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Hematology & Oncology Hepatology Infectious Disease Nephrology Neurology Preventive Medicine Psychiatry & Psychology Pulmonary Disease Rheumatology Women's Health DISEASE MANAGEMENT PROJECT MAIN Chapter Index Editorial Board Editorial Policy Text-based CME cases Disease Management Project Clinical Decisions Published: August 2010

Heart Failure
Robert Hobbs Andrew Boyle

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Definition and etiology Prevalence and risk factors Pathophysiology and natural history Signs and symptoms Diagnosis Treatment

Prevention and screening Considerations in special populations Summary References

Definition and etiology

doxorubicin. alcohol). Paget's disease. whereas in diastolic heart failure there is impaired cardiac relaxation and abnormal ventricular filling (Fig. In many patients. herceptin.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. pregnancy. arteriovenous fistulae. Other common causes of LV systolic dysfunction include idiopathic dilated cardiomyopathy. 1). most cases are a result of end-stage coronary artery disease. Back to Top Prevalence and risk factors . infiltrative. valvular heart disease. 2A). Figure 2: Click to Enlarge Right ventricular systolic dysfunction is usually a consequence of LV systolic dysfunction. 2B). yet viable. both processes are present simultaneously (Fig. toxin-induced cardiomyopathies (e. Other causes include restrictive. In this category. pulmonary hypertension. In systolic heart failure. or severe chronic anemia. myocardium. Inadequate filling of the right ventricle can result from pericardial constriction or cardiac tamponade.. Figure 1: Click to Enlarge The most common cause of heart failure is left ventricular (LV) systolic dysfunction (about 60% of patients). and hypertrophic cardiomyopathies. or arrhythmogenic right ventricular dysplasia. It can also develop as a result of right ventricular infarction. there is reduced cardiac contractility. and congenital heart disease (seeFig. This may be further subdivided into systolic or diastolic heart failure. Diastolic LV dysfunction (impaired relaxation) usually is related to chronic hypertension or ischemic heart disease. either with a history of myocardial infarction or with a chronically underperfused. chronic severe tricuspid regurgitation. A less-common cause of heart failure is high-output failure caused by thyrotoxicosis. hypertensive heart disease.g.

particularly in patients with New York Heart Association (NYHA) Class IV symptoms. valvular regurgitation. The sympathetic nervous system increases heart rate and contractility. approximately 2% of the population. An increased aldosterone level. coronary artery disease. catecholamines aggravate ischemia.Heart failure is a common syndrome. potentiate arrhythmias. in turn. causing reabsorption of water in the renal collecting duct. 1 Patients at high risk for developing heart failure are those with hypertension. and another 2 million patients have heart failure as a secondary diagnosis. and organ fibrosis. promote cardiac remodeling. endothelial dysfunction. Some patients die from end-organ failure resulting from inadequate systemic organ perfusion. hypocholesterolemia. and are directly toxic to myocytes. Currently. Although these neurohormonal pathways initially are compensatory . 5 million Americans are afflicted with heart failure. and stimulates secretion of renin from the juxtaglomerular apparatus of the kidney. cachexia. the body activates several neurohormonal pathways to increase circulating blood volume. Stimulation of the renin-angiotensin system as a result of increased sympathetic stimulation and decreased renal perfusion results in further arteriolar vasoconstriction. most have at least some residual LV systolic dysfunction. Patients with combined systolic and diastolic LV dysfunction also have a worse prognosis than patients with either in isolation. and obesity. family history of cardiomyopathy. especially in older adults. sodium and water retention. low serum sodium level. which can lead to heart failure. In heart failure. Back to Top Pathophysiology and natural history Although much progress has been made in the treatment of heart failure. use of cardiotoxins. One third of these patients are readmitted within 90 days for recurrent decompensation. and marked LV dilation. particularly to the kidneys. there is a high overall annual mortality (5%20%). although one half die from sudden cardiac death. baroreceptor and osmotic stimuli lead to vasopressin release from the hypothalamus. diabetes mellitus. ventricular arrhythmias. lower LV ejection fraction (LVEF). Although more patients survive acute myocardial infarction because of reperfusion therapy. 3 2 In LV systolic dysfunction. leads to sodium and water retention. Many patients succumb to progressive pump failure and congestion. Indicators of poor cardiac prognosis include renal dysfunction. Unfortunately. high catecholamine and B-type natriuretic peptide (BNP) levels. higher NYHA heart failure class. causes arteriolar vasoconstriction in nonessential vascular beds. Patients with heart failure account for about 1 million hospital admissions annually. and release of aldosterone.

