Management of arrhythmias in heart failure

Arrhythmias continue to contribute significantly to morbidity and mortality in heart failure. Implantable defibrillators have assumed an increasingly important role in preventing sudden death and are recommended for patients who have been resuscitated from cardiac arrest, have unexplained syncope, or exhibit inducible ventricular tachycardia in the setting of prior myocardial infarction. The extension of survival conferred by implantable defibrillators is likely to be limited in patients with advanced heart failure. Ongoing trials will help define the use of these devices in heart failure populations, in whom atrial fibrillation is common and rate control and anticoagulation are of major importance. Among pharmaceutical options, amiodarone and dofetilide are the major agents for maintenance of sinus rhythm. The complexity of coexistent heart failure and arrhythmia management warrants close collaboration between heart failure and arrhythmia specialists.     

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.     

Ventricular arrhythmias in heart failure patients

Ventricular arrhythmia represents a significant cause of mortality and morbidity. Its pathophysiologic mechanisms and electroanatomic substrates are slowly being elucidated. Clinical management in patients with heart failure has progressed from antiarrhythmic drugs to device therapy. Catheter ablation is an effective adjunct in the management of ventricular arrhythmia but remains a significant challenge. Advances in robotic and magnetic catheter manipulation may shorten procedural time and increase safety. Incorporation of imaging technologies such as CT, MRI, or ultrasound with electroanatomic mapping can enhance the ability to map and ablate ventricular arrhythmia. Novel imaging modalities may provide rapid characterization of the substrate for ventricular dysfunction and arrhythmia development and the capacity for serial assessment of the disease progression, improving risk stratification for ventricular dysfunction and arrhythmia development and the capacity for serial assessment of the disease progression, improving risk stratification.     

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.     

Mechanisms of ventricular arrhythmias in heart failure

Congestive heart failure continues to be a leading cause of mortality and morbidity worldwide. In approximately 50% of these patients, the mode of death is sudden. Ventricular tachycardia and fibrillation represent the majority of arrhythmias; the mechanisms responsible are heterogeneous and complex. Myocardial scar, a potent environment for reentry, is likely to contribute to many of the ventricular arrhythmias in ischemic heart failure. Altered calcium handling and changes in potassium currents may contribute to the increase in early and delayed afterdepolarizations seen in the failing heart. In addition, compensatory mechanisms may become deleterious and potentially arrhythmogenic via a variety of mechanisms. This article provides a general overview of the mechanisms thought to be responsible for ventricular arrhythmias in chronic heart failure.     

Cardiac arrhythmias in chronic heart failure.

It has been proven that treatment of chronic heart failure (CHF) with some modern drugs is able to reduce mortality in groups of patients with the severest grades of this disease. The risk of sudden death has been unchanged, however. Out of 49 patients on long-term follow-up, 28 patients are surviving (group A) and 21 died (group B). 52.3% of the dead patients died suddenly. Eight patients in NYHA classes I-II died, all of them suddenly. Contrary to this, sudden death was the cause of death only in three of 13 patients in NYHA classes III-IV (p < 0.001). More severe heart failure was present in group B (NYHA class 2.95 +/- 0.96 vs. 2.18 +/- 0.48 in group A--p < 0.1). Antiarrhythmic drugs were given more frequently in group B (in 47.6% of pts vs. 17.9% in group A--p < 0.05). It is concluded that the occurrence of sudden death is higher in patients with less severe forms of CHF and has not been reduced by the means employed. Use of antiarrhythmic drugs may be dangerous and their indication should be based on results of a comprehensive examination. Use of the implantable cardioverter-defibrillator seems to be the most promising approach in indicated cases.     

The impact of arrhythmias in acute heart failure

BACKGROUND: Arrhythmias are common in chronic heart failure and affect outcomes. The incidence and significance of new arrhythmias in acute heart failure, however, are largely unknown. METHODS AND RESULTS: The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations study randomized 949 patients with decompensated heart failure to receive intravenous milrinone or placebo. In the study, patients were divided into 2 groups based on the occurrence of a new arrhythmic event during their index hospitalization and analyzed for outcome. There were 59 new arrhythmic events occurring in 6% of the population. Of these, 49% were atrial fibrillation/flutter. The primary endpoint of days hospitalized for cardiovascular causes within 60 days after randomization was 30.9+/-22.7 for those in the arrhythmia group and 11.3+/-12.7 days for those with no arrhythmias (P=.0001). Mortality during index hospitalization was 26% in the arrhythmia group and 1.8% in the no arrhythmia group (P=.001). Death or hospitalization at 60 days was also worse in the arrhythmia group (35 versus 8.2%, P=.0001; 57 versus 34%, P=.001, respectively). Cox proportional hazard analysis identified new arrhythmias as an independent risk factor for the primary endpoint and death at 60 days. CONCLUSION: New arrhythmia during an exacerbation of heart failure identifies a high-risk group with higher intrahospital and 60-day morbidity and mortality.     

