Published: March 2014
Heart failure is a clinical syndrome characterized by systemic perfusion inadequate to meet the body's metabolic demands as a result of impaired cardiac pump function. This may be further subdivided into systolic or diastolic heart failure. In systolic heart failure, there is reduced cardiac contractility, whereas in diastolic heart failure there is impaired cardiac relaxation and abnormal ventricular filling (Figures 1A and 1B).
The most common cause of heart failure is left ventricular (LV) systolic dysfunction (about 60% of patients). In this category, most cases are a result of end-stage coronary artery disease, either with a history of myocardial infarction or with a chronically underperfused, yet viable, myocardium. In many patients, both processes are present simultaneously (Figure 2A). Other common causes of LV systolic dysfunction include idiopathic dilated cardiomyopathy, valvular heart disease, hypertensive heart disease, toxin-induced cardiomyopathies (e.g., doxorubicin, herceptin, alcohol), and congenital heart disease (Figure 2B).
Right ventricular systolic dysfunction is usually a consequence of LV systolic dysfunction. It can also develop as a result of right ventricular infarction, pulmonary hypertension, chronic severe tricuspid regurgitation, or arrhythmogenic right ventricular dysplasia. A less-common cause of heart failure is high-output failure caused by thyrotoxicosis, arteriovenous fistulae, Paget's disease, pregnancy, or severe chronic anemia.
Diastolic LV dysfunction (impaired relaxation) usually is related to chronic hypertension or ischemic heart disease. Other causes include restrictive, infiltrative, and hypertrophic cardiomyopathies. Inadequate filling of the right ventricle can result from pericardial constriction or cardiac tamponade.
Heart failure is a common syndrome, especially in older adults. Although more patients survive acute myocardial infarction because of reperfusion therapy, most have at least some residual LV systolic dysfunction, which can lead to heart failure. Currently, 5.7 million Americans are afflicted with heart failure, approximately 2% of the population.1 Patients with heart failure account for about 1 million hospital admissions annually, and another 2 million patients have heart failure as a secondary diagnosis. Many of these patients are readmitted within 90 days for recurrent decompensation.
Patients at high risk for developing heart failure are those with hypertension, coronary artery disease, diabetes mellitus, family history of cardiomyopathy, use of cardiotoxins, and obesity.
Although much progress has been made in the treatment of heart failure, there is a high overall annual mortality (5% to 20%), particularly in patients with New York Heart Association (NYHA) Class IV symptoms.2 Many patients succumb to progressive pump failure and congestion, although one half die from sudden cardiac death. Some patients die from end-organ failure resulting from inadequate systemic organ perfusion, particularly to the kidneys. Indicators of poor cardiac prognosis include renal dysfunction, cachexia, valvular regurgitation, ventricular arrhythmias, higher NYHA heart failure class, lower LV ejection fraction (LVEF), high catecholamine and B-type natriuretic peptide (BNP) levels, low serum sodium level, hypocholesterolemia, and marked LV dilation. Patients with combined systolic and diastolic LV dysfunction also have a worse prognosis than patients with either in isolation.3
In LV systolic dysfunction, the body activates several neurohormonal pathways to increase circulating blood volume. The sympathetic nervous system increases heart rate and contractility, causes arteriolar vasoconstriction in nonessential vascular beds, and stimulates secretion of renin from the juxtaglomerular apparatus of the kidney. Unfortunately, catecholamines aggravate ischemia, potentiate arrhythmias, promote cardiac remodeling, and are directly toxic to myocytes. Stimulation of the renin-angiotensin system as a result of increased sympathetic stimulation and decreased renal perfusion results in further arteriolar vasoconstriction, sodium and water retention, and release of aldosterone. An increased aldosterone level, in turn, leads to sodium and water retention, endothelial dysfunction, and organ fibrosis.
In heart failure, baroreceptor and osmotic stimuli lead to vasopressin release from the hypothalamus, causing reabsorption of water in the renal collecting duct. Although these neurohormonal pathways initially are compensatory and beneficial, eventually they are deleterious, and neurohormonal modulation is the basis for modern medical treatment of heart failure.
