renin, mediated by decreased stretch of the glomerular afferent arteriole, reduce delivery of chloride to the macula densa and increase beta1-adrenergic activity as a response to decreased cardiac output. This results in an increase in angiotensin II (Ang II) levels and, in turn, aldosterone levels, causing stimulation of the release of aldosterone. Ang II, along with ET-1, is crucial in maintaining effective intravascular homeostasis mediated by vasoconstriction and aldosterone-induced salt and water retention. The concept of the heart as a self-renewing organ is a relatively recent development.[3] This new paradigm for myocyte biology has created an entire field of research aimed directly at augmenting myocardial regeneration. The rate of myocyte turnover has been shown to increase during times of pathologic stress.[1] In heart failure, this mechanism for replacement becomes overwhelmed by an even faster increase in the rate of myocyte loss. This imbalance of hypertrophy and death over regeneration is the final common pathway at the cellular level for the progression of remodeling and heart failure. Ang II Research indicates that local cardiac Ang II production (which decreases lusitropy, increases inotropy, and increases afterload) leads to increased myocardial energy expenditure. Ang II has also been shown in vitro and in vivo to increase the rate of myocyte apoptosis.[4] In this fashion, Ang II has similar actions to norepinephrine in heart failure. Ang II also mediates myocardial cellular hypertrophy and may promote progressive loss of myocardial function. The neurohumoral factors above lead to myocyte hypertrophy and interstitial fibrosis, resulting in increased myocardial volume and increased myocardial mass, as well as myocyte loss. As a result, the cardiac architecture changes, which, in turn, leads to further increase in myocardial volume and mass. Myocytes and myocardial remodeling In the failing heart, increased myocardial volume is characterized by larger myocytes approaching the end of their life cycle. As more myocytes drop out, an increased load is placed on the remaining myocardium, and this unfavorable environment is transmitted to the progenitor cells responsible for replacing lost myocytes. Progenitor cells become progressively less effective as the underlying pathologic process worsens and myocardial failure accelerates. These features, namely the increased myocardial volume and mass, along with a net loss of myocytes, are the hallmark of myocardial remodeling. This remodeling process leads to early adaptive mechanisms, such as augmentation of stroke volume (Starling mechanism) and decreased wall stress (Laplace mechanism), and later, to maladaptive mechanisms, such as increased myocardial oxygen demand, myocardial ischemia, impaired contractility, and arrhythmogenesis. As heart failure advances, there is a relative decline in the counterregulatory effects of endogenous vasodilators, including nitric oxide (NO), prostaglandins (PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP). This occurs simultaneously with the increase in vasoconstrictor substances from the RAAS and the adrenergic system. This fosters further increases in vasoconstriction and thus preload and afterload, leading to cellular proliferation, adverse myocardial remodeling, and antinatriuresis, with total body fluid excess and worsening heart failure (HF) symptoms. Systolic and diastolic failure Systolic and diastolic heart failure each result in a decrease in stroke volume. This leads to activation of peripheral and central baroreflexes and chemoreflexes that are capable of eliciting marked increases in sympathetic nerve traffic.2 of 30 9/3/2011 8:27 AM
  3. 3. Heart Failure http://emedicine.medscape.com/article/163062-overview While there are commonalities in the neurohormonal responses to decreased stroke volume, the neurohormone- mediated events that follow have been most clearly elucidated for individuals with systolic heart failure. The ensuing elevation in plasma norepinephrine directly correlates with the degree of cardiac dysfunction and has significant prognostic implications. Norepinephrine, while directly toxic to cardiac myocytes, is also responsible for a variety of signal-transduction abnormalities, such as down-regulation of beta1-adrenergic receptors, uncoupling of beta2- adrenergic receptors, and increased activity of inhibitory G-protein. Changes in beta1-adrenergic receptors result in overexpression and promote myocardial hypertrophy. ANP and BNP ANP and BNP are endogenously generated peptides activated in response to atrial and ventricular volume/pressure expansion. ANP and BNP are released from the atria and ventricles, respectively, and both promote vasodilation and natriuresis. Their