Heart Failure

Heart Failure

http://emedicine.medscape.com/article/163062-overview

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 Author: Ioana Dumitru, Dumitru, MD; MD; Chief Editor: Henry H Ooi, MB, MB, MRCPI more... Updated: Apr 5, 2013

Pract Practice ice Ess Essentials entials Heart failure failure is when the heart, via an an abnormality abnormality of cardiac function (detectable (detec table or not), fails to pump blood blo od at a rate commensurat comme nsurate e with the the requirements o f the metabolizing tissues o r is able to do d o so only with with an elevated diastolic filling pressure.

Essential update: FDA approves imaging agent for cardiac risk evaluation in heart failure patients In March 2013, the FDA approved the scintigra sc intigraphic phic imaging agent iobenguane I 123 12 3 injection (AdreView) for the evaluation of myocardial sympathetic innervation in patients with NYHA class 2–3 heart failure with an LVEF ≤35%. The radionuclide tracer, which which functions mole cularly cularly as a norep inephrine inephrine analog, can show relative levels of norepinephrine uptake uptake in the cardiac s ympathetic nervous system and contribut co ntribute e to risk stratification in heart heart failure failure patient p atients. s. Improved I mproved [1] reuptake of norepinephrine is associated with a better prognosis.

Signs and symptoms Signs and symptoms of heart failure failure include the followin fo llowing: g: Exertional dyspnea and/or dyspnea at rest Orthopnea  Acute pulmonary edema edem a Chest pain/ p ain/press pressure ure and palpitations Tachycardia Fatigue and weakness Nocturia and oliguria  Anorexia, weight weight loss, nausea nausea Exophthalmos and/or visible visible p ulsation ulsation of eyes Distention of neck nec k veins Weak, rapid, and thready pulse Rales, wheezing wheezing S3 gallop and/or pulsus alternan alternans s Increased intensity of P2 heart sound Hepatojugular Hepatojugular reflux  Ascites , hepatomegaly, hepatomegaly, and/or and/or anasarca anasarca Central or peripheral cyanosis, pallor  See Clinical Presenta Prese ntation tion for  for more detail.

Diagnosis Heart failure criteria, classification, and staging

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The Framingham criteria for the diagnosis of heart failure consists of the concurrent presence of either 2 major criteria or  1  1 major and 2 minor criteria.[2] Major Major criteria include the f ollowing: Paroxysmal nocturnal nocturnal dyspnea d yspnea Weight loss of 4.5 kg in 5 days in response to treatment Neck vein distention Rales  Acute pulmonary edema edem a Hepatojugular Hepatojugular reflux S3 gallop Central venous pressure greater g reater than than 16 c m water  Circulation time of 25 seconds Radiographic cardiomegaly Pulmonary edema, edem a, visceral congestion, or cardiomegaly cardiome galy at autopsy autopsy Minor Minor criteria are as follows: Nocturnal Nocturnal co ugh Dyspnea on o rdinary rdinary exertion  A decrease dec rease in vital vital capacity by one third third the the maximal value value recorded record ed Pleural effusion Tachycardia (rate (rate of 120 bpm) Bilateral ankle ankle edema edem a The New York York Heart Association (NYHA) (NYHA) classif ication system catego rizes heart failure failure on a s cale of I to IV,[3] as follows: Class I : No limitation limitation of physical activity activity Class I I: Slight limitation of p hysical activity activity Class I II: Marked Marked limitation of physical activity Class IV: I V: Symptoms oc cur even at rest; disco mfort with any any physical activity activity The American College of Cardiology/American Heart Association (ACC/AHA) staging system is defined by the following 4 stages[4, 5] : Stage A: High risk of heart failure but no structural structural heart disease or symptoms sympto ms of o f heart failure Stage B: Structural heart heart disease but b ut no symptoms of o f heart failure Stage C: Structural heart heart disease and symptoms sympto ms of heart failure failure Stage D: Refractory R efractory heart failure requiring requiring spec s pecializ ialized ed interventions Testing

The following fo llowing basic tests may be useful in the initial initial evaluation evaluation for suspected susp ected heart failure failure[4, 6, 7] : Complete blood c ount (CBC) (CBC) Urinalysis Electrolyte levels Renal and liver function studies Fasting blood glucose levels Lipid profile Thyroid stimulating stimulating hormone (TSH) levels B-type natriuretic natriuretic peptide levels N-terminal N-terminal pro-B-type natriuretic natriuretic pep tide Electrocardiography Chest radiography 2-dimensional (2-D) echocardiography Maximal Maximal exercise testing Pulse oximetry or arterial blood gas See Workup Workup for  for more detail.