In contrast, natriuretic peptides are hormones released by secretory granules in cardiac myocytes in response to myocardial stretching. They have a beneficial influence in heart failure, including systemic and pulmonary vasodilation, possible enhancement of sodium and water excretion, and suppression of other neurohormones.
With continuous neurohormonal stimulation, the left ventricle undergoes remodeling consisting of LV dilation and hypertrophy, such that stroke volume is increased without an actual increase in EF. This is achieved by myocyte hypertrophy and elongation. LV chamber dilation causes increased wall tension, worsens subendocardial myocardial perfusion, and can provoke ischemia in patients with coronary atherosclerosis. Furthermore, dilation of the LV chamber can cause mitral annular dilatation and functional mitral regurgitation, leading to pulmonary congestion.
In diastolic dysfunction, the primary abnormality is impaired LV relaxation, causing high diastolic pressures and poor filling of the ventricle. To increase diastolic filling, left atrial and pulmonary capillary pressures increase and pulmonary edema ensues. As a result, patients are often symptomatic with exertion when increased heart rate reduces LV filling time and circulating catecholamines worsen diastolic dysfunction. LV filling may also be very dependent on normal left atrial function. The loss of atrial function, as occurs with atrial fibrillation, may lead to a sudden worsening of LV filling and pulmonary congestion.
The American College of Cardiology (ACC) and American Heart Association (AHA) have developed a classification of heart failure based on stages of the syndrome (Table 1).4 Stage A includes patients who are at risk for developing heart failure but who have no structural heart disease at present. The management strategy in this group is prevention of heart failure. Stage B includes patients with structural heart disease but no symptoms. The management goal is prevention of further LV remodeling leading to heart failure and the promotion of LV reverse remodeling. Stage C includes patients with structural heart disease with current or prior symptomatic heart failure. Diuretics, digoxin, and aldosterone antagonists may be added to angiotensin-converting enzyme (ACE) inhibitors and beta blockers, depending on the severity of symptoms. Cardiac resynchronization therapy (CRT) also may be considered. Stage D includes patients with severe refractory heart failure. Physicians should consider either end-of-life care or high-technology therapies such as cardiac transplantation or mechanical circulatory support, based on individual cases.
|A: High risk for developing heart failure||Hypertension, diabetes mellitus, CAD, family history of cardiomyopathy|
|B: Asymptomatic heart failure||Previous MI, LV dysfunction, valvular heart disease|
|C: Symptomatic heart failure||Structural heart disease, dyspnea and fatigue, impaired exercise tolerance|
|D: Refractory end-stage heart failure||Marked symptoms at rest despite maximal medical therapy|
CAD, coronary artery disease; LV, left ventricular; MI, myocardial infarction.
There is a wide spectrum of potential clinical manifestations of heart failure.5 Most patients have signs and symptoms of fluid overload and pulmonary congestion, including dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Patients with right ventricular failure have jugular venous distention, peripheral edema, hepatosplenomegaly, and ascites. Others, however, do not have congestive symptoms but have signs and symptoms of low cardiac output, including fatigue, effort intolerance, cachexia, and renal hypoperfusion. The NYHA functional classification scheme is used to assess the severity of functional limitations and correlates fairly well with prognosis (Table 2).
|NYHA Class||Level of Impairment|
|I||No symptom limitation with ordinary physical activity|
|II||Ordinary physical activity somewhat limited by dyspnea (e.g., long-distance walking, climbing two flights of stairs)|
|III||Exercise limited by dyspnea with moderate workload (e.g., short-distance walking, climbing one flight of stairs)|
|IV||Dyspnea at rest or with very little exertion|
On physical examination, patients with decompensated heart failure may be tachycardic and tachypneic, with bilateral inspiratory rales, jugular venous distention, and edema. They often are pale and diaphoretic. The first heart sound usually is relatively soft if the patient is not tachycardic. An S3 and often an S4 gallop will be present. Murmurs of mitral or tricuspid regurgitation may be heard. Paradoxical splitting of S2 may be present because of delayed mechanical or electrical activation of the left ventricle. Patients with compensated heart failure will likely have clear lungs but a displaced cardiac apex. Patients with decompensated diastolic dysfunction usually have a loud S4 (which may be palpable), rales, and often systemic hypertension.
