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Chronic Heart Failure:10 Questions Physicians Often Ask


The past several years have witnessedimportant advances in the evaluationand management of chronic heart failure(HF). Drugs such as β-blockersand spironolactone have been shownto reduce morbidity and mortality, andstrategies that employ new devices,such as pacing and defibrillator therapy,are evolving. This has promptedthe American College of Cardiology(ACC)/American Heart Association(AHA) to update guidelines first publishedin 1995.1 The guidelines highlightthe importance of early and accuraterecognition of the clinical syndromeof chronic HF and offer anoutline for evidence-based therapeuticdecision making.

The past several years have witnessed important advances in the evaluation and management of chronic heart failure (HF). Drugs such as β-blockers and spironolactone have been shown to reduce morbidity and mortality, and strategies that employ new devices, such as pacing and defibrillator therapy, are evolving. This has prompted the American College of Cardiology (ACC)/American Heart Association (AHA) to update guidelines first published in 1995.1 The guidelines highlight the importance of early and accurate recognition of the clinical syndrome of chronic HF and offer an outline for evidence-based therapeutic decision making.

In this article, we address 10 frequently asked questions about chronic HF. Our answers are based on the ACC/AHA guidelines, analysis of the current literature, and our own clinical experience.

Which diagnostic tests should be included in the initial assessment?
There is no single algorithm for the evaluation of chronic HF. An accurate assessment still relies on such basic clinical skills as a comprehensive history taking and physical examination. Only after careful synthesis of information from this workup can a decision be made about which diagnostic tests to perform.

Textbooks usually provide an exhaustive list of tests for initial assessment. The general rule is to ascertain whether there are any correctable causes of HF, as well as to determine comorbidities and complications (from the disease itself as well as from drug therapy for other conditions). The rationale for obtaining a thyroid function test, general chemistry panel, and complete blood cell count is that they are inexpensive and may provide valuable information. An ECG can assess underlying rhythm or conduction abnormalities and detect evidence of myocardial infarction (MI). Chest radiography is not generally helpful in the absence of clinical congestion. Routine Holter monitoring, invasive evaluation of right heart pressures, and endomyocardial biopsy are un- necessary unless clearly indicated in specific circumstances.

Echocardiography. Perhaps the single most important test to be performed is the standard echocardiogram. This test should be performed in every patient with clinical signs and symptoms that suggest chronic HF to determine the extent of structural abnormality of the heart.1

The importance of left ventricular ejection fraction (LVEF) has sometimes been exaggerated. In reality, determination of LVEF is qualitative and very much depends on the loading condition and pulse rate of the heart. Beyond the assessment of the degree of contractile impairment, other important echocardiographic measurements- such as the extent of cardiac remodeling (ventricular dimensions and wall thickness), diastolic properties (evidence of diastolic dysfunction), and valvular integrity (presence of primary valvular disease and degrees of tricuspid and mitral regurgitation)- should be determined.

Another common misconception is that low ejection fraction is synonymous with HF. In fact, almost half of all patients with chronic HF have preserved left ventricular (LV) systolic function; these patients are said to have diastolic HF. There is still no generally accepted definition of this condition; patients typically are elderly women, often overweight and with a long history of systemic hypertension and/or diabetes mellitus with associated LV hypertrophy. 2 Echocardiography frequently demonstrates some mitral regurgitation and a thick left ventricle with a small LV cavity. At present, the only effective way to treat diastolic HF is to interrupt the pathophysiologic mechanisms of the underlying cause. This can be achieved by meticulous control of blood pressure in patients with hypertension and careful glycemic control in those with diabetes.

At the other end of the spectrum are patients with no symptoms of HF but evidence of LV dysfunction who may require appropriate medical therapy and clinical monitoring. Often referred to as asymptomatic LV dysfunction, this condition may be characterized by subclinical symptoms that can be detected only with exercise testing or careful history taking.