Management Treatment includes includes the following: Nonpharmacologic Nonpharmacologic therapy: Oxygen Oxygen and noninvasive noninvasive positive p ositive pres sure ventilation, ventilation, dietary sodium sod ium and fluid

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restriction, physical activity as approp riate, and attention to weight gain Pharmacotherapy: Diuretics, vasodilators, inotropic agents, anticoagulants, beta blockers, and digoxin Surgical options

Surgical treatment options include the following: Electrophysiologic intervention Revascularization procedures Valve replacement/repair  Ventricular restoration Extracorporeal membrane oxygenation Ventricular assist devices Heart transplantation Total artificial heart See Treatment and Medication for more detail.

Image library

This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute heart failure.

Background Heart failure is the pathophysiologic state in which the heart, via an abnormality of cardiac function (detectable or not), fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure. Heart failure (see the images below) may be caused by myocardial failure but may also occ ur in the presence of  near-normal cardiac function under co nditions of high demand. Heart failure always causes circulatory failure, but the converse is not necessarily the case, because various noncardiac conditions (eg, hypovolemic shock, septic shock) can produce circulatory failure in the presence of normal, modestly impaired, or even supranormal cardiac function. To maintain the pumping f unction of the heart, compensatory mechanisms increase blo od volume, cardiac filling pressure, heart rate, and cardiac muscle mass. However, despite these mechanisms, there is progressive decline in the ability of the heart to contract and relax, resulting in worsening heart failure.

This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute heart failure.

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 A 28-year-old woman presented with acute heart failure secondary to chronic hypertension. The enlarged cardiac silhouette on this anteroposterior (AP) radiograph is caused by acute heart failure due to the effects of chronic high blood pressure on the left ventricle. The heart then becomes enlarged, and fluid accumulates in the lungs (ie, pulmonary congestion).

This magnetic resonance image shows a scar in the anterior cardiac wall, which may be indicative of a previous myocardial infarction (MI). MIs can precipitate heart failure.

Signs and symptoms of heart failure include tachycardia and manifestations of venous congestion (eg, edema) and low cardiac output (eg, fatigue). Breathlessness is a cardinal symptom of left ventricular (LV) failure that may manifest with progressively increasing se verity. Heart failure can be classif ied according to a variety of factors (se e Heart Failure Criteria and Classification).The New York Heart Association (NYHA) classification for heart failure comprises 4 classes, based on the relationship between symptoms and the amount of effort required to provoke them, as follows[3] : Class I patients have no limitation of physical activity Class I I patients have slight limitation of physical activity Class I II patients have marked limitation of p hysical activity Class I V patients have symptoms even at rest and are unable to carry on any physical activity without discomfort The American College of Cardiology/American Heart Association (ACC/AHA) heart failure guidelines complement the NYHA classification to reflect the progression of disease and are divided into 4 stages, as follows[4, 5] : Stage A patients are at high risk for heart failure but have no structural heart disease or symptoms of heart failure Stage B patients have structural heart disease but have no symptoms of heart failure Stage C patients have structural heart disease and have symptoms of heart failure Stage D patients have ref ractory heart failure requiring specialized interventions Laboratory studies for heart failure should include a complete blood count (CBC), electrolytes, and renal function studies. Imaging studies such as chest radiography and 2-dimensional echocardiography are recommended in the initial evaluation of patients with known or suspected heart failure. B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic pep tide (NT-proBNP) levels can be useful in differentiating cardiac and noncardiac causes of  dyspnea. (See the Workup Section for more information.) In acute heart failure, patient care consists o f stabilizing the patient's clinical condition; establishing the diagnosis, etiology, and precipitating factors; and initiating therapies to provide rapid symptom relief and survival benefit. Surgical options f or heart failure include revascularization procedures, electrophysiologic intervention, cardiac resynchronization therapy (CRT), implantable cardioverter-defibrillators (IC Ds), valve replacement or repair, ventricular restoration, heart transplantation, and ventricular assist devices (VADs). (See the Treatment Section for mo re information.) The goals of pharmacotherapy are to increase survival and to prevent comp lications. Along with oxygen, medications assisting with symptom relief include diuretics, digo xin, inotropes, and morphine. Drugs that can exacerbate heart failure should be avoided (nonsteroidal anti-inflammatory drugs [NSAIDs], calcium channel blockers [CCBs], and most antiarrhythmic drugs). (See the Medication Section fo r more information.) For further information, see the Medscape Reference articles Pediatric Congestive Heart Failure, Congestive Heart Failure Imaging, Heart Transplantation, Coronary Artery Bypass Grafting, and Implantable Cardioverter-Defibrillators.