The initial evaluation of new-onset heart failure should include an electrocardiogram, chest radiograph, and BNP assay. EKG findings of LV hypertrophy, left bundle branch block, intraventricular conduction delay, and nonspecific ST-segment and T wave changes support a diagnosis of heart failure. Q waves in contiguous leads strongly implicate a previous myocardial infarction and coronary artery disease as the cause. Chest radiographic findings of heart failure include cardiomegaly, pulmonary vascular redistribution, pulmonary venous congestion, Kerley B lines, alveolar edema, and pleural effusions.
The single most useful diagnostic test is the echocardiogram, which can distinguish between systolic and diastolic dysfunction. If systolic dysfunction is present, regional wall motion abnormalities or LV aneurysm suggest an ischemic basis for heart failure, whereas global dysfunction suggests a nonischemic cause. Echocardiography is helpful in determining other causes, such as valvular heart disease, cardiac tamponade, or pericardial constriction, and provides useful clues about infiltrative and restrictive cardiomyopathies. Echocardiography can also provide meaningful prognostic information about diastolic function, severity of hypertrophy, chamber size, and valvular abnormalities. In many cases, however, the exact cause of the heart failure cannot be discerned from the echocardiogram.
Cardiac catheterization can detect coronary atherosclerosis as the cause of heart failure. Severe coronary artery disease is so prevalent that coronary angiography routinely should be performed to exclude this cause and, if found, should lead to an assessment of myocardial viability, with a goal of revascularization. Coronary computed tomographic angiography or radionuclide myocardial imaging might also be suitable alternatives to exclude coronary artery disease in select patients.
Magnetic resonance imaging is useful in assessing for arrhythmogenic right ventricular dysplasia, myocardial viability, and infiltrative cardiomyopathies.
Objective information about functional capacity can be obtained from metabolic (cardiopulmonary) exercise testing. This test can distinguish ventilatory from cardiac limitations in patients with exertional dyspnea. A peak oxygen consumption or VO2max higher than 25 mL/kg/min is normal for middle-age adults, but a value lower than 14 mL/kg/min indicates severe cardiac limitation and poor prognosis.
A useful diagnostic test for the detection of heart failure is the BNP assay.6,7 BNP levels correlate with severity of heart failure and decrease as a patient reaches a compensated state. This blood test may be useful for distinguishing heart failure from pulmonary disease. Because smokers often have both these clinical diagnoses, differentiating between them may be challenging.
The routine use of invasive hemodynamic monitoring to guide the management of decompensated heart failure has not proved to be beneficial. However, invasive hemodynamic monitoring may be warranted if the diagnosis is uncertain, if the patient fails to respond to therapy, or if advanced therapies (heart transplant or mechanical circulatory support) are being considered.
Dietary sodium and fluid restrictions should be implemented in all patients with congestive heart failure. Limiting patients to 2 g/day of dietary sodium and 2 L/day of fluid will lessen congestion and decrease the need for diuretics. Patient education guidelines are listed in Box 1.
|Box 1: Patient Education Guidelines
|2-g Sodium diet|
|Monitoring weight daily|
|2-L Fluid restriction|
|Monitoring blood pressure|
|Light aerobic exercise|
|Knowing whom to call|
|Achieving ideal weight|
Cardiac rehabilitation can improve symptoms and exercise tolerance in patients with heart failure. This will also reduce or prevent skeletal muscle atrophy that could worsen exercise tolerance. Weight loss is encouraged in obese patients. Patients should be counseled about smoking cessation.