possible enhancement of sodium and water excretion. and neurohormonal modulation is the basis for modern treatment of heart failure. Stage B includes patients with structural heart disease but no symptoms. With continuous neurohormonal stimulation. digoxin. In contrast. and suppression of other neurohormones. As a result. Diuretics. worsens subendocardial myocardial perfusion. Furthermore. and can provoke ischemia in patients with coronary atherosclerosis. and aldosterone antagonists may be added to angiotensin-converting enzyme (ACE) 4 . the primary abnormality is impaired LV relaxation. This is achieved by myocyte hypertrophy and elongation. patients are often symptomatic with exertion when increased heart rate reduces LV filling time and circulating catecholamines worsen diastolic dysfunction. causing high diastolic pressures and poor filling of the ventricle. Stage C includes patients with structural heart disease with current or prior symptomatic heart failure. LV chamber dilation causes increased wall tension. natriuretic peptides are hormones released by secretory granules in cardiac myocytes in response to myocardial stretching. Stage A includes patients who are at risk for developing heart failure but who have no structural heart disease at present. They have a beneficial influence in heart failure. In diastolic dysfunction. The management goal is prevention of LV remodeling leading to heart failure. such that stroke volume is increased without an actual increase in EF. dilation of the LV chamber can cause mitral annular dilatation and mitral regurgitation. the left ventricle undergoes remodeling consisting of LV dilation and hypertrophy. leading to pulmonary congestion. left atrial and pulmonary capillary pressures increase and pulmonary edema ensues. The management strategy in this group is prevention of heart failure.and beneficial. eventually they are deleterious.++ - +-* 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). To increase diastolic filling. including systemic and pulmonary vasodilation.



Cardiac resynchronization therapy also may be considered. Table 1: American College of Cardiology–American Heart Association Classification of Chronic Heart Failure Stage A****++ Description Hypertension. depending on the severity of symptoms. Physicians should consider either end-oflife care or high-technology therapies such as cardiac transplantation or mechanical circulatory support. diabetes mellitus.inhibitors and beta blockers. based on individual cases. family history of cardiomyopathy . Stage D includes patients with severe refractory heart failure. CAD.


climbing one flight of stairs) IV Dyspnea at rest or with very little exertion On physical examination. with bilateral inspiratory rales. effort intolerance. and paroxysmal nocturnal dyspnea. They often are pale and diaphoretic.g. coronary artery disease. do not have congestive symptoms but have signs and symptoms of low cardiac output. including fatigue. Most patients have signs and symptoms of fluid overload and pulmonary congestion. and renal hypoperfusion. and ascites.. MI. orthopnea. impaired exercise tolerance Marked symptoms at rest despite maximal medical therapy CAD. Others. long-distance walking. Patients with right ventricular failure have jugular venous distention. peripheral edema.: High risk for developing heart failure B: Asymptomatic heart failure C: Symptomatic heart failure D: Refractory end-stage heart failure Previous MI. An S 3 and often an S4 gallop will be present. hepatosplenomegaly. left ventricular. climbing two flights of stairs) III Exercise limited by dyspnea with moderate workload (e. patients with decompensated heart failure may be tachycardic and tachypneic. dyspnea and fatigue. Murmurs of . valvular heart disease Structural heart disease. jugular venous distention. The NYHA functional classification scheme is used to assess the severity of functional limitations and correlates fairly well with prognosis (Table 2). including dyspnea. however. short-distance walking. LV dysfunction. LV. 5 Table 2: New York Heart Association (NYHA) Heart Failure Symptom Classification System NYHA Level of Impairment Class I II No symptom limitation with ordinary physical activity Ordinary physical activity somewhat limited by dyspnea (e.. cachexia. and edema. Back to Top Signs and symptoms There is a wide spectrum of potential clinical manifestations of heart failure.g. myocardial infarction. The first heart sound usually is relatively soft if the patient is not tachycardic.