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 do es

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heart failure ensue.[8, 9, 10, 11, 12]

 Adaptations Most important among the adaptations are the following[13] : 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 d ilatation, in which the mass of contractile tissue is augmented  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 m echanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels b ecome maladaptive when trying to sustain adequate cardiac performance.[14] The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration.[15] 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.[16] The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendoc rine systems, most notably the above-mentioned adrenergic systems and RAAS.[17] The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases calcium afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytoso lic 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 myoc ardial 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 expe nditure leads to myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of f urther 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 de livery of chloride to the macula densa and increase be ta1-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 conce pt of the heart as a self -renewing organ is a relatively recent development.[18] This new paradigm for  myocyte biolog y 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.[15] 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 rege neration is the f inal 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 b een shown in vitro and in vivo to increase the rate of myocyte apoptosis.[19] In this fashion, Ang I I 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 myoc ardial mass, as well as myocyte los s. As a result, the cardiac architecture changes, which, in turn, leads to further increase in myocardial volume and mass.

Myocytes and myoc ardial remodeling

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In the failing heart, increased myocardial volume is characterized by larger myocytes app roaching the end of their life cycle.[20] 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 (Frank-Starling mechanism) and dec reased wall stress (Laplace's law), 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 o f endogenous vasodilators, including nitric oxide (NO), prostaglandins (PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP). This decline occurs simultaneously with the increase in vasoconstrictor substances from the RAAS and the adrenergic system, which fosters further increases in vasoconstriction and thus preload and afterload. This results in ce llular prolife ration, adverse myocardial remodeling, and antinatriuresis, with total body fluid excess and worsening of heart failure symptoms.

Systolic and diastolic failure Systolic and diastolic heart failure each result in a decrease in stroke volume. This leads to activation of pe ripheral and central baroreflexes and chemoreflexes that are capable of eliciting marked increases in sympathetic nerve traffic. While there are commonalities in the neurohormonal responses to decreased stroke volume, the neurohormonemediated 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 recep tors, uncoupling of be ta2adrenergic recep tors, and increased activity of inhibitory G-protein. Changes in beta1-adrenergic receptors result in overexpression and promote myocardial hypertrophy.

 ANP and B NP  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, respe ctively, and both promote vasodilation and natriuresis. Their hemodynamic effe cts are med iated by decreases in ventricular filling pressures, owing to reductions in cardiac preload and afterload. BNP, in particular, produce s selective aff erent arteriolar vasodilation and inhibits sodium reabso rption in the proximal convoluted tubule. It also inhibits renin and aldosterone release and, therefore, adrenergic activation. ANP and BNP are elevated in chronic heart failure. BNP, in particular, has potentially important diagnostic, therapeutic, and prognostic implications. For more information, see the Medscape Reference article 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 f actor-alpha (TNF-alpha).[21] ET, a substance produced by the vascular endothelium, may contribute to the regulation of myoc ardial function, vascular tone, and peripheral resistance in heart failure. Elevated levels of ET-1 close ly correlate with the severity of heart failure. ET-1 is a potent vasoconstrictor and has exaggerated vasoconstrictor ef fects in the renal vasculature, reducing renal plasma blood flow, glomerular filtration rate (GFR), and s odium 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. Some studies sugg est that local production of T NF-alpha may have toxic eff ects on the myocardium, thus worsening myocardial systolic and diastolic f unction. In individuals with systolic dysfunction, therefore, 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 progres sion of myocardial dysfunction in the long term.

