青壮年猝死综合征心传导系统及心肌HHF35免疫组化研究

为了探讨青壮年猝死综合征（SMDS）的死亡原因与心性猝死之间的关系，作者对SMDS、冠心病、非心血管疾病死亡（正常对照）三组共23例心脏标本进行H．E和HHF35免疫组化观察．结果：9例SMDS中，8例心传导系统及心肌细胞出现小灶性HHF35阴性缺染区，而H．E染色未发现明显梗死灶；冠心病组7例均出现不同程度的心肌细胞缺染，呈广泛大面积分布；对照组心肌细胞、心传导系统及血管壁里均匀一致的阳性染色．表明部分SMDS死前已有早期心肌缺血或梗死等病变，其死亡原因应为急性心功能不全而致猝死．     

心传导系统病变猝死1例

心传导系统病变导致猝死的公认病变是心传导系统肿瘤,炎症及出血,而国内法医实践中往往把心传导系统的退行性病变作为其死因诊断标准,但病理学者则有不同认识,关于这个问题,作者复习相关文献,结合案例,阐述对其诊断标准的看法,以供同仁参考。1案例某男,48岁,法国人。某年2月4日曾在某医院因心悸、胸闷就诊。心电图检查示窦性心动过速(HR125次·min-1),完全性右束支传导阻滞。胸部X线检查示:左肺中野外带少许小结节影。诊断为哮喘。次日在成都住家死亡。2月7日对死者进行尸体解剖。尸长180cm,发育正常、营养良好,尸斑分布于双耳后、项部、…     

急性心肌梗死心传导系统的免疫组化实验观察

观察急性心肌梗死时心传导系统的形态学改变。取急性心肌梗死死亡者的心传导系统标本6例,运用抗纤维连接蛋白抗体、肌红蛋白抗体、血管内皮生长因子抗体进行免疫组化染色。结果发现,纤维连接蛋白染色有3例呈现强阳性,2例出现阳性,1例出现弱阳性;血管内皮生长因子染色均呈弱阳性;肌红蛋白染色呈脱失改变。提示纤维连接蛋白检测量敏感性强,稳定性好,易于观察,可作为在心肌梗死时了解心传导系统受损害的指标之一。     

心肌炎侵及心传导系统病理学观察

本研究采用已建立的人体心脏传导系统简易取材法,对6例心肌炎的案例进行了传导组织的病理学观察,结果发现6例心肌炎患者CCS均有明显炎症,尤以SAN、AVN病变为主;推测CCS炎症可能为心肌炎患者猝死的主要原因。因此,本文提出对怀疑心性猝死案例应作常规传导系统检查。     

心传导系统的常见疾病(讲座3)

心脏传导系统疾病常是全身或心脏病变的一部分 ,也可以是独立的发生。心脏传导系统疾病虽不多见 ,但它可诱发心律失常导致猝死。心源性猝死是法医学中的重要组成部分 ,故法医应该了解、掌握心脏传导系统病变 ,以便在损伤与疾病并存中作出准确鉴定 ,为执法部门提供量刑定罪的依据。日常尸体解剖中 ,常规心脏传导系统检查 ,都可见到心脏传导系统存在某些异常变化 ,但不要随意轻率地定为猝死原因 ,认定心脏传导系统疾病是其死亡原因 ,需具备以下条件 :1 没有可致死的暴力损伤 ,排除暴力致死 ;2 排除中毒致死 ;3 排除心脏外疾病致死 ;4 排除心…     

心传导系统取材及组织形态观察的实验研究

收集32例人体心脏标本，分为两组，每组16例，介绍并比较心传导系统的不同取材方法。一组采用与窦房结、房里结长轴相垂直切面取材（横切法）；另一组采用与窦房结、房室结相平行的水平切面取材（纵切法）。通过石蜡切片，HE染色后于光镜下观察其形态结构。结果显示：横切取材较易掌握，不需间断连续切片，16例心脏在显微镜下全部显示出窦房结、房室结结构；纵切面16例心脏有7例没有取中窦房结，9例没有取中房室结，操作方法较难掌握。提倡心传导系统取材采用横切法。     

青壮年猝死综合征心肌心钠素免疫组化研究

研究青壮年猝死综合征病理形态学诊断依据。应用免疫组化LSAB,观察10例SMDS及10例非心性死亡对照组死者ANP变化情况。结果发现,SMDS中7例ANP呈阴性,3例呈弱阳性;10例非心性死亡ANP呈强阳性。研究表明,SMDS死者心房内ANP数量减少是导致死亡的重要因素,可通过ANP免疫组化观察找到SMDS死亡的形态学依据。     