and nonspecific ST-segment and T wave changes support a diagnosis of heart failure. In many cases. and infiltrative cardiomyopathies. whereas global dysfunction suggests a nonischemic cause. Kerley B lines. the exact cause of the heart failure cannot be discerned from the echocardiogram. Paradoxical splitting of S2 may be present because of delayed mechanical or electrical activation of the left ventricle. with a goal of revascularization. Q waves in contiguous leads strongly implicate a previous myocardial infarction and coronary atherosclerosis as the cause. Cardiac catheterization can detect coronary atherosclerosis as the cause of heart failure. and BNP assay. Patients with compensated heart failure will likely have clear lungs but a displaced cardiac apex. If systolic dysfunction is present. Echocardiography is helpful in determining other causes. A peak oxygen . Objective information about functional capacity can be obtained from metabolic (cardiopulmonary) exercise testing. if found. Back to Top Diagnosis The initial evaluation of new-onset heart failure should include an electrocardiogram. severity of hypertrophy. should lead to an assessment of myocardial viability. and pleural effusions.mitral or tricuspid regurgitation may be heard. which can distinguish between systolic and diastolic dysfunction. Patients with decompensated diastolic dysfunction usually have a loud S4(which may be palpable). however. Echocardiography can also provide meaningful prognostic information about diastolic function. and valvular abnormalities. cardiac tamponade. pulmonary vascular redistribution. myocardial viability. such as valvular heart disease. left bundle branch block. EK6 findings of LV hypertrophy. and provides useful clues about infiltrative and restrictive cardiomyopathies. alveolar edema. rales. This test can distinguish ventilatory from cardiac limitations in patients with exertional dyspnea. Coronary computed tomographic angiography (CTA) might also be a suitable alternative to exclude coronary artery disease in select patients. pulmonary venous congestion. Chest radiographic findings of heart failure include cardiomegaly. chest radiograph. or pericardial constriction. regional wall motion abnormalities or LV aneurysm suggest an ischemic basis for heart failure. Magnetic resonance imaging (MRI) is useful in assessing for arrhythmogenic right ventricular dysplasia. The single most useful diagnostic test is the echocardiogram. Severe coronary artery disease is so prevalent that coronary angiography routinely should be performed to exclude this cause and. and often systemic hypertension. chamber size. intraventricular conduction delay.

Back to Top Summary      Jugular venous distention is a useful physical sign of heart failure. Echocardiography is the single most useful diagnostic modality. Box 1: Patient Education Guidelines 2-g Sodium diet Monitoring weight daily 2-L Fluid restriction . 6.consumption higher than 25 mL/kg/min is normal for middle-age adults. This blood test may be useful for distinguishing heart failure from pulmonary disease. However. Because smokers often have both these clinical diagnoses. invasive hemodynamic monitoring may be warranted if unanticipated responses to therapies are observed or for diagnostic purposes if the diagnosis is uncertain. 7 BNP levels correlate with severity of heart failure and decrease as a patient reaches a compensated state. The lungs usually are clear in chronic heart failure. Patient education guidelines are listed in Box 1. Back to Top Treatment Lifestyle Modifications Dietary sodium and fluid restrictions should be implemented in all patients with congestive heart failure. differentiating between them may be challenging. Coronary angiography confirms or excludes coronary artery disease as the cause. but a value lower than 14 mL/kg/min indicates severe cardiac limitation and poor prognosis. The routine use of invasive hemodynamic monitoring to guide the management of decompensated heart failure has not proved to be beneficial. Limiting patients to 2 g/day of dietary sodium and 2 L/day of fluid will lessen congestion and decrease the need for diuretics. A useful diagnostic test for the detection of heart failure is the BNP assay. The BNP assay improves the accuracy of diagnosing heart failure.

ACE inhibitors are useful in preventing heart failure in patients at high risk who have atherosclerotic cardiovascular disease. which can necessitate change to an angiotensin II receptor blocker (ARB). exercise tolerance. or hypertension with associated cardiovascular risk factors (stage A). 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. ACE inhibitors and beta blockers should be used for all patients with a history of myocardial infarction. Medical Options Angiotensin-Converting Enzyme Inhibitors 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). heart failure symptoms.Monitoring blood pressure Medications Smoking cessation Light aerobic exercise Knowing whom to call Achieving ideal weight Follow-up visits 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. Table 3: Angiotensin-Converting Enzyme Inhibitor Dosing Agent Target Dose (mg) Frequency . both necessitate immediate cessation of the drug. Weight loss is encouraged in obese patients. The main side effect from ACE inhibition is a dry hacking cough. Patients should be counseled about smoking cessation. diabetes mellitus. Vasodilation and neurohormonal modulation with ACE inhibitors improve mortality. and LVEF as well as reduce emergency room visits and hospitalizations. Approximately 10% to 20% of patients do not tolerate ACE inhibitors. Two uncommon side effects of ACE inhibitors are angioedema and acute renal failure (caused by bilateral renal artery stenosis). regardless of LVEF. 8-10 The dose of ACE inhibitors should be titrated to the maximum tolerated dose 11 or the target dose as listed in Table 3.

