心脏猝死的危险分层及无创检测

心脏猝死（SCD）是指任何心脏疾病引起的发生在院外、急诊室内的突然死亡,并且死亡时间必须在有症状出现后1h内通常称瞬间死亡。SCD可能由于室速（VT）／室颤（VF）、心脏停搏或者非心律失常性原因所致。但在近期心脏死亡病例中显示,多数SCD并非像术语解释的那样瞬间死亡,而是在其之前的相当长一段时间内即有预警信号出现,只是未被患者或医生引起注意而已。     

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.     

ICD年代室性心律失常的抗心律失常药物的地位与评价

对于室性恶性的心律失常和心源性猝死(SCD)的主要治疗为埋藏式心脏复律除颤器(ICD),ICD比抗心律失常药物(AAD)的疗效好,总体死亡率可降低23-55%.ICD虽然从远期来说,降低了心源性猝死的死亡率,但仍不能完全替代AAD,中止室性心律失常的急性发作仍需要依赖AAD,心脏停搏的除颤、复律治疗后,必须要有药物的辅助,无药物的辅助其成功率不高.     

氧合血与冷晶体心肌停搏液保护心肌的临床研究

目的：比较氧合血心肌停搏液与冷晶体心肌停搏液对心肌的保护效果。方法：心脏瓣膜直视术病人120例，随机分为氧合血心肌停博液组（I组）、冷晶体心肌停博液组（Ⅱ组）各60例。I组采用4：1高钾冷血停搏液（4℃-8℃）灌注诱导心肌停跳，术中每隔20min用4：1高钾冷血停搏液维持，在开放升主动脉钳之前用温血灌注。Ⅱ组采用4℃冷晶体心肌停搏液灌注，术中每20min复灌1次。结果：I组心脏自动复跳率明显高于Ⅱ组（P＜0．001）；术后低心排综合征和室性心律失常的发生率明显低于Ⅱ组（P＜0．01）；术后应用心肌正性肌力药物量及时间明显少于Ⅱ组（P＜0．05）。结论：氧合血心肌停博液较冷晶体心肌停搏液具有更好的保护心肌效果。     

室性心律失常诊断和治疗进展

室性心律失常（verltriculararrhythmia VA）是一种十分常见的心律失常。根据血流动力学状态可分为血流动力学稳定和不稳定型VA。前者包括完全无症状和有轻微症状VA。后者包括晕厥、先兆晕厥、心脏性猝死（SCD）和心脏骡停。根据心电图表现分为非持续性和和持续性室速、束支折返型室速、双向性室速、尖端扭转型室速、心室扑动和心室颤动。     

重组人脑利钠肽对急性失代偿性心力衰竭患者室性心律失常的影响

心力衰竭（CHF）患者发生心脏性猝死（SCD）的危险性极高,而85％以上的SCD是由于持续性室性心律失常（VA）所致。重组人脑利钠肽（rh-BNP）是一种应用生物重组技术生产的,与人类B型利钠肽等同的肽类物质,对急性失代偿性心力衰竭（ADHF）患者安全有效。而其是否影响CHF患者VA尚缺少研究。本研究旨在探讨rh-BNP治疗对ADHF患者VA的影响。     

永久心脏起搏器植入术中心律失常的护理要点

总结363例患者行各类起搏器植入术术中心律失常的护理要点。对介入室护士开展岗前培训,心理护理贯穿起搏器植入手术的全过程,术中严密观察患者主诉及心电监护心律失常的表现,及时发现恶性心律失常并配合医生处理;普通起搏器植入术中心律失常以缓慢型多见,埋藏式心脏自动转复除颤器（ICD）和心脏再同步治疗（CRT或CRT-D）以室性心律失常多见,经有效护理干预均能顺利完成手术;起搏器参数测试时的护理主要注意是否出现长时间停搏或室性心动过速、室性颤动等恶性心律失常,随时准备好抢救药品,及时配合医生抢救”一;本组患者术中发生各类心律失常共38例,经积极处理均顺利完成手术。     

胺碘酮治疗慢性心力衰竭合并室性心律失常疗效观察

患者合并室性心律失常发生心脏性猝死（SCD）的危险性很高，因而及时、有效地治疗室性心律失常显得犹为重要。现将我科应用胺碘酮治疗慢性心衰合并室性心律失常的病例报道如下。     

