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.     

Treatment of arrhythmias in patients with congestive heart failure

Both ventricular and atrial arrhythmias are commonly encountered in patients with ventricular dysfunction. In fact, roughly half of the deaths occurring in patients with ventricular dysfunction are caused by ventricular arrhythmias. Atrial arrhythmias in this patient population compromise left ventricular filling and if uncontrolled can exacerbate (and in some cases cause) the underlying myopathic process. Consequently, the diagnosis and treatment of these complex, and often life-threatening, arrhythmias is a critical component in the management of congestive heart failure (CHF). As the complexity of pharmacologic and nonpharmacologic antiarrhythmic therapy evolves, it has become increasingly important to understand the potential benefits and limitations of the various treatment modalities in the setting of patients with CHF. The management of arrhythmias in patients with CHF includes conventional drug therapies, as well as therapies directed specifically at treating the arrhythmias that are encountered. The treatment of atrial arrhythmias may include anticoagulation, drugs for rate control, rhythm control, or radiofrequency ablation. The treatment of ventricular arrhythmias, conversely, uses the implantable cardioverter-defibrillator to prevent sudden death, with adjuvant drug therapy or ablation for refractory ventricular tachycardia. This article provides an overview of the current state-of-the-art arrhythmia management in patients with CHF.     

Arrhythmia and sudden death in congestive heart insufficiency

The author emphasizes the current reawakening of interest of clinicians and investigators in congestive heart failure (CHF) as a consequence of the known bad prognosis of this syndrome and the new diagnostic techniques and drugs they may use in patients with this syndrome. The central topic of the paper deals with the relation between arrhythmias and sudden death (SD) in patients with CHF and is subdivided in five points: 1. Prevalence of SD in patients suffering from CHF; 2. Prevalence of ventricular arrhythmias in patients with CHF; 3. Prognostic value of ventricular arrhythmias on survival in patients with CHF; 4. Effect of antidysrhythmic drugs on survival in patients suffering from CHF; and 5. Different repercussion of drug therapy on rhythmic profile of patients with CHF. The analysis of these five points is supported by a revision of the literature on this subject and leads to some final comments, in which the author tries to do the state-of-the-art of the problem of the relation between arrhythmias and SD in patients suffering from CHF.     

Safety of encainide for the treatment of ventricular arrhythmias

A data base of 1,245 patients treated for ventricular arrhythmias, most of whom had serious cardiac disease, was reviewed. Only 2.9% of these patients had benign ventricular arrhythmias without structural heart disease. The overall incidence of proarrhythmia in this population was 9.2% (115/1,245), but was as frequent as 16% in patients with a history of cardiomyopathy. The proarrhythmic form was new sustained ventricular tachycardia in 22 patients (1.8%). Only 2 of 71 patients (2.8%) with primary arrhythmia had a proarrhythmic event. The incidence has decreased markedly over the past years as reduced doses and gradual titration have been used. There were 137 deaths in the data base of which 82 were sudden, all in patients with advanced (79) or moderately severe (3) cardiac disease. High initial doses, prior myocardial infarction and congestive heart failure (CHF) were positively associated with sudden cardiac death. There were no deaths among the 71 patients with benign arrhythmias. Death rates were related to the severity of the arrhythmia being treated. Comparisons with published survival curves indicated modest improvement; in no case was survival decreased. Invasive and noninvasive measures of left ventricular function indicated no adverse hemodynamic effects. There was only 1 case of new and 3 cases of worsened CHF probably related to encainide. Only 5 patients discontinued for CHF or related signs and symptoms. The most frequent drug-related noncardiac adverse reactions were dizziness (26%), abnormal or blurred vision (19%), QRS interval prolongation (5%), taste perversion (4%) and tremor (3%). In conclusion, the use of reduced doses and gradual titration of encainide has markedly decreased the incidence of proarrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Factors causing arrhythmias in chronic congestive heart failure

Severe congestive heart failure (CHF) is a common syndrome with a high mortality rate (about 50% in 1 year among patients with symptoms at rest). Severity of left ventricular dysfunction is the most important adverse prognostic factor. Serious arrhythmias are common in CHF and also increase the mortality rate. Sudden death is the mode of death in about 40% of patients with severe heart failure. Multiple factors contribute to arrhythmias in CHF, including left ventricular dysfunction, myocardial ischemia, catecholamines, electrolyte disturbances, and drugs used to treated the heart failure. Minimizing or correcting these influences may be important in reducing serious arrhythmias. Antiarrhythmic drugs may be important in reducing the incidence of sudden doath among patients with severe heart failure, although this has not yet been proved.     

