Use of Left Ventricular Ejection Fraction or Wall-Motion Score Index in Predicting Arrhythmic Death in Patients Following an Acute Myocardial Infarction

All-cause mortality and morbidity following an acute myocardial infarction (AMI) are correlated to LV systolic dysfunction. The correlation is closest with mortality and morbidity associated with congestive heart failure (CHF). Prediction of arrhythmic death in patients with AMI relies on the correlation between arrhythmic death and "sudden unexpected death" defined as death within 1 hour of onset of new symptoms. Assessment of late potentials, heart rate variability (HRV), T wave alternans, arrhythmias seen on Holter monitoring or during exercise testing, electrophysiological testing, and baroreceptor assessment have all proven to be useful in the prediction of sudden death even when LV systolic function is known. In selected populations HRV is superior to LV systolic function assessment in predicting sudden death and/or arrhythmic events, and may even predict all-cause mortality with the same precision. Comparisons of other methods with LV function assessment should be interpreted with care because most methods have been evaluated in subgroups of infarct patients with a low risk of death. Results from a large series of high risk patients with AMI (the TRAndolapril Cardiac Evaluation study) have shown that even in patients with severe depressed LV systolic function around one-third of the patients will die suddenly. The current situation is that LV function appears to be the best method of predicting death whereas other methods appear very promising for detecting arrhythmic death in more selected populations. The optimal method for selecting patients at high risk of arrhythmic death has not yet been developed, but a combination of LV function and another method, i.e., HRV, appears promising. This may ensure that the enrolled patients have an increased risk of death and that this risk will be due to arrhythmic events. Patients with LVEF of 10% or less can be excluded as they will most likely not die suddenly.     

Heart Rate Dynamics and Vulnerability to Ventricular Tachyarrhythmias

Sudden arrhythmic death is the most common mode of death in Western countries. An increased understanding of the pathophysiology and trigger mechanisms of life-threatening ventricular tachyarrhythmias in patients with structural heart disease can provide a logical basis for improved therapeutic strategies in the prevention of sudden death. Analysis of heart rate variability (HRV) from ambulatory electrocadiographic recordings can identify the patients at increased risk for arrhythmic death after an acute myocardial infarction. Despite the epidemiological evidence of an association between low HRV and sudden arrhythmic death, the pathophysiological link of this association has not been completely understood. An important approach to understand this association is to investigate the heart rate dynamics before the spontaneous onset of life-threatening arrhythmias. Analysis of heart rate behaviour preceding the spontaneous onset of ventricular tachyarrhythmias has shown that overall HRV is impaired in patients who develop spontaneous ventricular tachycardia during the Holter recording. Recently, quantitative analysis of Poincare plots of successive R-R intervals has shown that reduced long-term R-R interval variability, associated with episodes of beat-to-beat sinus alternans, is a specific sign of a propensity for spontaneous onset of ventricular tachycardia. These studies suggest that abnormal heart rate behaviour reflects an electrical instability favoring the onset of life-threatening arrhythmia and provide evidence that altered neurohumoral or autonomic regulation is an important trigger mechanism for the spontaneous onset of life-threatening arrhythmia. Future research in larger patient populations will reveal whether analysis of dynamic behaviour of cardiac electrical signals will give new insights into the mechanisms of life-threatening arrhythmias and help in the development of new therapeutic options for the prevention of sudden arrhythmic death.     

Drug and drug-device therapy in heart failure patients in the post-COMET and SCD-HeFT era

Reduced left ventricular ejection fraction and heart failure are the most important risk factors for sudden cardiac death. Recent trials have contributed to the knowledge base of critical therapies for the treatment of left ventricular systolic dysfunction and heart failure as it relates to arrhythmic and sudden cardiac death. Both pharmacologic and device therapies can reduce sudden cardiac death. The trials discussed in this paper have identified the pharmacologic and device interventions that are likely to improve the length and quality of life of the patient with left ventricular dysfunction and reduce the risk of sudden cardiac death. The mortality and anti-arrhythmic effects of angiotensin-converting enzyme inhibitors and beta-blockers have been confirmed in large-scale controlled clinical heart failure trials. Recent trials have evaluated which agents are most effective and which patients will derive the most benefit from device therapy in terms of the reduction in the risk of sudden cardiac death and in the amelioration of heart failure. The recent data from the Carvedilol or Metoprolol European Trial (COMET) and the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) are discussed as the latest in the series of landmark studies that have shaped the current approaches to treating patients with heart failure and that have altered the heart failure treatment paradigm.     