Angiography. A lack of consensus still exists regarding the need for routine coronary angiography in the initial assessment of chronic HF.1 Nevertheless, documentation of the presence or absence of coronary artery disease is very useful, because myocardial ischemia is an underlying cause of chronic HF in almost two thirds of patients. Of course, the hazards of invasive procedures must be considered, especially in stable patients who have no signs of active ischemia but are at significant risk for procedural complications (such as renal insufficiency). Noninvasive tests for myocardial ischemia are often nondiagnostic in patients with HF.

What is the role of B-type natriuretic peptide (BNP)? 2BNP belongs to a family of naturally occurring hormones that are synthesized in the cardiac ventricles. Plasma levels of BNP often correspond to the severity of underlying cardiac dysfunction and can provide relatively reliable prognostic information, thus making BNP measurement a potential “white cell count” for chronic HF.3A bedside BNP assay. The recently approved point-of-care BNP assay enables clinicians to measure plasma BNP levels at the bedside. Women and elderly patients usually have higher normal baseline values of BNP. The assay, which uses an arbi- trary cut-off of 100 pg/mL, is highly sensitive and specific in determining whether cardiac dysfunction is the cause of dyspnea.4 If a patient presents with dyspnea and low BNP levels, it is unlikely that cardiac causes are involved. However, some patients with stable, well-managed chronic HF or those with flash pulmonary edema at symptom onset may present with normal levels of plasma BNP.

Despite the utility of BNP assays in ruling out cardiac causes of dyspnea, plasma BNP levels vary widely in patients with established cardiac conditions (Table 1). In patients with decompensated HF, BNP levels are more than 50% above baseline, but a single measurement of plasma BNP may not accurately correlate with filling pressure or the degree of decompensation. Common conditions that may falsely elevate plasma BNP levels include age, significant renal dysfunction, and surgery (especially cardiothoracic procedures).

Significance of BNP levels. There is little doubt that elevated plasma BNP levels indicate a high risk of morbidity and mortality in patients with chronic HF5 or with acute coronary syndrome.6 Rehospitalization rates are usually lower among patients who achieve BNP levels below 400 pg/mL; those with BNP levels higher than 1000 pg/mL often have an especially poor prognosis.7 Additional laboratory-based BNP and Nterminal proBNP assays will soon be available for routine diagnostic use, but more data are needed to support the routine use of sequential plasma BNP assays to guide medical therapy.

Nesiritide. The BNP used for diagnosis is not to be confused with the vasodilator nesiritide, a human recombinant form of BNP given as a continuous infusion in patients with acute HF.8 A number of studies have established that nesiritide effectively lowers intracardiac pressures during acute exacerbations of HF and has a good safety profile. 9,10 The drug is relatively expensive; it costs about the same as milrinone but more than nitroglycerin or nitroprusside. Guidelines for patient selection for nesiritide therapy are still evolving.

What is the optimal dosage and titration sequence for angiotensinconverting enzyme (ACE) inhibitors and β-blockers in the treatment of chronic HF?
Consider both classes of drugs for every patient with chronic HF, regardless of disease severity.1 Tens of thousands of patients with chronic systolic HF have been treated with these agents in clinical studies worldwide; results show a remarkable improvement in morbidity and mortality. Nevertheless, these agents remain relatively underused, in part because they can be difficult to titrate. In addition, although ACE inhibitors and β- blockers are likely to benefit patients with diastolic HF, the guidelines for using these drugs in such patients are not well defined.

Target drug dosages to those used in the clinical trials (Table 2). Patients who experience adverse events from steady up-titration schedules may be able to tolerate a slower pace of increases. A schedule for up-titration of ACE inhibitors has never been clearly defined, but increasing the dosage on a weekly basis is reasonable.

The absence of clinical HF is not a compelling reason to stop up-titration, nor is mild to moderate renal insufficiency (serum creatinine levels of less than 3 mg/dL). Prerenal azotemia often occurs with ACE inhibitor up-titration, especially following aggressive diuresis. In such cases, the preferred strategy is slower up-titration and temporary discontinuation of diuretic therapy.