Evaluation of the patient with congestive heart failure and ventricular arrhythmias

Although vasodilators and new inotropic agents have been shown to improve ventricular function and reduce symptoms, their effect on mortality is uncertain. In view of our failure to reduce mortality in patients with congestive heart failure (CHF), the identification and amelioration of potentially reversible factors that might alter survival are crucial before initiating therapy. The first step is to establish the diagnosis of CHF and the presence or absence of dilated congestive cardiomyopathy. The extent of myocardial dysfunction, both right and left, must also be evaluated. In post-myocardial infarction patients, left ventricular ejection fraction is an important indicator of prognosis during the first 1 to 2 years. However, in patients with chronic CHF and dilated cardiomyopathy, right ventricular ejection fraction may be a more effective predictor of survival. The presence, frequency and complexity of ventricular arrhythmias must be determined, because these arrhythmias may independently increase the risk of sudden cardiac death in patients with ischemic cardiomyopathy. Their role in patients with idiopathic cardiomyopathy is less certain. In addition, myocardial ischemia, left ventricular dyskinesis or aneurysm, occult myocarditis and neurothrombosis formation must be ruled out. Detection and correction of serum electrolyte and neurohumeral abnormalities are essential. Our failure to reduce mortality in patients with CHF may not entirely lie in the lack of effective therapeutic agents but rather in our failure to apply properly the diagnostic and therapeutic approaches now available.     

Chemosensitivity in chronic heart failure

Augmented peripheral and central chemoreceptor sensitivity has recently been demonstrated in both experimental and clinical settings of chronic heart failure (CHF). As a result of the effects of chemoreflexes on the respiratory, circulatory and neurohormonal systems, changes in their activity may account for several pathophysiological features of CHF--predominantly augmented ventilation, abnormal cyclic respiratory pattern and sympathetic overactivity. Although the precise underlying mechanisms are not known, a heightened chemoreflex drive may constitute an ominous sign in CHF. Patients with abnormally elevated chemosensitivity demonstrate an augmented ventilatory response to exercise, a severely impaired autonomic regulation and suppression of baroreceptor function, and a higher prevalence of ventricular arrhythmias. All these factors may unfavorably influence the prognosis of CHF. In fact, we have recently confirmed in a group of patients with advanced CHF that high peripheral chemosensitivity is an independent predictor of death. New therapies are needed in CHF to improve prognosis and quality of life. Drugs, such as opiates, and oxygen administration have been shown to suppress chemosensitivity, which may further favorably influence exercise tolerance and modify periodic breathing in CHF patients. Treatment strategies targeted at peripheral and central chemoreceptors may be a promising option for further evaluation.     

Newer concepts in the medical management of patients with congestive heart failure

Congestive heart failure (CHF) remains a major cause of morbidity and mortality in the United States, especially among the elderly. Although an underlying disturbance in cardiac function can be identified in most patients, manifestations of the disease are greatly influenced by other factors, particularly neurohumoral and peripheral adaptive responses which occur secondary to impaired cardiac function. The renin-angiotensin system (RAS) is integrally involved in the pathophysiology of CHF. Originally considered a humoral system, the RAS is now known to exist and operate within cardiac and vascular tissues. The importance of tissue-specific renin-angiotensin systems in CHF is presently under investigation. Most patients with symptomatic CHF benefit from the administration of an ACE inhibitor. Certain asymptomatic patients, such as those with severe left ventricular (LV) dysfunction and those who are at high risk for LV remodeling after anterior wall myocardial infarction, may also benefit from ACE inhibitor therapy. Diuretics and nitrates improve symptoms and often cardiac output in many patients with CHF. Although many new inotropic agents have been tested in CHF patients, none appear clinically superior to digitalis glycosides. The efficacy of digitalis glycosides in CHF may in part result from sympathoinhibitory properties such as the activation of baroreceptor mechanisms. Despite the fact that many CHF patients die from arrhythmias, treatment of asymptomatic ventricular arrhythmias in these patients is not recommended. Patients with symptomatic or sustained ventricular arrhythmias are best treated by a physician experienced in cardiac electrophysiology. Therapy with beta-blocking drugs for CHF patients is controversial. Anticoagulants are recommended for selected patients with CHF. Finally, exercise therapy may improve functional capacity in some patients with CHF through its effects on peripheral blood vessels and skeletal muscle tissues.     