Late Gadolinium Enhancement in Patients with Nonischemic Dilated Cardiomyopathy

One‐third of all patients with heart failure have nonischemic dilated cardiomyopathy (NIDM). Five‐year mortality from NIDM is as high as 20% with sudden cardiac death (SCD) as the cause in 30% of the deaths. Currently, the left ventricular ejection fraction (LVEF) is used as the main criteria to risk stratify patients requiring an implantable cardioverter defibrillator (ICD) to prevent SCD. However, LVEF does not necessarily reflect myocardial propensity for electrical instability leading to ventricular tachycardia (VT) or ventricular fibrillation (VF). Due to the differential risk in various subgroups of patients for arrhythmic death, it is important to identify appropriate patients for ICD implantation so that we can optimize healthcare resources and avoid the complications of ICDs in individuals who are unlikely to benefit. We performed a systematic search and review of clinical trials of NIDM and the use of ICDs and cardiac magnetic resonance imaging with late gadolinium enhancement (LGE) for risk stratification. LGE identifies patients with NIDM who are at high risk for SCD and enables optimized patient selection for ICD placement, while the absence of LGE may reduce the need for ICD implantation in patients with NIDM who are at low risk for future VF/VT or SCD.     

Antiarrhythmic therapy in patients with heart failure

In patients with severe chronic heart failure, many deaths are sudden due to life-threatening ventricular arrhythmias. Supraventricular arrhythmias such as paroxysmal or chronic atrial fibrillation may also cause serious complications in those patients due to acute loss of atrial contraction, pump failure during rapid ventricular response and embolic events. Two therapeutic strategies are currently available for therapy and prevention of malignant ventricular arrhythmias and subsequent sudden arrhythmic death: antiarrhythmic drug therapy and implantable defibrillators. However, selection of the most beneficial strategy for the individual patient to reduce the risk of sudden death remains a major challenge in cardiology. Betablockers exert a favorable antiarrhythmic action without increasing proarrhythmia, thus betablockers may serve as a basic medication in patients at risk for sudden death. However, the general use of antiarrhythmic drug therapy for symptomatic ventricular arrhythmias is not recommended, as these drugs have been shown to increase mortality in patients with severe congestive heart failure due to proarrhythmic or negative inotropic effects (e.g. class Ia antiarrhythmics). Even class III antiarrhythmic drugs such as amiodarone, which has been studied sufficiently in patients with left ventricular dysfunction, is not effective enough for significant reduction of cardiac mortality in patients with symptomatic ventricular arrhythmias and depressed ventricular function (e.g. EMIAT, CAMIAT). But as a positive result of available studies, amiodarone does not increase mortality in those patients. Dofetilide has also not been shown to prolong life significantly by suppressing malignant ventricular arrhythmias (DIAMOND-Study). In patients with symptomatic ventricular arrhythmias or aborted sudden death, ICD therapy has been proven to be superior to antiarrhythmic drug therapy in cardiac mortality reduction as a secondary prevention strategy (e.g. AVID, CASH, CIDS). For primary prevention of sudden arrhythmic death in high risk patients, 2 studies (MADIT, MUSST) have already demonstrated favorable results, decreasing mortality by ICD therapy in selected patient populations with partly-reduced ventricular function and unsustained but inducible ventricular tachycardias. This topic is, however, undergoing further evaluation by ongoing trials (e.g. MADIT II, SCD-HeFT). From available data, antiarrhythmic drug therapy in high risk patients is not justified on a routine basis, whereas ICD therapy as a secondary and perhaps primary prevention strategy will significantly reduce cardiac mortality in patients with severe heart failure. Sotalol, a class III antiarrhythmic agent, has recently been shown to reduce ICD-shock delivery which indicates that concomitant drug therapy in patients with an ICD device already implanted may be beneficial in terms of reducing ICD discharges due to ventricular and supraventricular tachycardias. In patients with paroxysmal atrial fibrillation and congestive heart failure, restitution of sinus rhythm is the primary therapeutic goal which can be safely achieved by amiodarone and dofetilide (DIAMOND). In the latter, continuous monitoring of the patient is mandatory because of increased risk of torsade de pointes arrhythmias during the first days of drug administration. In patients with chronic atrial fibrillation rate control and anticoagulation with warfarin is the primary therapeutic option, which can be achieved with either drug treatment (Digoxin, betablockers, amiodarone) or by His bundle ablation with subsequent pacemaker insertion.     