Several mechanistic and largescale mortality studies failed to demonstrate a clear-cut benefit of highdose ACE inhibition over the more commonly used low-dose regimens. For example, the Assessment of Treatment With Lisinopril and Survival (ATLAS) trial showed only a slight improvement in a composite end point of mortality and hospital admissions when high doses of lisinopril (32.5 to 35 mg/d) were compared with low doses (2.5 to 5 mg/d).11

The usual practice is to titrate the ACE inhibitor first and then start the β-blocker. However, there is no set rule, and separate titration serves mainly as a convenient way to monitor drug tolerability. Sometimes these agents can be initiated together (especially when β-blockers are likely to be beneficial, as in a hypertensive patient with tachycardia). Many experts initiate β-blockers before ACE inhibitors are fully maximized. A slow increase in β-blocker dosage on a biweekly to monthly basis is reasonable.

Contraindications to β-blocker therapy include cardiogenic shock, bradycardia with a high degree of heart block, active wheezing (in patients with bronchospasm), severe emphysema, and sustained symptomatic hypotension. Adjustments to diuretic dosage (eg, an increase to reduce fluid retention) and ACE inhibitor dosages (eg, a reduction to maintain adequate blood pressure) are often required during β-blocker up-titration when symptoms of light-headedness or fluid retention develop.

Data on the effects of down-titration of ACE inhibitors or β-blockers are limited, although several observational series have suggested adverse outcomes. In cases of acute exacerbation of HF or acute renal insufficiency, temporary withdrawal of these drugs may be necessary.

Are all ACE inhibitors and β-blockers equivalent?
Probably not. Although all ACE inhibitors are thought to be equally effective, advocates of the newer “tissuespecific” ACE inhibitors, such as ramipril and quinapril, claim that these agents provide additional benefits. Head-to-head studies will probably not be done, so a definitive answer is unlikely. Our recommendation is thus to use those ACE inhibitors studied in the large clinical trials because of their proven efficacy (see Table 2). Captopril is usually a good choice in the inpatient setting because it has a short half-life and can be up-titrated easily to target dosages before a switch is made to longer-acting formulations to enhance compliance. In the outpatient setting, however, once-daily dosing of ramipril or lisinopril is quite reasonable.

Three β-blockers-carvedilol, metoprolol succinate, and bisoprolol- are currently approved for the treatment of chronic HF. It is thought that these agents differ somewhat, although their major inotropic and chronotropic effects (mediated via the β1-adrenergic receptor) are similar. Carvedilol, perhaps the most extensively studied, has the greatest hypotensive effect when therapy is initiated because of concomitant blockade of α1-adrenergic receptors.12 Metoprolol succinate was tolerated as well as placebo in the Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure (MERIT-HF).13 However, generic metoprolol tartrate should not be substituted for the proprietary agent, because its efficacy has not yet been demonstrated. A study comparing carvedilol and metoprolol succinate (the Carvedilol and Metoprolol European Trial [COMET]) is now under way in Europe.

Can an angiotensin II receptor blocker (ARB) be used instead of an ACE inhibitor?
No; these 2 classes are not equivalent. Small mechanistic studies have suggested similar improvement in surrogate end points (eg, LV remodeling), but survival data are not comparable so far.14 Two large-scale randomized controlled trials of losar- tan (Losartan Heart Failure Survival Study [ELITE II]15) and valsartan (Valsartan Heart Failure Trial [Val- HeFT]16) failed to show that these agents reduced mortality more than standard doses of ACE inhibitors. ACE inhibitors should therefore remain first-line agents for chronic HF unless contraindicated.

Routine combined use of ARBs, ACE inhibitors, and β-blockers is not recommended; patients in this tripletherapy subgroup in the Val-HeFT study had a higher overall mortality. This observation warrants further testing (eg, in the upcoming Valsartan in Acute Myocardial Infarction [VALIANT] trial).

