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Heart FailureRobert Hobbs

Andrew Boyle

Definition and etiology

Heart failure is a clinical syndrome characterized by systemic perfusion inadequate to meet the body's metabolicdemands as a result of impaired cardiac pump function. This may be further subdivided into systolic or diastolicheart failure. In systolic heart failure, there is reduced cardiac contractility, whereas in diastolic heart failurethere is impaired cardiac relaxation and abnormal ventricular filling (Fig. 1).

The most common cause of heart failure is left ventricular (LV) systolic dysfunction (about 60% of patients). Inthis category, most cases are a result of end-stage coronary artery disease, either with a history of myocardialinfarction or with a chronically underperfused, yet viable, myocardium. In many patients, both processes arepresent simultaneously (Fig. 2A). Other common causes of LV systolic dysfunction include idiopathic dilatedcardiomyopathy, valvular heart disease, hypertensive heart disease, toxin-induced cardiomyopathies (e.g.,doxorubicin, herceptin, alcohol), and congenital heart disease (see Fig. 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 causedby thyrotoxicosis, arteriovenous fistulae, Paget's disease, pregnancy, or severe chronic anemia.

Diastolic LV dysfunction (impaired relaxation) usually is related to chronic hypertension or ischemic heartdisease. Other causes include restrictive, infiltrative, and hypertrophic cardiomyopathies. Inadequate filling of the right ventricle can result from pericardial constriction or cardiac tamponade.

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Prevalence and r isk factors

Heart failure is a common syndrome, especially in older adults. Although more patients survive acutemyocardial infarction because of reperfusion therapy, most have at least some residual LV systolic dysfunction,which can lead to heart failure. Currently, 5 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, andanother 2 million patients have heart failure as a secondary diagnosis. One third of these patients are readmittedwithin 90 days for recurrent decompensation.

Patients at high risk for developing heart failure are those with hypertension, coronary artery disease, diabetesmellitus, family history of cardiomyopathy, use of cardiotoxins, and obesity.

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Pathophysiology and natural history

Al though much progress has been made in the treatment of heart failure, there is a high overall annual mortali ty

(5%-20%), particularly in patients with New York Heart Association (NYHA) Class IV symptoms.2 Many

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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 thekidneys. Indicators of poor cardiac prognosis include renal dysfunction, cachexia, valvular regurgitation,ventricular arrhythmias, higher NYHA heart failure class, lower LV ejection fraction (LVEF), highcatecholamine and B-type natriuretic peptide (BNP) levels, low serum sodium level, hypocholesterolemia, andmarked 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 bloodvolume. The sympathetic nervous system increases heart rate and contractility, causes arteriolar vasoconstrictionin nonessential vascular beds, and stimulates secretion of renin from the juxtaglomerular apparatus of thekidney. 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 increasedsympathetic stimulation and decreased renal perfusion results in further arteriolar vasoconstriction, sodium andwater 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, causingreabsorption of water in the renal collecting duct. Although these neurohormonal pathways initially arecompensatory and beneficial, eventually they are deleterious, and neurohormonal modulation is the basis for modern treatment of heart failure.

In contrast, natriuretic peptides are hormones released by secretory granules in cardiac myocytes in response tomyocardial stretching. They have a beneficial influence in heart failure, including systemic and pulmonaryvasodilation, possible enhancement of sodium and water excretion, and suppression of other neurohormones.

With continuous neurohormonal stimulation, the left ventricle undergoes remodeling consisting of LV dilationand hypertrophy, such that stroke volume is increased without an actual increase in EF. This is achieved bymyocyte hypertrophy and elongation. LV chamber dilation causes increased wall tension, worsenssubendocardial myocardial perfusion, and can provoke ischemia in patients with coronary atherosclerosis.Furthermore, dilation of the LV chamber can cause mitral annular dilatation and mitral regurgitation, leading topulmonary congestion.

In diastolic dysfunction, the primary abnormality is impaired LV relaxation, causing high diastolic pressures andpoor filling of the ventricle. To increase diastolic filling, left atrial and pulmonary capillary pressures increaseand pulmonary edema ensues. As a result, patients are often symptomatic with exertion when increased heartrate reduces LV filling time and circulating catecholamines worsen diastolic dysfunction.