河豚毒素对缺血再灌注大鼠心肌细胞凋亡及相关蛋白表达的影响

目的 研究河豚毒素（TTX）心脏停搏液对缺血再灌注大鼠心肌细胞凋亡及凋亡相关蛋白表达的影响。     

自体冷血心脏停搏液婴儿体外循环心脏直视手术1050例

目的：探讨自体冷血心脏停搏液对婴幼儿体外循环心脏直视手术未成熟心肌细胞的保护作用。方法：选取年龄≤10个月行体外循环室间隔缺损修补术的患儿1380例,随机分成自体冷血停搏液组（A组,n=1050）、冷血停搏液组（B组,n=280）和晶体停搏液（HTK）组（C组,n=50）。于术前、术后1、12、24、48h分别测量左心室Tei指数、心脏指数（CI）及左心室射血分数（LVEF）,监测CI术中记录复跳时间及复跳率,正性肌力药物依赖情况。结果：A组自动复跳率及时间、正性肌力药物依赖均明显减少（P〈0.05）。A组CI及LVEF较B、C组升高更明显（P〈0.05）,A组左心室Tei指数较B、C组降低更明显（P〈0.05）。结论：自体冷血停搏液利于婴儿体外循环直视手术心脏功能恢复,对未成熟心肌有良好的保护作用,值得临床推广。     

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。     

Role of antiarrhythmic therapy in patients at risk for sudden cardiac death: an evidence-based review

Sudden cardiac death (SCD) accounts for more than half of all cardiac deaths occurring each year in the United States. Although it has several causes, patients at greatest risk are those with coronary artery disease and impaired left ventricular function, heart failure secondary to ischemia or idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy, documented sustained ventricular tachycardia or ventricular fibrillation, and survivors of cardiac arrest. The presence of asymptomatic ventricular arrhythmias, positive signal-averaged electrocardiogram (ECG), low heart rate variability index, or inducible ventricular tachycardia or ventricular fibrillation increases the risk. In primary prevention trials in patients with ischemic heart disease, beta-blockers reduced both total mortality and SCD, whereas class I antiarrhythmic drugs, especially class IC, increased mortality. Among class III agents, d,l-sotalol and dofetilide have a neutral effect on mortality, whereas d-sotalol increases mortality. Amiodarone has a neutral effect on total and cardiac mortality but does reduce the risk of arrhythmic death and cardiac arrest. Three primary prevention trials in patients with ischemic heart disease were conducted with implantable cardioverter-defibrillators (ICDs). Patients with low ejection fractions (EFs), asymptomatic ventricular arrhythmias, and inducible ventricular tachycardia or ventricular fibrillation had significant reductions in total, cardiac, and arrhythmic death with ICDs compared with either no drug therapy or conventional antiarrhythmic agents. The ICDs did not reduce mortality in patients with low EFs and a positive signal-averaged ECG undergoing coronary bypass graft. In those with heart failure, beta-blockers reduced total and SCD mortality, but dofetilide and amiodarone had a neutral effect on mortality. In the secondary prevention of SCD, antiarrhythmic drugs alone generally are not thought to improve survival. In three trials in patients with documented sustained ventricular tachycardia or ventricular fibrillation, or survivors of SCD, ICDs reduced cardiac and arrhythmic mortality. Total mortality, however, was significantly reduced in only one of these trials. The role of antiarrhythmic drugs in secondary prevention of SCD is limited to patients in whom ICD is inappropriate or in combination with ICD. Antiarrhythmics can be given selectively with ICDs to decrease episodes of ventricular tachycardia or fibrillation to reduce ICD discharges, to suppress episodes of nonsustained ventricular tachycardia that trigger ICD discharges, to slow the rate of ventricular tachycardia to increase hemodynamic stability, to allow effective antitachycardia pacing, or to suppress supraventricular arrhythmias.     

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。     

Assessing QT interval prolongation and its associated risks with antipsychotics

Several antipsychotics are associated with the ventricular tachycardia torsade de pointes (TdP), which may lead to sudden cardiac death (SCD), because of their inhibition of the cardiac delayed potassium rectifier channel. This inhibition extends the repolarization process of the ventricles of the heart, illustrated as a prolongation of the QT interval on a surface ECG. SCD in individuals receiving antipsychotics has an incidence of approximately 15 cases per 10,000 years of drug exposure but the exact association with TdP remains unknown because the diagnosis of TdP is uncertain. Most patients manifesting antipsychotic-associated TdP and subsequently SCD have well established risk factors for SCD, i.e. older age, female gender, hypokalaemia and cardiovascular disease. QT interval prolongation is the most widely used surrogate marker for assessing the risk of TdP but it is considered somewhat imprecise, partly because QT interval changes are subject to measurement error. In particular, drug-induced T-wave changes (e.g. flattening of the T-wave) may complicate the measurement of the QT interval. Furthermore, the QT interval depends on the heart rate and a corrected QT (QTc) interval is often used to compensate for this. Several correction formulas have been suggested, with Bazett's formula the most widely used. However, Bazett's formula overcorrects at a heart rate above 80 beats per minute and, therefore, Fridericia's formula is considered more appropriate to use in these cases. Several other surrogate markers for TdP have been developed but none of them is clinically implemented yet and QT interval prolongation is still considered the most valid surrogate marker. Although automated QT interval determination may offer some assistance, QT interval determination is best performed by a cardiologist skilled in its measurement. A QT interval >500?ms markedly increases the risk for TdP and SCD, and should lead to discontinuation of the offending drug and, if present, correction of underlying electrolyte disturbances, particularly serum potassium and magnesium derangements. Before prescribing antipsychotics that may increase the QTc interval, the clinician should ask about family and personal history of SCD, presyncope, syncope and cardiac arrhythmias, and recommend cardiology consultation if history is positive.     