Generally, patients with severe rash or intolerable cough resulting from ACE inhibitor use (about 5% to 8%) should be switched to an ARB. Because cough can sometimes be associated with the heart failure syndrome, careful evaluation is warranted before the switch is made. A similar incidence of renal insufficiency (serum creatinine greater than 3 mg/dL) and hyperkalemia (serum potassium greater than 6 mEq/dL) has been observed with ARBs and ACE inhibitors. Angioedema has also occurred with both agents, especially in African Americans. Consider a hydralazine-nitrate combination in patients with this potentially life-threatening side effect. It is unclear whether angioedema is likely to occur with an ARB if it has occurred with an ACE inhibitor, but such a cross-reaction is possible.

What is the role of spironolactone?
There is increasing recognition that aldosterone antagonists play an important role in chronic HF. Spironolactone has a long history in the treatment of this disease, but it has been used mainly as an adjunctive diuretic. To date, there has been only 1 large-scale clinical study of spironolactone (the Randomized Aldactone Evaluation Study [RALES]).17 It demonstrated a 35% reduction in morbidity and mortality in patients with advanced HF (LVEF, 35% or less; New York Heart Association [NYHA] class III or IV) randomly assigned to spironolactone, 25 mg/d. However, the typical patient treated with spironolactone in this study was very ill. Patients enrolled in the study also were very closely monitored to ensure a relatively low rate of renal insufficiency and hyperkalemia. Further safety and efficacy studies are needed, especially to support the routine use of spironolactone in patients with stable mild to moderate HF.

Spironolactone can be added to the regimen of patients with advanced HF-for example, following recurrent HF exacerbation despite optimal ACE inhibitor (and β-blocker) therapy.

Some caveats. Serious adverse events have been associated with spironolactone. One common error is to initiate the drug without close follow- up of clinical and renal function. Dosages of 25 mg once daily or less are recommended, and blood chemistry values should be checked at regular intervals (eg, at 1, 4, 8, and 12 weeks following initiation). Reduce the dosage of spironolactone (to alternative days or half-doses) or withhold the drug if there is a significant rise in serum potassium levels (greater than 6 mEq/dL) or creatinine levels (greater than 3 to 4 mg/dL) following drug initiation. Concomitant administration with NSAIDs is not recommended because of potential synergistic nephrotoxic effects.

Some patients who take spironolactone have breast discomfort and/or gynecomastia and must discontinue it. This effect was noted in 10% of men in the RALES trial. Advise patients to discontinue the drug temporarily if diarrhea or vomiting occurs, to avoid electrolyte imbalance. A newer, more specific aldosterone antagonist is being evaluated in clinical trials; it may provide the benefits of spironolactone with a better sideeffects profile.

Is anticoagulation routinely recommended in patients with advanced chronic HF?
It was once thought that oral anticoagulation was warranted because of the heightened risk of clot formation in the failing myocardium, but this therapy is not advocated in the latest guidelines.1 Some experts suggest a benefit for patients at high risk, such as those with a history of atrial fibrillation, mitral regurgitation, stroke, LV thrombus, or large anterior MI.18 A large-scale clinical study (the Warfarin and Antiplatelet Therapy in Chronic Heart Failure [WATCH] trial) is now under way to determine whether anticoagulation with warfarin, clopidogrel, or aspirin will reduce morbidity and mortality in patients with chronic HF.

Even though concerns regarding concomitant use of ACE inhibitors and aspirin have emerged from several post-hoc analyses and small-scale clinical trials, many experts believe that this drug combination poses minimal risk.19 However, aspirin may offset some of the benefits of ACE inhibitors.20Until definitive evidence dictates otherwise, aspirin should not be withheld from patients with ischemic cardiomyopathy.

