178例心源性猝死法医组织病理学诊断分析

目的探讨心源性猝死(SCD)的病理特点与鉴别要点。方法对四川华西法医学鉴定中心2000—2005年尸检出的178例SCD死亡案例进行回顾性分析,主要对其病因、年龄、诱因及病理改变进行分析。结果本组资料显示冠心病、心传导系统病变、心肌炎、心肌病等在SCD中占有较大比例。冠心病猝死是中老年人SCD的最主要原因,青壮年人SCD的病因以非冠心病为主。如传导系统病变、心肌炎、心肌病。在儿童的SCD中先天性心脏病、传导系统病变及心肌炎占主导地位。结论不同的病因,其病理特点不同,其病理变化是法医学鉴定的主要依据。     

97例心性猝死的法医病理学分析

目的探讨心性猝死（SCD）的特点、病理基础及致死因素和诱因等。方法对本系2002年12月至2006年12月期间，所作450例法医病理检案的97例心性猝死案例进行分析研究。结果97例SCD患者中，冠心痛猝死38例，心肌炎23例，心肌痛16例，高血压性心脏病12例，主动脉瘤破裂4例，肺栓塞4例。结论SCD病程短骤、凶险，以老年男性多见，冠心病占首位。由于猝死的因素繁多，因此对猝死事件的法医学鉴定要根据其发生特征和变化规律，作出客观、全面、准确的签定结论。     

病毒性心肌炎和扩张性心肌病中Dystrophin蛋白的表达

目的探讨病毒性心肌炎和扩张性心肌病的发病机制及相互关系,从而提高心性猝死法医学鉴定的可靠性和准确性。方法对17例对照(包括正常心脏、冠心病、高血压性心脏病等),25例病毒性心肌炎和28例扩张性心肌病的心肌组织进行改良的病理学dystrophin免疫组织化学研究。结果dystrophin蛋白在对照组,病毒性心肌炎组和扩张性心肌病组中阳性表达率分别为100%,88%,57%,三组表达差异有显著性(P<0.05),且在病毒性心肌炎和扩张性心肌病组间表达有显著差异(P<0.05),经Spearman等级相关分析呈显著负相关(r=-0.526)。结论病毒性心肌炎和扩张性心肌病心肌中细胞骨架蛋白均有破坏,且随着由病毒性心肌炎进展为扩张性心肌病,dystrophin蛋白表达逐渐降低,说明在病毒性心肌炎和扩张性心肌病的发病机制中可能与dystrophin的被破坏有关,病毒感染并破坏心肌细胞骨架蛋白并最终导致心肌细胞坏死,心功能受损,从而使病毒性心肌炎进展为扩张性心肌病。     

300例心源性猝死案例的法医学鉴定分析

目的探讨心源性猝死案例的病因、诱发因素及法医病理学特点,以期为心源性猝死案件的法医病理诊断提供参考。方法收集法医病理检案中的心源性猝死案例,对其年龄、性别、死亡时间、死因、诱因及场所等流行病学特点进行回顾分析。结果 300例心源性猝死案例中男性多于女性,18~45岁发病最多;病因包括冠心病(129例),心肌病(78例),心肌炎(36例)等;应激为SCD最常见的诱发因素(157例)。结论 1应激和冠心病是心源性猝死的重要危险因素。2心源性猝死的法医学鉴定除了要进行系统的尸检及病理学检查外,还要对死者的相关资料如:基础疾病、诱因、死亡时间、死亡经过等进行全面系统的分析以明确死因。     

成人心脏性猝死的心脏大体病理学测量数据报告

目的 分析不同原因心脏性猝死(sudden cardiac death,SCD)的大体病理学数据,为不明原因的猝死鉴定提供证据支持。方法 收集南京医科大学司法鉴定所2010—2020年行法医病理鉴定的167例成人SCD案件,汇总SCD案例的大体病理学检验数据,统计分析不同死因的特征。结果 男、女性SCD案例比例3.4∶1。冠状动脉粥样硬化性心脏病是引起SCD的首要原因,主要分布于40岁以上的人群。心肌炎导致的猝死主要分布于年轻群体,平均死亡年龄为(34.00±9.55)岁。分析不同原因SCD的心脏病理学参数差异发现,主动脉瘤或动脉夹层猝死者的主动脉瓣瓣环周径多呈明显扩张(P<0.05)。男性主动脉瘤或动脉夹层和合并死因组的心脏质量增大,合并死因组的肺动脉瓣和三尖瓣瓣环均扩张(P<0.05)。结论 不同原因SCD存在多个大体病理学测量指标差异,在心脏性猝死的原因推断中具有参考价值。     

