Morning sudden cardiac death

A circadian variation of cardiac function with peak in the early morning was documented about twenty years ago. A circadian rhythm of platelet aggregability, in the same time of the day, was demonstrated in healthy young male subjects. The morning hours were also reported as crucial for sympathetic nervous system activity, for heart rate variability, and for the abrupt rise in blood pressure. Altogether, these trigger factors may explain the high incidence of sudden cardiac death during the morning. In the primary prevention of sudden death in patients with high cardiovascular risk, many strategies were proposed, such as implantable cardioverter-defibrillators, antiarrhythmic and antihypertensive therapies, particularly beta-blockers and more recently, aspirin. Also in subjects without cardiovascular risk factors, it is predictable that early and continuous administration of low-dose aspirin, by inhibiting platelet aggregation and thrombin formation, particularly in morning hours, may represent an effective therapy for the prevention of myocardial infarction and morning sudden cardiac death.     

Therapeutic developments in sudden cardiac death

Sudden cardiac death is characterised by the unexpected death of a patient who has been clinically stable. It is frequently due to the development of ventricular tachyarrhythmias. With appropriate treatment, patients can be appropriately resuscitated. Clinically, it is essential to develop treatment strategies to prevent such an episode, as most patients do not survive out-of-hospital cardiac arrest. β-Blockers are an effective pharmacological therapy in patients following myocardial infarction and in those with congestive heart failure. They may also be effective in other types of heart disease. Anti-arrhythmic agents are not useful as prophylactic drug therapy for reducing mortality in patients at risk for sudden cardiac death. Amiodarone is a notable exception, which may have some benefit, particularly in some subgroups. The implantable cardioverter-defibrillator has emerged as the most effective therapy for preventing sudden cardiac death in high-risk patients. Further work is required to enhance the characterisation of high-risk patients. Genetic analyses in patients with cardiovascular disorders may also identify new approaches to the prevention of sudden cardiac death.     

Therapeutic developments in sudden cardiac death

Sudden cardiac death is characterised by the unexpected death of a patient who has been clinically stable. It is frequently due to the development of ventricular tachyarrhythmias. With appropriate treatment, patients can be appropriately resuscitated. Clinically, it is essential to develop treatment strategies to prevent such an episode, as most patients do not survive out-of-hospital cardiac arrest. beta-Blockers are an effective pharmacological therapy in patients following myocardial infarction and in those with congestive heart failure. They may also be effective in other types of heart disease. Anti-arrhythmic agents are not useful as prophylactic drug therapy for reducing mortality in patients at risk for sudden cardiac death. Amiodarone is a notable exception, which may have some benefit, particularly in some subgroups. The implantable cardioverter-defibrillator has emerged as the most effective therapy for preventing sudden cardiac death in high-risk patients. Further work is required to enhance the characterisation of high-risk patients. Genetic analyses in patients with cardiovascular disorders may also identify new approaches to the prevention of sudden cardiac death.     

心脏性猝死病因及高危因素分析

目的探讨心脏性猝死(SCD)的病因及高危因素。方法回顾性分析97例SCD临床资料。结果冠心病69例(71.1%),其中急性心肌梗死(AMI)35例(36.1%)、慢性充血性心力衰竭(CHF)53例(54.6%),其中纽约心功能分级(NY-HA)Ⅱ～Ⅲ级占86.7%,左室射血分数(LVEF)测定57例,LVEF<55%占84.2%,B型利钠肽(BNP)明显升高26例(26.8%)、临终前心电图示室性心律失常73例(75.3%)、低钾血症26例(26.8%)、冬季SCD最常见(42.2%)、其中6:00—12:00时SCD发生率最高(38.1%)。结论冠心病是SCD最常见的病因;SCD发生有明显的季节性和昼夜差;室性心律失常、心力衰竭、LVEF降低、BNP升高、低钾血症是SCD的高危因素。     

心脏性猝死的危险因素分析

目的探讨心脏性猝死的危险因素,为针对性预防提供参考。方法通过对惠州中心医院80例心脏性猝死患者的发病诱因和原因以及大量文献资料从而归纳心脏性猝死的危险因素。结果经过临床结果的推论和文献资料的查阅,证实在干预或消除其危险因素后,心脏性猝死的发生率明显减少。结论心血管疾病危险因素对心脏性猝死有直接影响,所以,应当及时干预、治疗,增强体质和健康指数,这样,才能有效减少心脏性猝死的发病率。     