充血性心力衰竭病人室性心律失常的发生机制

充血性心力衰竭中室性心律失常的发生率高、致死率高、且治疗也相当困难 ,因此 ,阐明其发生机制就显得非常重要。目前 ,这一领域的研究范围很广 ,成果很多 ,本文将就有关研究作一简要综述     

Cellular basis of triggered arrhythmias in heart failure

Ventricular tachycardia in nonischemic heart failure (HF) initiates by a nonreentrant mechanism that appears to be due to triggered activity primarily from delayed afterdepolarizations that arise from altered cellular Ca handling and ionic currents. In HF, factors that conspire to enhance triggered arrhythmias include upregulated Na/Ca exchange, preserved beta-adrenergic responsiveness, and decreased I(K1). Overall, the further delineation of key factors that underlie triggered arrhythmias in HF will provide the basis for new therapeutic strategies directed toward novel targets that can reduce the high incidence of sudden death in patients with HF.     

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.     

心力衰竭并发的常见心律失常

尽管对于治疗慢性心力衰竭(chronic heart failure,CHF)已经取得了重大的进展,但是CHF的病死率仍然很高,轻度CHF每年有5%～15%的病死率,而重度CHF患者每年的病死率可高达20%～50%.     

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.     

Drug-related arrhythmias during therapy of congestive heart failure

Summary It is now recognized that ventricular and supraventricular arrhythmias are serious complications of congestive heart failure. There are four possible drug-related mechanisms: diuretic-induced electrolyte imbalance; digitalis-induced arrhythmias; use of sympathomimetic agents; and drug interactions with digoxin. In selecting optimal therapy for congestive heart failure all these drug interactions need to be borne in mind.     

Effect of enalapril on ventricular arrhythmias in congestive heart failure

Twenty-four-hour Holter electrocardiographic recordings were used to measure the effects of a converting-enzyme inhibitor, enalapril, given for 12 weeks, on the frequency of cardiac arrhythmias in 10 patients with congestive heart failure (New York Heart Association functional class II to III) receiving maintenance therapy with digoxin and furosemide. Nine patients were given placebo, and both study groups were conducted in a double-blind, parallel manner. The placebo group had no change in the frequency of arrhythmias, whereas enalapril-treated patients showed a significant decrease in the frequency of premature ventricular complexes, ventricular couplets and ventricular tachycardia. A minor, nonsignificant reduction in atrial premature complexes was seen in patients who received enalapril. Compared with placebo patients, those who received enalapril had an increase in plasma potassium levels of 0.33 mmol/liter, a decrease in plasma digoxin, and decreases in pulmonary artery wedge, mean pulmonary artery and right atrial pressures. However, none of these indexes were correlated with the concomitant decline in cardiac arrhythmias. It is concluded that enalapril reduces the frequency of ventricular arrhythmias in congestive heart failure, although the underlying mechanisms are not known.     

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.     

缬沙坦对心力衰竭患者心律失常的影响研究

目的 探讨慢性心力衰竭患者缬沙坦治疗后,血浆镁浓度(PMC)、红细胞镁含量(EMC)和红细胞Na /Mg2 交换速率与心律失常的相关性.方法 收集2006年3月至2007年3月哈尔滨医科大学第一临床医学院心内科128例充血性心力衰竭病例并随机分为两组,常规治疗加缬沙坦组(观察组)和不加缬沙坦组(对照组),采用原子吸收光谱火焰法测定两组治疗前、治疗6个月后PMC、EMc以及Na /Mg2 交换速率,以Holter检测两组治疗6个月时心律失常发生情况.结果 (1)治疗前两组PMC、EMC、VTmax(红细胞总镁外流量最大速度)、VNImax (红细胞非钠依赖性镁外流最大速度)、VNDmax(红细胞钠依赖性镁外流最大速度)比较差异无统计学意义(P>0.05).(2)治疗6个月后,观察组PMC、EMC与对照组比较差异均有统计学意义(P＜0.05,P＜0.01);观察组VNImax与对照组比较差异无统计学意义(P>0.05);观察组VTmax、VNDmax与对照组比较均明显降低,差异均有统计学意义(P＜0.01).(3)两组治疗6个月后,观察组各种心律失常的发生较对照组显著减少.结论 (1)心衰治疗加缬沙坦后,Na /Mg2 交换速率降低,PMC与EMC增加,并由此减少了各种心律失常的发生.(2)缬沙坦的抗心律失常作用可能与增加了细胞的Mg2 稳态有关.     

Mechanisms underlying the development of atrial arrhythmias in heart failure

There is an important association between heart failure and the development of atrial arrhythmias. Although most often associated with atrial fibrillation, there is some evidence to suggest an association between heart failure and other atrial arrhythmias and, in particular, atrial flutter and atrial tachycardia. The mechanisms by which these common atrial arrhythmias may arise in patients with heart failure are discussed.