Photoshop软件在法医学鉴定冠脉狭窄中的应用

<正>冠心病猝死(sudden coronary death,SCD)在法医学鉴定中经常遇到,其发生率在猝死案例中约占40%～60%,其中男性明显多于女性,比例约为3～5∶1,男性以30～49岁者居多,女性年龄则较男性晚[1]。SCD的鉴定需要对冠状动脉(以下简称冠脉)狭窄程度进行判断,冠脉狭窄程度以管腔面积的缩小程度来度量,一般分为4级,Ⅰ级为管腔面积缩小1%     

冠状动脉内弹力膜缺损与冠心病猝死的关系

目的探讨冠状动脉内弹力膜(IEL)病变与冠心病猝死(SCD)的关系。方法从本单位近5年尸检案例中挑选60例病例和心脏标本,分为SCD组、对照组A和B组。每例分别在冠状动脉左前降支近段取材,常规制片,HE和双重组合特殊染色,显微镜下观察冠状动脉IEL,并用图像分析技术对特殊染色的IEL进行形态定量分析。结果60例中,SCD组(男性24例,女性6例,年龄30~83岁)的冠状动脉IEL缺失明显(缺失率=41.64%),未缺失的IEL失去原有弯曲度而变平直;对照组A(冠心病非猝死者,男性13例、女性2例,年龄41~80岁)的冠状动脉IEL缺失程度较SCD组稍轻(缺失率=30.53%);对照组B(无冠心病的其他死者,男性8例,女性7例,年龄17~54岁)的冠状动脉IEL仅有轻度缺失(缺失率=15.67%),多保持原有波浪状结构。统计学分析显示,SCD组与对照组、SCD组与对照组B、对照组A与对照组B之间IEL缺损率的差异均具有极显著性意义;SCD组与对照组A在IEL缺损率上的差异有显著性意义。结论SCD与其冠状动脉IEL缺损率的大小密切相关。     

冠心病猝死心肌纤维连接蛋白免疫组化染色观察

目的研究纤维连接蛋白（FN）免疫组化染色对冠心病猝死（SCD）的病理学诊断价值。方法用兔抗人FN多克隆抗体对人SCD心肌、颅脑损伤和病毒性心肌炎致死者心肌进行FN-SP免疫组化染色观察，用图像分析处理系统对FN免疫组织化学染色阳性反应产物面积定量，所得数据进行统计分析。结果SCD组16例心肌组织内FN大量沉积；颅脑损伤致死组心肌细胞内FN染色阴性，病毒性心肌炎致死组部分心肌细胞内FN阳性；3组心肌细胞内的阳性反应面积存在显著性差异（P〈0．05）。冠心病猝死组阳性反应面积（μm^2）为54143．28±8474．92；颅脑损伤致组阳性反应面积（μm^2）为527．99±105．04；病毒性心肌炎组阳性反应面积（μm^2）为5483．53±1219．91。结论冠心病猝死者心肌FN免疫组化检测可为死因诊断提供可靠依据。     

病毒性心肌炎和扩张性心肌病心肌中β-sarcoglycan的免疫组化染色观察

目的探讨病毒性心肌炎(viralmyocarditis,VCM)和扩张型心肌病(dilatedcardiomyopathy,DCM)的发病机制及相互关系,从而提高心性猝死法医学鉴定的可靠性和准确性。方法对17例对照组(包括冠心病、高血压性心脏病和正常心脏等),25例VCM和28例DCM的心肌组织进行改良的β-sarcoglycan免疫组织化学染色观察,并对其阳性反应率进行χ2检验及相关分析。结果β-SG蛋白在对照组,VCM组和DCM组中阳性反应率分别为100%,80%,46.4%。经χ2检验,3组阳性反应率差异有显著性意义(P<0.05);用χ2分割法分析,VCM和DCM组间差异有显著意义(P<0.05),且Spearman等级相关分析呈显著负相关(rs=-0.605)。结论病毒性心肌炎和扩张性心肌病病变与β-SG的被破坏有关;随着VCM病变程度的加重,其可能发展为DCM。     

219例损伤与疾病关系的尸检案例分析

目的探讨损伤与疾病关系案例的特点。方法对本教研室近20年的219例涉及损伤与疾病关系的尸检案例进行回顾性研究。结果①219例中,20~59岁青壮年占71.7%;伤后<24h死亡占48.9%。②损伤以拳、足等钝器伤为主,以擦伤和挫伤多见,主要位于头、胸部。③疾病以心血管疾病最多,CNS疾病次之。④损伤与疾病相关的案例占71.2%,最常见的是“疾病为主、损伤为辅”。结论损伤与疾病关系案例的死者多为男性青壮年,冠心病和病理性脑出血是两个主要的疾病;将损伤与疾病关系分为“单纯损伤致死、单纯疾病致死、损伤为主疾病为辅和疾病为主损伤为辅”四类简单而实用。     

