Arrhythmias in Patients with Heart Failure

Opinion statement Both atrial and ventricular arrhythmias are very common in patients with congestive heart failure, and their presence is associated with symptoms, significant morbidity, and mortality. Studies have attempted to determine the prognostic significance of atrial and ventricular arrhythmias in patients with heart failure. Whether atrial fibrillation is an independent risk factor of mortality remains controversial. The presence of ventricular arrhythmias in patients with ischemic cardiomyopathy identifies patients at high risk for sudden death. However, in patients with nonischemic cardiomyopathy there is not a strong correlation between ventricular arrhythmias and increased risk for sudden death. Multiple trials using antiarrhythmic drugs, pharmacologic therapy, and implantable cardioverter defibrillators have been performed in an attempt to improve survival in patients 1) post-myocardial infarction; 2) with congestive heart failure, with and without nonsustained ventricular tachycardia; and 3) with sustained ventricular tachycardia and those who have survived an out-of-hospital cardiac arrest. The purpose of this article is to present an overview of arrhythmias in patients with heart failure and discuss the prevalence, prognostic significance, complications, mechanisms, and trials that have formed the current therapies presently used.     

Ventricular arrhythmias in congestive heart failure

Despite advances in the treatment of congestive heart failure (CHF), the mortality rate continues to be high. A large number of the deaths are sudden, presumably due to ventricular arrhythmias. Complex ventricular arrhythmias are recorded in as many as 80% of patients with CHF, with nonsustained ventricular tachycardia occurring in 40%. The latter appears to be an independent predictor of mortality. Chronic structural abnormalities responsible for CHF may be the basis for the capability of a ventricle to support life-threatening arrhythmias, which are triggered by premature ventricular contractions. The pathogenesis of arrhythmias is multifactorial. Electrolyte abnormalities, ischemia, catecholamines, inotropic and antiarrhythmic drugs may worsen arrhythmias and increase susceptibility of a ventricle to sustained arrhythmias. Beta-adrenergic blockers and angiotensin-converting enzyme inhibitors have a beneficial effect. The role of various drugs in the pathogenesis and treatment of ventricular arrhythmias is discussed. The efficacy of antiarrhythmic therapy targeted to asymptomatic nonsustained ventricular tachycardia, in order to prevent sudden death, is controversial. Pharmacotherapy guided by electrophysiologic testing is the treatment of choice for patients who have manifest sustained ventricular tachycardia, but patients resuscitated from ventricular fibrillation may require automatic implantable cardioverter defibrillator.     

Ventricular arrhythmias in heart failure.

Heart failure is an increasingly common disorder leading to reduced quality and expectancy of life. Asymptomatic and symptomatic ventricular arrhythmias are a frequent complication and have been found to be independent prognostic predictors for sudden cardiac death in patients with heart failure. Unfortunately, the positive predictive failure for this finding is low, but in patients with sustained ventricular arrhythmias, variables indicating impaired pump function are the most important predictors of sudden and of nonsudden cardiac death. Arrhythmias in heart failure may have many different underlying mechanisms. Indications for, and mode of treatment of, arrhythmias in heart failure depend on the symptoms and prognostic significance of the arrhythmia. Primarily, pump function should be optimized and antiarrhythmic drug therapy instituted only when the arrhythmia persists. In poorly tolerated and life-threatening arrhythmias, implantable devices allowing pacing and defibrillation must be considered. No data are presently available indicating a protective role of antiarrhythmic drugs in the prevention of sudden cardiac death in heart failure. Future directions should concentrate on the development of better stratification of risk for sudden death, better delineation of mechanisms of arrhythmias in heart failure (allowing the development of mechanism-specific antiarrhythmic drugs), and research into new nonpharmacologic techniques such as cardiomyoplasty and molecular biologic techniques to rebuild the failing heart muscles.     