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 atrisk for developing heart failure but who have no structural heart disease at present. The management strategy inthis group is prevention of heart failure. Stage B includes patients with structural heart disease but no symptoms.The management goal is prevention of LV remodeling leading to heart failure. Stage C includes patients withstructural heart disease with current or prior symptomatic heart failure. Diuretics, digoxin, and aldosteroneantagonists may be added to angiotensin-converting enzyme (ACE) inhibitors and beta blockers, depending onthe severity of symptoms. Cardiac resynchronization therapy also may be considered. Stage D includes patientswith severe refractory heart failure. Physicians should consider either end-of-life care or high-technologytherapies such as cardiac transplantation or mechanical circulatory support, based on individual cases.

Table 1: American College of Cardiology–American Heart Association Classification of Chronic Heart Failure

Stage Description

A: High risk for developing heartfailure

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.

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Signs and symptoms

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 nocturnaldyspnea. Patients with right ventricular failure have jugular venous distention, peripheral edema,hepatosplenomegaly, and ascites. Others, however, do not have congestive symptoms but have signs andsymptoms of low cardiac output, including fatigue, effort intolerance, cachexia, and renal hypoperfusion. TheNYHA functional classification scheme is used to assess the severity of functional limitations and correlatesfairly well with prognosis (Table 2).

Table 2: New York Heart Association (NYHA) Heart Failure Symptom Classification System

NYHAClass

Level of Impairment

I No symptom l imitation with ordinary physical activity

II Ordinary physical activity somewhat limited by dyspnea (e.g., long-distance walking, climbingtwo flights of stairs)

III Exercise limited by dyspnea with moderate workload (e.g., short-distance walking, climbingone flight of stairs)

IV Dyspnea at rest or with very l ittle exertion

On physical examination, patients with decompensated heart failure may be tachycardic and tachypneic, withbilateral inspiratory rales, jugular venous distention, and edema. They often are pale and diaphoretic. The firstheart 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 diastolicdysfunction usually have a loud S4 (which may be palpable), rales, and often systemic hypertension.

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Diagnosis

The initial evaluation of new-onset heart failure should include an electrocardiogram, chest radiograph, andBNP assay. EK6 findings of LV hypertrophy, left bundle branch block, intraventricular conduction delay, andnonspecific ST-segment and T wave changes support a diagnosis of heart failure. Q waves in contiguous leadsstrongly implicate a previous myocardial infarction and coronary atherosclerosis as the cause. Chestradiographic 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 anddiastolic dysfunction. If systolic dysfunction is present, regional wall motion abnormalities or LV aneurysmsuggest 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 heartfailure cannot be discerned from the echocardiogram.

Cardiac catheterization can detect coronary atherosclerosis as the cause of heart failure. Severe coronary arterydisease 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. Coronarycomputed tomographic angiography (CTA) might also be a suitable alternative to exclude coronary arterydisease in select patients.





Magnetic resonance imaging (MRI) i s useful in assessing for arrhythmogenic right ventricular dysplasia,myocardial viabil ity, and infil trative cardiomyopathies.

Objective information about functional capacity can be obtained from metabolic (cardiopulmonary) exercisetesting. This test can distinguish ventilatory from cardiac limitations in patients with exertional dyspnea. A peakoxygen consumption higher than 25 mL/kg/min is normal for middle-age adults, but a value lower than14 mL/kg/min indicates severe cardiac l imitation and poor prognosis.

A useful diagnostic test for the detection of heart failure is the BNP assay.6, 7 BNP levels correlate with severityof 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 failurehas not proved to be beneficial. However, invasive hemodynamic monitoring may be warranted if unanticipatedresponses to therapies are observed or for diagnostic purposes if the diagnosis is uncertain.

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Summary

Jugular venous distention is a useful physical sign of heart failure.The lungs usually are clear in chronic heart failure.The BNP assay improves the accuracy of diagnosing heart failure.Echocardiography is the single most useful diagnostic modality.Coronary angiography confirms or excludes coronary artery disease as the cause.

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Treatment

Lifestyle Modifications

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 wi ll lessen congestion and decrease the needfor 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 pressureMedications

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 alsoreduce or prevent skeletal muscle atrophy that could worsen exercise tolerance. Weight loss is encouraged inobese patients. Patients should be counseled about smoking cessation.