Chemoreflexsensitivity in Patients with Survived Sudden Cardiac Arrest and Prior Myocardial Infarction

For evaluation of patients with an increased risk of sudden cardiac death, the analyses of ventricular late potentials, heart rate variability, and baroreflexsensitivity are helpful. But so far, the prediction of a malignant arrhythmic event is not possible with sufficient accuracy, For a better risk stratification other methods are necessary. In this study the importance of the ChRS for the identification of patients at risk for ventricular tachyarrhythmic events should be investigated. Of 41 patients included in the study, 26 were survivors of sudden cardiac arrest. Fifteen patients were not resuscitated, of whom 6 patients had documented monomorphic ventricular tachycardia and 9 had no ventricular tachyarrhythmias in their prior history. All patients had a history of an old myocardial infarction (> 1 year ago). For determination of the ChRS the ratio between the difference of the RR intervals in the ECG and the venous pO₂ before and after a 5-minute oxygen inhalation via a nose mask was measured (ms/mmHg). The 26 patients with survived sudden cardiac death showed a significantly decreased ChRS compared to those patients without a tachyarrhythmic event (1.74 ± 1.02 vs 6.97 ± 7.14 ms/mmHg, P < 0.0001). The sensitivity concerning a survived sudden cardiac death amounted to 88% for a ChRS below 3.0 ms/mmHg. During a 12-month follow-up period, the ChRS was significantly different between patients with and without an arrhythmic event (1.64 ± 1.06 vs 4.82 ± 5.83 ms/mmHg, P < 0.01). As a further method for evaluation of patients with increased risk of sudden cardiac death after myocardial infarction the analysis of ChRS seems to be suitable and predicts arrhythmias possibly more sensitive than other tests of neurovegetative imbalance. The predictive importance has to be examined by prospective investigations in larger patient populations.     

Prediction of arrhythmic events with positron emission tomography: PAREPET study design and methods

BACKGROUND: In medically-treated patients with ischemic cardiomyopathy, myocardial viability is associated with a worse prognosis than scar. The risk is especially great with hibernating myocardium (chronic regional dysfunction with reduced resting flow), and the excess mortality appears to be due to sudden cardiac death (SCD). Hibernating myocardium also results in sympathetic nerve dysfunction, which has been independently associated with risk of SCD. OBJECTIVES: PAREPET is a prospective, observational cohort study funded by NHLBI. It is designed to determine whether hibernating myocardium and/or inhomogeneity of sympathetic innervation by positron emission tomography imaging identifies patients with ischemic cardiomyopathy who are at high risk for SCD and cardiovascular mortality. METHODS: Patients with documented ischemic cardiomyopathy, an ejection fraction of 相似文献   

Prognosis, risk stratification,and management of asymptomatic individuals with Brugada syndrome: A systematic review

Brugada syndrome (BrS) is a primary electrical disease associated with increased risk of sudden cardiac death due to polymorphic ventricular arrhythmias. The prognosis, risk stratification, and management of asymptomatic individuals remain the most controversial issues in BrS. Furthermore, the decision to manage asymptomatic patients with an implantable cardioverter‐defibrillator should be made after weighing the potential individual risk of future arrhythmic events against the risk of complications associated with the implant and follow‐up of patients living with such devices, and the accompanying impairment of the quality of life. Several clinical, electrocardiographic, and electrophysiological markers have been proposed for risk stratification of subjects with BrS phenotype, but the majority have not yet been tested in a prospective manner in asymptomatic individuals. Recent data suggest that current risk factors are insufficient and cannot accurately predict sudden cardiac death events in this setting. This systematic review aims to discuss contemporary data regarding prognosis, risk stratification, and management of asymptomatic individuals with diagnosis of Brugada electrocardiogram pattern and to delineate the therapeutic approach in such cases.     