心源性猝死的危险因素和预警因子的探讨

心源性猝死以冠心病患者最为多见,约占75%,急性心肌梗死是医院内发生心源性猝死的最主要原因。冠状动脉粥样硬化和心肌病变是发生猝死的基础,心肌一过性的功能障碍和电生理的改变,是导致心跳骤停的原因,也有人是因为冠状动脉发育畸形、冠状动脉有炎症而发生猝死。除冠心病外,尤以原发性心肌病中肥厚型心肌病最多见;各种严重的心律失常;急性心肌炎等多种心脏病。     

Psychotropic drugs,cardiac arrhythmia,and sudden death

A variety of drugs targeted towards the central nervous system are associated with cardiac side effects, some of which are linked with reports of arrhythmia and sudden death. Some psychotropic drugs, particularly tricyclic antidepressants (TCAs) and antipsychotic agents, are correlated with iatrogenic prolongation of the QT interval of the electrocardiogram (ECG). In turn, this is associated with the arrhythmia (TdP). This review discusses the association between psychotropic agents, arrhythmia and sudden death and, focusing on TCAs and antipsychotics, considers their range of cellular actions on the heart; potentially pro-arrhythmic interactions between psychotropic and other medications are also considered. At the cellular level TCAs, such as imipramine and amitriptyline, and antipsychotics, such as thioridazine, are associated with inhibition of potassium channels encoded by In many cases this cellular action correlates with ECG changes and a risk of TdP. However, not all psychotropic agents that inhibit HERG at the cellular level are associated equally with QT prolongation in patients, and the potential for QT prolongation is not always equally correlated with TdP. Differences in risk between classes of psychotropic drugs, and between individual drugs within a class, may result from additional cellular effects of particular agents, which may influence the consequent effects of inhibition of repolarizing potassium current.     

患者心源性猝死相关诱因的分析与对策

目的通过总结分析患者发生心源性猝死（SCD）的相关诱因和护理方法,为临床防治提供依据。方法回顾性调查2004年5月至2009年5月在我院住院发生SCD心血管疾病患者33例,对33例猝死病例的资料进行统计和原因分析,并对护理方法进行探讨。结果本组SCD患者29例有明显相关诱发因素,占87．88％;发生于各种诊疗护理活动过程和大小便后的分别有16例（占48．48％）、11例（占33．33％）。1：00～8：00时间段为一天中猝死最高时间段（占42．42％）。33例均有不同程度的心力衰竭,其中急性左心衰17例（占51．51％）。结论大小便、各种诊疗护理活动时患者恐慌心理为SCD常见相关诱因,心力衰竭为高危因素,猝死时间分布有较明显的昼夜节律。因此,对于心血管疾病患者,应重视患者大小便的护理,特别注意提高各种诊疗护理活动的及时性和有效性,重视对患者的心理护理,同时加强夜间巡视与病情观察。     

心源性猝死64例临床分析

目的探讨心源性猝死的病因、诱发因素,并提出有效的预防措施。方法对发生心源性猝死的64例患者进行回顾性临床分析。结果冠心病是心源性猝死的最常见病因,6～12时及18～24时是猝死的易发时间,3～6月及11～12月是猝死的易发季节。猝死常见的直接原因是室性心律失常。结论控制多种危险因素,有效控制室性心律失常将可减少心源性猝死的发生。     

老年人心脏性猝死65例临床分析

目的 探讨老年人心脏性猝死（SCD）的危险因素.方法 对65例老年SCD患者进行心电图、心电监护、Holter、彩色多普勒超声心动图检查、电解质等检测,并与对照组比较.结果 老年人SCD复杂性室性期前收缩、左室收缩功能不全、低血钾症、心脏扩大病例数多于对照组（均P＜0.05）.结论 老年人SCD与复杂性室性期前收缩、左室收缩功能不全、低血钾、心脏扩大相关.     

门急诊发生的心脏性猝死68例临床分析

目的探究心脏性猝死（suddencardiacdeath,SCD）的危险因素及预防措施。方法回顾性分析河南省人民医院2010年1月-2013年6月收治的SCD患者的临床资料,根据患者病历资料并询问现场医务人员和知情家属,采集SCD患者的诱发因素、猝死前征兆、直接原因及高危因素等数据资料。利用SPSS13．0统计软件对相应观察指标进行统计分析。结果肺部感染是SCD事件发生的主要诱因（26％）;恶性心律失常是绝大多数SCD事件直接原因（96％）,其中心室颤动占71％;既往存在冠心病病史是SCD事件发生的高危因素（79％）;在时间分布方面SCD多发生在01：00～12：00（93％）。结论提高高危患者与家属的知晓率,并以生物、心理、社会医学模式为指导全方位预防;同时强化医护人员专业素质,提高抢救效奎,最终可改善SCD患者预后。     

