猝死与冠状动脉肌桥

冠状动脉肌桥临床上的表现，血管造影，诊断以及治疗得到医生的普遍认可，但在导致猝死尚还没有引起法医同仁的注意。通过复习相关的文献，本文主要对冠状动脉肌桥的研究状况、致死机制以及由此引起猝死的病理特点等进行阐述。     

冠状动脉肌桥与心源性猝死

冠状动脉肌桥也称冠脉肌桥或心肌桥,是一种先天性冠状动脉分布走行的发育畸形,为冠状动脉某一段或其分支的某一段走行于心外膜下的心肌层内。这种先天性冠状动脉分布走行的发育畸形可以引起猝死,在尸体解剖中也较为常见。本文对冠脉肌桥的形态学特点、临床影像学与心电图改变、猝死机制以及法医学鉴定中需要注意的问题等方面进行了阐述。     

26例冠状动脉肌桥法医病理学研究

人或某些动物冠状动脉主干某一段有时穿行于心肌纤维中,这段被心肌纤维覆盖的血管称壁冠状动脉(muralcoronaryartery,MC),而被覆血管的心肌束称为冠状动脉肌桥(myocardialbridge,MB),冠状动脉肌桥影响心脏的血液动力学,可导致胸痛、心率失常,甚至猝死等[1-4],有关冠状动脉肌桥病理学的研究报道较少,本文对我们尸检中的26例冠状动脉肌桥进行法医病理学研究报道。1资料与方法资料来源于我院1988年1月～2001年12月尸检档案中750例死亡案例,其中冠状动脉肌桥26例,每一案例均有完整的临床资料及案情资料,进行了系统尸检,每例尸检均在死后24小时…     

3例冠状动脉肌桥与急死尸检材料

<正> 冠状动脉肌桥(Coronary Artery Myocardial Bridging)是指跨越冠状动脉表面的心肌纤维束。传统观点认为,这是少数人的正常解剖变异。近年来,法医病理学和病理学的报告认为,冠状动脉肌桥是引起人体急死的原因之一。     

冠状动脉肌桥致急死1例

冠状动脉肌桥存在于极少数人中,系正常解剖学变异。随着病理学研究的进展,目前认为心肌纤维束跨越冠状动脉表面所形成的冠状动脉肌桥压迫,可引起冠状动脉供血障碍致心脏性急死。笔者在检案中见到1例,现报道如下:简要案情1990年12月10日晚,马某酒后与他人发生纠纷,事后马某被他人从其床上拖至地下,拳打脚踢其头部、左腰和用砍刀背打击其左胸部等处,马因处于醉酒嗜睡状态未能反抗。当时发现马某面     

冠状动脉畸形引起猝死1例

猝死是指貌似健康的人，因潜在的疾病或重要器官急性功能障碍导致的意外突然死亡。心血管疾病是引起猝死最常见的疾病，其中以冠心病和高血压性心脏病最多见，冠状动脉畸形引起猝死的案例报道较少见。笔者检验了一起因冠状动脉开口畸形引起猝死的案例，报道如下。     

冠状动脉瘤引起猝死一例

<正> 冠状动脉瘤的发病率文献报告为1.4%～2.5%。因冠状动脉瘤发生猝死者则极为罕见。最近日本的 Murai 报告1例冠状动脉瘤引起猝死,国内王纪芳曾报告3例冠状动脉夹层动脉瘤,但冠状动脉瘤(真性)引起猝死尚无报道:病例报告男,47岁,农民。4月25日全天参加运沙劳动,无不适。下午收工后于4时30分进晚餐,饭后还同其他民工闲谈。晚7时,外出快速步行约400m,觉不适,出汗,口渴,5～10分钟后,在返回工棚的途中突然倒地,目击者见其在地上翻动,并发出呻吟声,很快死亡。     

冠心病猝死193例尸检分析

本文对193例因冠心病而猝死的尸检材料进行以分析,并对冠状动脉粥样硬化好发部位,病理改变,心脏病理变化,以及冠心病猝死发生机理和诱因等进行讨论。     

心肌桥的研究现状及法医学意义

心肌桥是一种少见的解剖学异常,可引起猝死,近年来已成为临床和法医工作者的一个研究热点。本文依据文献资料从心肌桥的发生率、解剖学特征、病理生理变化、临床表现及法医学意义等方面进行综述。     