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.     

Congestive heart failure and arrhythmias: an overview

Arrhythmias are common in patients with congestive heart failure (CHF), especially those with concomitant ischemic heart disease. The degree of left ventricular dysfunction is the most important indicator of prognosis in patients with severe heart failure. In general, the better the patient's ventricular function, the greater his chance of survival. In addition, the severity of arrhythmias is also related to survival; patients with simple arrhythmias have higher survival rates than those with complex arrhythmias. All drugs used in the treatment of CHF have a potential proarrhythmic effect. In a study involving the new class of positive inotropic agents, a trend toward higher mortality was evident in CHF patients with ischemic heart disease compared with those with congestive dilated cardiomyopathy. A subgroup of patients also treated with antiarrhythmic agents had lower sudden death rates than those not receiving antiarrhythmics. A double-blind clinical trial of antiarrhythmic agents for patients with CHF is warranted.     

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.     

The prevalence and prognostic significance of arrhythmias in Duchenne type muscular dystrophy.

To investigate the prevalence and prognostic significance of cardiac arrhythmias in Duchenne type muscular dystrophy 24-hour ambulatory ECG was performed in 80 patients with Duchenne type muscular dystrophy, and they were followed up for 5 years. Various arrhythmias were observed in 63.8% (51 of 80) of the patients. Ventricular premature beats were found in 30% (24 of 80), and the incidence of ventricular premature beats increased as the clinical severity of skeletal muscle involvement advanced. Forty-seven patients survived for 5 years, but the incidence of arrhythmias increased from 38.3% (18 of 47) to 74.5% (35 of 47) (p < 0.001). During the 5-year period, four of 33 deaths were sudden. Malignant ventricular premature beats (ventricular couplets, ventricular tachycardia, and R-on-T-type ventricular premature beats) were observed in three of these four patients. It appears that cardiac arrhythmias are a common complication of Duchenne type muscular dystrophy and that the incidence of ventricular arrhythmias increases with the progression of myocardial involvement. There is an association between ventricular arrhythmias and sudden death, but the reduction of ventricular arrhythmias may not reduce the incidence of episodes of sudden death.     

Ambulatory ventricular arrhythmias in patients with heart failure do not specifically predict an increased risk of sudden death. PROMISE (Prospective Randomized Milrinone Survival Evaluation) Investigators

BACKGROUND: Ventricular arrhythmias are a frequent finding in congestive heart failure (CHF) patients and a cause of concern for physicians caring for them. Previous studies have reached conflicting conclusions regarding the importance of ventricular arrhythmias as predictors of sudden death in patients with CHF. This study examined the independent predictive value of ventricular arrhythmias for sudden death and all-cause mortality in PROMISE (Prospective Randomized Milrinone Survival Evaluation). METHODS AND RESULTS: Ventricular arrhythmias were analyzed and quantified by use of prespecified criteria on baseline ambulatory ECGs from 1080 patients with New York Heart Association (NYHA) class III/IV symptoms and a left ventricular ejection fraction 相似文献   

