Management of Ventricular Tachycardia in Heart Failure

Ventricular tachyarrhythmias are common in patients with congestive heart failure. The clinical presentation ranges from an asymptomatic incidental electrocardiographic finding to palpitations, syncope, and sudden cardiac death. Although implantable cardioverter defibrillators successfully prevent sudden cardiac death associated with ventricular fibrillation and ventricular tachycardia, recurrent implantable cardioverter defibrillators shocks remain a clinical management challenge. In this review, we discuss management strategies of ventricular tachycardia in congestive heart failure, including drug therapy, radiofrequency catheter ablation (RFCA), and recent RFCA advances.     

Significance and control of cardiac arrhythmias in patients with congestive cardiac failure

A wide spectrum of ventricular and supraventricular tachyarrhythmias occurs in the setting of congestive cardiac failure. However, the two most clinically significant are atrial fibrillation and ventricular tachycardia and fibrillation.In the past there has been much emphasis on premature ventricular contractions and more recently, on nonsustained ventricular tachycardia. For the most part, these arrhythmias are asymptomatic in heart failure. They are markers of sudden arrhythmic death but their suppression by antiarrhythmic drugs have not resulted in a reduction of total mortality. Two approaches have been used to this end. The first is the use of beta-adrenergic blocking drugs and antiarrhythmic agents such as amiodarone. Beta-blockers have been shown to significantly reduce sudden death as well as total mortality, while the effects of amiodarone have been less decisive. The prospective role of the implantable cardioverter defibrillator (ICD) is undergoing critical evaluation in patients with cardiac failure at high risk for sudden death. The elective role of the ICD is well established as first-line therapy in patients with heart failure resuscitated from sudden death and in those with sustained ventricular tachycardia in conjunction with conventional therapies for cardiac decompensation.The prevalence of atrial fibrillation rises as a function of severity of cardiac failure, but it is also in known that persistent atrial fibrillation with an uncontrolled ventricular response may induce heart failure. Controlled ventricular response may prevent congestive heart failure and improve left ventricular function. The two most common causes of atrial fibrillation in cardiac failure in Europe and America are ischemic heart disease and hypertension, while mitral valve disease remains the prevalent cause elsewhere. The choice of antiarrhythmic drugs for maintaining sinus rhythm is critical in the prevention of heart failure aggravation and proarrhythmic reactions of antiarrhythmic drugs. Amiodarone and dofetilide are most widely used in this context.     

Treatment and prevention of sudden cardiac death: effect of recent clinical trials.

Tremendous strides have been made in recent years in the treatment and prevention of sudden cardiac death. Large scale trials have now established several interventions that may improve survival in patients susceptible to sudden cardiac death. In patients who have had a sustained ventricular tachyarrhythmia, the current therapy of choice is an implantable cardioverter defibrillator. For prophylaxis of sudden cardiac death in patients without a previous event, several approaches should be considered. Beta-Adrenergic blocking agents are an effective pharmacologic therapy in patients following myocardial infarction, and their efficacy has also most recently been demonstrated in patients with congestive heart failure. There is no Vaughan Williams class I or III antiarrhythmic drug that has demonstrated efficacy as a prophylactic agent to reduce mortality in these populations, with the possible exception of amiodarone. The best therapeutic approach for prophylactic therapy to prevent sudden cardiac death appears to be the implantable cardioverter defibrillator; however, its use can be justified only in patients at high risk for developing sudden cardiac death. Further work is needed to identify the high risk populations in which this therapy is warranted.     

Risk stratification and prevention of sudden death in patients with heart failure

Patients with heart failure can die of progressive refractory heart failure or sudden cardiac death. This article reviews the major clinical predictors of sudden death in patients with heart failure due to left ventricular systolic dysfunction. Although earlier studies have identified many independent univariate predictors of reduced survival in these patients, the positive predictive value of most of them is low. Cardioverter defibrillator implantation has been shown to be the most effective therapy in patients resuscitated after cardiac arrest caused by ventricular fibrillation or poorly tolerated ventricular tachycardia. Low left ventricular ejection fraction, low New York Heart Association functional class, unsustained ventricular tachycardia and inducibility of ventricular arrhythmia in electrophysiological studies may also identify high-risk patients who are candidates for cardioverter defibrillator implantation. The role of amiodarone in preventing sudden death in high-risk patients with heart failure seems to be small. Further studies are needed to improve risk stratification criteria to select patients with heart failure who are candidates for cardioverter defibrillator implantation.     