hemodynamic effects are mediated by decreases in ventricular filling pressures, owing to reductions in cardiac preload and afterload. BNP, in particular, produces selective afferent arteriolar vasodilation and inhibits sodium reabsorption in the proximal convoluted tubule. BNP inhibits renin and aldosterone release and, therefore, adrenergic activation as well. ANP and BNP are elevated in chronic heart failure. BNP, in particular, has potentially important diagnostic, therapeutic, and prognostic implications. For more information, see Natriuretic Peptides in Congestive Heart Failure. Other vasoactive systems Other vasoactive systems that play a role in the pathogenesis of heart failure include the ET receptor system, the adenosine receptor system, vasopressin, and tumor necrosis factor-alpha (TNF-alpha). ET, a substance produced by the vascular endothelium, may contribute to the regulation of myocardial function, vascular tone, and peripheral resistance in heart failure. Elevated levels of ET-1 closely correlate with the severity of heart failure. ET-1 is a potent vasoconstrictor and has exaggerated vasoconstrictor effects in the renal vasculature, reducing renal plasma blood flow, glomerular filtration rate (GFR), and sodium excretion. TNF-alpha has been implicated in response to various infectious and inflammatory conditions. Elevations in TNF-alpha levels have been consistently observed in heart failure and seem to correlate with the degree of myocardial dysfunction. Experimental studies suggest that local production of TNF-alpha may have toxic effects on the myocardium, thus worsening myocardial systolic and diastolic function. Thus, in individuals with systolic dysfunction, the neurohormonal responses to decreased stroke volume result in temporary improvement in systolic blood pressure and tissue perfusion. However, in all circumstances, the existing data support the notion that these neurohormonal responses contribute to the progression of myocardial dysfunction in the long term. Heart failure with normal ejection fraction In diastolic heart failure (heart failure with normal ejection fraction [HFNEF]), the same pathophysiologic processes leading to decreased cardiac output that occur in systolic heart failure also occur, but they do so in response to a different set of hemodynamic and circulatory environmental factors that depress cardiac output. In HFNEF, altered relaxation, and increased stiffness of the ventricle (due to delayed calcium uptake by the myocyte sarcoplasmic reticulum and delayed calcium efflux from the myocyte) occur in response to an increase in ventricular afterload (pressure overload). The impaired relaxation of the ventricle leads to impaired diastolic filling of the left ventricle (LV). Morris et al found that RV subendocardial systolic dysfunction and diastolic dysfunction, as detected by echocardiographic strain rate imaging, are common in patients with HFNEF. This dysfunction is potentially associated with the same fibrotic processes that affect the subendocardial layer of the LV and, to a lesser extent, with RV pressure overload. This may play a role in the symptomatology of patients with HFNEF.[5] LV chamber stiffness An increase in LV chamber stiffness occurs secondary to any one of the following 3 mechanisms or to a combination thereof: Rise in filling pressure Shift to a steeper ventricular pressure-volume curve Decrease in ventricular distensibility3 of 30 9/3/2011 8:27 AM
  4. 4. Heart Failure http://emedicine.medscape.com/article/163062-overview A rise in filling pressure is the movement of the ventricle up along its pressure-volume curve to a steeper portion, as may occur in conditions such as volume overload secondary to acute valvular regurgitation or acute LV failure due to myocarditis. A shift to a steeper ventricular pressure-volume curve results most commonly not only from increased ventricular mass and wall thickness, as observed in aortic stenosis and long-standing hypertension, but also from infiltrative disorders (eg, amyloidosis), endomyocardial fibrosis, and myocardial ischemia. Parallel upward displacement of the diastolic pressure-volume curve is generally referred to as a decrease in ventricular distensibility. This is usually caused by extrinsic compression of the ventricles. Concentric LV hypertrophy Whereas volume overload, as observed in chronic aortic and/or mitral valvular regurgitant disease, shifts the entire diastolic pressure-volume curve to the right, indicating increased chamber stiffness, pressure overload that leads to concentric LV hypertrophy (LVH, as occurs in aortic stenosis, hypertension, and hypertrophic cardiomyopathy) shifts the diastolic pressure-volume curve to the left along its volume axis so that at any diastolic volume ventricular diastolic pressure is abnormally elevated, although chamber stiffness may or may not be altered. Increases in diastolic pressure lead to increased myocardial energy expenditure, remodeling of the ventricle, increased myocardial oxygen demand, myocardial ischemia, and eventual progression of the maladaptive mechanisms of the heart that lead to decompensated heart failure. Arrhythmias While life-threatening rhythms are more common in ischemic versus nonischemic cardiomyopathy, arrhythmia imparts a significant burden in all forms of heart failure. In fact, some arrhythmias even perpetuate heart failure. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias. Structural substrates for ventricular arrhythmias common in heart failure, regardless of the underlying cause, include the following: Ventricular dilatation Myocardial hypertrophy Myocardial fibrosis At the cellular level, myocytes may be exposed to increased stretch, wall tension, catecholamines, ischemia, and electrolyte imbalance. The combination of these factors contributes to an increased incidence of arrhythmogenic sudden cardiac death in patients with heart failure. Etiology Most patients who present with significant heart failure do so because of an inability to provide adequate cardiac output in that setting. This is often a combination of the causes listed below in the setting of an abnormal myocardium. The list of causes responsible for presentation of a patient with heart failure exacerbation is very long, and searching for the proximate cause to optimize therapeutic interventions is important. From a clinical standpoint, classifying the causes of heart failure into the following 3 broad categories is useful: Underlying causes Fundamental causes Precipitating causes Underlying causes Underlying causes include structural abnormalities (congenital or acquired) that affect the peripheral and coronary arterial circulation, pericardium, myocardium, or cardiac valves, thus leading to the increased hemodynamic burden or myocardial or coronary insufficiency responsible for heart failure. Specific underlying factors in various forms of heart failure include systolic heart failure, diastolic heart failure, acute heart failure, high-output heart failure, and right heart failure. Systolic heart failure includes the following: Coronary artery disease4 of 30 9/3/2011 8:27 AM
  5. 5. Heart Failure http://emedicine.medscape.com/article/163062-overview Diabetes mellitus Hypertension Valvular heart disease (stenosis or regurgitant lesions) Arrhythmia (supraventricular or ventricular) Infections and inflammation (myocarditis) Peripartum cardiomyopathy Congenital heart disease Drug induced (either recreational like alcohol and cocaine, or therapeutic drugs with cardiac side effects like doxorubicin) Idiopathic cardiomyopathy Rare conditions (endocrine abnormalities, rheumatologic disease, neuromuscular conditions) Diastolic heart failure includes the following: Coronary artery disease Diabetes mellitus Hypertension Valvular disease (aortic stenosis) Hypertrophic cardiomyopathy Restrictive cardiomyopathy (amyloidosis) Constrictive pericarditis Acute heart failure includes the following: Acute valvular (mitral or aortic) regurgitation Myocardial infarction Myocarditis Arrhythmia Drug induced (eg, cocaine, calcium channel-blocker or beta-blocker overdose) Sepsis High-output heart failure includes the following: Anemia Systemic arteriovenous fistulas Hyperthyroidism Beriberi heart disease Paget disease of bone Albright syndrome (fibrous dysplasia) Multiple myeloma Pregnancy Glomerulonephritis Polycythemia vera Carcinoid syndrome Right heart failure includes the following: Left ventricular failure Coronary artery disease (ischemia) Pulmonary hypertension Pulmonary valve stenosis Pulmonary embolism Chronic pulmonary disease Neuromuscular disease Fundamental causes Fundamental causes include the biochemical and physiologic mechanisms, through which either an increased hemodynamic burden or a reduction in oxygen delivery to the myocardium results in impairment of myocardial contraction. Precipitating causes of heart failure5 of 30 9/3/2011 8:27 AM