Captopril* Enalapril* Lisinopril* Ramipril* Quinapril* Fosinopril* Benazepril* Trandolapril† * 50 20 40 5 20 20 20 4 tid bid qd bid bid bid qd qd FDA-approved for treatment of heart failure. † ACE inhibitors should be used in combination with beta blockers in most patients. In clinical trials. ARBs may have morbidity benefits for patients with diastolic heart failure. 12 ARBs are recommended as second-line therapy in patients who do not tolerate ACE inhibitors because of cough or angioedema (stages B to D). these agents were found to be superior to placebo but no better than ACE inhibitors in improving mortality. Angiotensin Receptor Blockers ARBs block the effects of angiotensin II at the receptor level (Table 4). 13 Table 4: Angiotensin Receptor Blocker Dosing Agent Valsartan* Candesartan* Losartan Irbesartan Telmisartan Eprosartan Olmesartan Initial Dose (mg) 80 4 25 75 40 400 20 Maximum Dose (mg) 320 32 100 300 80 800 40 . FDA-approved for treatment of post–myocardial infarction heart failure. Either agent may be started first. ARBs should not be substituted for ACE inhibitors in cases of hyperkalemia or renal dysfunction.

A large. but it does not reduce mortality. and bisoprolol —have been shown to improve survival in patients with heart failure (Table 5). 14-16 Metoprolol tartrate is not U. it inhibits renin release. metoprolol succinate (Toprol XL). but it likely involves antiarrhythmic. and peripheral arterial disease are not contraindications to beta blocker use. controlled trial has shown that the use of digoxin reduces the rate of hospitalization for heart failure.S Food and Drug Administration (FDA)17 approved for heart failure and was less effective than carvedilol in preventing sudden death.5 mg qd 2. Diabetes mellitus. Table 5: Beta Blocker Dosing Beta Blocker Carvedilol* Initial Dose (mg) 3. 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. as well as improved beta receptor pathway function. anti-ischemic. randomized. In the central nervous system. this inhibition increases myocardial contractility. Beta blockers may be used in stable NYHA Class IV patients who are euvolemic. but either agent may be initiated first. and antiapoptotic properties. so dose adjustment is necessary in cases of renal failure (Table 6). In heart failure patients. All stable patients with reduced LVEF should receive a beta blocker unless it is contraindicated (stages B. and in the kidney. Myocardial oxygen consumption is reduced with beta blockers. it reduces sympathetic outflow. Beta Blockers Three beta blockers—carvedilol.125 mg bid Target Dose 50 mg bid if >75 kg 25 mg bid if <75 kg Metoprolol succinate* Bisoprolol * 12. C and D). The exact mechanism of beta blocker action is unclear. A low dose of digoxin (0. primarily because of a reduction in heart rate. antiremodeling. 2 Digoxin Digoxin is a neurohormonal modulating agent that inhibits the enzyme Na /K -ATPase in various organs. although patients with severe bronchospasm and hypotension might not tolerate the drug.125 mg daily) .* FDA-approved for treatment of heart failure. In cardiac cells. chronic obstructive pulmonary disease. 18 + + Digoxin is excreted by the kidneys.5 mg qd 200 mg qd 10 mg qd FDA-approved for treatment of heart failure. Beta blockers usually are given in combination with an ACE inhibitor.

