Cocaine and sudden "natural" death

The cardiovascular effects of cocaine may culminate in clinical episodes of angina pectoris, myocardial infarction, arrhythmias, and intracranial hemorrhage. To clarify whether or not cocaine causes fatalities by these mechanisms, we studied 24 cases of sudden, apparently natural deaths as a result of coronary arteriosclerosis (15 cases), hypertensive cardiovascular disease (4 cases), and intracranial hemorrhage (5 cases) associated with cocaine use. In 11 cases, cocaine was found in the blood (average concentration: 0.57 mg/L, range: 0.05 to 1.45 mg/L), whereas in the remainder, cocaine or its major metabolite was found in the urine or other tissues. In the majority of decedents, autopsy disclosed the existence of severe natural disease which could have been exacerbated by the administration of stimulant drugs, including cocaine. These data, and a review of the current medical literature, indicate that cocaine may precipitate the sudden death of an individual with undiagnosed cardiovascular disease. A contributory role of cocaine should be considered in any apparently natural death occurring in a population where cocaine abuse is prevalent.     

Molecular genetics of sudden cardiac death

Sudden cardiac death (SCD) is one of the most common causes of death. An important number of sudden deaths, especially in the young, are due to genetic heart disorders, both with structural and arrhythmogenic abnormalities. In recent years, significant advances have been made in understanding the genetic basis of SCD. Identification of the genetic causes of sudden death is important because close relatives are also at potential risk of having a fatal cardiac condition. A comprehensive post-mortem investigation is vital to determine the cause and manner of death and provides the opportunity to assess the potential risk to the family after appropriate genetic counselling. In this paper, we present an update of the different genetic causes of sudden death, emphasizing their importance for the forensic pathologist due to his relevant role in the diagnosis and prevention of SCD.     

阴性解剖中的心脏性猝死

综述了近年来有关心脏性猝死的分子生物学和电生理学的研究进展,着重讨论了心震荡、先天性长QT间期综合征和Brugada综合征,可能诱发致死性心律失常,发生心脏性猝死。这些功能性病症死亡常可导致病理解剖时无明显客观器质性病理改变。提示法医和病理工作者在遇到阴性解剖猝死时,应注意了解猝死的诱因、继往病史和家族病史,注意排除可能存在的这些病症。     

窦房结中央动脉狭窄与心源性猝死

近年来国内外学者相继报道由单纯窦房结中央动脉狭窄引起的猝死。本文就窦房结中央动脉的解剖、组织学特点、病变特点进行综述,探讨窦房结动脉狭窄引起猝死的机制,以期为相关法医病理学死因鉴定提供理论基础。     

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.     

心脏性猝死的机制研究进展

世界范围内心脏病性猝死发病率正呈逐年升高趋势并已成为第一大死亡原因,因此国内外学者在这方进行了广泛而深入的研究。本文综述了心脏病性猝死的病理学、神经体液、电生理特别是其分子生物学发病机制的研究成果。     

Rupture of a cardiac diverticulum resulting in sudden death

Cardiac diverticula have been documented in approximately 80 patients. In over 70% of cases, this lesion is associated with midline thoracoabdominal defects or other congenital malformations of the heart. The diverticulum is thought to occur early in embryogenesis from an outpouching of the endomyocardium through a weak region in the left ventricular wall, but its exact etiology is uncertain. The case of a 6-year-old white boy who died suddenly while playing is presented. Autopsy revealed a ruptured diverticulum of the left ventricular apex with massive hemopericardium and cardiac tamponade. No other abnormalities were found. The pertinent literature is reviewed.     

RyR2相关心脏性猝死的研究进展

雷诺定受体2(ryanodine receptor 2,RyR2)是心肌细胞肌浆网上主要的钙释放通道,主要参与心肌的兴奋收缩耦联过程,其基因突变及调控异常可导致心肌舒张期钙漏引起心律失常,甚至猝死。本文重点综述RyR2基因突变及调控异常引起心脏性猝死的机制,并对以后的研究提出建议,旨在为心脏性猝死的法医学诊断提供一种新的思路。     

KCNE、KCNQ1与心性猝死的相关性研究进展

部分心性猝死由于缺乏明确的病理学改变,其鉴定工作一直是法医工作者的一大难题。近年来,与长QT综合征、心房颤动等致死性心律失常疾病相关基因（KCNE基因家族与KCNQl）等研究逐渐增多。国内外研究发现KCNE和KCNQ1基因编码心肌钾离子通道,其基因异常可引起严重的心律失常,甚至导致心性猝死。因此,死后KCNE和KCNQl的基因检测对于心性猝死鉴定具有重要意义。本文对KCNE、KCNQl与心性猝死的相关性研究进展进行综述,希望能为法医学研究和实践提供参考。     