Dilated cardiomyopathy: recent advances and current treatment

The combination of dilatation and systolic dysfunction of the left or both ventricles from idiopathic or specific origin define dilated cardiomyopathy (DC). It is an important cause of cardiac morbidity through congestive heart failure (CHF) or arrhythmias. Prevalence studies estimate a rate of left ventricular systolic dysfunction of 2% to 3% or more, and of 1.5% of CHF among the general population. Genetic studies on familial DC have identified at least 5 genetic locus. In addition, the role of virus, genetic abnormalities, immunologic responses and increased myocardial apoptosis are factors recognized factors that play a significant role in the pathogenesis of idiopathic DC. Mortality in severe CHF may reach 50% at 2 years after diagnosis. The introduction of "triple" therapy combining diuretics, digoxin and angiotensin converting enzyme inhibitors (ACEI) has significantly decreased this high mortality. Recent large, multicentric clinical trials on drugs aimed to diminish the neuroendocrine hyperactivity of patients in stable chronic CHF (betablockers and spirolactone) have resulted in an additional reduction in total mortality of about 35% in relation with control groups. Betablockers, compared to ACEI, also diminish the rate of sudden death prompting their almost mandatory indication in the absence of contraindications. Cardiac transplantation presently offers a survival rate of 66% at 5 years but donor scarcity has stabilized the number of procedures. In patients resuscitated from malignant arrhytmias the implantation of defibrillators offers a better survival than drugs. Future advances in the knowledge of the pathogenesis and especially of genetic mechanisms, may substantially change the understanding and treatment of these disorders.     

Effects of aerobic exercise training on indices of ventricular repolarization in patients with chronic heart failure.

BACKGROUND: Patients with chronic heart failure (CHF) have a markedly increased incidence of malignant ventricular arrhythmias. QT dispersion (QTd), defined as the difference between maximal and minimal QT intervals, reflects the regional inhomogeneity of ventricular repolarization dispersion and may mark the presence of malignant ventricular arrhythmias. PURPOSE: To determine the effects of exercise training on QTd in patients with CHF. PATIENTS: Fifteen patients with CHF and ejection fractions < 40% (mean, 28+/-9%) who were on a stable medical regimen. DESIGN AND INTERVENTION: Standardized 12-lead surface ECGs were obtained at the beginning and end of the exercise training program, and QT and JT intervals were measured manually and corrected for heart rate by using Bazett's formula. QTd, heart rate-corrected QTd (QTc-d), JT dispersion (JTd), and heart rate-corrected JTd (JTc-d) were measured in at least eight ECG leads in each patient. RESULTS: Following the cardiac rehabilitation and exercise training programs, patients with CHF had only slight improvements in exercise capacity (results were not significant). However, these patients had marked improvements in QTd (71+/-11 to 59+/-17 ms; p < 0.02), QTc-d (82+/-28 to 63+/-17 ms; p < 0.01), JTd (76+/-19 to 57+/-18 ms; p < 0.002), and JTc-d (84+/-23 to 61+/-18 ms; p < 0.001) following the exercise training programs. CONCLUSION: These data indicate that aerobic exercise training significantly reduces the indices of ventricular repolarization dispersion in patients with CHF. Further studies are needed to evaluate how effectively this reduction in ventricular repolarization dispersion decreases the risk of malignant ventricular arrhythmias and sudden death in patients with CHF.     

Age and Sex as Determinants of Ventricular Arrhythmic Events in Patients with Decompensated Congestive Heart Failure