Arrhythmias in heart failure: current concepts of mechanisms and therapy

About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may be prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing 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 because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy.     

Malignant idiopathic ventricular fibrillation “cured” by radiofrequency ablation

Idiopathic Ventricular Fibrillation is a rare cause of sudden cardiac death. It may be difficult to prospectively diagnose idiopathic ventricular fibrillation due to the episodic nature of the arrhythmias as well as the inability to induce the clinical tachycardia on electrophysiological studies. Although an implantable cardioverter defibrillator can terminate episodes of ventricular fibrillation, it cannot prevent recurrences. We describe a patient who underwent radiofrequency ablation of the culprit ectopics initiating ventricular fibrillation for frequent symptomatic episodes.     

Implantable cardioverter defibrillator: a review.

Sudden cardiac death claims 400,000 to 450,000 lives annually. It is believed that sudden cardiac death results predominantly from ventricular fibrillation or sustained ventricular tachycardia that deteriorates into ventricular fibrillation. Conventional treatments for patients who suffer from ventricular arrhythmias have been limited to antiarrhythmic drugs or surgery. These treatments have proved ineffective to a portion of arrhythmia sufferers. The implantable cardioverter defibrillator offers hope to a segment of ventricular arrhythmia sufferers whose disease is resistant to conventional therapies.     

The future of implantable defibrillator and cardiac resynchronization therapy trials

Implantable cardioverter defibrillator (ICD) trials were initially limited to survivors of sudden death. The focus of defibrillator trials in the last decade has been in prophylactic implantation of the device in high risk populations for the prevention of sudden cardiac death. It is the contention in this review that the new focus for implantable defibrillator trials in 2008 and beyond will be on more selective and focused use of this therapy. This could be achieved by selecting ICD patients based on their pathophysiologic and genetic risk. Increasing effort will also be placed on using the device for prevention of spontaneous malignant ventricular tachyarrhythmias and the index clinical sudden death event. Finally, implantable defibrillators will be used in combination in a “hybrid” therapy approach. ICDs will be increasingly combined either with ventricular tachycardia ablation or ventricular fibrillation ablation using catheter techniques. With the addition of cardiac resynchronization therapy in these devices, new clinical trials that use cardiac resynchronization therapy as an early intervention in specific high risk heart failure populations and refinement of the CRT technique to improved optimal results are in progress. Finally, combining ICD devices and regenerative medicine approaches to myocardial replacement therapy are being explored. Dr. Saksena is a consultant and/or investigator for Medtronic Inc., St. Jude Medical Inc., Sanofi Aventis, and Aryx Pharmaceuticals.     

Survival after cardiac arrest or sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy.

OBJECTIVES: The aim of this study was to evaluate the survival of patients with hypertrophic cardiomyopathy (HCM) after resuscitated ventricular fibrillation or syncopal sustained ventricular tachycardia (VT/VF) when treated with low dose amiodarone or implantable cardioverter defibrillators (ICDs). BACKGROUND: Prospective data on clinical outcome in patients with HCM who survive a cardiac arrest are limited, but studies conducted before the widespread use of amiodarone and/or ICD therapy suggest that over a third die within seven years from sudden cardiac death or progressive heart failure. METHODS: Sixteen HCM patients with a history of VT/VF (nine male, age at VT/VF 19 +/- 8 years [range 10 to 36]) were studied. Syncopal sustained ventricular tachycardia/ventricular fibrillation occurred during or immediately after exertion in eight patients and was the initial presentation in eight. One patient had disabling neurologic deficit after VT/VF. Before VT/VF, two patients had angina, four had syncope and six had a family history of premature sudden cardiac death. After VT/VF all patients were in New York Heart Association class I or II, three had nonsustained VT during ambulatory electrocardiography and 11 had an abnormal exercise blood pressure response. After VT/VF eight patients were treated with low dose amiodarone and six received an ICD. Prophylactic therapy was declined by two patients. RESULTS: Mean follow-up was 6.1 +/- 4.0 years (range 0.5 to 14.5). Cumulative survival (death or ICD discharge) for the entire cohort was 59% at five years (95% confidence interval: 33% to 84%). Thirteen (81%) patients were alive at last follow-up. Two patients died suddenly while taking low dose amiodarone, and one died due to neurologic complications of his initial cardiac arrest. Three patients had one or more appropriate ICD discharges during follow-up; the times to first shock after ICD implantation were 23, 197 and 1,124 days. CONCLUSIONS: This study shows that patients with HCM who survive an episode of VT/VF remain at risk for a recurrent event. Implantable cardioverter defibrillator therapy appears to offer the best potential benefit regarding outcome.     