gynecomastia Eplerenone 25 mg qd 50 mg qd Risk of hyperkalemia. risk of hyperkalemia. avoid in renal dysfunction. metabolic alkalosis. diuretics have not been shown to improve survival. no gynecomastia 25 mg qid 20 mg tid 100 mg qid 80 mg tid Use concurrently with nitrates to prevent coronary steal Also useful for angina pectoris 0. Digoxin may be prescribed for patients with LV systolic dysfunction who remain symptomatic while receiving standard medical therapy. Most patients with heart failure have some degree of symptomatic congestion and benefit from diuretic therapy. Table 6: Other Heart Failure Drugs Maximum Agent Initial Dose Dose Digoxin 0. oral and IV doses are the same Torsemide Ethacrynic acid Loop Loop 5-10 50 Best oral availability Only diuretic with no sulfhydryl group. Although useful for symptomatic relief. Table 7: Diuretic Dosing Initial Dose Generic Name Class (mg) Furosemide Bumetanide Loop Loop 20 0. particularly if they are in atrial fibrillation. can be given intravenously.should be prescribed to most patients. a loop diuretic is required. with amiodarone Guidelines Diuretics Diuretics should be used in combination with an ACE inhibitor (or ARB) and a beta blocker.25 mg qd Reduce dose in women with renal dysfunction. used if allergic to furosemide Special Considerations .125 mg qd Hydralazine Isosorbide dinitrate Spironolactone 25 mg qd 50 mg qd Weak diuretic. avoid in renal dysfunction.5 Can be given intravenously. hypokalemia. and they can cause azotemia. and elevation of neurohormone levels (Table 7). with the addition of a thiazide diuretic in patients refractory to the loop diuretic alone (diuretic resistance or cardiorenal syndrome). 19 Usually. PO equivalent is twice the IV dose Good oral bioavailability.

5. the addition of an aldosterone antagonist is reasonable for select patients with moderately severe to severe symptoms of heart failure and reduced LVEF who can be carefully monitored for preserved renal function and normal potassium concentration. Calcium channel antagonists have not been proved beneficial in heart failure . 21 Aldosterone inhibition can prevent sodium and water retention. Oncedaily dosing of ACE inhibitors is easier than giving nitrates three times daily and giving hydralazine four times daily (see Table 6).5 Weak diuretic. only available orally.5 mg/dL. Hydralazine also prevents nitrate tachyphylaxis (loss of effect).5 2. 22 Other Medical Therapies Patients with known coronary artery disease should be treated with aspirin and a statin to lower the low-density lipoprotein (LDL) level to 70 mg/dL. A fixed-dose combination tablet has been approved for treating heart failure in African Americans. 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. The combination of hydralazine and nitrate is inferior to an ACE inhibitor in improving survival.Hydrochlorothiazide Metolazone Thiazide Thiazide 12. With aldosterone antagonists. because patients can develop hyperkalemia (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. used mainly for hypertension Give /2 hr before furosemide. and so these drugs should be reserved for patients with moderately severe to severe heart failure. 20 A 15% reduction in the risk of death and hospitalization has been reported in patients who had heart failure and an LVEF lower than 40% after a myocardial infarction and who were treated with eplerenone. Hydralazine and Nitrates Hydralazine is an arterial dilator and nitrates are venous dilators. Data from studies of mild heart failure are lacking. These drugs should be avoided in patients with a creatinine level higher than 2. or renal insufficiency. Hydralazine and nitrate also may be added to ACE inhibitors and beta blockers when additional afterload reduction is needed or pulmonary hypertension is present. hyperkalemia. and myocardial fibrosis. high risk of hypokalemia 1 Aldosterone Antagonists Two aldosterone antagonists have been approved for patients with heart failure: spironolactone and eplerenone. diligent monitoring of serum potassium levels is mandatory. Therefore. Eight percent of men develop gynecomastia with spironolactone but not with eplerenone. endothelial dysfunction.

Specific therapies for treating atrial fibrillation. limited by vascular headache.75 µg/kg/min Special Considerations β receptor agonist. may provoke ischemia by coronary steal. and thyroid disease may improve the symptoms and functional limitations of heart failure. occasional hypotension Milrinone . 24 Intravenous (IV) dobutamine infusions. 23 The use of warfarin to prevent cardioembolic strokes remains controversial in the absence of atrial arrhythmias. anemia.01 µg/kg/min Fixed weight-based dose. ischemia Phosphodiesterase inhibitor. tolerance develops rapidly Nitroprusside 10-500 µg/min Thiocyanate accumulation in renal failure. vasodilator. The dose of dobutamine should always be titrated to the lowest dose compatible with hemodynamic stability to minimize adverse events. Dihydropyridines such as amlodipine have a neutral effect on heart failure and may be useful for treating concomitant hypertension or angina pectoris. chronic dobutamine infusions are reserved for palliative symptom relief or for patients who have an implantable cardioverter-defibrillator (ICD) and are awaiting heart transplantation. heart rate. then 0. As a result. should be given only in intensive care unit Nesiritide 2-µg/kg bolus. hypotension. cardiac thrombi. because the risk appears to be relatively low (1%-3% per year). may improve pulmonary hypertension. used for patients taking beta blockers. long-term infusions of dobutamine can increase mortality.patients. vasodilator. sleep apnea. may be useful for select patients with acute hypotensive heart failure or shock. Intravenous Inotropes and Vasodilators Dobutamine Dobutamine (Table 8) enhances contractility by directly stimulating cardiac β1 receptors. previous embolic event. vasodilator. or LV aneurysms. proarrhythmic. Intermittent outpatient infusions of dobutamine are not recommended for routine management of heart failure. obesity. As with many inotropes. sometimes guided by hemodynamic monitoring. Warfarin therapy is recommended for patients with atrial arrhythmias. Table 8: Intravenous Agents Used for Treatment of Heart Failure Drug Dobutamine Milrinone Dose 2-20 µg/kg/min 0. proarrhythmic Nitroglycerin 10-500 µg/min Anti-ischemic. principally because of its arrhythmogenic effect.25-0. vasodilator.