Management of arrhythmias in heart failure

The literature for coronary artery disease as well as ischemic and dilated cardiomyopathy suggests that ventricular arrhythmias and left ventricular dysfunction are independent risk factors for sudden death, but that the presence of organic heart disease provides the substrate for potentially lethal arrhythmias. Patients with a cardiomyopathy and ventricular tachycardia are at a high risk for sudden death as a group. The general risk, then, is high for the group with CHF and arrhythmias. The prognostic indices for hypertrophic cardiomyopathy are imprecise, but the risk for sudden death for the group is high in the young and remains high even among the adult survivors. Many conditions associated with CHF and its treatment may lead to arrhythmias and are potentially reversible. Most studies suggest that EPS and exercise provocation have limited power in predicting the risk to the individual patient. Therapeutically, reversible causes of arrhythmias should be sought and corrected. In general, antiarrhythmic drug therapy has been disappointing with adequate control being achieved in only about 30 per cent of patients and uncertainties about the effectiveness of such therapy in altering long-term prognosis. This is due to various causes including the inability to find an effective drug, problems with patient compliance, the failure of physicians to properly monitor drug levels, and changes in the anatomical and physiologic substrate due to disease and therapy. Surgical ablation or resection of arrhythmogenic foci is effective in selected patients. The AICD will become first-line therapy in patients at high risk for sudden death due to ventricular arrhythmias, with antiarrhythmic drugs and other approaches being used to minimize the frequency of the arrhythmias.     

Use of implantable cardioverter defibrillators in patients with left ventricular assist devices

Patients with left ventricular assist devices (LVADs) are at high risk of sustained ventricular arrhythmias, but these may be remarkably well tolerated and the association with sudden death is unclear. Many patients who receive an LVAD already have an implantable cardioverter defibrillator (ICD). While it is standard practice to reactivate a previously implanted ICD in an LVAD recipient, this should include discussion of the revised risks and benefits of ICD therapy following LVAD implantation. In particular, patients should be warned that they might receive a significant number of ICD shocks that may not be life saving. When ICDs are reactivated, device programming should minimize the risk of repeated shocks for non-sustained or well-tolerated ventricular arrhythmias. Implantation of a primary prevention ICD after implantation of an LVAD is not supported by current evidence, poses potential risks, and should be the subject of a clinical trial before it becomes standard practice.     

Treatment of Obstructive Sleep Apnea in Patients With Cardiac Arrhythmias

OPINION STATEMENT: Obstructive sleep apnea (OSA) is the most common form of sleep-disordered breathing that is prevalent in the population and frequently under diagnosed. Usually presenting with respiratory symptoms, the most significant consequences of OSA are cardiovascular, including arrhythmias. The pathophysiology of OSA through multiple mechanisms may promote bradyarrhythmias, atrial fibrillation, premature ventricular complexes, ventricular arrhythmias, and sudden death. These mechanisms may acutely trigger nocturnal arrhythmias and may chronically affect electrical and structural myocardial changes, causing arrhythmias. Numerous epidemiological data have identified an increased risk for atrial fibrillation, ventricular fibrillation and sudden death in subjects with OSA. Diagnosis of OSA should be considered in patients with arrhythmias. However, not all patients with arrhythmias need to undergo formal testing for sleep apnea. Patients who are observed to have nocturnal arrhythmias should be considered for evaluation for possible OSA. Also, if the arrhythmia is refractory to standard therapy and if other clinical indicators of OSA are also present, there should be a low threshold for pursuing the diagnosis of sleep apnea. The principal therapy for OSA is continuous positive airway pressure (CPAP). Currently, there are limited data to support the efficacy of CPAP for arrhythmia prevention or treatment. Randomized trials are necessary to determine the efficacy of OSA treatment on arrhythmia prevention.     

Role of the Automatic Implantable Cardioverter Defibrillator in the Post-myocardial Infarction Patient

Patients with a myocardial infarction are at an increased risk of sudden cardiac death largely due to ventricular arrhythmias associated with myocardial scarring. Implantable cardioverter defibrillators (ICDs) have been established as the best available treatment for the secondary prevention of an arrhythmic death in patients at high risk. This includes patients who have survived sudden cardiac death, have had sustained ventricular tachycardia or fibrillation, or have had syncope assumed to be due to a ventricular arrhythmia. High-risk features of patients with infarction without a previous arrhythmic event who qualify for a primary prevention ICD are an ejection fraction (EF) <30% or symptoms of Class II or III heart failure with an EF ≤ 35%. In addition, patients with nonsustained ventricular tachycardia, a positive electrophysiology study, and EF ≤ 40% are candidates under the current primary prevention guidelines. The current guidelines have specified the timing for ICD implantation as >40 days following the acute myocardial infarction. Despite the establishment of the guidelines, current clinical practice has revealed that ICDs are underutilized in patients who qualify. This article reviews the ICD implantation guidelines to encourage the appropriate use of the device.     