32例无心外原因猝死者传导系统病理学观察

在对32例无心外原因猝死者传导系统(CCS)组织学观察中,发现31例 CCS 有异常和病变,其中11例可致猝死。这些病变包括有急性炎症、出血、脂肪浸润和结内外神经病变,且与猝死有关。     

230例汉人心传导系统间质年龄变化统计分析

采用ＨＥ染色、部分用Ｍａｓｓｏｎ三色对照的半定量估算法，对２３０例中国汉人的心传导系统脂肪和纤维组织含量，分８个年龄组进行检测，按其含量不同分轻、中和重度三型，所得数据经统计学处理、分析，结果显示窦房结和房室束均在４０岁以后随年龄增大而增多，房室结３０岁出现脂肪组织，纤维组织则在６０岁开始出现，从而划分出生理和病理范围。     

心传导系统解剖组织学研究简史及法医学意义(讲座1)

人的胚胎从两个多月起开始有搏动 ,直至心脏停止跳动 ,人的生命也就终结。这奥秘被人类揭示才仅一百多年。1845年波兰教授Purkinje在有蹄类动物发现了一种位心内膜下、胞浆空虚的大细胞 (后人称Purkinje细胞 ) ,认为是心脏的运动装置。 1893年德国His教授在小鼠、狗和人的心脏发现了连接心房和心室的一束纤维 (被后人命名His束 )。190 6年此束纤维得到Tawara的详细叙述和图解 (包括房室结和房室束 ,后人合称之为His Tawarasystem)。至此 ,确定了从心房到心室迅速传递收缩冲动的肌束。同年夏 ,一位英国医学学生Flack在Keith的实验室做鼹…     

婴儿猝死综合征的法医学鉴定

近20多年来,婴儿猝死综合征（sudden infant death syndrome,SIDS）一直是西方发达国家医学界尤其是法医学和儿科学领域研究的热点。目前,随着对SIDS广泛而深入的研究,对其病因、发病特点、危险因素以及致病机制等都有了更明确的认识。虽说近年来SIDS的发病率已有明显下降,在欧美洲、澳洲等发达国家,SIDS仍然是导致1个月到1岁婴儿死亡的首要原因。在亚洲国家和地区,尤其是发展中国家SIDS的报道很少见。本文通过总结文献并结合美国马里兰州近20年（1990—2006）来对SIDS的调查研究资料,介绍SIDS的发展历史、研究现状和新的发展趋势,并对SIDS法医学鉴定程序及鉴定要素进行讨论。     

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.     

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。     

青壮年猝死综合征心肌细胞内纤维连接蛋白免疫组化观察初探

本文应用免疫组化ＬＳＡＢ法首次对５例青壮年碎死综合征和１１例非心性死亡对照组进行心肌细胞内纤维连接蛋白的研究。发现青壮年猝死综合征５例中有３例心肌细胞内纤维连接蛋白阳性。１１例非心性死、对照组心肌细胞内纤维连接蛋白均呈阴性。说明上述３例青壮年猝死综合征的心肌细胞已发生不可逆损伤，实属早期心肌梗死。该研究为青壮年猝死综合征的死因研究提供了一个新的方向和手段。     

The Institution of a Standardized Investigation Protocol for Sudden Infant Death in the Eastern Metropole,Cape Town,South Africa,,

The rate for the sudden infant death syndrome (SIDS) in Cape Town, South Africa, is estimated to be among the highest in the world (3.41/1000 live births). In several of these areas, including those of extreme poverty, only sporadic, nonstandardized infant autopsy, and death scene investigation (DSI) occurred. In this report, we detail a feasibility project comprising 18 autopsied infants with sudden and unexpected death whose causes of death were adjudicated according to the 1991 NICHD definitions (SIDS, n = 7; known cause of death, n = 7; and unclassified, n = 4). We instituted a standardized autopsy and infant DSI through a collaborative effort of local forensic pathology officers and clinical providers. The high standard of forensic investigation met international standards, identified preventable disease, and allowed for incorporation of research. We conclude that an effective infant autopsy and DSI protocol can be established in areas with both high sudden unexpected infant death, and elsewhere. (SUID)/SIDS risk and infrastructure challenges.     