Stressful events as a trigger of sudden death: a study of 43 medico-legal autopsy cases

The reports relating emotional stress to sudden death are largely anecdotal. In addition to experimental and electrophysiological studies, an opportunity for a better understanding of possible stress-related sudden death (SSD) may be provided by medico-legal autopsies. The goal of our autopsy study was to analyze cardiovascular pathologic findings in cases of SSD and if possible identify mechanisms by which the stressful event (SE) could be the cause. Forty three cases were studied (29 males and 14 females). In all cases, the SE and the death were witnessed. The age range was 22 to 90 years in males (mean, 52) and 30 to 92 years in females (mean, 64). Death occurred in all cases without premonitory symptoms. In 20 cases, death occurred during the SE and in the other 23 cases occurred within 2 h of the event. SE included fear, 15 cases; altercation, 21 cases; sexual activity, 3 cases; police questioning or arrest, 4 cases. According to police reports, in 40 cases (90%), the victims had no previous clinical history of cardiovascular disease. At autopsy, the heart weight in males ranged from 255 to 1000 g with a mean of 517 g and in females the range was 250–700 g with a mean of 417 g. In only 3 cases, gross and microscopic examination of the heart was normal. In 2 of the remaining 40 cases the subjects died of subarachnoid hemorrhage. In 38 cases, a cardiac cause of death was found as follows: coronary heart disease, 27 cases; cardiomyopathy, 6 cases; aortic valvular stenosis, 2 cases and right ventricular dysplasia, 3 cases. A coronary artery thrombosis was found in 8 cases of sudden coronary death. Post myocardial infarction fibrosis was present in 25 cases (92%) of sudden coronary death. In conclusion, it appears from our autopsy study that SSD occurs primarily in those individuals with severe heart disease, especially coronary heart disease.     

Impact of Myocardial Infarction and Abnormalities of Cardiac Conduction System on Sudden Cardiac DeathCSCD

Sudden cardiac death (SCD), most commonly seen in coronary heart disease, is a kind of sudden death caused by series of cardiac parameters, which usually combines with myocardial infarction. However, some SCDs (including early myocardial infarction) happen suddenly and cause death in a very short time. In these circumstances, typical morphological changes are lack in macroscopic or microscopic fields, which make such SCDs become the emphasis and difficulty in the present research. SCD caused by myocardial infarction and abnormalities of cardiac conduction system (CCS) is related to atherosclerosis of coronary artery closely. This paper reviews cardiac dysfunction caused by myocardial infarction and diseases of CCS from morphology and molecular biology, and explores potential relationship between them. This paper aims to provide clues to the mechanism of myocardial infarction related sudden death and possible assistance for forensic diagnosis of SCD. © 2017 by the Editorial Department of Journal of Forensic Medicine.     

冠心病猝死心肌mcl-1蛋白检测及其意义

目的观察冠心病猝死(SCD)心肌mcl-1蛋白产物,探讨其免疫组化检测及其对SCD诊断的意义。方法运用免疫组织化学SABC法,对46例SCD和40例非猝死心肌(有冠心病和无冠心病)中mcl-1蛋白产物进行检测和观察,并比较其差异。结果(1)自症状出现至死亡,时间超过30min的SCD(36例),其心肌组织均出现mcl-1蛋白阳性染色;(2)自症状出现至死亡,时间短于30min的SCD(10例),其心肌组织mcl-1蛋白呈弱阳性染色;(3)冠心病非猝死样本(20例),4例心肌出现微弱的mcl-1蛋白阳性染色,无冠心病非猝死样本(20例)几乎没有出现阳性染色。结论心肌mcl-1蛋白的免疫组化检测可诊断自症状出现至死亡时间超过30min的SCD。     

Sudden cardiac death in young adults: environmental risk factors and genetic aspects of premature atherosclerosis

Familial hypercholesterolemia (FH) is a genetic disorder that may lead to premature coronary heart disease (CHD) and sudden cardiac death (SCD). Mutations in the LDLR or APOB genes cause FH. We have screened the LDLR and the ligand-binding region of APOB genes in 52 cases of SCD. Deceased patients were younger than 40 years of age and were suspected of having FH. The LDLR and APOB genes were examined via PCR, high-resolution melting, and DNA sequencing. Therein, it was observed that 7.7% of the screened patients exhibited a rare sequence variant in the LDLR gene, with 5.7% suspected of being pathogenic mutations. Lipid profiles and genetic testing for FH could be considered when autopsy reveals significant atherosclerosis of the coronary arteries in young adults. First-degree family members are advised to seek medical advice and testing to determine their own risks of atherosclerosis to prevent premature CHD and SCD.     