Heart failure with normal ejection f raction In diastolic heart failure (heart failure with normal ejection fraction [HFNEF]), the same pathophysiologic processes occur that lead to decreased cardiac output in systolic heart failure, but they do so in response to a different set of  hemodynamic and circulatory environmental factors that depress cardiac output.[22]

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In HFNEF, altered relaxation and increased s tiffness of the ventricle (due to delayed calcium uptake by the myocyte sarcoplasmic reticulum and delayed calcium eff lux from the myocyte) occur in response to an increase in ventricular  afterload (pressure o verload). The impaired relaxation of the ventricle then leads to impaired d iastolic 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 p atients with HFNEF. This dysfunction is potentially associated with the same fibrotic processes that affect the subendo cardial layer of the LV and, to a lesser extent, with RV pressure overload. This may play a role in the symp tomatology of patients with HFNEF.[23]

LV chamber stiffness  An increase in LV chamber stiffness occurs seco ndary to any one of, or any combination of, the following 3 mechanisms: Rise in filling pressure Shift to a steeper ventricular pressure-volume curve Decrease in ventricular distensibility  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 s uch 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 stenos is 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 Pressure o verload that leads to concentric LV hypertrophy (LVH), as occurs in aortic stenosis, hypertension, and hypertrophic cardiomyopathy, shifts the diastolic pres sure-volume curve to the lef t along its volume axis. As a result, ventricular diastolic press ure is abnormally elevated, although chamber stiff ness may or may not be altered. Increases in diastolic pressure lead to increased myocardial energy expenditure, remodeling of the ventricle, increased myoc ardial oxygen demand, myocardial ischemia, and eventual progress ion of the maladaptive mechanisms of the heart that lead to decompensated heart failure.

 Arrh ythmias While life-threatening rhythms are more common in ischemic cardiomyopathy, arrhythmia imparts a significant burden in all forms of heart failure. In fact, s ome arrhythmias even perpetuate heart failure. The most s ignificant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias. Structural substrates for ventricular  arrhythmias that are common in heart failure, regardless of the underlying cause, include ventricular dilatation, myocardial hypertrophy, and myoc ardial 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 f or prese ntation of a patient with heart failure exacerbation is very long, and searching for the proximate cause to optimize therapeutic interventions is imp ortant. From a clinical standpoint, classifying the causes of heart failure into the following 4 broad c ategories is useful: Underlying causes: Underlying causes of heart failure include structural abnormalities (congenital or acquired) that affect the peripheral and coronary arterial circulation, pericardium, myocardium, or c ardiac valves, thus leading to increased hemo dynamic burden or myocardial or coronary insufficiency 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 myoc ardial contraction

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Precipitating causes: Overt heart failure may be prec ipitated by progres sion of the underlying heart disease (eg, f urther narrowing of a stenotic aortic valve or mitral valve) or various co nditions (fever, anemia, infection) or  medications (chemo therapy, NSAIDs ) that alter the homeostasis of heart failure patients Genetics of cardiomyopathy: Dilated, arrhythmic right ventricular and restrictive cardiomyopathies are known genetic causes of heart failure.

Underlying causes Specific underlying factors cause various forms of heart failure, such as systolic heart failure (most commo nly, left ventricular systolic dysfunction), heart failure with preserved LVEF, acute heart failure, high-output heart failure, and right heart failure. Underlying causes of systolic heart failure include the following: Coronary artery disease Diabetes mellitus Hypertension Valvular heart disease (stenosis or regurgitant lesions)  Arrhythmia (supraventricular or ventricular) Infections and inflammation (myocarditis) Peripartum cardiomyopathy Congenital heart disease Drugs (either recreational, such as alcohol and coc aine, or therapeutic drugs with cardiac side effects, such as doxorubicin) Idiopathic cardiomyopathy Rare conditions (endocrine abnormalities, rheumatologic disease , neuromuscular conditions) Underlying causes of diastolic heart failure include the following: Coronary artery disease Diabetes mellitus Hypertension Valvular heart disease (aortic stenosis) Hypertrophic cardiomyopathy Restrictive cardiomyopathy (amyloidosis, sarcoidosis) Constrictive pericarditis Underlying causes of acute heart failure include the f ollowing:  Acute valvular (mitral or aortic) regurgitation Myocardial infarction Myocarditis  Arrhythmia Drugs (eg, cocaine, calcium channel blockers, or beta-blocker overdose) Sepsis Underlying causes of high-output heart failure include 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 Underlying causes of right heart failure include the fo llowing: Left ventricular failure Coronary artery disease (ischemia) Pulmonary hypertension Pulmonary valve stenosis Pulmonary embolism Chronic pulmonary disease