Sudden cardiac death in adults with congenital heart disease

Sudden cardiac death is one of the leading causes of death in patients with congenital heart disease, especially in patients with repaired cyanotic and left heart obstructive lesions. While the overall annual incidence of sudden cardiac death is relatively low, estimated at 0.09% per year, this nonetheless represents a many-fold increase over that of comparable age-matched control populations. The most frequent cause of sudden cardiac death is believed to be arrhythmic, usually ventricular arrhythmia. Most studies investigating risk factors for ventricular arrhythmia and/or sudden cardiac death have focused on patients with repaired tetralogy of Fallot and patients with Mustard/Senning repair for complete transposition of the great arteries. Despite a multitude of risk factors, their predictive value for the occurrence of sudden cardiac death is relatively low. Current experience with implantable cardioverter defibrillators in this patient population is limited to observational studies and the selection of patients for prophylactic implantable cardioverter defibrillator implantation is impeded both by the absence of randomized trials and weak predictors. Catheter ablation of ventricular tachycardia has emerged as a promising therapy for abolishing or reducing the burden of arrhythmia but experience is still limited and the impact on long-term outcome uncertain. Future studies will have to focus on improving risk stratification of patients with congenital heart disease.     

Rhythm disorders in isolated left ventricular noncompaction

Abstract

Both supraventricular and ventricular rhythm disorders are frequently observed in patients with isolated left ventricular noncompaction (IVNC). Most importantly, these patients are prone to develop life-threatening ventricular arrhythmias, which are amongst their most frequent causes of death. Data regarding risk stratification of ventricular arrhythmias, however, are scarce due to the rareness of the disease. Indeed, even invasive electrophysiological studies may be of limited value in this regard in the majority of patients. Implantable cardioverter defibrillators (ICDs) have been demonstrated to be highly effective for the prevention of sudden arrhythmic death in IVNC and should be considered in patients who are clinically judged to be at high risk for ventricular tachyarrhythmias. These include patients with a severely reduced ejection fraction as well as those with a prior history of sustained ventricular tachycardia or fibrillation, recurrent syncope of unknown etiology, or a family history of ventricular tachyarrhythmias or sudden cardiac death. This review summarizes the electrocardiographic and electrophysiological findings in patients with IVNC and discusses possibilities for risk stratification as well as the rationale for ICD implantation for the prevention of sudden cardiac death.     

Rhythm disorders in isolated left ventricular noncompaction

Both supraventricular and ventricular rhythm disorders are frequently observed in patients with isolated left ventricular noncompaction (IVNC). Most importantly, these patients are prone to develop life-threatening ventricular arrhythmias, which are amongst their most frequent causes of death. Data regarding risk stratification of ventricular arrhythmias, however, are scarce due to the rareness of the disease. Indeed, even invasive electrophysiological studies may be of limited value in this regard in the majority of patients. Implantable cardioverter defibrillators (ICDs) have been demonstrated to be highly effective for the prevention of sudden arrhythmic death in IVNC and should be considered in patients who are clinically judged to be at high risk for ventricular tachyarrhythmias. These include patients with a severely reduced ejection fraction as well as those with a prior history of sustained ventricular tachycardia or fibrillation, recurrent syncope of unknown etiology, or a family history of ventricular tachyarrhythmias or sudden cardiac death. This review summarizes the electrocardiographic and electrophysiological findings in patients with IVNC and discusses possibilities for risk stratification as well as the rationale for ICD implantation for the prevention of sudden cardiac death.     

Out-of-hospital cardiac arrest in patients with cardiac amyloidosis: presenting rhythms, management and outcomes in four patients

Primary systemic amyloidosis (AL) is a well-recognized systemic disease, and cardiac amyloidosis accounts for 10% of all nonischemic cardiomyopathies [J S C Med Assoc 97 (2001) 201-206]. The median survival of patients with symptomatic congestive heart failure secondary to cardiac amyloidosis is 4 months [New Engl J Med 336 (1997) 1202-1207; Am J Med 100 (1996) 290-298]. The cause of death in most patients is refractory congestive heart failure or sudden arrhythmic [Mayo Clin Proc 59 (1984) 589-597]. While there are reports of in-hospital arrhythmic deaths in these patients, there are no detailed reports that describe the presentation and management of patients with cardiac amyloidosis who have experienced an out-of-hospital cardiac arrest (OHCA). We describe here our experience with four patients with AL who had an OHCA, including presenting rhythms, interventions, and outcomes.     