肥厚型心肌病猝死尸检一例

肥厚型心肌病（HypertrophicCardiomy－opaty，HCM）可引起猝死。现结合一例尸检讨论其主要病理变化、猝死机制及法医学鉴定注意事项。案例报告王某，女，7岁，某日体育课短跑时突然“晕厥”，摔倒在地，神志不清，5分钟后送到医院发现已死亡。据查死者既往史、家族史均无特殊。尸检见：心脏呈球形，重220g（同龄女性正常为100g），心外膜光滑，外膜下脂肪组织无明显增多。冠状动脉各支及心瓣膜正常，心内膜光滑，左心室乳头肌、肉柱明显肥大，心空腔缩小，心室壁切面见肌束交织，纹理粗糙如“纹绸”（Wateredsilk）外观。室间隔不对称性…     

Sudden Cardiac Death in a Young Man with Migraine-associated Arrhythmia

A 31-year-old man with migraine-induced syncope and bradycardia with subsequent pacemaker implantation died unexpectedly. Clinically unsuspected cardiac anomalies were found at autopsy including myocardial bridging of the left anterior descending artery and shelf-like coronary artery ostia. Nortriptyline was identified by toxicologic analysis. A review of the autopsy findings, the historical information, and the effects of the possible arrhythmogenic circumstances is undertaken and the potential contributions to the death are discussed. Cardiac arrhythmias have been documented during migraines. Coronary artery bridging has been known to lead to ischemia and infarction, ventricular tachycardia, and sudden death; however, these are very rare sequelae. Congenital coronary artery anomalies have been linked to sudden cardiac death, but only rarely cause death in people younger than 31 years. Migraines and the autopsy findings described have been associated with cardiac arrhythmia and sudden death. Altogether, they led to the unexpected death of this young man.     

IMA和H-FABP在心源性猝死法医学诊断中的应用

急性心肌缺血的发生是心源性猝死的最常见原因,而如何认定早期急性心肌缺血是法医学研究的热点,同时也是临床预防心肌梗死发生的重要环节。本文通过对缺血修饰白蛋白(ischemia modified albumin,IMA)和心型脂肪酸结合蛋白(heart-type fatty acid binding protein,H-FABP)的结构、功能、临床应用价值及法医学中的应用前景进行综述,旨在分析二者是否可作为早期心肌缺血的生化检测指标用于心源性猝死的诊断,并为今后选择心源性猝死的科研方向提供借鉴。     

早期心肌梗死死后诊断的法医病理学研究进展

心源性猝死在成人猝死的死因中占首位,心肌梗死是冠心病猝死的主要机制之一,由于早期心肌梗死发生突然,且可在短时间内死亡,肉眼和镜下都缺乏典型的形态学改变,一直都是法医实践中研究的热点,本文回顾多年来心肌梗死的研究成果在法医学中的应用及局限,展望新的临床指标在法医工作中的可行性,期望提高死后心肌梗死诊断的准确率。     

原发性心肌病猝死心肌mtDNA~(4977)缺失变化

目的探讨原发性心肌病(PCM)猝死者心肌线粒体DNA(m tDNA4977)缺失情况及其与猝死的关系。方法对18例PCM猝死和28例对照组病例心肌组织蜡块,用常规方法提取心肌m tDNA,以PCR、琼脂糖紫外凝胶成像技术确定扩增产物激光密度,初步定量检测m tDNA4977缺失率。结果PCM猝死18例中,检见13例m tDNA4977缺失,占72.44%。对照组28例中,检见3例m tDNA4977缺失,占10.71%;两组病例m tDNA4977缺失率均值分别为0.5795和0.0744,差异有非常显著性意义。结论多数PCM,特别是扩张型心肌病猝死者心肌可检见m tDNA4977缺失;提示其心肌m tDNA4977缺失变化与PCM猝死的发生可能有一定关系。     