Sodium Nitroprusside Sodium nitroprusside (see Table 8) is a nitric oxide donor and a potent short-acting arterial and venous dilator. The effectiveness of prolonged infusions is limited by the development of tachyphylaxis (loss of effect) within the first 24 hours. The OPTIME (Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure) study. the by-product of hepatic metabolism of nitroprusside. which is excreted by the kidney. which shunts blood away from the ischemic myocardium to well-perfused muscle. During nitroprusside infusions. Figure 3: Click to Enlarge . Nitroprusside should be avoided in patients with active ischemia because of its potential for coronary steal syndrome. 25 Similar to dobutamine. intermittent outpatient milrinone infusions are not recommended for routine management of heart failure. failed to show clinical benefit and was associated with an increased risk of atrial arrhythmias and hypotension.Milrinone (see Table 8) is a phosphodiesterase inhibitor that enhances contractility. Nitroprusside infusions generally are reserved for patients in an intensive care unit. in contrast to dobutamine. IV nitroglycerin requires dose titration to achieve therapeutic goals. ARBs. making it useful for patients with heart failure and myocardial ischemia. Milrinone is useful for patients with low-output heart failure and pulmonary hypertension because it is a more potent pulmonary vasodilator than dobutamine. Sodium nitroprusside should be infused for a short duration in patients with severe renal disease to prevent accumulation of thiocyanate. Milrinone. lowering intracardiac pressures and alleviating pulmonary congestion. Nitroglycerin also dilates coronary arteries. Nitroglycerin Nitroglycerin (see Table 8) is a nitric oxide donor that causes vasodilation. or hydralazine and a nitrate. is also useful for patients on chronic oral beta blocker therapy who develop acute heart failure. patients should be converted to oral vasodilators such as ACE inhibitors. involving the routine intravenous infusion of milrinone for 48 hours during hospitalization for decompensated heart failure. It is a venodilator at low doses and an arterial dilator at higher doses.

26 Nesiritide increases cardiac output by afterload reduction without increasing heart rate or oxygen consumption.Nesiritide Nesiritide (see Table 8). as is often the case. synthetic BNP. 27. and reduction of mitral regurgitation. a third electrode is implanted in a left cardiac vein via the coronary sinus so that the right and left ventricles are paced in a synchronous fashion (Fig. 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. Optimal synchronization of atrial and ventricular contraction is achieved with echocardiographic guidance. 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. Nesiritide is administered as a weight-based bolus followed by continuous IV infusion in patients who have acutely decompensated heart failure and who have dyspnea at rest or with minimal activity. 29-32 Current indications for defibrillator therapy are listed in Box 3. It may be started in the emergency department and does not require invasive hemodynamic monitoring or frequent titration. It modulates the vasoconstrictor and sodium-retaining effects of other neurohormones. Device Therapies for Heart Failure Cardiac Resynchronization Therapy Several clinical trials have shown the potential benefit of cardiac resynchronization therapy (CRT) for patients with severe symptomatic heart failure and a wide QRS complex. 3). Cardiac resynchronization therapy can be combined with an ICD as a single device if the patient meets criteria for both therapies. Guidelines for resynchronization therapy are listed in Box 2. is an arterial and venous vasodilator with modest diuretic and natriuretic properties. Intermittent outpatient infusions of nesiritide are not recommended for the routine management of heart failure. Tolerance to the drug does not occur and it is not arrhythmogenic. ventricular reverse-remodeling. . 28 Symptomatic improvement is achieved in approximately 70% of patients because of improved ventricular contraction. With cardiac resynchronization therapy (biventricular pacing). intraventricular conduction delay) Evidence of dyssynchrony Defibrillator Therapy Approximately 50% of patients with heart failure die suddenly. left bundle branch block.