Update of implantable cardioverter/defibrillator and cardiac resynchronization therapy in heart failure

PURPOSE OF REVIEW: Heart failure prevalence is reaching epidemic proportion in the United States and is associated with significant morbidity and mortality. A large proportion of the mortality is the result of sudden cardiac death (SCD). Clinical trials have demonstrated the superiority of the implantable cardioverter/defibrillator (ICD) compared with antiarrhythmic drugs for secondary prevention of sudden cardiac death. RECENT FINDINGS: Recently, several clinical trials in primary prevention of sudden cardiac death in both ischemic and nonischemic heart failure have been completed. The 2002 guidelines for implantable cardioverter/defibrillator implantation were recently released as well. Adjunct therapy consisting of antiarrhythmic drugs or radiofrequency ablation is necessary in the subset of patients with implantable cardioverter/defibrillator that have frequent or intractable ventricular arrhythmias. An emerging new therapy in the heart failure population is cardiac resynchronization therapy, which coordinates right and left ventricular pacing in a subset of patients with interventricular conduction delay. SUMMARY: Several randomized clinical trials have demonstrated improvements in heart failure-related symptoms, exercise tolerance, and reversal of ventricular remodeling. Meta-analysis of these trials has also demonstrated mortality benefit. Patient selection, left ventricular pacing site, and optimal device programming are issues that need further investigation. Recent trials have also studied the compatibility between cardiac resynchronization therapy and implantable cardioverter/defibrillator as a single device. Finally, the DAVID trial has raised concerns of conventional right ventricular pacing and the risk of heart failure in a subset of patients.     

A critical appraisal of indications for the implantable cardioverter defibrillator (ICD).

The implantable cardioverter defibrillator (ICD) is a remarkably effective therapy for reducing sudden cardiac death in patients with malignant ventricular arrhythmias. The indications for implantation of the ICD were approved in 1985 by the United States Food and Drug Administration; it could be implanted in patients who have experienced cardiac arrest or in those with recurrent ventricular arrhythmias which are not suppressed by anti-arrhythmic drugs in the electrophysiology laboratory. These established indications have not changed in the last seven years. In the near future, the release of third-generation ICDs (with antitachycardia pacing) will likely further expand indications for the device. Many patients with stable ventricular tachycardia who have not had syncope or cardiac arrest will receive a third-generation defibrillator. Also, three clinical trials now in progress--CABG-PATCH, Multicenter Automatic Defibrillator Implantation Trial (MADIT) and Multicenter Unsustained Tachycardia Trial (MUSTT)--are studying "pre-event" patients with low ejection fraction and electrical instability; some of the patients in each trial are being prospectively randomized to the ICD. Within the next five years we will have a better understanding of the role of ICD therapy in such patients. Until these studies are completed, it is important that the indications for the ICD not be expanded.     

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.     

恶性室性心律失常埋藏式心脏复律除颤器与药物治疗的对比研究

观察埋藏式心脏复律除颤器 (ICD)与药物对恶性室性心律失常的治疗效果 ,探讨其对心源性猝死的预防。94例患者 ,均有室性心动过速 (简称室速 )和 /或心室颤动等恶性室性心律失常发作史 ,其中冠心病 68例、原发性扩张型心肌病 2 6例。根据电生理心室程序刺激结果将患者分为药物治疗组 (A组 )、ICD组 (B组 )和慢频率室速药物治疗组 (C组 )。分别给予胺碘酮和 /或阿替洛尔药物治疗和ICD治疗。观察随访 1 ,2 ,5年的总生存率 ,不同左室射血分数 (EF)值亚组的生存率和心律失常性死亡的发生率。结果显示 ,随访 5年的总生存率C组明显低于A、B两组(P <0 .0 5 ) ,B组的低EF(≤ 0 .40 )值亚组的 5年生存率明显高于A、C两组的低EF值亚组 (P <0 .0 5 )。B组随访期间无心律失常死亡者 ,其心律失常性死亡事件的发生率明显低于A、C两组 (P <0 .0 5 )。结论 :ICD对于合并有恶性室性心律失常的心脏病人预防猝死的总体效果优于 β 阻断剂和胺碘酮等药物治疗。这尤其见于长期随访 (≥ 5年 )和伴有心功能不全 (EF值≤ 0 .40 )的病人。对于有过恶性室性心律失常发作史的患者 ,若心电生理检查不能诱发室速 ,在没有条件安装ICD时 ,胺碘酮与 β 阻断剂联合应用仍可在一定程度上减少心源性猝死的发生。     