Background: The propensity to develop specific arrhythmias varies between the sexes and is influenced by age. Patients with congestive heart failure (CHF) have a high prevalence of ventricular ectopy. However, in the setting of CHF, it is not known whether sex‐related or age‐dependent differences exist in the susceptibility to arrhythmias. Methods: The study population included 134 men and 73 women (mean age 61 ± 14 years) admitted for decompensated CHF. The severity of ventricular arrhythmias was assessed by 24‐hour Holter monitoring. None of the patients were on parenteral vasoactive therapy during Holter recording. Results: All measures of ventricular ectopy were markedly lower in women. The average hourly premature ventricular contractions (PVCs), the frequency of ventricular pairs, the mean hourly repetitive ventricular beats, and the frequency of ventricular tachycardia episodes per 24 hours were 40%, 62%, 65%, and 78% lower in women, respectively. Multivariate logistic regression revealed that the risk of developing > 3 ventricular pairs per 24‐hour period (OR = 2.2, Cl = 1.1–4.2, P = 0.03), > 3 repetitive ventricular beats/hour (OR = 2.5, Cl = 1.2–5.3, P = 0.01), or an episode of ventricular tachycardia (OR = 2.1, CI = 1.2–3.9, P = 0.01) were significantly higher in men. Patients in the higher fertile age group had a higher risk for the presence of > 3 ventricular pairs per 24‐hour period (OR = 2.3, CI = 1.1–4.2, P = 0.03), and the presence of > 3 repetitive ventricular beats per hour (OR = 5.9, CI = 2.7–13.3, P < 0.0001), compared with patients in the lower age fertile. Conclusion: Male sex and age are associated with complex ventricular ectopy in patients with CHF. Further understanding of the mechanisms involved in the relative protection conferred by female sex would advance our understanding about arrhythmias in heart failure. A.N.E. 2002;7(3):234–241     

Dofetilide in patients with left ventricular dysfunction and either heart failure or acute myocardial infarction: Rationale,design, and patient characteristics of the DIAMOND studies

Background: Attempts to prolong life with antiarrhythmic drugs in patients at increased risk of sudden cardiac death have so far been disappointing or inconclusive. Hypothesis: The Danish Investigations of Arrhythmia and Mortality ON Dofetilide (DIAMOND) encompass two survival studies testing the prophylactic use of the selective potassium-channel blocker, dofetilide, in patients at high risk of sudden death. Methods: The first study includes patients admitted to hospital with congestive heart failure (CHF), the other includes patients with acute myocardial infarction (MI) within the previous 7 days. In both studies patients must have left ventricular systolic dysfunction (ejection fraction 35%) determined by echocardiography. Each of the two studies are planned to enroll 1500 patients. Consecutive hospitalized patients with MI or CHF are screened in 37 Danish hospitals. Eligible patients are randomized to receive dofetilide or matching placebo. All patients are continuously monitored by telemetry for the first 3 days of the study to detect possible arrhythmic events and to ensure resuscitation in case of serious arrhythmias. Minimum duration of follow-up is 12 months. Results: Between November 1993 and July 1996, a total of 5812 consecutive patients with CHF and 8688 consecutive patients with MI was screened for entry. Of these, 1518 patients were included in the CHF study and 1510 patients in the MI study. Overall 1-year mortality of randomized patients were 28 and 22%, respectively. Conclusion: DIAMOND will provide important data on the safety and efficacy of dofetilide in high-risk patients with left ventricular dysfunction and either CHF or MI, as well as evaluate tolerability in these populations.     

Prevalence and prognostic significance of exercise-induced ventricular arrhythmias after coronary artery bypass grafting

Exercise-induced ventricular arrhythmias occur often after coronary artery bypass grafting (CABG), but their prognostic significance is unknown. Two hundred patients examined by exercise electrocardiography and cardiac catheterization (including left ventriculography, bypass graft and native coronary artery angiography) before and 3 months after CABG were prospectively followed up. Exercise-induced ventricular arrhythmias occurred more often after (49 of 200 patients, 24.5%) than before (32 of 200 patients, 16.0%) CABG (p less than 0.05). There were no differences between the patients with and without ventricular arrhythmias in the prevalence of graft patency (79 vs 80%) or the postoperative ejection fraction (57 +/- 9 vs 57 +/- 12%). Ten cardiac deaths occurred during the mean follow-up time of 61 +/- 19 months, 8 of which were witnessed sudden cardiac deaths. All cardiac deaths occurred in patients who did not have exercise-induced ventricular arrhythmias after CABG. The postoperative ejection fraction was lower in the cardiac death patients (42 +/- 16%) than in the survivors (58 +/- 10%) (p less than 0.01). No other clinical or angiographic variable predicted the occurrence of cardiac death. Thus, the prevalence of exercise-induced ventricular arrhythmias increases after CABG, but the occurrence of ventricular arrhythmias does not indicate an increased risk of cardiac death.     