Serum concentrations of cardiac troponin T in sudden death

Ischemic heart disease is the most common cause of sudden death of natural causes in most western countries. By autopsy, there may be no gross or histologic evidence of acute myocardial damage unless the patient survived for several hours following the event. Cardiac troponin in serum has become the recommended biochemical marker for myocardial injury in the clinical setting. We performed a prospective study on 102 autopsied subjects at the Central Hospital of Rogaland, Stavanger, Norway. Femoral blood was sampled for subsequent analysis of cardiac troponin T (cTnT). In the subjects with morphologic evidence of recent myocardial injury (n = 34), the mean serum cTnT level was 1.95 microg/L compared with 0.16 microg/L in the subjects with a noncardiac cause of death (n = 35) and 0.61 microg/L in the group with probable sudden cardiac death without morphologic signs of acute myocardial injury (n = 33). The observed differences in mean serum cTnT levels between the groups were statistically significant (P < 0.0001). These data suggest that elevated postmortem serum concentration of cTnT reflects ongoing myocardial damage and may support a diagnosis of cardiac-related death in cases associated with sparse or inconclusive morphologic findings postmortem.     

大鼠急性心肌缺血后肌浆网RyR2 mRNA表达变化

目的 研究大鼠急性心肌缺血后心肌肌浆网兰尼碱受体蛋白2(ryanodine receptor 2,RyR2)mRNA表达的变化.方法 将SD大鼠分为正常对照组、心肌缺血组和缺血性猝死组.采用腹腔注射垂体后叶素的方法复制大鼠急性心肌缺血和猝死模型,对心肌进行半定量荧光RT-PCR检测,观察RyR2 mRNA表达水平的变化.结果 与正常对照组相比,不同时间和不同程度的急性心肌缺血后心肌肌浆网RyR2 mRNA表达均显著降低(P<0.05).结论 心肌缺血性损伤可诱导心肌钙调控蛋白RyR2 mRNA表达下调.     

大鼠心肌缺血后SERCA和PLB基因表达变化的观察

目的观察大鼠心肌缺血后，肌浆网钙调节蛋白SERCA和PLB基因表达水平变化，探讨其在早期心肌缺血诊断上的应用价值。方法25只大鼠随机分为正常对照组、缺血5、10、15min及缺血性猝死组，建立大鼠急性心肌缺血模型；利用荧光标记逆转录聚合酶链反应技术（RT—PCR）检测不同时间大鼠心肌缺血后，SERCA和PLB的基因表达变化，并与缺血性猝死组相比较。结果心肌缺血5min即可检测到SERCA和PLBmRNA表达相对下降，且随着缺血时间的延长，呈逐渐下降趋势，心肌缺血组与缺血性猝死组表达存在显著性差异。结论大鼠心肌缺血后SERCA和PLB基因表达变化呈一定规律性。对早期心肌缺血的诊断具有法医学意义。     

A Case of Sudden Infant Death Due to Incomplete Kawasaki Disease

Although Kawasaki disease (KD) is a self‐limiting disease, it may cause sudden cardiac death. Diagnosis of KD is principally based on clinical signs; however, some infant cases do not meet the criteria. Such cases are identified as incomplete KD. The sudden death risk in incomplete KD cases is similar to conventional KD. In our 5‐month‐old case, he had been admitted to a hospital for a fever and suppuration at the site of Bacille de Calmette et Guerin (BCG) vaccination. However, after discharge from the hospital, his C‐reactive protein (CRP) levels declined, he got indisposed and died suddenly. A medico‐legal autopsy revealed myocarditis, coronaritis, platelet‐aggregated emboli in coronary arteries, and myocardial degeneration, suggesting that the fatal myocardial infarction was due to thrombus emboli in the coronary arteries. Forensic pathologists therefore should pay attention to the cardiac pathology originated from incomplete KD as a potential cause in cases of sudden infant death.     

Relationship of ischemic heart disease to sudden death

A clinicopathological synthesis is presented of the relationship of ischemic heart disease to sudden cardiac death. The immediate pathophysiological process responsible for sudden cardiac death is a lethal arrhythmia, usually ventricular fibrillation. Although significant coronary atherosclerosis is present in most cases of naturally occurring sudden death, available evidence indicates that several mechanisms can be operative in the pathogenesis of the fatal event. These are (1) acute myocardial infarction in a minority of cases; (2) myocardial ischemia, without infarction, which is initiated either by (a) an exertion-induced increase in myocardial oxygen demand or (b) an acute coronary event often involving plaque degeneration and platelet aggregation; and (3) a primary arrhythmia, usually resulting from altered electrical conduction in the setting of a previous myocardial infarction.