心室颤动治疗策略的思考

心源性猝死(sudden cardiac death,SCD)是目前公共卫生事业所面临的重大课题和挑战。美国每年有30万～60万人因SCD而死亡。我国目前尚无大规模的流行病学资料的报道,但发生SCD的人数呈逐年上升趋势。回顾性资料显示,80%以上SCD患者最终由恶性室性心律失常所引起。心室颤动(ventricular fibrillation,VF)是恶性室性心律失常的一种临床类型,也是其他恶性室性心律失常发展的趋势和结果。恶性室性心律失常复发率较高,每次发作均可能发展为VF,危及患者生命,因此,积极地防治VF是预防SCD的基本策略。1抗心律失常药物的作用20世纪80～90年…     

普罗帕酮

普罗帕酮(心律平)是I型C组抗心律失常药,作用强,疗效好,副作用弱。治疗主动性异位性室性和室上性心律失常的效果很好。特别适用于充血性心力衰竭合并致死性室性心律失常患者。与Ⅰa、Ⅰb、Ⅱ、Ⅲ型抗心律失常药并用的疗效尤佳,是当前最理想的抗心律失常药。     

心力衰竭患者心源性猝死的预警和治疗策略

心源性猝死（SCD）是指心脏的临床状态突然变化而发生在1h内的死亡或瞬间死亡。SCD的分类包括心律失常死亡（SAD）和非心律失常事件死亡。心力衰竭患者的SCD发生率是普通人群的6～9倍,而SCD的预警和治疗则是临床医生所面临的棘手问题。在过去的20年里,尽管心力衰竭的治疗已有了较大进展,但心力衰竭患者的4年存活率却低于公众对照组的50％。     

心力衰竭患者心源性猝死的预警和治疗策略

心源性猝死(SCD)是指心脏的临床状态突然变化而发生在1h内的死亡或瞬间死亡.SCD的分类包括心律失常死亡(SAD)和非心律失常事件死亡[1].心力衰竭患者的SCD发生率是普通人群的6～9倍,而SCD的预警和治疗则是临床医生所面临的棘手问题.在过去的20年里,尽管心力衰竭的治疗已有了较大进展,但心力衰竭患者的4年存活率却低于公众对照组的50%.现已确定在严重充血性心力衰竭患者中室性心律失常的发生率高达85%以上.埋藏式心脏复律除颤器(ICD)是终止致命性室性心动过速最有效的方法,而且在选择性高危患者中已证实ICD降低死亡率的费用-效果最佳.在公众人群中心力衰竭约占1%～2%,而且数量还在增加 .目前,确定心力衰竭合并有高度心律失常危险性的患者,及时置入ICD并采取其他抗心律失常措施是一个重大挑战[2].     

抗心律失常药与尖端扭转型室速

近十年来,抗心律失常药发展迅速,许多新药不断问世,心律失常的药物治疗效果也同时得到较大提高。但随着抗心律失常药广泛的临床应用,其在心脏方面的不良反应也日渐突出。研究发现,许多抗心律失常药本身也具有促心律失常作用(proarrhythmia),表现为使原有的心律失常加重或出现新的心律失常。Torsade de Pointes(TdP)意为“尖端扭转型室速”,即多形性室性心动过速(polymorphic ventricular tachyarrhythmia),是一致命的心律失常,常于患者接受药物(尤其是抗心     

心力衰竭中的室性心律失常

心力衰竭患者,生活质量和存活率均降低。心力衰竭经常伴发的室性心律失常,特别是持续性室速,是心脏猝死的独立预后指标。心力衰竭中的室性心律失常可能有多种不同的机理,在给予抗心律失常药前必须将泵衰竭和心肌缺血控制在最佳状态。至于抗心律失常药预防心力衰竭病例心脏猝死的效果,尚待证实。     

10年心脏颤动——挑战及其逐步解决

<正>本世纪之初,大多数的心律失常都已有了疗效肯定的治疗。但2种常见而重要的心律失常仍存在着很大的威胁:心脏猝死(SCD)和心房颤动(AF)。上世纪末,广泛使用一种埋藏体内的仪器,预防猝死,但实际上可能并不真正地降低死亡率。Bardy团队比较收缩性心力衰竭病人(已知它发生SCD高危)用amiodarone(最有效的抗心律失常药),一种ICD(埋藏式心脏转复除颤器)和安慰剂。结     