Careful screening to target interventions to prevent sudden cardiac death

1. Cardiac death is due not only to coronary artery disease, but also to left ventricular (LV) abnormalities (fibrosis, dysfunction) and arrhythmogenic triggers, such as autonomic imbalance. 2. Nitric oxide deficiency could be a key mediator leading not only to coronary atherosclerosis, but also to LV abnormalities and autonomic imbalance. 3. It may be possible to screen for the above abnormalities (e.g. echocardiography and brain natriuretic peptide levels for LV abnormalities, 24 h tapes for autonomic imbalance and QT interval analysis). 4. Once individuals are identified as being at high risk, a range of interventions is possible (e.g. intensive statin therapy or angiotensin-converting enzyme inhibitors if LV abnormalities or autonomic imbalance are found).     

Antipsychotic-induced sudden cardiac death: examination of an atypical reaction

Following the publication of a recent study, which linked antipsychotics to sudden cardiac death, the safety of both typical and atypical antipsychotics has once again been questioned. Sudden cardiac death resulting from ventricular arrhythmias remains a significant public health concern, with over 300,000 deaths per year in the US alone. Long QT syndrome (LQTS) is an important cause of sudden cardiac death in which both congenital and acquired lesions in cardiac ionic channels impair myocardial repolarization and predispose the heart to developing lethal ventricular rhythms, including torsade de pointes, which may degenerate into ventricular fibrillation. Congenital LQTS is a relatively rare condition; however, acquired LQTS and arrhythmogenesis occurring through the unwanted pharmacological effects of a wide range of medications has become one of the largest problems facing the pharmaceutical industry today. This article examines recent findings linking antipsychotics to ventricular arrhythmias and explores potential new strategies to reduce the incidence of drug-induced sudden cardiac death.     

Calstabin2 - a new target in sudden cardiac death

Sudden cardiac death is occasionally observed in people with structurally normal hearts. Calstabin2 stabilises the ryanodine receptor (RyR)2, preventing aberrant activation of the sarcoplasmic reticulum calcium channel during the resting phase of the cardiac muscle. Calstabin2-deficient mice have structurally normal hearts, but exhibit exercise-induced cardiac ventricular arrhythmias that cause sudden death. In three models of arrhythmias, the calstabin2 stabiliser JTV519 did not prevent arrhythmias in calstabin2(-/-) mice, but reduced the arrhythmias in calstabin2(+/-) mice, illustrating the antiarrhythmic potential of stabilising calstabin2. Familial polymorphic ventricular tachycardia (FPVT) has been linked to three missense mutants (P2328S, Q4201R and V4653F) in the hRyR2 gene of Finnish families. In HEK293 cells, these RyR2 mutants showed less binding of (35)S-calstabin2 than the wild-type, indicating a reduced binding affinity. JTV519 rescues the gain-of-function defect in the RyR2-P2328S channels via increased binding of calstabin2 to the channel complex. In heart failure (HF), there is excessive disassociation of calstabin2 from the RyR2 receptor, and JTV519 has been shown to be beneficial in an animal model of HF. In conclusion, calstabin2 is an important new target in sudden cardiac death associated with either FPVT or HF.     

Current concepts and animal models of sudden cardiac death for drug development

Sudden cardiac death (SCD) or sudden coronary death, occurring in patients with unstable angina (angina at rest), myocardial ischemia with or without myocardial infarction (MI), and congestive heart failure (CHF), emerges as one of the most important challenges in cardiovascular medicine at present. Of the 1.5 million cases of myocardial infarction that occur each year in the U.S., about 540,000 patients will die and more than 300,000 of these will die before they reach a hospital, mostly due to ventricular fibrillation (VF) and/or SCD. About 4.8 million people alive in the U.S. have a history of myocardial infarction, angina pectoris, or both and are prime candidates for SCD. About 3 million people in the U.S. have congestive heart failure (CHF) and about 400,000 new cases are reported each year. One year mortality due to CHF is 33–58% and about 45% of the deaths are sudden. These patients were not those who had deleterious hemodynamic parameters whose demise could be predicted; they were those that died suddenly and unexpectedly of VF. Current pharmacological intervention in patients with a documented myocardial infarction with marketed antiarrhythmic agents has not reduced the overall mortality of SCD significantly. This suggests that an efficacious antiarrhythmic/antifibrillatory agent for the prevention of SCD does not exist at present and that there is an urgent need for such an agent.