  6. 6. Heart Failure http://emedicine.medscape.com/article/163062-overview Overt heart failure may be precipitated by progression of the underlying heart disease. A previously stable, compensated patient may develop heart failure that is clinically apparent for the first time when the intrinsic process has advanced to a critical point, such as with further narrowing of a stenotic aortic valve or mitral valve. Alternatively, decompensation may occur as a result of failure or exhaustion of the compensatory mechanisms but without any change in the load on the heart in patients with persistent, severe pressure or volume overload. The most common cause of decompensation in a previously compensated patient with heart failure is inappropriate reduction in the intensity of treatment, whether dietary sodium restriction, physical activity reduction, drug regimen reduction, or, most commonly, a combination of these measures. Arrhythmias, particularly ventricular arrhythmias, can be life threatening. Systemic infection or the development of unrelated illness can also lead to heart failure. Systemic infection precipitates heart failure by increasing total metabolism as a consequence of fever, discomfort, and cough, increasing the hemodynamic burden on the heart. Septic shock, in particular, can precipitate heart failure by the release of endotoxin-induced factors that can depress myocardial contractility. Cardiac infection and inflammation can also endanger the heart. Myocarditis or infective endocarditis may directly impair myocardial function and exacerbate existing heart disease. The anemia, fever, and tachycardia that frequently accompany these processes are also deleterious. In the case of infective endocarditis, the additional valvular damage that ensues may precipitate cardiac decompensation. Patients with heart failure, particularly when confined to bed, are at high risk of developing pulmonary emboli, which can increase the hemodynamic burden on the right ventricle by further elevating right ventricular (RV) systolic pressure, possibly causing fever, tachypnea, and tachycardia. Intense, prolonged physical exertion or severe fatigue, such as may result from prolonged travel or emotional crisis, is a relatively common precipitant of cardiac decompensation. The same is true of exposure to severe climate change (ie, the individual comes in contact with a hot, humid environment or a bitterly cold one). Excessive intake of water and/or sodium and the administration of cardiac depressants or drugs that cause salt retention are other factors that can lead to heart failure. Because of increased myocardial oxygen consumption and demand beyond a critical level, the following high-output states can precipitate the clinical presentation of heart failure: Profound anemia Thyrotoxicosis Myxedema Paget disease of bone Albright syndrome Multiple myeloma Glomerulonephritis Cor pulmonale Polycythemia vera Obesity Carcinoid syndrome Pregnancy Nutritional deficiencies (eg, thiamine deficiency, beriberi) In particular, consider whether the patient has underlying coronary artery disease or valvular heart disease. Patients with one form of underlying heart disease that may be well compensated can develop heart failure when a second form of heart disease ensues. For example, a patient with chronic hypertension and asymptomatic LVH may be asymptomatic until a myocardial infarction (MI) develops and precipitates heart failure. Epidemiology United States statistics According to the American Heart Association, heart failure affects nearly 5.7 million Americans of all ages and is responsible for more hospitalizations than all forms of cancer combined. It is the number 1 cause for hospitalization among Medicare patients. With improvement in survival of acute MIs and a population that continues to age, heart failure will continue to increase in prominence as a major health problem in the United States.6 of 30 9/3/2011 8:27 AM
  7. 7. Heart Failure http://emedicine.medscape.com/article/163062-overview Heart failure statistics for the United States are as follows[6] : Heart failure is the fastest-growing clinical cardiac disease entity in the United States, affecting 2% of the population. In 2006, 1.1 million patients were admitted to the hospital for acute decompensated heart failure in the United States, almost double the number seen 15 years prior. In addition, there were 3.4 million outpatient visits for heart failure. 550,000 new cases of heart failure are diagnosed and 300,000 deaths are caused by heart failure each year. Rehospitalization rates[7] during the 6 months following discharge are as much as 50%. Nearly 2% of all hospital admissions in the United States are for decompensated heart failure; and heart failure is the most frequent cause of hospitalization in patients older than 65 years, with an annual incidence of 10 per 1,000. The average duration of hospitalization is about 6 days. In 2008, the estimated total cost of heart failure in the United States was $37.2 billion. This represented 1-2% of all healthcare expenditures. The incidence and prevalence of heart failure are higher in African Americans, Hispanics, Native Americans, and recent immigrants from developing nations, Russia, and the former Soviet republics. The higher prevalence of heart failure in African Americans, Hispanics, and