Regional Cardiac Sympathetic Nervous System Evaluation Using 123I-mIBG SPECT in Patients with Heart Failure

BackgroundHeart failure (HF) involves both mechanical and autonomic nervous system dysfunction that can lead to sudden cardiac death. In the failing human heart, there is increased release of norepinephrine from neurons and reduced uptake. Iodine-123–labeled metaiodobenzylguanidine (123I-mIBG) demonstrates reduced global uptake and increased washout associated with increased mortality in HF. This research examined the potential benefits of single-photon emission computed tomography (SPECT) regional quantitation in risk stratification of HF patients and its role in prediction of cardiac morbidity and mortality.MethodsTwenty-two clinically diagnosed HF patients were recruited into this study. The subjects underwent myocardial perfusion SPECT and cardiac sympathetic imaging with 123I-mIBG. Early (at 15 min after injection) and delayed (four hours after injection) planar and SPECT were performed. Visual and semiquantitative analysis was conducted, and global (from planar imaging) and regional (from SPECT imaging) uptake and washout indices determined. The patients were clinically followed for up to two years, and the cardiac events (CEs) in these patients were recorded and correlated with the various parameters.ResultsThe occurrence of a CE in HF was independent of the patients' demographics or the cause of HF. Genetic biomarkers were unable to reliably predict CEs. Global or regional uptake had limited ability to predict a CE, whereas regional washout from the inferior wall (P = .005) was a statistically significant predictor of CEs. Similarly, a high washout of 40% or more from the peri-infarcted and noninfarcted segments on myocardial perfusion scintigraphy was also a significant predictor of CEs (P = .035).ConclusionHF is a complex, multifactorial, progressive disease that appears to begin regionally. 123I-mIBG provides a valuable tool in imaging the global and regional sympathetic nervous system innervation of the heart. This may allow early identification and stratification of patients at risk of sudden cardiac death.     

Arrhythmogenic right ventricular cardiomyopathy/dysplasia: a review and update

Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a predominantly genetically determined and heritable form of cardiomyopathy that is characterized pathologically by the replacement of myocytes by adipose and fibrous tissue and leads to right ventricular failure, arrhythmias, and sudden cardiac death. The estimated prevalence of ARVC/D in the general population ranges from 1 in 2,000 to 1 in 5,000, men are more frequently affected than women, with an approximate ratio of 3:1. ARVC/D can be inherited as an autosomal dominant disease with reduced penetrance and variable expression, autosomal recessive inheritance is also described. There have been 12 genes identified which are linked to ARVC/D, encoding several components of the cardiac desmosome. Dysfunctional desmosomes resulting in defective cell adhesion proteins, such as plakoglobin (JUP), desmoplakin (DSP), plakophilin-2 (PKP-2), and desmoglein-2 (DSG-2) consequently cause loss of electrical coupling between cardiac myocytes, leading to myocyte cell death, fibrofatty replacement and arrhythmias. Diagnosis is based on the finding a combination of characteristic abnormalities in family history, electrocardiography, cardiac imaging as well as endomyocardial biopsy (original task force criteria). Therapeutic options remain limited because of the progressive nature of ARVC/D. Competitive athletics should be avoided. Patients with ARVC/D with a history of having been resuscitated from sudden cardiac death, patients with syncope, very young patients, and those who have marked right ventricular involvement are at the highest risk for arrhythmic death and also, the presence of left ventricular involvement is a risk factor. Several authors concluded that patients who meet the Task Force criteria for ARVC/D are at high risk for sudden cardiac death and should undergo ICD placement for primary and secondary prevention, regardless of electrophysiologic testing results. The role of electrophysiologic study and VT catheter ablation in ARVC/D remains poorly defined, and is frequently used as a palliative measure for patients with refractory VT. The progressive nature of ARVC/D suggests that catheter ablation would not be a long-term curative procedure. Sotalol proved to be highly effective in patients with ARVC/D and inducible as well as non-inducible ventricular tachycardia; if it is ineffective in inducible ventricular tachycardia response to other antiarrhythmic drugs is unlikely and therefore non-pharmacological therapy without further drug testing should be considered. Orthotopic heart transplantation is considered in patients with progressive heart failure and intractable recurrent ventricular arrhythmias     

Prognosis of hypertrophic and dilated cardiomyopathy

Hypertrophic and dilated cardiomyopathies are a heterogeneous disease, both clinically and genetically. Hypertrophic cardiomyopathy(HCM) is important causes of sudden cardiac death and death from congestive heart failure, although HCM has a relatively benign prognosis. The prognosis of dilated cardiomyopathy(DCM) has improved due to advances in earlier diagnosis and therapy, however, sudden cardiac death and death from congestive heart failure still occur in DCM. Accordingly, it is of importance to know possible risk factors on risk stratification for a high-risk group in HCM and DCM. Possible risk factors may contribute to the construction of therapeutic strategies for the prevention of sudden cardiac death or death from congestive heart failure in patients with HCM and DCM.     