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Neuromuscular disease

Precipitating causes of heart failure  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. In particular, consider whether the patient has underlying coronary artery disease or valvular heart disease. The most commo n cause of decompensation in a previously compensated patient with heart failure is inappropriate reduction in the intensity of treatment, such as dietary sodium res triction, physical activity reduction, or drug regimen reduction. Uncontrolled hypertension is the second most common cause of decompensation, followed closely by cardiac arrhythmias (most commonly, atrial fibrillation). Arrhythmias, particularly ventricular arrhythmias, can be life threatening. Also, patients with one form of underlying heart disease that may be well compensated can develop heart failure when a second form o f heart disease ensues. Fo r example, a patient with chronic hypertension and asymptomatic LVH may be asymptomatic until a myocardial infarction (MI) develops and prec ipitates heart failure. 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 infec tive endocarditis may directly impair myocardial function and exacerbate existing heart dis ease. T he 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 decomp ensation. Patients with heart failure, particularly when confined to bed, are at high risk of developing pulmonary emboli, which can increase the hemod ynamic burden on the right ventricle by further elevating right ventricular (RV) systolic pressure, possibly causing f ever, 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 depress ants 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 prec ipitate 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 def iciencies (eg, thiamine deficiency, beriberi) Longitudinal data from the Framingham Heart Study suggests that antecedent subclinical left ventricular systolic o r  diastolic dysf unction is associated with an increased incidence of heart failure, supporting the notion that heart failure is a progressive syndrome.[24, 25] 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.[26]

Genetics of cardiomyopathy  Autosomal dominant inheritance has been demonstrated in dilated cardiomyopathy and in arrhythmic right ventricular  cardiomyopathy. Restrictive cardiomyopathies are usually sporadic and assoc iated with the gene for cardiac troponin I. Genetic tests are available at major genetic centers f or cardiomyopathies.[27]

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In families with a first-degree relative who has bee n diagnosed with a cardiomyopathy leading to heart failure, the at-risk patient should be screened and followed.[27] The recommended screening consists of an electrocardiogram and an echocardiogram. If the patient has an asymptomatic left ventricular dysfunction, it should be treated.[27]

Epidemiology United States statistics  According to the American Heart Assoc iation, heart failure affects nearly 5.7 million Americans of all ages[28] and is responsible for more hospitalizations than all forms of cancer combined. It is the number 1 cause of hospitalization for  Medicare patients. With improved s urvival of patients with acute myocardial infarction and with a population that continues to age, heart failure will continue to increase in prominence as a major health problem in the United States.[29, 30, 31, 32]  Analysis of national and regional trends in hospitalization and mortality among Medicare beneficiaries from 19 98-2008 showed a relative decline of 29.5% in heart failure hospitalizations[33] ; however, wide variations are noted between states and races, with black men having the slowest rate of decline. A relative decline of 6.6% in mortality was also observed, although the rate was uneven across states. The length of stay decreased from 6.8 days to 6.4 days, despite an overall increase in the comorbid conditions.[33] Heart failure statistics for the United States are as f ollows: Heart failure is the fastest-growing clinical cardiac disease entity in the United States, affecting 2% of the population Heart failure accounts for 34% of cardiovascular-related deaths[28] [28]  Approximately 670,000 new cases o f heart failure are diagnosed each year  [28]  About 277,000 deaths are caused by heart failure each year  Heart failure is the most frequent cause of hospitalization in patients older than 65 years, with an annual incidence of 10 per 1,000[28] Rehospitalization rates during the 6 months following discharge are as much as 50%[34] Nearly 2% of all hospital admissions in the United States are fo r decompensated heart failure, and the average duration of hospitalization is about 6 days In 2010, the estimated total cos t of heart failure in the United States was $39.2 billion,[35] representing 1-2% of  all health care expenditures The incidence and prevalence of heart failure are higher in blacks, Hispanics, Native Americans, and recent immigrants from developing nations, Russia, and the former Soviet republics. The higher prevalence of heart failure in blacks, 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 acce ss to health care and by substandard preventive health care available to the most indigent of individuals in these and other groups; in addition, many persons in these groups do not have adequate health insurance. The higher incidence and prevalence of heart failure in recent immigrants from de veloping nations are largely due to a lack of prior preventive health care, a lack of treatment, or substandard treatment for common conditions, such as hypertension, diabetes, rheumatic fever, and ischemic heart disease. Men and women have the same incidence and the s ame prevalence of heart failure. However, there are still many differences between men and women with heart failure, such as 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 to a rate of 10% for perso ns older than 75 years. Nonetheless, heart failure can occ ur at any age, depending on the cause.