Medical Options

Angiotensin-Converting Enzyme Inhibitors

Al l patients with LV systolic dysfunction should be treated with an ACE inhibitor unless they have acontraindication or intolerance to the drug (stages B to D). ACE inhibitors are useful in preventing heart failurein 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 patientswith a history of myocardial infarction, regardless of LVEF. Vasodilation and neurohormonal modulation with ACE inhibitors improve mortali ty, 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 inTable 3. Approximately 10% to 20% of patients do not tolerate ACE inhibitors. The main side effect from ACEinhibition 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 ACEinhibitors are angioedema and acute renal failure (caused by bilateral renal artery stenosis); both necessitateimmediate cessation of the drug.

Table 3: Angiotensin-Converting Enzyme Inhibitor Dosing

Agent Target Dose (mg) Frequency

Captopril* 50 tid

Enalapril* 20 bid

Lisinopril* 40 qd

Ramipril* 5 bid

Quinapril* 20 bid

Fosinopril* 20 bid

Benazepril* 20 qd

Trandolapril 4 qd

*FDA-approved for treatment of heart failure.

FDA-approved for treatment of post–myocardial infarction heart failure.

ACE inhibitors should be used in combination with beta blockers in most patients. Either agent may be startedfirst.

Angiotensin Receptor Blockers

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 arerecommended as second-line 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 morbidity benefits for patients with diastolic heart failure. 13

Table 4: Angiotensin Receptor Blocker Dosing

Agent Initial Dose (mg) Maximum Dose (mg)

Valsartan* 80 320

Candesartan* 4 32

Losartan 25 100

Irbesartan 75 300





Telmisartan 40 80

Eprosartan 400 800

Olmesartan 20 40


Beta Blockers

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.

Table 5: Beta Blocker Dosing

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


Al l stable patients with reduced LVEF should receive a beta blocker unless it is contraindicated (stages B, C andD). Diabetes mellitus, chronic obstructive pulmonary disease, and peripheral arterial disease are notcontraindications 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 heartfailure patients, a beta blocker should be initiated before hospital discharge or on an outpatient basis at a lowdose and titrated slowly to target levels or maximally tolerated doses. Beta blockers usually are given incombination with an ACE inhibitor, but either agent may be initiated first.

Digoxin

Digoxin is a neurohormonal modulating agent that inhibits the enzyme Na+/K+-ATPase in various organs. Incardiac cells, this inhibition increases myocardial contractility. In the central nervous system, it reducessympathetic 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 patientswith LV systolic dysfunction who remain symptomatic while receiving standard medical therapy, particularly if they are in atrial fibrillation.

Table 6: Other Heart Failure Drugs

Agent Initial DoseMaximumDose

Guidelines

Digoxin 0.125 mgqd

0.25 mg qd Reduce dose in women with renal dysfunction, withamiodarone

Hydralazine 25 mg qid 100 mg qid Use concurrently with nitrates to prevent coronary steal

Isosorbidedinitrate

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 renaldysfunction; gynecomastia

Eplerenone 25 mg qd 50 mg qd Risk of hyperkalemia, avoid in renal dysfunction; nogynecomastia

Diuretics

Diuretics should be used in combination with an ACE inhibitor (or ARB) and a beta blocker. Most patients withheart failure have some degree of symptomatic congestion and benefit from diuretic therapy.19 Usually, a loopdiuretic 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 beenshown to improve survival, and they can cause azotemia, hypokalemia, metabolic alkalosis, and elevation of neurohormone levels (Table 7).

Table 7: Diuretic Dosing

Generic Name ClassInitial Dose(mg)

Special Considerations

Furosemide Loop 20 Can be given intravenously; PO equivalent is twice the IVdose

Bumetanide Loop 0.5 Good oral bioavailability; can be given intravenously; oraland 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 tofurosemide

Hydrochlorothiazide Thiazide 12.5 Weak diuretic; used mainly for hypertension

Metolazone Thiazide 2.5 Give 1/2 hr before furosemide; only available orally; high

risk of hypokalemia

Aldosterone Antagonists

Two aldosterone antagonists have been approved for patients with heart failure: spironolactone and eplerenone. A 30% reduction in mortali ty 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 2.5.20 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.21