Is there progress in the autopsy diagnosis of sudden unexpected death in adults?

Sudden death is now currently described as natural unexpected death occurring within 1h of new symptoms. Most studies on the subject focused on cardiac causes of death because most of the cases are related to cardiovascular disease, especially coronary artery disease. The incidence of sudden death varies largely as a function of coronary heart disease prevalence and is underestimated. Although cardiac causes are the leading cause of sudden death, the exact incidence of the other causes is not well established because in some countries, many sudden deaths are not autopsied. Many risk factors of sudden cardiac death are identified: age, gender, heredity factors such as malignant mutations, left ventricular hypertrophy and left ventricle function impairment. The role of the police surgeon in the investigation of sudden death is very important. This investigation requires the interrogation of witnesses and of the family members of the deceased. The interrogation of physicians of the rescue team who attempted resuscitation is also useful. Recent symptoms before death and past medical history must be searched. Other sudden deaths in the family must be noted. The distinction between sudden death at rest and during effort is very important because some lethal arrhythmia are triggered by catecholamines during stressful activity. The type of drugs taken by the deceased may indicate a particular disease linked with sudden death. Sudden death in the young always requires systematic forensic autopsy performed by at least one forensic pathologist. According to recent autopsy studies, coronary artery disease is still the major cause of death in people aged more than 35 years. Cardiomyopathies are more frequently encountered in people aged less than 35 years. The most frequent cardiomyopathy revealed by sudden death is now arrhythmogenic right ventricular cardiomyopathy also known simply as right ventricular cardiomyopathy (RVC). The postmortem diagnosis of cardiomyopathies is very important because the family of the deceased will need counseling and the first-degree relatives may undergo a possible screening to prevent other sudden deaths. In each case of sudden death, one important duty of the forensic pathologist is to inform the family of all autopsy results within 1 month after the autopsy. Most of the recent progress in autopsy diagnosis of sudden unexpected death in the adults comes from molecular biology, especially in case of sudden death without significant morphological anomalies. Searching mutations linked with functional cardiac pathology such as long-QT syndrome, Brugada syndrome or idiopathic ventricular fibrillation is now the best way in order to explain such sudden death. Moreover, new syndromes have been described by cardiologists, such as short-QT syndrome and revealed in some cases by a sudden death. Molecular biology is now needed when limits of morphological diagnosis have been reached.     

心脏性猝死心肌组织N-Cadherin、Bax表达变化及评价

目的观察心脏性猝死者(SCD)心肌组织的神经性钙粘附蛋白(N-Cadherin)和Bax的表达变化,探讨其法医学意义。方法分别选取心脏性猝死和排除心脏疾病死因的尸检案例心肌组织标本各33例、29为SCD组和对照组。光镜下观察心肌组织病理学改变,检测N-Cadherin和Bax在心肌组织中的表达变化,并进行统计学分析。结果 N-Cadherin在SCD组心肌中表达呈弱阳性,排列紊乱,显著低于正常心肌,正常心肌组织中N-Cadherin呈强阳性表达,细胞间界限明显,排列整齐。Bax在SCD组表达呈阳性,显著高于正常心肌。结论 N-Cadherin和Bax的变化表达对心脏性猝死鉴定有意义。     

基质金属蛋白酶2在冠心病猝死心肌中的表达

目的探讨基质金属蛋白酶2（mmp2）在冠心病猝死（SCD）心肌细胞和间质中的表达与SCD的关系。方法选取本教研室2003年51例死亡鉴定病例,分为SCD组,患有冠心病但非SCD组（对照组1）,无严重冠脉粥样硬化（As）病变和其它心血管疾病组（对照组2）,无严重As病变但有其它心脏病组（对照组3）。采用免疫组化SABC法染色及图像分析技术,检测mmp2在各组心肌细胞和间质内表达的阳性率（R值）和平均灰度值（H值）,并比较各组间的差异。结果SCD组与3个对照组之间心肌细胞内romp2H值的差异均有显著性意义;SCD组与对照组2和3之间心肌间质内mmp2H值的差异有显著性意义;镜下各组心肌间质及心肌细胞内表达的阳性率差别明显。结论心肌间质及心肌细胞内mmp2同相表达增高与SCD的发生有密切关系,联合检测心肌和间质mmp2的表达对诊断SCD有重要意义。