心力衰竭患者心律失常的药物治疗

心力衰竭(简称心衰)患者易发各类心律失常,其中,以合并心房颤动(简称房颤)和室性心动过速(简称室速)为最常见。对于心衰并发心律失常的患者而言,胺碘酮和β受体阻滞剂是既有效、又安全的药物选择,Ⅰ类抗心律失常药不宜使用。其他非抗心律失常药物,如他汀类、血管紧张素转换酶抑制剂、血管紧张素Ⅱ受体拮抗剂等,对心衰并发心律失常的患者也是大有裨益的。     

心律平治疗充血性心力衰竭合并室性心律失常的疗效与安全性

目的　观察心律平治疗充血性心力衰竭 ( CHF)合并室性心律失常 ( VA)的疗效与安全性。方法　将 80例 CHF合并 VA患者随机分成两组 ,均停用抗心律失常药物 5个半衰期 ,两组病人抗心力衰竭治疗相同 ,试验组应用心律平抗心律失常 ,对照组不使用抗心律失常药物 ,疗程 4周 ,观察临床疗效、室性心律失常及左心室射血分数 ( L VEF)变化。结果　治疗后试验组临床疗效低于对照组 ( P<0 .0 1) ,VA减少两组差异无显著性 ( P>0 .0 5 ) ,对照组 L VEF值增加优于试验组 ( P<0 .0 5 ) ,试验组有 6例出现新的心律失常 ,停用心律平后恢复。结论　 CHF合并 VA时不宜应用心律平     

院内心脏性猝死177例临床回顾分析

目的　分析院内心脏性猝死 (SCD)的临床特点。方法　以 1999年 1月至 2 0 0 1年 12月 177例院内SCD的临床资料进行回顾性研究。结果　院内SCD事件中 0～ 14岁占 8 5 % ,6 0岁及以上占 6 3 9%。导致院内SCD的常见病因是冠心病 (47 5 % )、风心病 (11 3% )和先心病 (11 3% )。导致院内冠心病性猝死的常见病因是急性心肌梗死 (AMI) (5 3 6 % )和不稳定型心绞痛 (UAP) (30 9% )。 75 1%的院内SCD合并心力衰竭 (HF)。心脏骤停即时检测示室性心律失常占 6 7 8% ,心室颤动占 5 2 0 %。结论　院内SCD事件以老年人所占比例最大 ,最防治重点 ,同时也应注意到儿童占有较高比例 ;对于AMI、UAP及HF患者应警惕其SCD的高度危险性 ;尽早除颤是提高院内SCD事件抢救成功率的关键之一。     

Pharmacotherapy to reduce arrhythmic mortality

Fatal ventricular arrhythmias and heart failure are the common modes of death in patients with cardiovascular diseases. Intracardiac defibrillator (ICD) implantation reduces arrhythmic mortality to a significant extent in the high risk patient. However, there continues to be a need for effective drug therapy to reduce the arrhythmic and overall mortality in patients with or without an ICD. Although anti-arrhythmic drugs (AAD) appear inferior to ICD, the role of beta-blockers and to an extent amiodarone along with non AAD like angiotensin converting enzyme inhibitors (ACE-I), mineralocorticoid blockers (MRB) and HMG-CoA reductase inhibitors (statins) need to be emphasized. There have been many drug trials and meta-analysis to this effect and we review the role of drugs especially in their ability to reduce arrhythmic mortality and sudden cardiac death (SCD). The focus is on post myocardial infarction (MI) and heart failure patients with a brief overview of role of drugs in channelopathies.     

Structural pathways and prevention of heart failure and sudden death

We review the macroscopic and microscopic anatomy of myocardial disease associated with heart failure (HF) and sudden cardiac death (SCD) and focus on the prevention of SCD in light of its structural pathways. Compared to patients without SCD, patients with SCD exhibit 5- to 6-fold increases in the risks of ventricular arrhythmias and SCD. Epidemiologically, left ventricular hypertrophy by ECG or echocardiography acts as a potent dose-dependent SCD predictor. Dyslipidemia, a coronary disease risk factor, independently predicts echocardiographic hypertrophy. In adult SCD autopsy studies, increases in heart weight and severe coronary disease are constant findings, whereas rates of acute coronary thrombi vary remarkably. The microscopic myocardial anatomy of SCD is incompletely defined but may include prevalent changes of advanced myocardial disease, including cardiomyocyte hypertrophy, cardiomyocyte apoptosis, fibroblast hyperplasia, diffuse and focal matrix protein accumulation, and recruitment of inflammatory cells. Hypertrophied cardiomyocytes express "fetospecific" genetic programs that can account for acquired long QT physiology with risk for polymorphic ventricular arrhythmias. Structural heart disease associated with HF and high SCD risk is causally related to an up-regulation of the adrenergic renin-angiotensin-aldosterone pathway. In outcome trials, suppression of this pathway with combinations of beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin-II receptor blockers, and mineralocorticoid receptor blockers have achieved substantial total mortality and SCD reductions. Contrarily, trials with ion channel-active agents that are not known to reduce structural heart disease have failed to reduce these risks. Device therapy effectively prevents SCD, but whether biventricular pacing-induced remodeling decreases left ventricular mass remains uncertain.     