Aldosterone inhibition can prevent sodium and water retention, endothelial dysfunction, and myocardialfibrosis. With aldosterone antagonists, diligent monitoring of serum potassium levels is mandatory, becausepatients can develop hyperkalemia (seeTable 6). These drugs should be avoided in patients with a creatininelevel higher than 2.5 mg/dL. Eight percent of men develop gynecomastia with spironolactone but not with

eplerenone. Data from studies of mild heart failure are lacking, and so these drugs should be reserved for patients with moderately severe to severe heart failure. Therefore, the addition of an aldosterone antagonist isreasonable for select patients with moderately severe to severe symptoms of heart failure and reduced LVEFwho can be carefully monitored for preserved renal function and normal potassium concentration.

Hydralazine and Nitrates

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.22 Once-daily dosing of ACE inhibitors is easier than giving nitrates three times daily and givinghydralazine four times daily (see Table 6). The combination of hydralazine and nitrate is reasonable for patientswho 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 nitrate also may beadded to ACE inhibitors and beta blockers when additional afterload reduction is needed or pulmonaryhypertension is present. A fixed-dose combination tablet has been approved for treating heart failure in African Americans.





Other Medical Therapies

Patients with known coronary artery disease should be treated with aspirin and a statin to lower the low-densitylipoprotein (LDL) level to 70 mg/dL. Calcium channel antagonists have not been proved beneficial in heartfailure patients. Dihydropyridines such as amlodipine have a neutral effect on heart failure and may be useful for

treating concomitant hypertension or angina pectoris.23

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%-3% per year). Warfarin therapy is recommended for patientswith atrial arrhythmias, previous embolic event, cardiac thrombi, or LV aneurysms.

Specif ic therapies for treating atrial fibrillation, sleep apnea, anemia, obesity, and thyroid disease may improvethe symptoms and functional limitations of heart failure.

Intravenous Inotropes and Vasodilators

Dobutamine

Dobutamine (Table 8) enhances contractility by directly stimulating cardiac β1 receptors.24 Intravenous (IV)

dobutamine infusions, sometimes guided by hemodynamic monitoring, may be useful for select patients withacute hypotensive heart failure or shock. The dose of dobutamine should always be titrated to the lowest dosecompatible with hemodynamic stability to minimize adverse events. As with many inotropes, long-terminfusions of dobutamine can increase mortality, principally because of its arrhythmogenic effect. As a result,chronic dobutamine infusions are reserved for pall iative symptom relief or for patients who have an implantablecardioverter-defibrillator (ICD) and are awaiting heart transplantation. Intermittent outpatient infusions of dobutamine are not recommended for routine management of heart failure.

Table 8: Intravenous Agents Used for Treatment of Heart Failure

Drug Dose Special Considerations

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 improvepulmonary 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 provokeischemia by coronary steal; vasodilator; should be given onlyin intensive care unit

Nesiritide 2-µg/kg bolus; then0.01 µg/kg/min

Fixed weight-based dose; vasodilator; occasional hypotension

Milrinone

Milrinone (seeTable 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 pulmonaryvasodilator than dobutamine. Milrinone, in contrast to dobutamine, is also useful for patients on chronic oralbeta 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 intravenousinfusion 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.25 Similar todobutamine, intermittent outpatient milrinone infusions are not recommended for routine management of heartfailure.

Nitroglycerin

Nitroglycerin (seeTable 8) is a nitric oxide donor that causes vasodilation. It is a venodilator at low doses andan 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 myocardialischemia. IV nitroglycerin requires dose titration to achieve therapeutic goals. The effectiveness of prolongedinfusions is limited by the development of tachyphylaxis (loss of effect) within the first 24 hours.

Sodium Nitroprusside

Sodium nitroprusside (seeTable 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 nitroprussideinfusions, patients should be converted to oral vasodilators such as ACE inhibitors, ARBs, or hydralazine and anitrate.

Sodium nitroprusside should be infused for a short duration in patients with severe renal disease to preventaccumulation of thiocyanate, the by-product of hepatic metabolism of nitroprusside, which is excreted by thekidney. Nitroprusside should be avoided in patients with active ischemia because of i ts potential for coronarysteal syndrome, which shunts blood away from the ischemic myocardium to well-perfused muscle.