Use of Cardiac Injury Markers in the Postmortem Diagnosis of Sudden Cardiac Death

In the daily practice of forensic pathology, sudden cardiac death (SCD) is a diagnostic challenge. Our aim was to determine the usefulness of blood biomarkers [creatine kinase CK‐MB, myoglobin, troponins I and T (cTn‐I and T), and lactate dehydrogenase] measured by immunoassay technique, in the postmortem diagnosis of SCD. Two groups were compared, 20 corpses with SCD and 8 controls. Statistical significance was determined by variance analysis procedures, with a post hoc Tukey multiple range test for comparison of means (p < 0.05). SCD cases showed significantly higher levels (p < 0.05) of cTn‐T and cTn‐I compared to the control group. Although only cases within the first 8 h of postmortem interval were included, and the control group consisted mainly of violent death cases, our results suggest that blood troponin levels may be useful to support a diagnosis of SCD.     

Sudden Death Due to Infiltration of Left Bundle Branches by Interventricular Septal Cardiac Fibroma

Cardiac fibromas are benign conditions; however, their location and size may cause ventricular arrhythmias and sudden cardiac death. We report a case of a 68‐year‐old female who died suddenly. Postmortem investigation detected a huge cardiac fibroma in the pars muscularis of the interventricular septum, occupying almost the entire muscular septum, and restricting the volume of left ventricular chamber. Histological examination revealed numerous foci of calcification in the alternating complex interlacing or strictly parallel collagenous fiber mass. Tumor mass was mainly demarcated, but in some places, fibrous infiltration of surrounding working cardiac muscle was found. We present a case when direct tumor involvement in the descending left bundle branches was evidenced. Mainly, the branches of septal fascicle were disrupted, entrapped, and degenerated by the tumor mass. This case report emphasizes that postmortem histological examination of conduction system in all sudden cardiac death cases may substantially improve the accuracy of postmortem diagnosis.     

Tyrosine Hydroxylase TH01 9.3 Allele in the Occurrence of Sudden Infant Death Syndrome in Swiss Caucasians

Catecholamines, especially noradrenalin, are essential in the control of respiration and arousal. Thus, an impaired production of these neurotransmitters may contribute to the occurrence of sudden infant death syndrome (SIDS). The first step of the noradrenergic synthesis pathway is catalyzed by the enzyme tyrosine hydroxylase (TH). The TH‐encoding gene contains a tetrameric short tandem repeat in intron 1 (TH01), with allele 9.3 reported to be associated with SIDS in German infants. We investigated the allelic frequency of the TH01 marker in 171 Swiss SIDS infants and 500 healthy and gender‐matched Caucasian adults. In our study population, the allelic frequency of the 9.3 allele is similarly distributed in SIDS cases and controls (27.2% vs. 25.6%; p‐value = 0.562). Nevertheless, the TH‐encoding gene is only one of several genes involved in the noradrenergic biosynthesis pathway. Therefore, further genetic investigations are required with focus on the whole noradrenergic signaling system.     

窖蛋白与不明原因心源性猝死的相关性研究进展

不明原因心源性猝死(unexpected sudden cardiac death,USCD)因其不伴有心脏结构的异常,尸体解剖呈阴性改变,一直是法医病理学鉴定的热点难题。USCD可能与部分致死性心律失常有关,该类心律失常多由心脏离子通道蛋白或其相关蛋白发生异常所致。窖蛋白可以通过其脚手架区域与多种心肌离子通道蛋白结合,在维持心肌动作电位的去极化和复极化中起到关键作用。当窖蛋白由于基因突变或蛋白表达异常等因素导致其结构和功能受到影响时,受其调控的心肌离子通道的功能也受到损害,继而引起多种离子通道病的发生,出现心律失常甚至心源性猝死。研究窖蛋白对离子通道功能的影响对于探索恶性心律失常及心源性猝死的发生机制具有重要意义。     

Morphometrical investigations into alterations of the wall thickness of small pulmonary arteries after birth and in cases of sudden infant death syndrome (SIDS)

In 1973 Naeye was the first to demonstrate that, in cases of SIDS, the small pulmonary arteries have more smooth muscle than in controls and suggested that this is a consequence of chronic alveolar hypoxia. Seventy-five cases have been investigated morphometrically in order to obtain quantitative data on the alterations of wall thickness of the small pulmonary arteries after birth and in cases of SIDS. The investigations comprise seven cases of stillbirth, 19 cases of newborn, 33 cases of SIDS and 16 controls. In each case the thickness of the media, the external diameter of the artery and the media area have been measured planimetrically for 90 arteries ranging between 50 μm and 500 μm. A media index was calculated as the ratio of the thickness of the media to the diameter of the artery. Using this index a thickening of the media of the small pulmonary arteries, corresponding to the situation in fetal and neonatal life, has been confirmed for cases of SIDS. The normal postnatal changes in the small pulmonary arteries, media thinning and enlargement of the lumen, could not be observed in SIDS cases in the first year of life.