Sudden cardiac death risk stratification in patients with heart failure

The multiplicity of mechanisms contributing to arrhythmogenesis in patients with heart failure carries obvious implications for risk stratification. If patients having the propensity to develop arrhythmias by these different mechanisms are to be identified, tests must be devised that reveal the substrates or other factors that relate to each mechanism. In the absence of this, efforts to risk stratify patients are likely to be neither cost-effective nor accurate. This article reviews the current knowledge base of risk stratification for sudden death in patients with heart failure, while acknowledging several limitations in the studies examined.     

Levosimendan versus dobutamine in heart failure patients treated chronically with carvedilol

Introduction : Although beta‐blockers are highly effective in the treatment of heart failure (HF), many patients with HF receiving a beta‐blocker continue to become decompensated and require hospitalization for worsening HF. Levosimendan and dobutamine are used to manage decompensated HF, but their comparative effects on left ventricular (LV) function in patients prescribed beta‐blockers are unknown. Aims : The aim of this study was to compare the effects of dobutamine and levosimendan on LV systolic and diastolic functions in chronic HF patients treated chronically with carvedilol. Forty patients with chronic HF who had NYHA class III to IV symptoms, a LV ejection fraction (LVEF) <40%, and ongoing treatment with carvedilol were enrolled in this randomized (1:1), dobutamine controlled, open‐label study. Before and 24 h after treatment, LVEF, mitral inflow peak E and A wave velocity, E/A ratio, the deceleration time of the E wave (DT), isovolumic relaxation time (IVRT), peak systolic (Sm) and early diastolic (Em) mitral annular velocity, and systolic pulmonary artery pressure (SPAP) were measured by echocardiography. Results : Levosimendan produced a statistically significant increase in LVEF (28 ± 5% vs. 33 ± 3%), Sm (6.5 ± 1.2 cm/s vs. 7.4 ± 0.9 cm/s), DT (120 ± 10 ms vs. 140 ± 15 ms), and Em (7.5 ± 0.4 cm/s vs. 8.1 ± 0.5 cm/s) and significant decrease in E/A ratio (2.1 ± 0.3 vs. 1.7 ± 0.4) and SPAP (55 ± 5 mmHg vs. 40 ± 7 mmHg). No significant change occurred in LV systolic and diastolic function parameters, or SPAP with dobutamine treatment. Levosimendan did not significantly alter the heart rate (72 ± 4 bpm vs. 70 ± 3 bpm), systolic (105 ± 5 mmHg vs. 102 ± 4 mmHg), or diastolic blood pressure (85 ± 5 mmHg vs. 83 ± 5 mmHg) whereas with dobutamine treatment, all these parameters significantly increased. Conclusions : Dobutamine and levosimendan have different effects on LV functions in patients treated chronically with carvedilol. These differences should be considered when selecting inotropic therapy for decompensated HF receiving long‐term carvedilol.     

卡维地洛对慢性心力衰竭心功能和ANP及BNP的影响

目的观察卡维地洛(达利全)对慢性心力衰竭(CHF)患者心功能和ANP/BNP的影响。方法60例CHF患者,在常规治疗病情基本稳定的基础上,增加服用卡维地洛,从每次3.125mg开始,2次/d,缓慢递增。治疗前后分别进行心率、血压、心功能分期评估和血清ANP/BNP测定。结果与治疗前相比,治疗5个月后,心率明显下降(P<0.01),心功能分级明显改善,血清ANP/BNP明显下降(P<0.01)。66.7%患者服用卡维地洛剂量可达到目标剂量25mg,2次/d;33.3%患者使用中等剂量12.5mg,2次/d,维持治疗。结论长期服用卡维地洛能改善心功能,降低血清ANP和BNP水平。     

Sudden cardiac arrest with shockable rhythm in patients with heart failure

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Sudden death prophylaxis in heart failure

Sudden cardiac death (SCD) is the leading cause of mortality in heart failure (HF). Today the implantable cardioverter-defibrillator (ICD) has become a commonplace therapy around the world for patients with both ischemic and non-ischemic cardiomyopathy and an ejection fraction (EF) < or = 35%. However, EF alone does not discriminate between the modes of death from HF (sudden arrhythmic death vs. non-sudden death). Other risk statifiers, such as electrophysiologic study and microvolt T-wave alternans testing, should therefore be used in the appropriate settings to minimize the number of unnecessary device implants. In addition, left ventricular mechanical dyssynchrony has now become recognized as an additional major marker of cardiac mortality. Its assessment should entail echocardiography rather than measurement of the QRS duration. This will allow us to better integrate the ability of cardiac resynchronization therapy (CRT) in enhancing cardiac function with the ability of an ICD in preventing SCD. This review aims to: 1) give a synthesis of the published evidence regarding the value of implantable ICDs and CRT in the primary prophylaxis of SCD in HF; 2) discuss controversial clinical issues in this area; and 3) recommend practical device-based management strategies.     