Arrhythmogene rechtsventrikuläre Kardiomyopathie

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetically determined heart muscle disease and a major cause of sudden cardiac death and ventricular tachyarrhythmia in young, apparently healthy individuals and athletes. Patients affected by ARVC should be excluded from competitive sports and vigorous training. To provide optimal treatment, early diagnosis and risk stratification are mandatory and genetic counseling of families is recommended. Tailored treatment strategies aim at the prevention of ventricular tachyarrhythmia and sudden death as well as the preclusion of disease progression and symptomatic heart failure. Patients with a low risk of sudden death need either no specific treatment or can be treated with beta blockers or antiarrhythmic drugs, depending on the clinical manifestation of the arrhythmia. Catheter ablation in ARVC constitutes a symptom-oriented and palliative approach for frequently relapsing ventricular tachycardia refractory to antiarrhythmic medication. However, despite good acute results of catheter ablation, there is a high incidence of recurrence during long-term follow-up. In patients with ARVC at high risk of sudden death, implantation of an implantable cardioverter defibrillator (ICD) improves long-term survival by detection and termination of life-threatening ventricular arrhythmias. In the long term, however, the cumulative incidence of mainly lead-related complications of ICD therapy must be considered in the young population with ARVC, particularly when the indications are for primary prevention of sudden death or life-threatening arrhythmias. The proposed algorithm of therapeutic management in ARVC is under constant validation, development and refinement.     

Arrhythmogenic Right Ventricular Cardiomyopathy: Risk Stratification and Indications for Defibrillator Therapy

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetically determined disease which predisposes to life-threatening ventricular arrhythmias. The main goal of ARVC therapy is prevention of sudden cardiac death (SCD). Implantable cardioverter defibrillator (ICD) is the most effective therapy for interruption of potentially lethal ventricular tachyarrhythmias. Despite its life-saving potential, ICD implantation is associated with a high rate of complications and significant impact on quality of life. Accurate risk stratification is needed to identify individuals who most benefit from the therapy. While there is general agreement that patients with a history of cardiac arrest or hemodynamically unstable ventricular tachycardia are at high risk of SCD and needs an ICD, indications for primary prevention remain a matter of debate. The article reviews the available scientific evidence and guidelines that may help to stratify the arrhythmic risk of ARVC patients and guide ICD implantation. Other therapeutic strategies, either alternative or additional to ICD, will be also addressed.     

Lack of long-term ventricular arrhythmia reduction by enalapril in heart failure

Previous studies have indicated that angiotensin-converting enzyme inhibitors may reduce the frequency of ventricular arrhythmias in patients with heart failure. These reports were mostly small and of short duration. We prospectively studied 734 patients recruited in 11 universities for 1 year who were enrolled in the Studies of Left Ventricular Dysfunction (SOLVD) to determine the long-term effects of enalapril and placebo on the frequency and complexity of ventricular arrhythmias in patients with symptomatic (treatment trial) or asymptomatic (prevention trial) heart failure and depressed left ventricular function (ejection fraction ≤35%). Five hundred fifty-three patients from the prevention trial and 181 from the treatment trial of SOLVD underwent ambulatory electrocardiographic monitoring at baseline, and then at 4 and 12 months of double-blind therapy with either placebo or enalapril (2.5 to 10 mg twice daily). The prospectively defined primary analysis was by intent-to-treat and revealed no significant differences in ventricular premature complexes between the placebo and enalapril groups at baseline (87 ± 13 vs 84 ± 13/hour), 4 months (100 ± 15 vs 85 ± 12/hour), or 12 months (80 ± 12 vs 90 ± 14/hour). Likewise, there was no difference between the placebo and enalapril groups in runs of nonsustained ventricular tachycardia: baseline (8.3 ± 4.1 vs 1.9 ± 0.4 runs/day), 4 months (16 ± 12 vs 7.2 ± 4.1 runs/day), or after 12 months of blinded therapy (11 ± 7.0 vs 6.1 ± 4.4 runs/day). Over the 1 -year trial, an equal number of patients in the placebo and enalapril groups developed new ventricular arrhythmias or had comparable reductions in ventricular arrhythmias which had been present at baseline. Our conclusion is that enalapril has no antiarrhythmic effect in a spectrum of patients with heart failure representing New York Heart Association classes I to III. These observations are consistent with the absence of any observed effect of enalapril on sudden death or hospitalization for arrhythmias in the 6,797 patients enrolled in SOLVD.     