International statistics Heart failure is a worldwide problem. The most common cause of heart failure in industrialized countries is ischemic cardiomyopathy, with other causes, including Chagas disease and valvular cardiomyopathy, assuming a more important role in developing c ountries. However, in developing nations that have become more urbanized and more

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affluent, eating a more p rocessed diet and leading a more sed entary lifestyle have resulted in an increased rate of  heart failure, along with increased rates of diabetes and hypertension. This change was illustrated in a population study in Soweto, South Africa, where the c ommunity transformed into a more urban and westernized city, followed by an increase in diabetes, hypertension, and heart failure.[36] In terms of treatment, one study showed few important differences in uptake of key therapies in European countries with widely diff ering cultures and varying 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 specif ic populations.[37, 38] For example, in some countries, hypertensive heart failure carries a 25% 1-year mortality rate, and human immunodeficiency virus (HIV)–associated c ardiomyopathy generally progresses to death within 100 days of  diagnosis in patients who are not treated with antiretroviral drugs. While data regarding developing nations are not as robust as studies of W estern soc iety, the following trends in developing nations 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 having been postulated, ranging from tuberculous pericardial disease to lung disease and pollution

Prognosis In general, the mortality following hospitalization for p atients with heart failure is 10.4% at 30 days, 22% at 1 year, and 42.3% at 5 years, de spite marked improvement in medical and device therapy.[28, 39, 40, 41, 42, 43] Each rehospitalization increases mortality by about 20-22%.[28] Mortality is greater than 50% for patients with NYHA class I V, ACC/AHA stage D heart failure. Heart failure associated with acute MI has an inpatient mortality of 20 -40%; mortality approaches 80% in patients who are also hypotensive (eg, cardiogenic s hock). (See Heart Failure Criteria and Classification). Numerous demographic, clinical and biochemical variables have been reported to provide important prognostic value in patients with heart failure, and several predictive models have bee n developed.[44]  A study by van Diepen et al suggests that patients with heart failure or atrial fibrillation have a significantly higher risk of  noncardiac postoperative mortality than patients with coronary artery disease; this risk should be considered even if a minor procedure is planned.[45]  A study by Bursi et al found that among community patients with heart failure, pulmonary artery systolic press ure (PASP), assessed by Doppler echocardiography, can strongly predict death and can provide incremental and clinically significant prognostic information independent of known outcome predictors.[46] Higher concentrations of galectin-3, a marker of cardiac fibrosis , were associated with an increased risk for incident heart failure (hazard ratio: 1.28 p er 1 SD increase in log galectin-3) in the Framingham Offspring Cohort. Galectin-3 was also asso ciated with an increased risk f or all-cause mortality (multivariable-adjusted hazard ratio: 1.15).[47]

Patient Educ atio n To help prevent recurrence of heart failure in patients in whom heart failure was caused by dietary factors o r  medication noncompliance, counsel and educate such patients about the importance of proper diet and the necessity of medication compliance. Dunlay et al examined medication use and adherence among community-dwelling patients with heart failure and found that medication adherence was suboptimal in many patients, often be cause of cost.[48] A randomized controlled trial of 605 patients with heart failure reported that the incidence of all-cause hospitalization or  death was not reduced in patients receiving multi-session self -care training compared to those rec eiving a single session intervention. The optimum method f or patient education remains to be established. It appears that more intensive interventions are not neces sarily better.[49] For patient education information, see the Heart Health Center , Cholesterol Center , and Diabetes Center , as well as Congestive Heart Failure, High Cholesterol, Chest Pain, Heart Rhythm Disorde rs, Coronary Heart Disease, and Heart  Attack.

