886例人心传导系统形态变异研究

探讨划分心传导系统 (CCS)变异与发育异常的界限。用本组建立的CCS检查法[1] ,连续切片 ,HE或Masson三色染色 ,光镜检查 ,对非心源性死亡组 (737例 )和心源性猝死组 (14 9例 )进行形态学及死因对比分析。结果显示 :(1)人CCS具有大小、位置和形态的先天性变异 ;(2 ) 4例心源性猝死者的房室结、房室束发育异常。房室束分叉部向室间隔膜部内移位、偏向于室间隔左侧、向左下侧移位 ,以及不足 1/2房室结移位至中心纤维体内、普通心肌移位至房室束或左束支内等应属变异 ;成年人胎儿型房室结及房室结全部移位至中心纤维体内或房室束完全分成 3束以上 ,房室束分叉部移位至三尖瓣根部应视为发育异常     

一种简便的心脏传导系统检查法

<正> 心脏传导系统包括窦房结、房室结、房室束(His 束)、左右束支及其末稍等部分。其中窦房结和房室结是起搏的主要成分。猝死常与窦房结、房室结、房室束和束支结构异常或病变有关,尤以窦房结和房室结更为重要。半个世纪以来,国内外检查心传导系统的传统方法,主要是与其长轴方向垂直切取若干块组织,作连续切片,每例需检查数百甚至     

青年人CCS脂肪超前变化致猝死

为研究心传导系统（CCS）与猝死的相互关系，对120例心性猝死者CCS作常规检查，光镜下作半定量计算其脂肪含量。结果发现：9例经一般常规尸检未找到任何致死原因的青年人（30岁以下），其房室结（AVN）与房室束（HB）的脂肪组织含量为70％，比同龄人明显增多，致使结、束肌细胞被脂肪分割中断或压迫萎缩。结内外细胞连接不足或缺失是构成心电不稳的病理基础。此外本文尚对其脂肪浸润的病因发病，猝死机理作了探讨。     

心脏传导系统变异及发育异常(讲座2)

心脏传导系统变异与发育异常是完全不同的两个概念 ,前者是属个体间的形态差异系生理性变化 ,后者是属病理性畸形 ,划清这两种界线对一个基层法医工作者有着重要的实用意义。1　CCS的变异CCS与人体其它系统、器官一样 ,亦具有某些形态变异 ,这些变异并不影响CCS的正常功能。根据产生变异的机理可分两种 :( 1)个体发育差异 :变异 (Variation)是指正常心脏的CCS位置或形态学的个体差异。表现为过大、过小 (正常中国人窦房结 10～ 15mm× 3～ 5mm× 1～ 2mm、房室结 8mm×4mm× 1mm、房室束 1mm× 1mm× 2 0mm )、变形 (如房室结变成薄片…     

心传导系统结动脉结细胞的定量分析

采用显微图像分析技术，定量观察35例人体心脏传导系统结细胞直径、结动脉管径及管壁厚度，探讨其与年龄变化的关系。结果显示：窦房结（SAN）动脉的血管内径较房室结、房室束供血动脉之内径粗大，反映出窦房结在心传导组织中地位显要；SAN动脉管壁菲薄，中层无完整环行平滑肌，组织构筑上提示SAN动脉对血压波动敏感；结细胞直径在40岁前随年龄增长而变大，40岁后则随年龄增长而逐渐缩小，与人体其它脏器生长发育的规律相一致。意味着年龄老化，心传导系统功能减退。     

房室结间皮瘤一例

房室结间皮瘤是一种原发于房室结区的罕见的良性肿瘤。自1911年Armstrong首次报告以来，迄今仅有4O余例，我国曾报告过3例[1,2]。4年多来，我们在对421例尸体心脏作传导系统常规检查中遇见1例，现报告如下。实例报告王XX，男，8岁。在自行车上被汽车冲撞死亡。尸体解剖：身长115cm，发育正常，营养中等。体表有数处挫擦伤。枕骨、颅底骨折，伴有对冲性脑挫伤（预叶）、硬膜下血肿形成，心重145g，外形无异常。心外膜光滑，心肌阳红色，有光泽，各心瓣膜正常。塞房结、房室结局部肉眼检查未见肿瘤，但见房间隔下部切面增厚达3．6mm－4mm（…     

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…     

6例肥厚性心肌病猝死者心传导系统病变

1958年，DonaldTears首次描述了肥厚性心肌病（HypertrophicCardiomyopathy，HCM）。其后40年来，虽有许多有关HCM的临床、超声心动电图和病理学的研究屡见报道，但对其。已脏传导系统的研究尚少，我们遇到6例HCM摔死者，现对其尸检材料的研究报告如下。材料与方法6例选自近4年来法医破案P检材料。全部尸检在死后低温保存36小时内进行。尸体解剖检查除心脏外未见有其它病变。切取心脏在心室组织4块（左前壁、外侧壁、室间隔上1／3部和中部各1块）；窦房结（SAN）、房室结（AVN）、房室束（HB）和左右束支（LBB、RBB）共6块（SA…     

急性心肌梗死时人心脏房室结细胞糖蛋白表达

目的观察急性心肌梗死时心传导系统糖蛋白表达。方法运用花生凝集素(PNA),对8例急性心肌梗死亡者的心传导系统标本进行亲和组化染色。结果PNA有7例呈现强阳性,1例出现弱阳性。结论房室结传导细胞在缺血时细胞膜表达PNA受体,提示急性心肌梗死时房室结细胞和工作心肌都不同程度受累,并且细胞病理改变机制可能相关或类似。     