Sudden death in idiopathic dilated cardiomyopathy.

Approximately 30% of deaths among patients with IDCM are sudden. Although ventricular tachyarrhythmias are responsible for many of these deaths, bradyarrhythmias may also play a significant role. Patients with a previous history of sustained ventricular arrhythmias are at high risk for sudden death. In patients without prior symptomatic ventricular arrhythmias a history of unexplained syncope, severely impaired right ventricular hemodynamics, frequent spontaneous ventricular ectopy or NSVT, and inducible SMVT may help identify those at greatest risk of dying suddenly. With the exception of angiotensin-converting enzyme inhibitor therapy, attempts at pharmacologic prevention of sudden death have had limited efficacy. The implantable defibrillator offers promising results in survivors of previous sustained ventricular arrhythmias; its prophylactic use in other high-risk subgroups is the subject of active investigation.     

Sudden cardiac death in Chagas' heart disease in the contemporary era

This article reviews epidemiology, clinical-morphological aspects, and primary and secondary prevention of sudden cardiac death in patients with chronic Chagas' heart disease in the current era. Chagas' disease patients with life-threatening ventricular tachyarrhythmias are at risk of sudden cardiac death. No evidence-based support is available for guiding prophylaxis of sudden cardiac death in patients with this condition. Therefore, measurements for sudden cardiac death prevention in Chagas' disease patients have been derived from data obtained in non-Chagas' disease patients as well as on expertise of physicians dealing with this disorder in areas where Chagas' disease is endemic. For primary prevention, therefore, we suggest that patients with non-sustained VT be referred to programmed ventricular stimulation. Patients with inducible VT will be better treated with Implantable Cardioverter-Defibrillator (ICD) than with amiodarone therapy. For secondary prevention, we suggest that patients with malignant ventricular tachyarrhythmias with hemodynamic instability receive ICD therapy. For patients with life-threatening ventricular arrhythmias and no hemodynamic instability, however, secondary prevention can be accomplished with ICD therapy or catheter ablation in those with a left ventricular ejection fraction (LVEF) of 30% or less, and with electrophysiologic testing-guided drug therapy or empiric treatment with amiodarone in those with a LVEF of 30% or high.     

Antiarrhythmic therapy in heart failure

Heart failure is the term used for a cardiovascular syndrome whose definition lacks uniform criteria. It is associated with a very high mortality rate. Approximately 50% of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT). In severe heart failure, death may also occur due to bradyarrhythmias. Other arrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation, and sustained or non-sustained VT. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations (such as fibrosis) may be prominent. Re-entrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. The treatment of the underlying disease process and optimal management of heart failure is of major importance. Revascularization, beta-blocker therapy, and angiotensin converting enzyme inhibitors are all essential to appropriate therapy. Treatment of arrhythmias is performed either because patients are symptomatic or to reduce the risk of sudden cardiac death. The implantable cardioverter-defibrillator (ICD) is the best available therapy to prevent sudden cardiac death from VT. Devices with back-up pacing also offer protection against bradyarrhythmias. There is evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy (e.g. amiodarone) because of atrial fibrillation or non-sustained VT that may activate the device.     

Patients with supraventricular tachycardia presenting with aborted sudden death: incidence, mechanism and long-term follow-up

A total of 13 (4.5%) of 290 patients with aborted sudden death had either documented (7; 54%) or strong presumptive evidence of supraventricular tachycardia that deteriorated into ventricular fibrillation. Six (46%) of the 13 had an accessory conduction pathway and either atrial fibrillation (5 patients) or paroxysmal atrioventricular (AV) reentrant tachycardia (1 patient) that deteriorated into ventricular fibrillation. Three patients with AV node reentrant tachycardia and four with atrial fibrillation and enhanced AV node conduction presented with supraventricular arrhythmias that deteriorated into ventricular fibrillation. Patients were treated with medical, surgical or catheter ablative procedures designed to prevent recurrences of supraventricular arrhythmias. Four patients received an implanted automatic defibrillator, but none had an appropriate device discharge. Over a follow-up period of 41.6 +/- 33.6 months, 12 patients are alive without symptomatic arrhythmias. One patient died because of severe chronic lung disease and heart failure. Supraventricular tachycardia was the cause of aborted sudden death in approximately 5% of patients referred for evaluation of sudden cardiac death. Treatment directed at prevention of supraventricular tachycardia was associated with an excellent prognosis. Current treatment techniques appear to obviate the need for automatic defibrillator therapy in these patients.     