Ventricular arrhythmia in congestive heart failure.

The importance of ventricular arrhythmia is based on its association with sudden death. In certain groups of patients, ventricular arrhythmia--primarily runs of nonsustained ventricular tachycardia (NSVT)--is associated with an increased risk for sudden death. Although this relationship has been most often reported in patients with recent myocardial infarction, it has also been recognized in patients with dilated cardiomyopathy, regardless of etiology. Therefore, ventricular arrhythmia is common in patients with CHF due to cardiomyopathy. A number of studies have reported that 70-95% of patients with cardiomyopathy and congestive heart failure (CHF) have frequent ventricular premature beats, and 40-80% will manifest runs of NSVT. Many factors are responsible for ventricular arrhythmia in such patients, including structural abnormalities, electrolyte imbalance, hemodynamic impairment, activation of neurohormonal mechanisms, and pharmacologic therapy. Many studies have reported a high yearly mortality in patients with cardiomyopathy and CHF; greater than 40% of deaths are sudden, most often the result of sustained ventricular tachyarrhythmia. Most studies have noted an association between presence (and frequency) of NSVT and risk of sudden cardiac death in these patients. Unfortunately, other techniques--such as the signal-averaged electrocardiogram and electrophysiologic testing--are not helpful in identifying the individual at risk. Although several drug interventions will reduce mortality from progressive CHF, these drugs have not been shown to reduce sudden death and, indeed, have a variable effect on ventricular arrhythmia. Although NSVT is a marker for increased risk for sudden death, it is uncertain if antiarrhythmic drugs will prevent this outcome. Antiarrhythmic drugs have not been shown to be effective for preventing sudden death, although there are as yet no well-controlled randomized trials. Several studies suggest that amiodarone and beta blockers are beneficial, but this requires confirmation. For patients who have been resuscitated following an episode of sudden death due to a sustained ventricular tachyarrhythmia, antiarrhythmic therapy guided by invasive and noninvasive techniques appears to reduce risk of recurrent arrhythmia. However, the response rate to antiarrhythmic agents is low and side effects are common in patients with CHF. Especially important is the increased risk of precipitating CHF and aggravating the arrhythmia being treated. For many such patients who have had serious ventricular tachyarrhythmia, the automatic implantable cardioverter defibrillator may prove a better option. Other drugs used for management of CHF reduce overall mortality, but not risk of sudden death.     

Comparison of the occurrence of ventricular arrhythmias in patients with acutely decompensated congestive heart failure receiving dobutamine versus nesiritide therapy.

Ventricular arrhythmias are common in patients with congestive heart failure (CHF) and may be exacerbated by positive inotropic therapy. Because human B-type natriuretic peptide (nesiritide), an arterial and venodilator, inhibits sympathetic activity, it may decrease the incidence of arrhythmias. Our investigation compares the arrhythmogenicity of dobutamine with nesiritide. A total of 305 patients with decompensated CHF requiring intravenous vasoactive therapy were randomized to receive standard therapy (n = 102) or nesiritide (0.015 microg/kg/min [n = 103] or 0.030 microg/kg/min [n = 100]) to gain additional data on the relative safety and efficacy of nesiritide compared with standard parenteral care. Dobutamine was chosen as the standard care agent in 58 subjects. During study drug infusion, all patients had continuous clinical hemodynamic and electrocardiographic monitoring. The dobutamine and nesiritide groups were similar with respect to baseline use of antiarrhythmic agents, including beta blockers. Serious arrhythmias and the incidence of cardiac arrest were more common in patients who received dobutamine than in those taking nesiritide: sustained ventricular tachycardia, 4 (7%) versus 2 (1%), respectively (p = 0.014); nonsustained ventricular tachycardia, 10 (17%) versus 23 (11%), respectively (p = 0.029); cardiac arrest, 3 (5%) versus 0, respectively (p = 0.011). We conclude that among patients with decompensated CHF for whom dobutamine is selected as standard therapy, the incidence of serious ventricular arrhythmias and cardiac arrest is significantly greater than the incidence of these events in patients randomized to nesiritide.