Native Americans is directly related to the higher incidence and prevalence of hypertension and diabetes. This problem is particularly exacerbated by a lack of access to health care and to substandard preventive health care among the most indigent of individuals in these and other groups; many persons in these groups are without adequate health insurance coverage. The higher incidence and prevalence of heart failure among recent immigrants from developing nations is largely due to a lack of prior preventive health care and to a lack of treatment or to substandard treatment for common conditions, such as hypertension, diabetes, rheumatic fever, and ischemic heart disease. Men and women have equivalent incidence and prevalence of heart failure. However, many differences between men and women are observed, including the following: Women tend to develop heart failure later in life than men do. Women are more likely than men to have preserved systolic function. Women develop depression more commonly than men do. Women have signs and symptoms of heart failure similar to those of men, but they are more pronounced in women. Women survive longer with heart failure than men do. The prevalence of heart failure increases with age. The prevalence is 1-2% of the population younger than 55 years and increases dramatically to a rate of 10% for persons older than 75 years. Nonetheless, heart failure can occur at any age, depending on the cause. Longitudinal data from the Framingham Heart Study suggests that antecedent subclinical left ventricular systolic or diastolic dysfunction is associated with an increased incidence of heart failure, supporting the notion that heart failure is a progressive syndrome.[8] Another analysis of over 36,000 patients undergoing outpatient echocardiography reported that moderate or severe diastolic dysfunction, but not mild diastolic dysfunction, is an independent predictor of mortality.[9] International statistics Heart failure is a worldwide problem, but little accurate financial data are available. The most common cause of heart failure in industrialized countries is ischemic cardiomyopathy. Other causes, including Chagas disease and valvular cardiomyopathy, assume a more important role in developing countries than in the United States. However, as developing nations urbanize and become more affluent, the rate of heart failure increases in concordance with rates of diabetes, hypertension, a more processed diet, and a more sedentary lifestyle. This was illustrated in a population study in Soweto, South Africa. As the community transformed into a more urban and westernized city, an increase in diabetes and hypertension was met with an increased rate of heart failure.[10] In terms of treatment, a 2006 study of European nations showed few important international differences in uptake of key therapies among European countries with widely differing cultures and economic status for patients with heart failure. In contrast, studies of sub-Saharan Africa, where health care resources are more limited, have shown poor outcomes in certain populations.[11] For instance, hypertensive heart failure carries a 25% 1-year mortality rate in some countries, and human immunodeficiency virus (HIV)–associated cardiomyopathy generally progresses to death within7 of 30 9/3/2011 8:27 AM
  8. 8. Heart Failure http://emedicine.medscape.com/article/163062-overview 100 days of diagnosis in patients who are not treated with antiretroviral drugs. While data in developing countries are not as robust as in Western society, the following trends are apparent: Causes tend to be largely nonischemic Patients tend to present at a younger age Outcomes are largely worse where health care resources are limited Isolated right heart failure tends to be more prominent, with a variety of causes, from tuberculous pericardial disease to lung disease and pollution, having been postulated Prognosis In general, the inpatient mortality rate for patients with heart failure is 5-20%, while outpatient mortality remains 20% at the end of the first year postdiagnosis and up to 50% at 5 years postdiagnosis, despite marked improvement in medical and device therapy (AHA published statistics). Each rehospitalization increases mortality by 20-30%. Cardiopulmonary stress testing can be useful in assessing the chances of a patient’s survival within the next year as well as in determining the need for referral for either cardiac transplantation or implantation of mechanical circulatory support. Patients with NYHA class IV, ACC/AHA stage D heart failure have more than 50% mortality at 1 year. A study by van Diepen et al suggests patients with heart failure or atrial fibrillation have a significantly higher risk of noncardiac postoperative mortality than patients with coronary artery disease; thus, patients and physicians should consider this risk, even if a minor procedure is planned.