The role of pharmacotherapy in the prevention of sudden cardiac death in patients with heart failure

Sudden cardiac death remains a significant threat to the survival of patients with heart failure. Long-term cardiac remodeling predisposes these patients to develop malignant ventricular arrhythmias. Permanent implantable and temporary external defibrillators remain a mainstay for the prevention of sudden cardiac death in this population. For decades, researchers have attempted to identify reliable drug therapies to avoid such arrhythmias; however, to date, success has been inconsistent. This review aims to explore the evidence defining the role of drug therapies for direct and indirect suppression of arrhythmias that may cause sudden cardiac death in patients with heart failure.     

Fighting against sudden death: A single or multidisciplinary approach

There are many causes of sudden death ranging from accidents and suicide to vascular events and arrhythmias. Most sudden deaths will occur in people who have not been diagnosed with a serious heart condition but at a very low annual rate. Many of these events are probably vascular and might be prevented by reducing the risk of developing coronary disease. Only a minority of sudden deaths occur in people with established cardiac disease, but in patients with major structural heart disease, the annual rate is high. The causes of sudden death are many in this clinical setting also, but dominated by ventricular arrhythmias and vascular events. There is good evidence that conventional treatments for heart failure, including ACE inhibitors, beta-blockers, aldosterone antagonists and cardiac resynchronisation devices reduce the risk of sudden death. Evidence that statins, aspirin or revascularisation are safe or effective in patients with heart failure is currently lacking. Implantable defibrillators confer a small but definite additional survival advantage by treating arrhythmias that have not been prevented.     

Prognostic significance of 24 hour ambulatory electrocardiographic monitoring in patients with hypertrophic cardiomyopathy: A prospective study

The prevalence and prognostic significance of ventricular arrhythmias identified on 24 hour ambulatory electrocardiographic monitoring was prospectlvely assessed in 99 patients with hypertrophie cardiomyopathy. In the absence of antlarrhythmic therapy, high grade ventricular arrhythmias (grade 3 and above) were common; that is, they were identified in 66 percent of the patients, including 19 percent with episodes of asymptomatic ventricular tachycardia.Clinical outcome was assessed 3 years after the initial 24 hour ambulatory electrocardiogram. Of the 84 patients who did not undergo ventricular septal myotomy-myectomy, 6 died suddenly or experienced cardiac arrest, 1 died of progressive congestive heart failure and the other 77 have survived without a cardiac catastrophe. The prevalence rate of sudden death or cardiac arrest during the follow-up period was the same (3 percent) in patients with high grade arrhythmias other than ventricular tachycardia (1 of 37) as in those with no or low grade arrhythmias (1 of 29). However, the occurrence of a sudden cardiac catastrophe was significantly more common in patients with asymptomatic ventricular tachycardia of brief duration on 24 hour electrocardiography (4 [24 percent] of 17) than in patients without ventricular tachycardia (2 [3 percent] of 66) (p <0.02).In summary, (1) high grade ventricular arrhythmias are commonly found on continuous 24 hour electrocardiographic monitoring in patients with hypertrophic cardiomyopathy; and (2) although sudden death is relatively uncommon in patients with high grade ventricular arrhythmias other than ventricular tachycardia (annual mortality rate 1 percent), the finding of ventricular tachycardia on 24 hour electrocardlography identifies a subgroup of patients at high risk for sudden death (annual mortality rate 8.6 percent). Although no conclusions can be drawn regarding the impact of therapy, our findings suggest that 24 hour electrocardiographic monitoring should be performed in patients with hypertrophic cardiomyopathy and that it may be reasonable to initiate antlarrhythmic therapy if ventricular tachycardia is identified.     