卡维地洛改善充慢性心力衰竭患者心功能的临床研究

目的:观察卡维地洛(Carvedilol)治疗慢性心力衰竭(CHF)的临床疗效.方法:将80例NYHA心功能Ⅱ～Ⅳ级CHF患者随机分为两组:Carvedilol组40例,采用常规治疗(ACEI、利尿剂、血管扩张剂、有或无洋地黄) Carvedilol;Betaloc组40例,常规治疗 Betaloc.随访1～2年,观察两组治疗前后血流动力学、左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)、左室射血分数(LVEF)、6 min步行距离(6-MWD)及心功能变化. 结果:两组治疗后心率(HR)、收缩压(SBP)、心肌耗氧量(HR×SBP)、LVEDD、LVESD、LVEF、左室短轴缩短分数(LVFS)、NYHA心功能分级均较治疗前显著改善(P＜0.01),而Carvedilol组在血流动力学及心功能改善上较Betaloc组更明显(P＜0.05);但治疗后组间HR降低无显著差异(P＞0.05).两组治疗后6-MWD也均较治疗前显著增加(P＜0.01),尤其Carvedilol组(P＜0.05).Carvedilol组无不良反应出现. 结论:联用Carvedilol治疗CHF安全有效.     

Sudden cardiac death in patients with diabetes

Sudden cardiac death (SCD) affects over 450,000 people in the United States annually. The mechanisms involved are poorly understood. The predictors currently known include traditional coronary heart disease risk factors, electrocardiographic abnormalities, cardiac autonomic neuropathy, left ventricular hypertrophy, cardiomyopathy, and conduction abnormalities. Diabetes mellitus and impaired glucose tolerance are of special importance due to their increased prevalence reaching epidemic proportions and the elevated risk of SCD in people with these disorders. This article reviews the current predictors of SCD with a focus on people with diabetes, hoping to offer physicians and researchers a better understanding of and a solid ground for further needed research on this important cause of premature death.     

卡维地洛改善充慢性心力衰竭患者心功能的临床研究

目的：观察卡维地洛(Carvedilol)治疗慢性心力衰竭(CHF)的临床疗效。方法：将80例NYHA心功能Ⅱ～Ⅳ级CHF患者随机分为两组：Carvedilol组40例,采用常规治疗(ACEI、利尿剂、血管扩张剂、有或无洋地黄)+Carvedilol；Betaloc组40例,常规治疗+Betaloc。随访1～2年,观察两组治疗前后血流动力学、左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)、左室射血分数(LVEF)、6min步行距离(6-MWD)及心功能变化。结果：两组治疗后心率(HR)、收缩压(SBP)、心肌耗氧量(HR×SBP)、LVEDD、LVESD、LVEF、左室短轴缩短分数(LVFS)、NYHA心功能分级均较治疗前显著改善(P＜0．01),而Carvedilol组在血流动力学及心功能改善上较Betaloc组更明显(P＜0．05)；但治疗后组间HR降低无显著差异(P＞0．05)。两组治疗后6-MWD也均较治疗前显著增加(P＜0．01),尤其Carvedilol组(P＜0．05)。Carvedilol组无不良反应出现。结论：联用Carvedilol治疗CHF安全有效。     