All patients with LV systolic dysfunction should be treated with an ACE inhibitor unless they have a contraindication or intolerance to the drug (stages B to D). ACE inhibitors are useful in preventing heart failure in patients at high risk who have atherosclerotic cardiovascular disease, diabetes mellitus, or hypertension with associated cardiovascular risk factors (stage A). ACE inhibitors and beta blockers should be used for all patients with a history of myocardial infarction, regardless of LVEF. Vasodilation and neurohormonal modulation with ACE inhibitors improve mortality, heart failure symptoms, exercise tolerance, and LVEF as well as reduce emergency room visits and hospitalizations.8–10
The dose of ACE inhibitors should be titrated to the maximum tolerated dose11 or the target dose as listed in Table 3. Approximately 10% to 20% of patients do not tolerate ACE inhibitors. The main side effect from ACE inhibition is a dry hacking cough, which can necessitate change to an angiotensin II receptor blocker (ARB). Most patients who cough on ACE inhibitors have this symptom because of congestive heart failure rather than ACE inhibitor intolerance and might improve with further diuresis. Two uncommon side effects of ACE inhibitors are angioedema and acute renal failure (in the setting of bilateral renal artery stenosis); both necessitate immediate cessation of the drug. ACE inhibitors should be used in combination with beta blockers in most patients. Either agent may be started first.
|Agent||Target Dose (mg)||Frequency|
* FDA-approved for treatment of heart failure.
ARBs block the effects of angiotensin II at the receptor level (Table 4). In clinical trials, these agents were found to be superior to placebo but no better than ACE inhibitors in improving mortality.12 ARBs are recommended as alternate therapy in patients who do not tolerate ACE inhibitors because of cough or angioedema (stages B to D). ARBs should not be substituted for ACE inhibitors in cases of hyperkalemia or renal dysfunction. ARBs may have some morbidity benefits for patients with diastolic heart failure.13
|Agent||Initial Dose (mg)||Maximum Dose (mg)|
* FDA-approved for treatment of heart failure.
Three beta blockers—carvedilol, metoprolol succinate (Toprol XL), and bisoprolol—have been shown to improve survival in patients with heart failure (Table 5).14–16 Metoprolol tartrate is not U.S Food and Drug Administration (FDA)-approved for heart failure and was less effective than carvedilol in preventing sudden death.17 The exact mechanism of beta blocker action is unclear, but it likely involves antiarrhythmic, anti-ischemic, antiremodeling, and antiapoptotic properties, as well as improved beta receptor pathway function. Myocardial oxygen consumption is reduced with beta blockers, primarily because of a reduction in heart rate.
|Beta Blocker||Initial Dose (mg)||Target Dose|
|Carvedilol*||3.125 mg bid||50 mg bid if >75 kg
25 mg bid if <75 kg
|Metoprolol succinate*||12.5 mg qd||200 mg qd|
|Bisoprolol||2.5 mg qd||10 mg qd|
* FDA-approved for treatment of heart failure.
All stable patients with reduced LVEF should receive a beta blocker unless it is contraindicated (stages B, C and D). Diabetes mellitus, chronic obstructive pulmonary disease, and peripheral arterial disease are not contraindications to beta blocker use, although patients with severe bronchospasm and hypotension might not tolerate the drug. Beta blockers may be used in stable NYHA Class IV patients who are euvolemic.2 In heart failure patients, a beta blocker should be initiated before hospital discharge or on an outpatient basis at a low dose and titrated slowly to target levels or maximally tolerated doses. Beta blockers usually are given in combination with an ACE inhibitor.
Digoxin is a neurohormonal modulating agent that inhibits the enzyme Na+/K+-ATPase in various organs. In cardiac cells, this inhibition increases myocardial contractility. In the central nervous system, it reduces sympathetic outflow, and in the kidney, it inhibits renin release. A large, randomized, controlled trial has shown that the use of digoxin reduces the rate of hospitalization for heart failure, but it does not reduce mortality.18 Digoxin is excreted by the kidneys, so dose adjustment is necessary in cases of renal failure (Table 6). A low dose of digoxin (0.125 mg daily) should be prescribed to most patients. Digoxin may be prescribed for patients with LV systolic dysfunction who remain symptomatic while receiving standard medical therapy, particularly if they are in atrial fibrillation.