[12] Heart failure associated with acute MI has an inpatient mortality rate of 20-40%; mortality approaches 80% in patients who are also hypotensive (eg, cardiogenic shock). Patient Education Stage A patients have risk factors for developing heart failure (eg, hypertension, diabetes mellitus, obesity, metabolic syndrome, sleep apnea, patients with a family history of dilated cardiomyopathy or using cardiotoxins). They should be treated with aggressive risk factor modification, education, and angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB) if diabetes mellitus or vascular disease is present (HOPE, SOLVD- prevention). To help prevent recurrence of heart failure, counsel and educate patients in whom heart failure was caused by dietary factors or medication noncompliance with regard to the importance of proper diet and the necessity of medication compliance. For excellent patient education resources, visit eMedicines Heart Center, Cholesterol Center, Diabetes Center. In addition, see eMedicines patient education articles Congestive Heart Failure, High Cholesterol, Chest Pain, Heart Rhythm Disorders, Coronary Heart Disease, and Heart Attack. Contributor Information and Disclosures Author Ioana Dumitru, MD Assistant Professor, Internal Medicine, Section of Cardiology, Founder and Medical Director, Heart Failure and Cardiac Transplant Program, University of Nebraska Medical Center; Assistant Professor, Internal Medicine, Section of Cardiology, Veterans Affairs Medical Center, Omaha, Nebraska Ioana Dumitru, MD is a member of the following medical societies: American College of Cardiology, Heart Failure Society of America, and International Society for Heart and Lung Transplantation Disclosure: Nothing to disclose. Coauthor(s) Mathue Baker, MD Fellow, Department of Internal Medicine, Division of Cardiology, University of Nebraska Medical Center, Omaha Disclosure: Nothing to disclose.8 of 30 9/3/2011 8:27 AM
  9. 9. Heart Failure http://emedicine.medscape.com/article/163062-overview David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Joseph Cornelius Cleveland Jr, MD Associate Professor, Division of Cardiothoracic Surgery, University of Colorado Health Sciences Center Joseph Cornelius Cleveland Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Geriatrics Society, American Physiological Society, American Society of Transplant Surgeons, Association for Academic Surgery, Heart Failure Society of America, International Society for Heart and Lung Transplantation, Phi Beta Kappa, Society of Critical Care Medicine, Society of Thoracic Surgeons, and Western Thoracic Surgical Association Disclosure: Thoratec Heartmate II Pivotal Tria; Grant/research funds Principal Investigator - Colorado; Abbott Vascular E-Valve E-clip Honoraria Consulting; Baxter Healthcare Corp Consulting fee Board membership; Heartware Advance BTT Trial Grant/research funds Principal Investigator- Colorado; Heartware Endurance DT trial Grant/research funds Principal Investigator-Colorado Kavita Garg, MD Professor, Department of Radiology, University of Colorado School of Medicine Kavita Garg, MD is a member of the following medical societies: American College of Radiology, American Roentgen Ray Society, Radiological Society of North America, and Society of Thoracic Radiology Disclosure: Nothing to disclose. Shamai Grossman, MD, MS Assistant Professor, Department of Emergency Medicine, Harvard Medical School; Director, The Clinical Decision Unit and Cardiac Emergency Center, Beth Israel Deaconess Medical Center Shamai Grossman, MD, MS is a member of the following medical societies: American College of Emergency Physicians Disclosure: Nothing to disclose. Jeffrey A Miller, MD Associate Adjunct Professor of Clinical Radiology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School; Faculty, Department of Radiology, Veterans Affairs of New Jersey Health Care System Jeffrey A Miller, MD is a member of the following medical societies: American Roentgen Ray Society, Society for Health Services Research in Radiology, and Society of Thoracic Radiology Disclosure: Nothing to disclose. John D Newell Jr, MD Professor of Radiology, Head, Division of Radiology, National Jewish Health; Professor, Department of Radiology, University of Colorado School of Medicine John D Newell Jr, MD is a member of the following medical societies: American College of Chest Physicians, American College of Radiology, American Roentgen Ray Society, American Thoracic Society, Association of University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology Disclosure: Siemens Medical Grant/research funds Consulting; Vida Corporation Ownership interest Board9 of 30 9/3/2011 8:27 AM