Nesiritide

Nesiritide (seeTable 8), synthetic BNP, is an arterial and venous vasodilator with modest diuretic and natriuretic

properties.26 Nesiritide increases cardiac output by afterload reduction without increasing heart rate or oxygenconsumption. It modulates the vasoconstrictor and sodium-retaining effects of other neurohormones. Nesiritideis administered as a weight-based bolus followed by continuous IV infusion in patients who have acutelydecompensated heart failure and who have dyspnea at rest or with minimal activity. It may be started in theemergency department and does not require invasive hemodynamic monitoring or frequent titration. Toleranceto the drug does not occur and it is not arrhythmogenic. Intermittent outpatient infusions of nesiritide are notrecommended for the routine management of heart failure.

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.27, 28 Symptomatic improvement is achieved inapproximately 70% of patients because of improved ventricular contraction, ventricular reverse-remodeling, andreduction of mitral regurgitation. With cardiac resynchronization therapy (biventricular pacing), a third electrodeis implanted in a left cardiac vein via the coronary sinus so that the right and left ventricles are paced in asynchronous fashion (Fig. 3). Optimal synchronization of atrial and ventricular contraction is achieved withechocardiographic guidance. 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

Defibrillator Therapy

Approximately 50% of patients with heart failure die suddenly. Implantation of an ICD can improve survival incertain subsets of heart failure patients and has been shown to be superior to antiarrhythmic drug therapy in

preventing sudden death.29-32 Current indications for defibrillator therapy are listed in Box 3. Cardiacresynchronization therapy 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.

9-month waiting period after diagnosis.

LVEF, left ventricular ejection fraction.

Ultrafiltration Therapy

Ultrafiltration therapy is an effective method for extracting sodium and fluid from volume overloaded heartfailure patients with resistance to diuretic therapy. A reduction in rehospitalization has been observed compared

with intravenous diuretic therapy.33

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.34, 35 At present, LV assist devices (LVADs) are used either as a bridge tocardiac transplantation in patients who are appropriate transplantation candidates or as destination therapy inpatients ineligible for transplantation. The inflow cannula of an LVAD is connected to the apex of the leftventricle. Blood is mechanically pumped by the device via the outflow cannula to the aorta (Fig. 4).Complications following LVAD implantation are common and often life threatening; these include stroke,

infection, perioperative coagulopathy and bleeding, and multisystem organ failure. Newer rotary continuous

flow LVADs have proven to be more durable and are associated with fewer complications.36

Ventricular Reconstruction Surgery

Ventricular reconstruction surgery, also called ventricular remodeling surgery or a Dor procedure, has been

performed for heart failure secondary to ischemic cardiomyopathy.37 It consists of several components: coronaryartery bypass grafting, mitral and tricuspid valve repair, resection of LV scar or aneurysm, reshaping the leftventricle from a spherical to an elliptic shape, and epicardial LV pacing lead placement (Fig. 5). The STICHtrial failed to show benefit over standard bypass or value surgery. Thus, the future of ventricular reconstructionsurgery is uncertain.

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. 6).38 Patients are excluded fromtransplantation if they have chronic medical comorbidities, pulmonary hypertension, active infection,psychosocial contraindications, or medical noncompliance. Survival after cardiac transplantation is about 85% at1 year, and median life expectancy is approximately 10 years. Complications limiting survival include rejection,infection, transplant coronary vasculopathy, and malignancy. Following cardiac transplantation, patients aresubjected to lifelong immunosuppression to prevent rejection, which in turn renders them susceptible to variousopportunistic infections and malignancies.

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Summary

Al l heart failure patients should receive an ACE inhibitor and a beta blocker.





Diuretics are needed in most patients to manage fluid retention.Digoxin is reserved for patients with signs and symptoms of heart failure. Aldosterone antagonists are used in patients with Class II I or IV heart failure. ARBs or a hydralazine plus nitrate may be added to standard therapy for additional benefi t.

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Prevention and screeningPatients classified as stage A are at high risk for heart failure but without structural heart disease or heart failuresymptoms. 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 lipiddisorders 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, butno symptoms of heart failure. These include patients with previous myocardial infarction, LV systolicdysfunction, and asymptomatic valvular disease. Therapies are prescribed to prevent LV remodeling. Theseinclude all preventive strategies for stage A, as well as ACE inhibitors and beta blockers for appropriatepatients.