|Agent||Initial Dose||Maximum Dose||Guidelines|
|Digoxin||0.125 mg qd||0.25 mg qd||Reduce dose in women, in renal dysfunction, and with amiodarone|
|Hydralazine||25 mg qid||100 mg qid||Use concurrently with nitrates|
|Isosorbide dinitrate||20 mg tid||80 mg tid||Also useful for angina pectoris|
|Spironolactone||25 mg qd||50 mg qd||Weak diuretic, risk of hyperkalemia, avoid in renal dysfunction; gynecomastia|
|Eplerenone||25 mg qd||50 mg qd||Risk of hyperkalemia, avoid in renal dysfunction; no gynecomastia|
Diuretics should be used in combination with an ACE inhibitor (or ARB) and a beta blocker. Most patients with heart failure have some degree of symptomatic congestion and benefit from diuretic therapy. Usually, a loop diuretic is required, with the addition of a thiazide diuretic in patients refractory to the loop diuretic alone (diuretic resistance or cardiorenal syndrome). Although useful for symptomatic relief, diuretics have not been shown to improve survival, and they can cause azotemia, hypokalemia, metabolic alkalosis, and elevation of neurohormone levels (Table 7).
|Generic Name||Class||Initial Dose (mg)||Special Considerations|
|Furosemide||Loop||20||Can be given intravenously; PO equivalent is twice the IV dose|
|Bumetanide||Loop||0.5||Good oral bioavailability; can be given intravenously; oral and IV doses are the same|
|Torsemide||Loop||5-10||Best oral availability|
|Ethacrynic acid||Loop||50||Only diuretic with no sulfhydryl group; used if allergic to furosemide|
|Hydrochlorothiazide||Thiazide||12.5||Weak diuretic; used mainly for hypertension|
|Metolazone||Thiazide||2.5||Give ½ hr before furosemide; only available orally; high risk of hypokalemia|
Two aldosterone antagonists have been approved for patients with heart failure: spironolactone and eplerenone. A 30% reduction in mortality and hospitalizations has been reported when spironolactone is added to standard therapy for patients with NYHA Class III or IV heart failure and a serum creatinine less than 2.5.19 A 15% reduction in the risk of death and hospitalization has been reported in patients who had NYHA Class II-IV heart failure and an LVEF lower than 40% after a myocardial infarction and who were treated with eplerenone.20
Aldosterone inhibition can prevent sodium and water retention, endothelial dysfunction, and myocardial fibrosis. With aldosterone antagonists, diligent monitoring of serum potassium levels is mandatory, because patients can develop hyperkalemia (see Table 6). These drugs should be avoided in patients with a creatinine level higher than 2.5 mg/dL. Eight percent of men develop gynecomastia with spironolactone but not with eplerenone. Recent clinical trial data demonstrated similar benefits in patients with mild heart failure. Therefore, the addition of an aldosterone antagonist is reasonable for select patients with mild to severe symptoms of heart failure and reduced LVEF who can be carefully monitored for preserved renal function and normal potassium concentration.
Hydralazine is an arterial dilator and nitrates are venous dilators. Hydralazine also prevents nitrate tachyphylaxis (loss of effect). The combination of hydralazine and nitrate is inferior to an ACE inhibitor in improving survival.21 Once-daily dosing of ACE inhibitors is easier than giving nitrates three times daily and giving hydralazine four times daily (see Table 6). The combination of hydralazine and nitrate is reasonable for patients who have current or prior symptoms of heart failure and reduced LVEF and who cannot be given an ACE or ARB because of drug intolerance, hyperkalemia, or renal insufficiency. Hydralazine and nitrates also may be added to ACE inhibitors and beta blockers when additional afterload reduction is needed or pulmonary hypertension is present.
Patients with known coronary artery disease should be treated with aspirin and a statin to lower the low-density lipoprotein level to 70 mg/dL. Calcium channel antagonists have been historically contraindicated in heart failure patients. However, dihydropyridine calcium channel blockers such as amlodipine have a neutral effect on heart failure and may be useful for treating concomitant hypertension or angina pectoris.22
The use of warfarin to prevent cardioembolic strokes remains controversial in the absence of atrial arrhythmias, because the risk appears to be relatively low (1% to 3% per year). Warfarin therapy is recommended for patients with atrial fibrillation or flutter, previous embolic events, cardiac thrombi, or LV aneurysms.
Specific therapies for treating atrial fibrillation, sleep apnea, anemia, obesity, and thyroid disease may improve the symptoms and functional limitations of heart failure.