Which patients should be considered for cardiac resynchronization therapy?
The association of asynchronous ventricular contraction and LV dysfunction has been recognized for many years, but only recently has it become an important therapeutic target. Patients who undergo cardiac resynchronization pacing therapy (so-called biventricular pacing) with synchro- nized pacing via right ventricular and coronary sinus leads may show significant hemodynamic and symptomatic improvement.21 Implantable cardioverter defibrillators (ICDs) are often used in association with biventricular pacing. Further studies on long-term morbidity and mortality are needed before this expensive (more than $30,000) form of therapy can be more routinely recommended.

It is still unclear which patients will benefit from resynchronization therapy. Clinical data and the results of randomized trials suggest that appropriate candidates may be those with moderate to severe chronic systolic HF (LVEF, less than 35%; NYHA class III or IV) and those with ventricular dyssynchrony manifested as a wide QRS of more than 120 to 150 milliseconds (especially with a left bundle branch block pattern) despite optimal drug therapy. However, preliminary studies did not show improvement in a subset of these patients. Collective experience has suggested that the most important determinant of good response to pacing therapy remains the “quality” of the resynchronization- that is, the optimization of lead placement site as well as timing of interventricular and atrioventricular delays.

When is ICD therapy recommended?
ICDs have evolved as an important treatment modality for primary and secondary prevention of sudden cardiac death (especially when chronic HF is attributable to ischemia). 22 Five randomized trials in patients with HF have demonstrated that ICDs lowered mortality to a greater degree than antiarrhythmic agents (such as amiodarone) in the following groups of patients:

•Survivors of ventricular fibrillation or sustained ventricular tachycardia (VT) that caused cardiac arrest, syncope, or significant hemodynamic compromise, or those with sustained VT, symptomatic HF, and an LVEF of less than 35%.23-25

•Those with ischemic cardiomyopathy (LVEF, less than 35%; NYHA class I to III) without prior events but with nonsustained VT on Holter monitoring and inducible VT on electrophysiologic testing.26,27

•Those who have a familial cardiac condition with a high risk of sudden death (such as long QT syndrome, hypertrophic cardiomyopathy, Brugada syndrome, arrhythmogenic right ventricular dysplasia, or following repair of tetralogy of Fallot).26

Patients with other reversible causes of ventricular arrhythmia, significant psychiatric illness, or a terminal illness with life expectancy of less than 6 months should not be considered for ICD therapy.28 Results from the second Multicenter Automatic Defibrillator Implantation Trial (MADIT-II) suggest that in patients with a prior MI and advanced cardiac dysfunction, prophylactic implantation of a defibrillator improved survival.29 This may further expand the current indications for ICD placement in patients with chronic HF. However, cost and personnel considerations will be major obstacles to more widespread use.

What are the key elements in an overall management program?
An essential-but often overooked-aspect of the management of chronic HF is to establish overall therapeutic goals in order to provide “rational polypharmacy.” This involves tailoring therapy by balancing beneficial and adverse drug effects and understanding how such drug regimens affect the natural history of HF for each patient.30 The management of a young patient with idiopathic dilated cardiomyopathy of acute onset is likely to be different from that of an elderly patient with moderate aortic regurgitation.

It is best to establish initially the level of aggressiveness and the cost-effectiveness of the pharmacotherapeutic protocol and to determine whether the focus of therapy is to improve survival, relieve symptoms, or both. Comorbidities such as lipid abnormalities and suboptimal blood pressure or glycemic control must be optimally managed. The cost of polypharmacy is becoming a major problem, not only because many of the drugs used to treat HF are proprietary agents but also because interactions between drugs used for HF and other agents (such as NSAIDs) may exacerbate the patients’ conditions or cause harm, especially in those with renal insufficiency.

Self-monitoring is a vital component of a successful treatment plan. Early patient education is necessary to foster an understanding of the importance of compliance with medication and dietary regimens. We always encourage patients to adhere to a lowsodium diet (less than 2 g/d) and weigh themselves every day. We also advise patients to adjust their diuretic dosages in order to maintain their dry weight, much as patients with diabetes can maintain glycemic control by adjusting insulin dosages. These measures may permit effective use of lower and safer diuretic dosages. Physical activity and cardiac rehabilitation are often beneficial; advise patients to continue their regular exercise regimen as tolerated.




Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to revise the 1995Guidelines for the Evaluation and Management of Heart Failure).

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Devereux RB, Roman MJ, Liu JE, et al. Congestive heart failure despite normal left ventricular systolic function in a population-based sample: theStrong Heart Study.

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Maisel A. B-type natriuretic peptide in the diagnosis and management of congestive heart failure.

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Dao Q, Krishnaswamy P, Kazanegra R, et al. Utility of B-type natriuretic peptide in the diagnosis of congestive heart failure in an urgent-care setting.

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Koglin J, Pehlivanli S, Schwaiblmair M, et al. Role of brain natriuretic peptide in risk stratification of patients with congestive heart failure.

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de Lemos JA, Morrow DA, Bentley JH, et al. The prognostic value of B-type natriuretic peptide in patients with acute coronary syndromes.

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Cheng V, Kazanagra R, Garcia A, et al. A rapid bedside test for B-type peptide predicts treatment outcomes in patients admitted for decompensated heart failure: a pilot study.

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Silver MA, Horton DP, Ghali JK, Elkayam U. Effect of nesiritide versus dobutamine on short-term outcomes in the treatment of patients with acutely decompensated heart failure.

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Packer M, Poole-Wilson PA, Armstrong PW, et al, for the ATLAS Study Group. Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure.




Packer M, Bristow MR, Cohn JN, et al, for the US Carvedilol Heart Failure Study Group. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure.

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MERIT-HF Study Group. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervention Trial in CongestiveHeart Failure (MERIT-HF).




Jamali AH, Tang WH, Khot UN, Fowler MB. The role of angiotensin receptor blockers in the management of chronic heart failure.

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Pitt B, Poole-Wilson PA, Segal R, et al. Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: randomized trial-the Losartan Heart Failure Survival Study ELITE II.




Cohn JN, Tognoni G. A randomized trial of the angiotensin-receptor blocker valsartan in chronic heart failure.

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Pitt B, Zannad F, Remme WJ, et al, for the Randomized Aldactone Evaluation Study Investigators. The effect of spironolactone on morbidity and mortality in patients with severe heart failure.

N Engl J Med.



Graham SP. To anticoagulate or not to anticoagulate patients with cardiomyopathy.

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Massie BM, Teerlink JR. Interaction between aspirin and angiotensin-converting enzyme inhibitors: real or imagined.

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Hall D. Controversies in heart failure. Are beneficial effects of angiotensin-converting enzyme inhibitors attenuated by aspirin in patients with heart failure?

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Pavia SV, Wilkoff BL. Biventricular pacing for heart failure.

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Sweeney MO, Ellison KE, Stevenson WG. Implantable cardioverter defibrillators in heart failure.

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Kuck KH, Cappato R, Siebels J, Ruppel R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest: the Cardiac Arrest Study Hamburg (CASH).




Connolly SJ, Gent M, Roberts RS, et al. Canadian implantable defibrillator study (CIDS): a randomized trial of the implantable cardioverter defibrillator against amiodarone.




The Antiarrhythmics versus Implantable Defibrillators (AVID) Investigators. A comparison of antiarrhythmic-drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias.

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Buxton AE, Lee KL, Fisher JD, et al, for the Multicenter Unsustained Tachycardia Trial Investigators. A randomized study of the prevention of sudden death in patients with coronary artery disease.

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Moss AJ, Hall WJ, Cannom DS, et al, for the Multicenter Automatic Defibrillator Implantation Trial Investigators. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia.

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Winters SL, Packer DL, Marchlinski FE, et al, for the North American Society of Electrophysiology and Pacing Group. Consensus statement on indications, guidelines for use, and recommendations for follow-up of implantable cardioverter defibrillators.

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Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction.

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