The role of antiarrhythmic drug therapy for the prevention of sudden cardiac death

Sudden cardiac death (SCD) accounts for more than 300,000 deaths annually in the United States alone. The utility of antiarrhythmic drugs in survivors of SCD (secondary prevention) is limited because of their incomplete efficacy and long-term toxicity. Efforts to target primary prevention of SCD have focused on left ventricular dysfunction in conjunction with congestive heart failure. Antiarrhythmic drugs are not able to decrease mortality in this patient population either; in fact, certain drugs may actually increase overall mortality. In both primary and secondary prevention patients, only implantable cardioverter-defibrillator implantation is associated with improved survival. Antiarrhythmic drugs like azimilide, dofetilide, sotalol, and amiodarone can be used as adjunct treatment for management of atrial arrhythmias and to decrease implantable cardioverter-defibrillator shocks. There is an unmet need for more effective and less toxic antiarrhythmic medications.     

Reducing the risk of sudden death in heart failure with beta-blockers

BackgroundHeart failure (HF) is a serious cardiovascular syndrome that affects nearly 5 million people in the United States. A review of clinical data demonstrates that sudden cardiac death (SCD) accounts for approximately one-third of all HF deaths. This fatal outcome typically involves an unexpected electrical event leading to sustained cardiac arrhythmias resulting in cardiovascular collapse.Methods and ResultsA systematic review of the literature was performed to serve as the basis for this review. Factors contributing directly to incidence of SCD in the HF population may include significant remodeling of the left ventricle (hypertrophy, dilation, and fibrosis) in addition to increased sympathetic activation. Using specific therapies to limit these mechanisms are beneficial in the HF patient by preventing SCD. β-blockers play a key role in the prevention of SCD for patients with HF by limiting the effects of circulating norepinephrine and by reducing left ventricular remodeling.ConclusionsThis review outlines the potential mechanisms and contributing factors of SCD in patients with HF and the impact of β-blocker usage in the prevention of this fatal outcome for this growing patient population.     

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.     

Neurohormonal Intervention to Reduce Sudden Cardiac Death in Heart Failure: What is the Optimal Pharmacologic Strategy?

Sudden cardiac death (SCD) accounts for up to 50% of deaths in patients with heart failure (HF), depending on severity of symptomatic impairment and left ventricular dysfunction. Neurohormonal therapy directed at the renin-angiotensin-aldosterone system may reduce the propensity to SCD through improved hemodynamic responsiveness, reduced sympathetic tone in the myocardium and inhibition of cardiac remodelling. Angiotensin converting enzyme (ACE) inhibitors reduce overall mortality in chronic HF, the greatest benefit appearing to arises from reduction of HF progression rather than SCD. In HF patients who experience myocardial infarction (MI) reduced incidence in SCD may make a more marked contribution to the mortality benefits of ACE inhibition. Addition of beta-blocker therapy to ACE inhibition has consistently resulted in a reduction in SCD in patients with either mild-to-moderate or severe HF, and in the presence or absence of MI; the reduction in SCD is of the order of one-third versus placebo. Aldosterone blockade reduces the risk of SCD in advanced chronic heart failure (when added to ACE inhibitor) and in HF associated with acute MI (when given in addition to both ACE inhibitor and beta blocker). The evidence base suggests that for maximal SCD risk reduction in HF, beta-blocker therapy is advisable in combination with standard ACE inhibitor therapy, with addition of aldosterone blockade to this regimen for particular groups of heart failure patients.     

Neurohormonal intervention to reduce sudden cardiac death in heart failure: what is the optimal pharmacologic strategy?