Dobutamine (Table 8) enhances contractility by directly stimulating cardiac β1 receptors.23 Intravenous (IV) dobutamine infusions, sometimes guided by hemodynamic monitoring, may be useful for select patients with acute hypotensive heart failure or shock. The dose of dobutamine should always be titrated to the lowest dose compatible with hemodynamic stability to minimize adverse events. As with many inotropes, long-term infusions of dobutamine can increase mortality, principally because of its arrhythmogenic effect. As a result, chronic dobutamine infusions are reserved for palliative symptom relief or for patients who have an implantable cardioverter-defibrillator (ICD) and are awaiting heart transplantation. Intermittent outpatient infusions of dobutamine are not recommended for routine management of heart failure.
|Dobutamine||2-20 µg/kg/min||β receptor agonist; proarrhythmic; heart rate; ischemia|
|Milrinone||0.25-0.75 µg/kg/min||Phosphodiesterase inhibitor; vasodilator; may improve pulmonary hypertension; used for patients taking beta blockers; proarrhythmic|
|Nitroglycerin||10-500 µg/min||Anti-ischemic; vasodilator; limited by vascular headache; hypotension, tolerance develops rapidly|
|Nitroprusside||10-500 µg/min||Thiocyanate accumulation in renal failure; may provoke ischemia by coronary steal; vasodilator; should be given only in intensive care unit|
|Nesiritide||2-µg/kg bolus; then 0.01 µg/kg/min||Fixed weight-based dose; vasodilator; occasional hypotension|
Milrinone (see Table 8) is a phosphodiesterase inhibitor that enhances contractility. Milrinone is useful for patients with low-output heart failure and pulmonary hypertension because it is a more potent pulmonary vasodilator than dobutamine. Milrinone, in contrast to dobutamine, is also useful for patients on chronic oral beta blocker therapy who develop acute heart failure. The OPTIME (Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure) study, involving the routine IV infusion of milrinone for 48 hours during hospitalization for decompensated heart failure, failed to show clinical benefit and was associated with an increased risk of atrial arrhythmias and hypotension.24 Similar to dobutamine, intermittent outpatient milrinone infusions are not recommended for routine management of heart failure.
Nitroglycerin (see Table 8) is a nitric oxide donor that causes vasodilation. It is a venodilator at low doses and an arterial dilator at higher doses, lowering intracardiac pressures and alleviating pulmonary congestion.
Nitroglycerin also dilates coronary arteries, making it useful for patients with heart failure and myocardial ischemia. IV nitroglycerin requires dose titration to achieve therapeutic goals. The effectiveness of prolonged infusions is limited by the development of tachyphylaxis (loss of effect) within the first 24 hours.
Sodium nitroprusside (see Table 8) is a nitric oxide donor and a potent short-acting arterial and venous dilator. Nitroprusside infusions generally are reserved for patients in an intensive care unit. During nitroprusside infusions, patients should be converted to oral vasodilators such as ACE inhibitors, ARBs, or hydralazine and a nitrate.
Sodium nitroprusside should be infused for a short duration in patients with severe renal disease to prevent accumulation of thiocyanate, the by-product of hepatic metabolism of nitroprusside, which is excreted by the kidney. Nitroprusside should be avoided in patients with active ischemia because of its potential to cause coronary steal syndrome, which shunts blood away from the ischemic myocardium to well-perfused muscle.
Nesiritide (see Table 8), synthetic BNP, is an arterial and venous vasodilator with modest diuretic and natriuretic properties. Nesiritide increases cardiac output by afterload reduction without increasing heart rate or oxygen consumption. Routine use of nesiritide infusion for acute decompensated heart failure is not associated with an improvement in survival or a reduction in rehospitalization and so is not recommended.25 Intermittent outpatient infusions of nesiritide are also not recommended for the routine management of heart failure.