房室结纤维和脂肪增多与房室结动脉狭窄的关系

目的探讨房室结纤维、脂肪含量与房室结动脉狭窄之间的关系,分析房室结内病理性纤维化和病理性脂肪浸润的原因。方法选取119例心源性猝死案例,用Image-pro plus图像分析软件检测组织切片,计算房室结面积,房室结动脉内径、房室结动脉管腔面积(lumen area,LA)、外周横截面积(perimeterarea,PA),纤维组织面积和脂肪组织面积。将所有案例分为动脉狭窄组和正常对照组组,观察房室结动脉PA/LA值及房室结纤维及脂肪含量的改变。结果狭窄组房室结动脉PA/LA值在21～40岁最大,40岁以下两组房室结脂肪含量和总间质含量差异有统计学意义。结论房室结动脉狭窄与房室结间质含量增多有一定关系。     

Age-related variation in the interstitial tissues of the cardiac conduction system; and autopsy study of 230 Han Chinese

The amount of fatty and fibrous tissues in 230 Han Chinese who died of noncardio-vascular diseases has been studied by a semi-quantitative method and analysed by chi-square test. The results have shown some consistency. Generally, in the sino-atrial node (SAN), fibrosis and fatty influtratin appear only after 40 years of age and increase one grade with every 20 years. The atrio-ventricular node (AVN) showed fatty change after 30 years of age and fibrosis appeared after 60. In the His bundle (HB), fatty infiltration and fibrosis appear after 40 years. The left bundle branch (LBB) showed similar changes. The appearance of fibrosis in the AVN seems to be later than that reported by Lev.     

6例心脏传导系统病变致交通事故的病理学观察

检查100例交通事故死亡者的心脏传导系统（CCS），发现大部分存在着程度不同的病变。其中6例的SAN、AVN、AVB及LBB、PBB起始部见明显的出血、炎症、脂肪浸润、纤维化、神经病变和结动脉狭窄等病变。结合案情与现场勘查，6例交通事故与CCS病变导致心律失常有关。     

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。     

NMDAR1在成人心脏中的分布及其法医学意义

目的 检测成人心脏中NMDAR1蛋白,观察其分布情况,并探讨法医学意义。方法以12例高坠死亡成人心脏为标本,提取左、右心室和心传导系统（窦房结、房室结、房室束及左右束支）组织作为实验组;取大脑额部组织作为阳性对照组。所取标本各两份,一份采用westernblot技术检测NMDAR1蛋白,另一份采用免疫组化染色法观察NMDAR1在成人心脏中的分布。结果两组中用westernblot均可检出NMDAR1蛋白表达,其强弱程度：脑组织最强,其次为窦房结和房室结,左右心室肌最弱;用免疫组化方法观察,结果在心脏传导系统可见NMDAR1阳性表达,而在心室肌中未见表达。结论成人心脏中存在NMDAR1,主要分布在心传导系统,NMDAR1可能在心脏电生理和病理生理中起作用。     

Histopathological findings of cardiac conduction system of 150 Finns

One hundred and fifty heart specimens were collected from the cases submitted for autopsy in the Department of Forensic Medicine in the University of Turku in March-May 1995 and May-July 1996, respectively. The cardiac conduction system (CCS) of these hearts were examined in order to find out the histopathological changes in the CCS of Finnish persons and their forensic pathological significance. There were 94 males and 56 females. Almost all age groups were included. The results revealed that in most of the persons the fibrous tissue and fatty tissue in the CCS increased with aging. In about half of the persons, there was deposition of calcium in the central fibrous body, pars membranacea, and the top of the musculature in the interventricular septum. In seven cases, the atrioventricular node (AVN), His bundle (HB) or bundle branches (RBB, LBB) were compressed by the calcium deposition. Hemorrhage, inflammation, amyloidosis, tumor, fatty infiltration and developmental malformations were observed in 31 cases. Twenty-eight cases died of myocardial infarct, among them, no involvement of the CCS could be observed. The authors concluded that routine examination of the CCS is helpful for revealing diseases of the CCS and improving the quality of forensic pathological diagnosis.     

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.     

Study by next generation sequencing of sudden cardiac death (SCD)

Sudden cardiac death (SCD) is one of the most common causes of death; most SCD are related to secondary arrhythmias, to structural heart disease, or to primary electrical abnormalities of the heart.A significant number of SCD, especially among young people, are due to genetic heart disorders, both with structural and arrhythmogenic abnormalities. However SCD occurs also in patients with negative clinical history, autopsy is not always conclusive for a diagnosis.Recent technological advances in DNA sequencing, have led to the commercialization of genetic testing now widely available in clinical practice. In particular, next generation sequencing, allows the large-scale and rapid assessment of entire genomes.Analysis of SCD with a NGS panel of 174 genes was performed in our laboratory in order to identify the genetic causes and thus to direct the clinician to an accurate clinical and genetic screening of relatives.Two SDC were studied:Case 1: female, 57, without story of syncope and no previously highlighted cardiac alteration, died post cardiac arrest; negative family history. Autopsy was apparently negative.Case 2: male, 52, who died during a football game; negative family history, neurological episodes occurred before death was reported by close relative. Autopsy was positive for ventricular hypertrophic.In both cases we made a genetic diagnosis.