Sudden cardiac death (SCD) accounts for up to 50% of deaths in patients with heart failure (HF), depending on severity of symptomatic impairment and left ventricular dysfunction. Neurohormonal therapy directed at the renin-angiotensin-aldosterone system may reduce the propensity to SCD through improved hemodynamic responsiveness, reduced sympathetic tone in the myocardium and inhibition of cardiac remodelling. Angiotensin converting enzyme (ACE) inhibitors reduce overall mortality in chronic HF, the greatest benefit appearing to arises from reduction of HF progression rather than SCD. In HF patients who experience myocardial infarction (MI) reduced incidence in SCD may make a more marked contribution to the mortality benefits of ACE inhibition. Addition of beta-blocker therapy to ACE inhibition has consistently resulted in a reduction in SCD in patients with either mild-to-moderate or severe HF, and in the presence or absence of MI; the reduction in SCD is of the order of one-third versus placebo. Aldosterone blockade reduces the risk of SCD in advanced chronic heart failure (when added to ACE inhibitor) and in HF associated with acute MI (when given in addition to both ACE inhibitor and beta blocker). The evidence base suggests that for maximal SCD risk reduction in HF, beta-blocker therapy is advisable in combination with standard ACE inhibitor therapy, with addition of aldosterone blockade to this regimen for particular groups of heart failure patients.     

Prediction of sudden death in elderly patients with heart failure

Most heart failure (HF) related mortality is due to sudden cardiac death (SCD) and worsening HF, particularly in the case of reduced ejection fraction. Predicting and preventing SCD is an important goal but most works include no or few patients with advanced age, and the prevention of SCD in elderly patients with HF is still controversial. A recent reduction in the annual rate of SCD has been recently described but it is not clear if this is also true in advanced age patients. Age is associated with SCD, although physicians frequently have the perception that elderly patients with HF die mainly of pump failure, underestimating the importance of SCD. Other clinical variables that have been associated to SCD are symptoms, New York Heart Association functional class, ischemic cause, and comorbidities (chronic obstructive pulmonary disease, renal dysfunction and diabetes). Some test results that should also be considered are left ventricular ejection fraction and diameters, natriuretic peptides, non-sustained ventricular tachycardias and autonomic abnormalities. The combination of all these markers is probably the best option to predict SCD. Different risk scores have been described and, although there are no specific ones for elderly populations, most include age as a risk predictor and some were developed in populations with mean age > 65 years. Finally, it is important to stress that these scores should be able to predict any type of SCD as, although most are due to tachyarrhythmias, bradyarrhythmias also play a role, particularly in the case of the elderly.     

Delayed and indirect effects of antiarrhythmic drugs in reducing sudden cardiac death

In the USA, two-thirds of sudden cardiac deaths (SCDs) are caused by sustained ventricular tachycardia and ventricular fibrillation. Implantable cardioverter defibrillator (ICD) therapy has been demonstrated to decrease mortality caused by these arrhythmias, when used both for primary and secondary prevention. However, ICD use is expensive, has proarrhythmic effects and does not prevent ventricular arrhythmias. Antiarrhythmic drugs (AADs) can be used for acute or chronic therapy to prevent ventricular arrhythmias and SCD. Most commonly, AADs are often used in patients with an ICD who have recurrent ICD shocks due to ventricular arrhythmias. Class I AADs are used in patients with a structurally normal heart and are contraindicated in patients with structural heart disease. β-blockers have been demonstrated to be beneficial in preventing mortality and malignant tachyarrhythmias in postmyocardial infarction and congestive heart failure patients, and in patients who have an ICD. Amiodarone has a neutral effect on mortality, while other class III drugs may increase mortality in certain subgroups of patients. Dronedarone, a new class III drug, may reduce mortality, but sufficient data are not available to allow for its use in the prevention of malignant tachyarrhythmias. Few drugs that are not classified as AADs can also prevent arrhythmias, via their beneficial effects on cardiovascular remodeling. These non-ADDs have delayed and indirect effects, which are mediated by the renin-angiotensin-aldosterone system and lipid metabolism - n-3 polyunsaturated fatty acids (fish oil), and statins, and can thus can reduce the likelihood of future malignant ventricular arrhythmias in patients with coronary artery disease or congestive heart failure. The role of chronic drug therapy alone for primary and secondary prevention of SCD is less than desirable because of proarrhythmic and adverse side effects. The non-ADDs are well tolerated and have no proarrhythmic actions, thus their benefit could outweigh risks, although currently there are no concrete data to suggest this.