卡维地洛对充血性心力衰竭患者心功能的影响

目的　探讨卡维地洛对充血性心力衰竭患者心功能的影响。　方法　充血性心力衰竭患者 6 2例(其中扩张性心肌病心力衰竭患者 15例 ,缺血性心脏病心力衰竭患者 4 7例 ) ,左室射血分数 (LVEF)≤ 4 0 % ,心功能(NYHA)Ⅱ～Ⅳ级 ,常规治疗 (洋地黄 ,利尿剂 ,ACEI)基础上随机分为卡维地洛试验组和安慰剂对照组。应用心脏彩色超声仪测定治疗前及治疗后 1个月 ,3个月左室结构和功能指标的变化。观察卡维地洛治疗三个月后对心功能的影响。　结果　卡维地洛平均用量为 2 1 1mg d± 9 6mg d。经过 3个月治疗 ,试验组症状和心功能改善 ,与对照组比较左室射血分数上升 (P <0 0 0 2 ) ,左室收缩末容积下降 (P <0 0 5 ) ;左室舒张末容积与对照组比较虽无统计学差异但与治疗前比较亦明显下降 (P <0 0 5 )。　结论　在洋地黄、利尿剂、ACEI的治疗基础上 ,应用卡维地洛能显著改善充血性心力衰竭患者的心功能 ,改善心室结构 ,且疗效与应用剂量无关。     

Exercise training reduces sympathetic nerve activity in heart failure patients treated with carvedilol

BACKGROUND: Evidence suggests that carvedilol decreases muscle sympathetic nerve activity (MSNA) in patients with heart failure (HF) but carvedilol fails to improve forearm vascular resistance and overall functional capacity. Exercise training in HF reduces MSNA and improves forearm vascular resistance and functional capacity. AIMS: To investigate whether the beneficial effects exercise training on MSNA are maintained in the presence of carvedilol. METHODS AND RESULTS: Twenty seven HF patients, NYHA Class II-III, EF <35%, peak VO(2) <20 ml/kg/min, treated with carvedilol were randomly divided into two groups: exercise training (n=15) and untrained (n=12). MSNA was recorded by microneurography. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. The four-month training program consisted of three 60-min exercise/week on a cycloergometer. Baseline parameters were similar between groups. Exercise training reduced MSNA (-14+/-3.3 bursts/100 HB, p=0.001) and increased forearm blood flow (0.6+/-0.1 mL/min/100 g, p<0.001) in HF patients on carvedilol. In addition, exercise training improved peak VO(2) in HF patients (20+/-6%, p=0.002). MSNA, FBF and peak VO(2) were unchanged in untrained HF patients on carvedilol. CONCLUSION: Exercise training reduces MSNA in heart failure patients treated with carvedilol. In addition, the beneficial effects of exercise training on muscle blood flow and functional capacity are still realized in patients on carvedilol.     

Epidemiology of sudden cardiac death in patients with heart failure

Mortality in congestive heart failure (CHF) usually occurs from either progressive worsening of cardiac pump failure or sudden cardiac death (SCD). Medical interventions that counter neurohormonal changes slow the progression of CHF and also prevent SCD. The benefits of medical therapy on SCD prevention have been variable, depending on the type of medical therapy. This article discusses the incidence, prediction, and prevention of SCD in CHF due to ischemic and nonischemic cardiomyopathy.     

Sudden death prevention in heart failure.

Heart failure is one of the main clinical entities in modern society, with a prevalence of 0.4 to 2% in Europe. It has an adverse prognosis, with 5 to 20% annual mortality, even when properly medicated. Mortality in heart failure is frequently due to sudden death, which means preventive strategies should be adopted. Risk stratification is essential in order to identify which patients will benefit most. The main risk factor for sudden death is low ejection fraction. However, ECG data, Holter monitoring and electrophysiological studies are also useful. In primary prevention, all reversible conditions and precipitating factors should be identified and heart failure treatment optimized. The best preventive strategy, after appropriate patient selection, is ICD implantation. Recently, devices with both cardioversion-defibrillation and cardiac resynchronization have proved beneficial in terms of morbidity, quality of life and survival.     

Sudden cardiac death in patients with rheumatoid arthritis

An increased cardiovascular morbidity and mortality, including the risk of sudden cardiac death(SCD), has been shown in patients with rheumatoid arthritis(RA). Abnormalities in autonomic markers such as heart rate variability and ventricular repolarization parameters, such as QTc interval and QT dispersion, have been associated with sudden death in patients with RA. The interplay between these parameters and inflammation that is known to exist with RA is of growing interest. In this article, we review the prevalence and predictors of SCD in patients with RA and describe the potential underlying mechanisms, which may contribute to this. We also review the impact of biologic agents on arrhythmic risk as well as cardiovascular morbidity and mortality.