left ventricular ejection fraction. LVEF ≤35% with symptoms * 40-day waiting period after myocardial infarction.Box 3: Indications for an Implantable Cardioverter-Defibrillator Cardiac arrest survivor Sustained ventricular tachycardia Inducible ventricular tachycardia Ischemic cardiomyopathy. † 9-month waiting period after diagnosis. LV assist devices (LVADs) are used either as a bridge to cardiac transplantation in patients who are appropriate transplantation candidates or as destination therapy in patients . A reduction in rehospitalization has been observed compared with intravenous diuretic therapy. * LVEF ≤35% Dilated cardiomyopathy†. bypass surgery. Ultrafiltration Therapy Ultrafiltration therapy is an effective method for extracting sodium and fluid from volume overloaded heart failure patients with resistance to diuretic therapy. 33 Figure 4: Click to Enlarge Surgical Options Left Ventricular Assist Devices (LVADs) Certain patients with end-stage heart failure and NYHA Class IV symptoms are referred to a tertiary care center for mechanical circulatory support. 35 At present. stenting. 34. LVEF.

and multisystem organ failure. infection. and epicardial LV pacing lead placement (Fig. has been performed for heart failure secondary to ischemic cardiomyopathy. Survival after cardiac transplantation is about 85% at 1 year. which in turn renders them susceptible to various opportunistic infections and malignancies. 36 Ventricular Reconstruction Surgery Ventricular reconstruction surgery. 6). Figure 5: Click to Enlarge Cardiac Transplantation Cardiac transplantation is reserved for otherwise healthy patients who have end-stage heart failure with severely impaired functional capacity despite optimal medical therapy (Fig. also called ventricular remodeling surgery or a Dor procedure. Complications limiting survival include rejection. psychosocial contraindications. these include stroke. 4). active infection. The STICH trial failed to show benefit over standard bypass or value surgery. and malignancy. Following cardiac transplantation. The inflow cannula of an LVAD is connected to the apex of the left ventricle. Back to Top Summary . 37 It consists of several components: coronary artery bypass grafting. pulmonary hypertension. 5). Blood is mechanically pumped by the device via the outflow cannula to the aorta (Fig. 38 Patients are excluded from transplantation if they have chronic medical comorbidities. and median life expectancy is approximately 10 years. reshaping the left ventricle from a spherical to an elliptic shape. Complications following LVAD implantation are common and often life threatening.ineligible for transplantation. resection of LV scar or aneurysm. transplant coronary vasculopathy. Newer rotary continuous flow LVADs have proven to be more durable and are associated with fewer complications. mitral and tricuspid valve repair. the future of ventricular reconstruction surgery is uncertain. infection. perioperative coagulopathy and bleeding. Thus. or medical noncompliance. patients are subjected to lifelong immunosuppression to prevent rejection.

is often related to hypertension. LV systolic dysfunction.     All heart failure patients should receive an ACE inhibitor and a beta blocker. Therapies are prescribed to prevent LV remodeling. Back to Top Prevention and screening Patients classified as stage A are at high risk for heart failure but without structural heart disease or heart failure symptoms. coronary artery disease. Diuretics are needed in most patients to manage fluid retention. Figure 6: Click to Enlarge Back to Top Considerations in special populations Heart failure is slightly more common in women than men. obesity. regular exercise. Patients with stage B heart failure have structural heart disease. smoking cessation. In women. diabetes mellitus. Digoxin is reserved for patients with signs and symptoms of heart failure. These include all preventive strategies for stage A. and asymptomatic valvular disease. Preventive therapies include treatment of lipid disorders and hypertension. avoidance of excess alcohol and illicit drugs. but no symptoms of heart failure. These include patients with previous myocardial infarction. as well as ACE inhibitors and beta blockers for appropriate patients. heart failure occurs later in life. and is often associated with preserved LV systolic function. Aldosterone antagonists are used in patients with Class III or IV heart failure. and ACE inhibitors in appropriate patients. They include patients with hypertension. or use of cardiotoxins and those with a family history of cardiomyopathy. ARBs or a hydralazine plus nitrate may be added to standard therapy for additional benefit. Women tend to have more prominent .