Contribut or Information and Disclosures  Author  Ioana Dumitru, MD Associate Profess or of Medicine, Division of Cardiology, Founder and Medical Director, Heart

Failure and Cardiac Transplant Program, University of Nebraska Medical Center; Assoc iate Profes sor of Medicine,

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Division of Cardiology, Veterans Affairs Medical Center  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 M Bak er, MD Cardiologist, BryanLGH Heart Institute and Saint Elizabeth Regional Medical Center 

Mathue M Baker, MD is a member of the following medical so cieties: American College of Cardiology Disclosure: Nothing to disclose. Chief Editor  Henry H Ooi, MB, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans

 Affairs Medical Center; Assistant Profess or of Medicine, Vanderbilt University School of Medicine Disclosure: Nothing to disclose.  Additional Contributors Barr y E B renn er, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program

Director, Emergency Medicine, Case Medical Center, University Hospitals, Case W estern Res erve 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 Academyof Sciences,and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair,

Department of E mergency 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 Prof essor, 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 Prof essor, 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 Soc iety, 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; Ab bott Vascular E-Valve E-clip Honoraria Consulting; Baxter Healthcare Corp Consulting fee Board me mbership; Heartware Advance BTT Trial Grant/research f unds Principal Investigator- Colorado; Heartware Endurance DT trial Grant/research funds Principal Investigator-Colorado Shamai Gross man, MD, MS Assistant Professor, Department of Emergency Medicine, Harvard Medical School;

Director, The Clinical Decision Unit and Cardiac Emergency Ce nter, Beth Israel Deaconess Medical Center  Shamai Grossman, MD, MS is a member of the following medical societies: American College of Emergency Physicians

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Disclosure: Nothing to disclose. Joh n D Newell Jr, MD Profe ssor o f 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 Board membership; TeraRecon Grant/research funds Consulting; Medsc ape Reference Honoraria Consulting; Humana Press Honoraria Other  Craig H Selzman, MD, FACS Associate Prof essor 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  Brett C Sheridan , MD, FACS Associate Prof essor of Surgery, University of North Carolina at Chapel Hill School of 

Medicine Disclosure: Nothing to disclose. 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 o f Cardiology, University of North Carolina Medical Ce nter  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 I nterventions Disclosure: Nothing to disclose. Franc isco Talavera, PharmD, PhD Adjunct Assis tant Professor, University of Nebraska Medical Center College

of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment  Additional Contributors Barr y E B renn er, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program

Director, Emergency Medicine, Case Medical Center, University Hospitals, Case W estern Res erve 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 Academyof Sciences,and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair,

Department of E mergency 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

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Disclosure: Nothing to disclose. William K Chiang, MD Associate Prof essor, 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 Prof essor, 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 Soc iety, 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; Ab bott Vascular E-Valve E-clip Honoraria Consulting; Baxter Healthcare Corp Consulting fee Board me mbership; Heartware Advance BTT Trial Grant/research f unds Principal Investigator- Colorado; Heartware Endurance DT trial Grant/research funds Principal Investigator-Colorado Shamai Gross man, MD, MS Assistant Professor, Department of Emergency Medicine, Harvard Medical School;

Director, The Clinical Decision Unit and Cardiac Emergency Ce nter, 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. Joh n D Newell Jr, MD Profe ssor o f 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 Board membership; TeraRecon Grant/research funds Consulting; Medsc ape Reference Honoraria Consulting; Humana Press Honoraria Other  Craig H Selzman, MD, FACS Associate Prof essor 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  Brett C Sheridan , MD, FACS Associate Prof essor of Surgery, University of North Carolina at Chapel Hill School of 

Medicine Disclosure: Nothing to disclose. 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 o f Cardiology, University of North Carolina Medical Ce nter 

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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 I nterventions Disclosure: Nothing to disclose. Franc isco Talavera, PharmD, PhD Adjunct Assis tant Professor, University of Nebraska Medical Center College

of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment

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