Heart Rate Variability and Major Arrhythmic Events in Patients with Idiopathic Dilated Cardiomyopathy

This prospective study of 71 patients with idiopathic dilated cardiomyopathy (IDC) and preserved sinus rhythm was designed to evaluate the relation between heart rate variability (HRV) and subsequent major arrhythmic events. Standard time- and frequency-domain HRV parameters were obtained from analysis of 24-hour Holter ECG recordings. During a mean follow-up of 15 ± 5 months, major arrhythmic events including sustained ventricular tachycardia, ventricular fibrillation, and sudden cardiac death occurred in 10 of the 71 study patients (14%). Neither time- nor frequency-domain indices of HRV differed significantly between patients with and patients without subsequent major arrhythmic events. However, there was a trend toward a lower standard deviation of the average normal RR interval for all 5-minute segments of the 24-hour recording (68 ± 17 ms vs 80 ± 31 ms; P = 0.06) in patients with major arrhythmic events. In addition, the percentage of adjacent normal RR intervals differing > 50 ms over the recording period tended to be lower in patients with major arrhythmic events (6%± 3% vs 9%± 6%; P = 0.08). Our results indicate a tendency toward attenuated parasympathetic activity in IDC patients with subsequent major arrhythmic events compared to arrhythmia-free patients. Larger studies with longer follow-up periods are necessary to clarify the role of HRV measurements for arrhythmia risk prediction in patients with IDC.     

Wearable defibrillator

Technological advances have increased life expectancy and improved quality of life for patients with heart disease. A new device, called the wearable defibrillator, is designed to provide monitoring and defibrillation capability for patients who have had an infarct and those awaiting heart transplantation. These two populations of patients are at increased risk of sudden cardiac death. This external wearable apparatus continuously monitors a patient's heart rhythm. The monitor is programmed to recognize the individual's heart rhythm. If the heart rhythm changes and meets criteria for a lethal dysrhythmia, the monitor will provide a series of alarms to the patient and bystanders. If the patient fails to respond to the alarms, because of loss of consciousness, the system delivers a shock to treat the life-threatening dysrhythmia. Although still in the investigational phase, this device holds promise as temporary protection for patients at risk for sudden cardiac death.     

Arrhythmias

There are several underlying factors including anatomical substrates (coronary artery disease, cardiomyopathy, valvular disease, congenital heart disease, WPW syndrome) and modulating factors(autonomic nervous system, electrolyte balance, drugs) which may induce sudden cardiac death. Although studies evaluating mechanisms of sudden cardiac death are increasing, evaluation of risk of each patient and effectiveness of preventive treatments are still inadequate. Sudden death due to life threatening arrhythmias in the out-of-hospital situation can be resuscitated by non-medical staff with automated external defibrillator. In these resuscitated high-risk patients implantable cardioverter and defibrillator could be used to prevent sudden death due to unpreventable further arrhythmic episodes. Widespread availability of automated external defibrillator is mandatory.     

Heart failure

Survival of patients with heart failure has improved over the past decade due to advances in medical therapy. However, sudden cardiac death continues to cause 35 to 65% of death. Ventricular arrhythmias are important causes of sudden cardiac death in patients with heart failure. The risks of antiarrhythmic drugs are increased in patients with heart failure. Therefore, in the absence of a clear indication, antiarrhythmic drug therapy should be avoided. A number of recent randomized trials have provided evidence that beta-adrenergic blockers, angiotensin-converting enzyme(ACE) inhibitors and angiotensin II receptor blockers(ARB) significantly reduces the risk of sudden death in patients with chronic congestive heart failure. For patients who have a history of sustained ventricular tachycardia(VT) or ventricular fibrillation(VF) amiodarone or an implantable cardioverter defibrillator(ICD) should be considered, and these therapy may benefit some high risk patients who have nonsustained VT.