Brugada综合征的电生理检查和置入性心脏复律除颤器治疗

目的　探讨Brugada综合征的电生理检查和置入性心脏复律除颤器 (ICD)治疗临床研究。方法　心电图自发性或普罗帕酮药物试验表现为Brugada波的 10例患者行电生理检查 ,均为男性 ,平均年龄 (41± 10 )岁 ,经超声心动图和冠状动脉造影检查未发现器质性心脏病。电生理检查诱发心室颤动 (室颤 )并对有条件者置入ICD治疗。结果　 3例有家族性心脏猝死史 ,4例有反复晕厥史 ,其中 2例晕厥发作时心电图记录到室颤。电生理检查 ,AH和HV间期分别为 5 0～ 12 4 (86± 2 1)ms和 4 1～ 84 (5 8± 15 )ms ,4例晕厥者诱发室颤 ,1例心悸者诱发房室折返性心动过速 ,3例有自发性或诱发心房颤动。 4例诱发室颤者中 ,3例置入ICD ;另 1例因经济原因未置入ICD ,随访中发生猝死。1例诱发房室折返性心动过速者作左侧房室旁路射频导管消融治疗。结论　有晕厥症状的Brugada综合征患者 ,经电生理检查 ,室颤有很高的诱发率 ,是猝死的高危人群 ,为了防止猝死应置入ICD治疗。     

Federal Guidelines for Prophylactic ICD Therapy in High Risk Populations for Sudden Cardiac Death: Is this a Necessary Course Correction?

Implantable cardiac devices have become firmly entrenched as important therapeutic tools for a variety of conditions. Pacemakers are the only available treatment for symptomatic bradycardia not due to reversible causes. Large randomized studies have demonstrated a small but statistically significant reduction in atrial fibrillation associated with pacing modes that maintain atrioventricular synchrony. In contrast, pacing mode appears to have a less dramatic effect in patients with atrioventricular block. Cardiac resynchronization with specialized left ventricular leads has been shown to reduce symptoms and improve survival in patients with symptomatic heart failure, systolic dysfunction, and widened QRS complexes. The implantable cardioverter defibrillator has become the standard therapy for protecting patients against sudden cardiac death. Two recent trials, Multicenter Automatic Defibrillator Trial II (MADIT II) and the Sudden Cardiac Death Heart Failure Trial (SCD-HEFT), demonstrated that the ICD is associated with a significant survival benefit for patients with reduced ejection fraction (< 0.30–0.35) particularly if heart failure symptoms are present. Finally the implantable loop recorder has become an important diagnostic tool for the patient with unexplained syncope. This brief overview summarizes the indications and follow-up of the wide array of implantable cardiac devices available to the clinical cardiologist.     

The role of prophylactic implantable cardioverter defibrillators in heart failure: Recent trials usher in a new era of device therapy

Sudden cardiac death (SCD) manifested as ventricular fibrillation or sustained ventricular tachycardia has been a major focus of cardiovascular research for more than three decades. Although mortality in patients with heart failure (HF) caused by left ventricular systolic dysfunction has declined in recent years through effective pharmacotherapeutic strategies, SCD remains the major cause of death in symptomatic HF, with little improvement by drug therapy. Although it is clear that the implantable cardioverter defibrillator (ICD) is efficacious and should be used to prevent a recurrence of sustained ventricular arrhythmia (secondary prevention) in most patients, the guidelines for prophylactic use of ICDs (primary prevention) are less well defined. The results of recent clinical trials examining the efficacy of prophylactic ICD therapy in HF patients have clarified the role of ICD treatment in this population. This article reviews these trials and summarizes our current approach to the prevention of SCD in HF.     