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Considerati ons in special populations

Heart failure is slightly more common in women than men. In women, heart failure occurs later in life, is oftenrelated to hypertension, and is often associated with preserved LV systolic function. Women tend to have moreprominent heart failure manifestations and more hospitalizations but better overall survival (except withcoronary artery disease) than men. Heart failure therapeutic agents are not gender specific.

African Americans appear to benefi t from a combination of hydralazine and nitrates when added to conventional

heart failure therapy.39

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References

1. American Heart Association. Heart Disease and Stroke Statistics—2008 Update. Dallas: American Heart Association, 2008. http://circ.ahajournals.org

2. Packer M, Coats AJ, Fowler MB, et al: Effect of carvedilol on survival in severe chronic heart failure. NEngl J Med. 2001, 344: 1651-1658.

3. Hansen A, Haass M, Zugck C, et al: Prognostic value of Doppler echocardiographic mitral inflowpatterns: Implications for risk stratification in patients with chronic congestive heart failure. J Am CollCardiol. 2001, 37: 1049-1055.

4. Hunt SA, Abraham WT, Chin MH, et al: American College of Cardiology; American Heart AssociationTask Force on Practice Guidelines; American College of Chest Physicians; International Society for Heartand Lung Transplantation; Heart Rhythm Society: ACC/AHA 2005 Guideline Update for the Diagnosisand 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 toUpdate the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed incollaboration with the American College of Chest Physicians and the International Society for Heart andLung Transplantation: Endorsed by the Heart Rhythm Society. Circulation. 2005, 112: e154-e235.

5. Swedberg K, Cleland J, Dargie H, et al: Guidelines for the diagnosis and treatment of chronic heartfailure: Executive summary (Update 2005). Eur Heart J. 2005, 26: 1115-1140.

6. Dao Q, Krishnaswamy P, Kazanegra R, et al: Uti lity of B-type natriuretic peptide in the diagnosis of

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Suggest Readings

Adams KF, Lindenfeld J, Arnold JMO, et al: Executive summary: HFSA 2006 comprehensive heartfailure practice guideline. J Cardiac Failure. 2006, 12: 10-38.

American Heart Association. Heart Disease and Stroke Statistics-2008 Update. Dallas: American Heart Association, 2008.

Bardy GH, Lee KL, Mark DB, et al: Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005, 352: 225-237.

Brater DC. Diuretic therapy. N Engl J Med. 1998, 339: 387-395.

Cleland JGF, Daubert JC, Erdman E, et al: The effect of cardiac resynchronization on morbidity andmortality in heart failure. N Engl J Med. 2005, 352: 1539-1549.

Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heartfailure. N Engl J Med. 1997, 336: 525-533.

Hjalmarson A, Goldstein S, Fagerberg B, et al: Effects of controlled-release metoprolol on total mortality,hospitalizations, and well-being in patients with heart failure: The Metoprolol CR/XL RandomizedIntervention Trial in congestive heart failure (MERIT-HF). JAMA. 2000, 283: 1295-1302.

Hunt SA, Abraham WT, Chin MH, et al: American College of Cardiology; American Heart AssociationTask Force on Practice Guidelines; American College of Chest Physicians; International Society for Heartand Lung Transplantation; 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 toUpdate the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed incollaboration with the American College of Chest Physicians and the International Society for Heart andLung Transplantation: Endorsed by the Heart Rhythm Society. Circulation. 2005, 112: e154-e235.

Mueller C, Scholer A, Laule-Kilian K, et al: Use of B-type natriuretic peptide in the evaluation andmanagement of acute dyspnea. N Engl J Med. 2004, 350: 647-654.

Pitt B, Remme W, Zannad F, et al: Eplerenone, a selective aldosterone blocker, in patients with leftventricular dysfunction after myocardial infarction. N Engl J Med. 2003, 348: 1309-1321.

Pitt B, Zannad F, Remme WJ, et al: The effect of spironolactone on morbidity and mortality in patientswith severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med. 1999,341: 709-717.

Swedberg K, Cleland J, Dargie H, et al: Guidelines for the diagnosis and treatment of chronic heartfailure: Executive summary (Update 2005). Eur Heart J. 2005, 26: 1115-1140.


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