分子生物学检查在猝死综合症患者法医学尸体检验中的应用

猝死综合症用来泛指急死后是用传统检查技术手段未能发现致死病变的情况。由于原因不明,其诊断和病因学的研究均十分困难。猝死综合症的诊断是法医学尸体检验实践中的难题之一。近年来,随着分子生物学技术和遗传学研究的不断深入,对于一些与猝死有关的发现不断报道,有希望用于法医学实践,用于将此类猝死进一步分型,并为进一步的深入研究提供准确的流行病学资料。     

118例心源性猝死分析

心源性猝死(sudden cardiac death,SCD)在成人猝死的死因中占首位,本文对1998-2005年陕西地区发生的118例SCD案例进行统计分析,结果显示男性是女性的5.9倍,其中冠心病占55.1%,心肌炎占17.8%,心肌病占9.3%,先天性心脏病、瓣膜病、主动脉夹层瘤破裂各占2.5%,其他疾病占4.5%。说明SCD多发于男性,冠心病仍是SCD的主要基础疾病,心肌炎是青少年SCD的主要原因,心肌病是青壮年SCD的危险因素,无结构异常的心脏病也同样严重威胁生命健康。     

分子生物学检查在猝死综合症患者法医学尸体检验中的应用

猝死综合症用来泛指急死后是用传统检查技术手段未能发现致死病变的情况。由于原因不明，其诊断和病因学的研究均十分困难。猝死综合症的诊断是法医学尸体检验实践中的难题之一。近年来。随着分子生物学技术和遗传学研究的不断深入，对于一些与猝死有关的发现不断报道，有希望用于法医学实践，用于将此类猝死进一步分型，并为进一步的深入研究提供准确的流行病学资料。     

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。     

Evaluation of eosin-fluorescence in the diagnosis of sudden cardiac death

The diagnostic significance of the eosin-fluorescence method was evaluated and compared with the enzymehistochemical β-hydroxybutyrate-dehydrogenase method (β-HBDH) and the degree of hyperchromasia in 568 samples from 24 β-HBDH-negative and β-HBDH-positive sudden cardiac deaths (SCD) and 23 non-cardiac deaths as controls. The effect of autolysis was investigated separately on isolated human hearts at +4°C and +22°C. All samples were examined without any knowledge of clinical or autopsy data. Normal olive-green fluorescence was observed in only five individuals of the control group and two in the β-HBDH-negative one. The frequency of the yellow-fluorescence and hyperchromasia increased from the control subjects towards the β-HBDH-positive-ones. The difference in frequency distribution of fluorescence between the groups was statistically highly significant (P < 0.001). The change in fluorescence did not correlate with the loss of β-HBDH-reaction or the distribution pattern of hyperchromasia. Postmortem autolysis did not change the fluorescence significantly but the 78% wrong positive subjects in the control group render this method too sensitive and unreliable for medicolegal purposes.     

Evaluation of eosin-fluorescence in the diagnosis of sudden cardiac death

The diagnostic significance of the eosin-fluorescence method was evaluated and compared with the enzymehistochemical beta-hydroxybutyrate-dehydrogenase method (beta-HBDH) and the degree of hyperchromasia in 568 samples from 24 bets-HBDH-negative and beta-HBDH-positive sudden cardiac deaths (SCD) and 23 non-cardiac deaths as controls. The effect of autolysis was investigated separately on isolated human hearts at +4 degrees C and +22 degrees C. All samples were examined without any knowledge of clinical or autopsy data. Normal olive-green fluorescence was observed in only five individuals of the control group and two in the beta-HBDH-negative one. The frequency of the yellow-fluorescence and hyperchromasia increased from the control subjects towards the beta-HBDH-positive-ones. The difference in frequency distribution of fluorescence between the groups was statistically highly significant (P less than 0.001). The change in fluorescence did not correlate with the loss of beta-HBDH-reaction or the distribution pattern of hyperchromasia. Postmortem autolysis did not change the fluorescence significantly but the 78% wrong positive subjects in the control group render this method too sensitive and unreliable for medicolegal purposes.     

Myocardial sarcoidosis as a rare cause of sudden cardiac death

Two relatively young women died suddenly due to myocardial sarcoidosis. Necropsy in both cases revealed compact infiltration of the ventricular septum by fibrous tissue. Histologic sections elucidated extensive granulomatous degeneration and giant cells of the Langhans' and foreign body type without central necrosis of the granulomas. Both women had been entirely free of symptoms, but in the second case of a 35-year-old, who had been 6 months pregnant, an ultrasound sonography of the heart had documented a suspicious area in the ventricular septum interpreted as a scar. Further investigations had been postponed until delivery. Isolated myocardial sarcoidosis should be taken into account as one possible cause of sudden death, especially in young people.