Clinical experience, complications, and survival in 70 patients with the automatic implantable cardioverter/defibrillator

Seventy patients received the automatic implantable defibrillator, five original devices and 72 modified second-generation devices using only bipolar rate sensing and delivering an R wave synchronous cardioverting/defibrillating shock, for either ventricular tachycardia or fibrillation. The primary clinical arrhythmia was sustained ventricular tachycardia in 32 patients, ventricular fibrillation in 20 patients, and both ventricular tachycardia and fibrillation in 18 patients. Before implantation of the device the patients had survived 3.1 +/- 2.3 arrhythmic episodes, including 1.9 +/- 1.7 cardiac arrest, and had received 4.0 +/- 2.1 antiarrhythmic drugs without improvement. Sixty-eight patients ultimately received devices. After a follow-up period of 8.9 +/- 7.7 months (range 1 to 33), 37 patients received a total of 463 discharges. Inability to determine the precise reason for most discharges and the unpleasant nature of the discharges were the major clinical problems encountered. Complications included postoperative death (one patient), lead problems (six patients), inadequate energy requiring explanation (two patients), and pocket infection (one patient. Life-table analysis revealed 6 and 12 month cardiovascular survival of 95.0% and 89.9% and sudden death survival of 98.2%. In our experience, survival with the automatic implantable cardioverter/defibrillator exceeds that with other forms of therapy.     

Baroreflex sensitivity and heart rate variability in the identification of patients at risk for life-threatening arrhythmias: implications for clinical trials

BACKGROUND: The need for accurate risk stratification is heightened by the expanding indications for the implantable cardioverter defibrillator. The Multicenter Automatic Defibrillator Implantation Trial (MADIT) focused interest on patients with both depressed left ventricular ejection fraction (LVEF) and the presence of nonsustained ventricular tachycardia (NSVT). Meanwhile, the prospective study Autonomic Tone and Reflexes After Myocardial Infarctio (ATRAMI) demonstrated that markers of reduced vagal activity, such as depressed baroreflex sensitivity (BRS) an heart rate variability (HRV), are strong predictors of cardiac mortality after myocardial infarction. METHODS AND RESULTS: We analyzed 1071 ATRAMI patients after myocardial infarction who had data on LVEF, 24-hour ECG recording, and BRS. During follow-up (21 +/- 8 months), 43 patients experienced cardiac death, 5 patients had episodes of sustained VT, and 30 patients experienced sudden death and/or sustained VT. NSVT, depressed BRS, or HRV were all significantly and independently associated with increased mortality. The combination of all 3 risk factor increased the risk of death by 22x. Among patients with LVEF<35%, despite the absence of NSVT, depressed BRS predicted higher mortality (18% versus 4.6%, P = 0.01). This is a clinically important finding because this grou constitutes 25% of all patients with depressed LVEF. For both cardiac and arrhythmic mortality, the sensitivity of lo BRS was higher than that of NSVT and HRV CONCLUSIONS: BRS and HRV contribute importantly and additionally to risk stratification. Particularly when LVEF is depressed, the analysis of BRS identifies a large number of patients at high risk for cardiac and arrhythmic mortalit who might benefit from implantable cardioverter defibrillator therapy without disproportionately increasing the number of false-positives.     

Induction of ventricular fibrillation predicts sudden death in patients treated with amiodarone because of ventricular tachyarrhythmias after a myocardial infarction.

OBJECTIVE--To examine the value of programmed electrical stimulation of the heart in predicting sudden death in patients receiving amiodarone to treat ventricular tachyarrhythmias after myocardial infarction. DESIGN--Consecutive patients; retrospective study. SETTING--Referral centre for cardiology, academic hospital. PATIENTS--106 patients with ventricular tachycardia (n = 77) or ventricular fibrillation (n = 29) late after myocardial infarction. INTERVENTIONS--Programmed electrical stimulation was performed while on amiodarone treatment for at least one month. MEASUREMENTS AND MAIN RESULTS--In 80/106 patients either ventricular fibrillation (n = 15) or sustained monomorphic ventricular tachycardia (n = 65) was induced. After a mean follow up of 50 (SD 40) months (1-144), 11 patients died suddenly and two used their implantable cardioverter debfibrillator. By multivariate analysis two predictors for sudden death were found: (1) inducibility of ventricular fibrillation under amiodarone treatment (P << 0.001), and (2) a left ventricular ejection fraction of < 40% (P < 0.05). The survival rate at one, two, three, and five years was 70%, 62%, 62%, and 40% respectively for patients in whom ventricular fibrillation was induced, and 98%, 96%, 94%, 94% for patients with induced sustained monomorphic ventricular tachycardia. Where there was no sustained arrhythmia, five year survival was 100%. CONCLUSIONS--In patients receiving amiodarone because of life threatening ventricular arrhythmias after myocardial infarction, inducibility of ventricular fibrillation, but not of sustained monomorphic ventricular tachycardia, indicates a high risk of sudden death.     

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.