Induced ion currents and the endothelin pathway as targets for anti-arrhythmic agents

The development of novel anti-arrhythmic drugs is necessary, specifically agents that do not cause torsades de pointes (Tdp). Ion channelopathy that is involved in mechanisms underlying sudden cardiac death (SCD) includes both ion channels in the membrane, and the calcium-releasing channels and the calcium uptake process in the sarcoplasmic reticulum. Advances in the understanding of abnormalities of ion channels in the myocardium caused by congenital defects or by a failing heart and cardiomyopathy offer further insights into the relationship between channelopathy and SCD. Enhanced L-type Ca2+ current (ICa.L) activity has been detected in the hearts of patients with a mutation of the Cav1.2 gene; these patients exhibit a high risk of SCD. Rats with thyroxin-induced cardiomyopathy demonstrate an increase in ICa.L activity that is responsible for exacerbated ventricular fibrillation (VF). This is suppressed by propranolol or CPU-86017, a class III anti-arrhythmic agent with potent antioxidant activity. Interestingly, an increase in rapidly (IKr) and slowly (IKs) activating delayed rectifying K+ currents is caused by gain-of-function mutations of the KCNH2 and KCNQ1 genes, respectively, in patients with short QT syndrome (SQT). Increased IKr and IKs, which are associated with exacerbated VF, are also found in models of thyroxin-induced cardiomyopathy and are suppressed by CPU-86017. ICa.L, IKr and IKs can also be induced in cardiomyocytes when incubated with isoproterenol. A reversal of upstream lesions by an endothelin receptor antagonist CPU-0213 provides suppression of ventricular tachyarrhythmias and upregulates FK506 binding protein 12.6. CPU-86017 and its chiral isomer SR-CPU-86017 relieve upstream lesions, with mild suppression of IKr and moderate suppression of IKs and ICa.L. These agents may be promising as anti-arrhythmic agents that produce less Tdp tachyarrhythmias.     

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.     

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。     

Familial and acquired long qt syndrome and the cardiac rapid delayed rectifier potassium current

1. Long QT syndrome (LQTS) is a cardiac disorder characterized by syncope, seizures and sudden death; it can be congenital, idiopathic, or iatrogenic. 2. Long QT syndrome is so-named because of the connection observed between the distinctive polymorphic ventricular tachycardia torsade de pointes and prolongation of the QT interval of the electrocardiogram, reflecting abnormally slowed ventricular action potential (AP) repolarization. Acquired LQTS has many similar clinical features to congenital LQTS, but typically affects older individuals and is often associated with specific pharmacological agents. 3. A growing number of drugs associated with QT prolongation and its concomitant risks of arrhythmia and sudden death have been shown to block the 'rapid' cardiac delayed rectifier potassium current (IKr) or cloned channels encoded by the human ether-a-go-go-related gene (HERG; the gene believed to encode native IKr). Because IKr plays an important role in ventricular AP repolarization, its inhibition would be expected to result in prolongation of both the AP and QT interval of the electrocardiogram. 4. The drugs that produce acquired LQTS are structurally heterogeneous, including anti-arrhythmics, such as quinidine, non-sedating antihistamines, such as terfenadine, and psychiatric drugs, such as haloperidol. In addition to heterogeneity in their structure, the electrophysiological characteristics of HERG/IKr inhibition differ between agents. 5. Here, clinical observations are associated with cellular data to correlate acquired LQTS with the IKr/HERG potassium (K+) channel. One strategy for developing improved compounds in those drug classes that are currently associated with LQTS could be to design drug structures that preserve clinical efficacy but are modified to avoid pharmacological interactions with IKr. Until such time, awareness of the QT-prolongation risk of particular agents is important for the clinician.