  10. 10. Heart Failure http://emedicine.medscape.com/article/163062-overview membership; TeraRecon Grant/research funds Consulting; eMedicine Honoraria Consulting; Humana Press Honoraria Other David A Nix, MD, PhD Staff Physician, Department of Emergency Medicine, Kaiser Santa Clara David A Nix, MD, PhD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Donald Schreiber, MD, CM Associate Professor of Surgery (Emergency Medicine), Stanford University School of Medicine Donald Schreiber, MD, CM is a member of the following medical societies: American College of Emergency Physicians Disclosure: Abbott Point of Care Inc Research Grant and Speakers Bureau Speaking and teaching; Nanosphere Inc Grant/research funds Research; Singulex Inc Grant/research funds Research; Abbott Diagnostics Inc Grant/research funds None Craig H Selzman, MD, FACS Associate Professor of Surgery, Surgical Director, Cardiac Mechanical Support and Heart Transplant, Division of Cardiothoracic Surgery, University of Utah School of Medicine Craig H Selzman, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American College of Surgeons, American Physiological Society, Association for Academic Surgery, International Society for Heart and Lung Transplantation, Society of Thoracic Surgeons, Southern Thoracic Surgical Association, and Western Thoracic Surgical Association Disclosure: Nothing to disclose. Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other Vibhuti N Singh, MD, MPH, FACC, FSCAI Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine Vibhuti N Singh, MD, MPH, FACC, FSCAI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Florida Medical Association Disclosure: Nothing to disclose. Specialty Editor Board George A Stouffer III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment10 of 30 9/3/2011 8:27 AM
  11. 11. Heart Failure http://emedicine.medscape.com/article/163062-overview Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Brett C Sheridan, MD, FACS Associate Professor of Surgery, University of North Carolina at Chapel Hill School of Medicine Disclosure: Nothing to disclose. Chief Editor Henry H Ooi, MBBCh Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine Henry H Ooi, MBBCh is a member of the following medical societies: American College of Cardiology, American Heart Association, Heart Failure Society of America, and International Society for Heart and Lung Transplantation Disclosure: Nothing to disclose. References 1. Kajstura J, Leri A, Finato N, Di Loreto C, Beltrami CA, Anversa P. Myocyte proliferation in end-stage cardiac failure in humans. Proc Natl Acad Sci U S A. Jul 21 1998;95(15):8801-5. [Medline]. [Full Text]. 2. Cohn JN. Structural basis for heart failure. Ventricular remodeling and its pharmacological inhibition. Circulation. May 15 1995;91(10):2504-7. [Medline]. 3. Anversa P, Nadal-Ginard B. Myocyte renewal and ventricular remodelling. Nature. Jan 10 2002;415(6868):240-3. [Medline]. 4. Leri A, Claudio PP, Li Q, Wang X, Reiss K, Wang S, et al. Stretch-mediated release of angiotensin II induces myocyte apoptosis by activating p53 that enhances the local renin-angiotensin system and decreases the Bcl-2-to-Bax protein ratio in the cell. J Clin Invest. Apr 1 1998;101(7):1326-42. [Medline]. [Full Text]. 5. Morris DA, Gailani M, Vaz Perez A, et al. Right ventricular myocardial systolic and diastolic dysfunction in heart failure with normal left ventricular ejection fraction. J Am Soc Echocardiogr. Aug 2011;24(8):886-97. [Medline]. 6. Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB, Flegal K, et al. Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. Jan 27 2009;119(3):480-6. [Medline]. 7. Jencks SF, Williams MV, Coleman EA. Rehospitalizations among patients in the Medicare fee-for-service program. N Engl J Med. Apr 2 2009;360(14):1418-28. [Medline]. 8. Lam CS, Lyass A, Kraigher-Krainer E, et al. Cardiac dysfunction and noncardiac dysfunction as precursors of heart failure with reduced and preserved ejection fraction in the community. Circulation. Jul 5 2011;124(1):24-30. [Medline]. 9. Halley CM, Houghtaling PL, Khalil MK, Thomas JD, Jaber WA. Mortality rate in patients with diastolic dysfunction and normal systolic function. Arch Intern Med. Jun 27 2011;171(12):1082-7. [Medline]. 10. Stewart S, Wilkinson D, Hansen C, Vaghela V, Mvungi R, McMurray J, et al. Predominance of heart failure in the Heart of Soweto Study cohort: emerging challenges for urban African communities. Circulation. Dec 2 2008;118(23):2360-7. [Medline]. 11. Damasceno A, Cotter G, Dzudie A, Sliwa K, Mayosi BM. Heart failure in sub-saharan Africa: time for action. J11 of 30 9/3/2011 8:27 AM
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