The Role of EP-Guided Therapy in Ventricular Arrhythmias: Beta-Blockers,Sotalol, and ICD's

Arrhythmic death can be reduced by antiarrhythmic drugs to a range of 2—4%. Electrophysiologic study by testing noninducibility of ventricular arrhythmia represents the classic method for evaluating the effectiveness of drug therapy.Several clinical studies have shown thaat sotalol suppresses VT induction and prevents arrhythmias recurrences at long term follow-up in 23% to 67% of patients. The efficacy of sotalol EP guided therapy in preventing VT/VF is not necessarily related to prevention of sudden death. In the ESVEM study the superiority of d,l-sotalol to other antiarrhythmic drugs was confirmed. The response to programmed ventricular stimulation was found to be strongly predictive for arrhythmia free state while the failure of sotalol therapy to suppress VT at the EP study was associated with an high recurrence rate (40%). However, EP study failes to predict freedom from sudden death. The beta-blocking activity of racemic sotalol may account for some of the observed survival benefit.Beta-blockers therapy reduces mortality in patients after myocardial infarction primarily by a reduction of sudden death. A reduction of death, worsening heart failure and life threatening ventricular arrhythmias was shown in a recent study on carvedilol. In the prospective study of Steinbeck the EP guided-therapy did not improve the overall outcome when compared to metoprolol. Suppression of inducible arrhythmias by antiarrhythmic drugs was associated with a better outcome. The effectiveness of defibrillator therapy in reducing overall mortality, has been uncertain since great clinical trials have been concluded. MADIT, AVID and CASH trials confirmed the superiority of ICD therapy over antiarrhythmic drugs therapy: ICD should be considered the first choice therapy in post-cardiac arrest patients.The ongoing BEST Trial will give us further responses about the interaction between EP study and metoprolol effect compared to ICD in patients post myocardial infarction also focusing on tolerability and compliance of the beta-blocking therapy in patients with low ejection fraction. In this study will be useful to optimize therapy in patients at high risk of sudden death     

Risk Stratification and Prevention of Sudden Death in Patients with Heart Failure

For almost the past decade, recommendations for the use of implantable cardioverter defibrillators (ICDs) for primary prevention of sudden cardiac death have been based upon the left ventricular ejection fraction (LVEF). Current guidelines recommend an ICD for heart failure patients with LVEF ≤35% and NYHA functional class of II or III; however, because the majority of heart failure patients who qualify for ICD implantation based on these criteria will never have an event requiring ICD therapy over several years of follow-up, additional methods of risk stratification for sudden death are clearly needed. Additionally, most of the nearly 300,000 cardiac arrests that occur each year occur in patients without heart failure or significant left ventricular dysfunction. To improve the identification of patients at risk for sudden death, several criteria other than ejection fraction have been proposed and studied. Markers of autonomic tone, including heart rate turbulence and QT dynamicity, have shown some ability to predict total mortality but not arrhythmic events. Microvolt T-wave alternans testing was initially thought to be highly predictive of life-threatening arrhythmias, but prospective large sub-studies of the MADIT II and SCD-HeFT trials have failed to show a predictive value for T-wave alternans testing. Newer markers for risk are based upon the detection of myocardial fibrosis, which forms the substrate for re-entrant and malignant ventricular tachyarrhythmias. Markers of collagen turnover or quantification of myocardial scar by MRI may hold the best promise for identifying patients at highest risk for sudden cardiac death and may also identify patients at high risk but with an ejection fraction above 35%, who are not currently recommended for ICD implantation.     

Current status of implantable cardioverter-defibrillator therapy in heart failure

Sudden cardiac arrest is one of the leading causes of death in patients with heart failure (HF). The implantable cardioverter-defibrillator (ICD) is the only evidence-based treatment strategy for patients who have survived a life-threatening ventricular arrhythmic event. Randomized clinical trials have shown that specific subsets of HF patients with ischemic and nonischemic dilated cardiomyopathy benefit from ICD therapy for primary prevention of sudden cardiac arrest. Cardiac resynchronization therapy has become the device-based therapy of choice for improving symptoms and survival in severe HF patients with evidence of ventricular dyssynchrony. This review summarizes the current status of ICD therapy in treating HF patients based on randomized clinical trials and current practice guidelines.