Several clinical trials have shown the potential benefit of CRT for patients with symptomatic heart failure and a wide QRS complex.26–28 Symptomatic improvement is achieved in approximately 70% of patients because of improved ventricular contraction, ventricular reverse-remodeling, and reduction of mitral regurgitation. It appears that patients with a QRS duration greater than 150 msec respond more favorably than those with lesser degrees of QRS prolongation. Recent clinical trial data indicate that patients with mild heart failure can also respond favorably to CRT. With CRT (biventricular pacing), a third electrode is implanted in a left-sided cardiac vein via the coronary sinus so that the right and left ventricles are paced in a synchronous fashion (Figure 3). Guidelines for resynchronization therapy are listed in Box 2.
|Box 2: Guidelines for Resynchronization Therapy|
|NYHA Class III or IV heart failure symptoms|
|Symptomatic despite medications|
|Left ventricular ejection fraction ≤35% (consider cardiac resynchronization therapy-defibrillator)|
|Wide QRS (>120 msec; left bundle branch block, intraventricular conduction delay)|
|Evidence of dyssynchrony|
Approximately 50% of patients with heart failure die suddenly. Implantation of an ICD can improve survival in certain subsets of heart failure patients and has been shown to be superior to antiarrhythmic drug therapy in preventing sudden death.29–31 Current indications for defibrillator therapy are listed in Box 3. CRT can be combined with an ICD as a single device if the patient meets criteria for both therapies, as is often the case.
|Box 3: Indications for an Implantable Cardioverter-Defibrillator|
|Cardiac arrest survivor|
|Sustained ventricular tachycardia|
|Inducible ventricular tachycardia|
|Ischemic cardiomyopathy*, LVEF ≤35%|
|Dilated cardiomyopathy†, LVEF ≤35% with symptoms|
* 40-day waiting period after myocardial infarction, stenting, bypass surgery.
† 3 to 9 month waiting period after diagnosis.
LVEF, left ventricular ejection fraction.
Ultrafiltration therapy is an effective method for extracting sodium and fluid from volume overloaded heart failure patients with resistance to diuretic therapy. A reduction in rehospitalization has been observed compared with IV diuretic therapy.32
Certain patients with end-stage heart failure and NYHA Class IV symptoms are referred to a tertiary care center for mechanical circulatory support.33 At present, LVADs are used either as a bridge to cardiac transplantation in patients who are appropriate transplantation candidates or as destination therapy in patients ineligible for transplantation. The inflow cannula of an LVAD is connected to the apex of the left ventricle. Blood is mechanically pumped by the device via the outflow cannula to the aorta (Figure 4). Complications following LVAD implantation are common and often life threatening; these include stroke, infection, coagulopathy, bleeding, and multisystem organ failure. Newer rotary continuous flow LVADs have proven to be more durable and are associated with fewer complications.34,35
Cardiac transplantation is reserved for otherwise healthy patients who have end-stage heart failure with severely impaired functional capacity despite optimal medical therapy (Figure 5). Patients are excluded from transplantation if they have chronic medical comorbidities, pulmonary hypertension, active infection, psychosocial contraindications, or medical noncompliance. Survival after cardiac transplantation is about 85% at 1 year, and median life expectancy is approximately 13 years. Complications limiting survival include rejection, infection, transplant coronary vasculopathy, and malignancy. Following cardiac transplantation, patients are subjected to lifelong immunosuppression to prevent rejection, which in turn renders them susceptible to various opportunistic infections and malignancies.
Patients classified as stage A are at high risk for heart failure but without structural heart disease or heart failure symptoms. They include patients with hypertension, diabetes mellitus, obesity, coronary artery disease, or use of cardiotoxins and those with a family history of cardiomyopathy. Preventive therapies include treatment of lipid disorders and hypertension, smoking cessation, regular exercise, avoidance of excess alcohol and illicit drugs, and ACE inhibitors in appropriate patients. Patients with stage B heart failure have structural heart disease, but no symptoms of heart failure. These include patients with previous myocardial infarction, LV systolic dysfunction, and asymptomatic valvular disease. Therapies are prescribed to prevent LV remodeling. These include all preventive strategies for stage A, as well as ACE inhibitors and beta blockers for appropriate patients.
Heart failure is slightly more common in women than men. In women, heart failure occurs later in life, is often related to hypertension, and is often associated with preserved LV systolic function. Women tend to have more prominent heart failure manifestations and more hospitalizations but better overall survival (except with coronary artery disease) than men. Heart failure therapeutic agents are not gender specific.
African Americans appear to benefit from a combination of hydralazine and nitrates when added to conventional heart failure therapy.36