. Packer M. Mueller C. Heart failure therapeutic agents are not gender specific. Coats AJ. 2004. Swedberg K. SOLVD Investigators. et al: Effect of carvedilol on survival in severe chronic heart failure. Abraham WT. 112: e154-e235. 350: 647-654. 2001. 37: 1049-1055. N Engl J Med. et al: Prognostic value of Doppler echocardiographic mitral inflow patterns: Implications for risk stratification in patients with chronic congestive heart failure. American College of Chest Physicians. 344: 1651-1658. Dao Q.ahajournals. J Am Coll Cardiol.heart failure manifestations and more hospitalizations but better overall survival (except with coronary artery disease) than men. 2005. Eur Heart J. 7. Heart Rhythm Society: ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: Endorsed by the Heart Rhythm Society. 8. 4. Heart Disease and Stroke Statistics—2008 Update. Hansen A. et al: Utility of B-type natriuretic peptide in the diagnosis of congestive heart failure in an urgent-care setting. 39 Back to Top References 1. Kazanegra R. African Americans appear to benefit from a combination of hydralazine and nitrates when added to conventional heart failure therapy. 26: 1115-1140. 37: 379-385. 3. Haass M. Scholer A. Circulation. 2001. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure (SOLVD). Cleland J. N Engl J Med. N Engl J Med. 6. Krishnaswamy P. http://circ. American Heart Association. Chin MH. Zugck C. American Heart Association Task Force on Practice Guidelines. et al: Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. International Society for Heart and Lung Transplantation. 325: 293-302.org 2. 5. Dargie H. et al: Guidelines for the diagnosis and treatment of chronic heart failure: Executive summary (Update 2005). 2001. Fowler MB. 2008. 2005. 1991. Laule-Kilian K. Dallas: American Heart Association. J Am Coll Cardiol. Hunt SA. et al: American College of Cardiology.

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JAMA. Chin MH. N Engl J Med. 2004. 352: 1539-1549. Goldstein S. Remme W.  Hjalmarson A. and well-being in patients with heart failure: The Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). Mark DB. International Society for Heart and Lung Transplantation. American Heart Association Task Force on Practice Guidelines.  Bardy GH. 2005. 1998. Erdman E. N Engl J Med. . 2006. Cohn JN.  American Heart Association. 2008. Back to Top Suggest Readings  Adams KF. 1997. N Engl J Med. 352: 225-237. Heart Disease and Stroke Statistics-2008 Update. Scholer A. Lindenfeld J. N Engl J Med. Laule-Kilian K. 2005. hospitalizations. The effect of digoxin on mortality and morbidity in patients with heart failure. Tam W. Circulation. Zannad F. N Engl J Med. 13: 331-339. Anard IS. 350: 647-654. Abraham WT.   Brater DC. Dallas: American Heart Association. et al: American College of Cardiology. 339: 387-395.39. et al: Executive summary: HFSA 2006 comprehensive heart failure practice guideline. 336: 525-533. 2000. et al: Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. Cleland JGF. N Engl J Med. J Cardiac Failure. 348: 1309-1321. in patients with left ventricular dysfunction after myocardial infarction.  Digitalis Investigation Group.  Hunt SA. Daubert JC. American College of Chest Physicians. et al: Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. J Cardiac Fail. 2007. et al: The effect of cardiac resynchronization on morbidity and mortality in heart failure. a selective aldosterone blocker. 2005.  Pitt B. et al: Eplerenone. 112: e154-e235. Arnold JMO. 283: 1295-1302. 12: 10-38. Fagerberg B. 2003.  Mueller C. Diuretic therapy. Heart Rhythm Society: ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: Endorsed by the Heart Rhythm Society. et al: Isosorbide dinitrate and hydralazine in a fixed-dose combination produces further regression of left ventricular remodeling in a well-treated block population with heart failure: Results from A-HeFT. et al: Effects of controlled-release metoprolol on total mortality. Lee KL.

Randomized Aldactone Evaluation Study Investigators. Pitt B. Eur Heart J. N Engl J Med. Cleland J. et al: The effect of spironolactone on morbidity and mortality in patients with severe heart failure. KK31. Cleveland. Dargie H. 341: 709717. Center for Continuing Education | 9500 Euclid Avenue. 2005. Remme WJ. Copyright © 2000-2013 The Cleveland Clinic Foundation. et al: Guidelines for the diagnosis and treatment of chronic heart failure: Executive summary (Update 2005). All Rights Reserved. OH 44195        Main Cleveland Clinic Website Accreditation with Commendation Awards Site Disclaimer Privacy Policy Feedback Sitemap . 1999.  Swedberg K. Zannad F. 26: 1115-1140.

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