成人心传导系统的超微结构

目的　进一步观察成人心传导系统的超微结构。方法　对窦房结、房室结采用纵切法 ,分别于其头、体、尾部切取 1mm3 组织各两块 ;房室束分叉部采用横切法切取其分叉部的近、远段组织各两块 ,用透射电镜观察。结果　 (1)窦房结头部或头体交界部见P细胞 3～ 4个环抱成团 ,团内细胞互相广泛连接 ,构成一个电传导装置 ;(2 )窦房结和房室结可见有功能下降的明细胞与代偿性功能增强的暗细胞相并列 ;(3)结细胞退行性变与纤维组织增生并举 ;(4)窦房结的退行性变化从外侧部、尾部开始。结论　推测窦房结的头部和头体交界部可能是窦房结的起搏中心     

人心房室结和房室束的光镜观察

本文对13例人心标本房室结和房室束的形态及位置,作了连续切片观察。1.房室结为一扁长形结构,其横切面呈右侧微凸的三角形,有时切面呈梭形或半卵圆形。成人房室结大小为3.5×3.3×1.1 mm~3。有5例房室结表面的右心房心内膜隆起。2.房室结位于二尖瓣与三尖瓣附着缘之间的房室隔内,成人房室结距冠状窦口1.8～5.8 mm,距右心房心内膜0.3～0.7 mm,距三尖瓣隔侧瓣上缘3.3～7.5 mm。结左侧紧贴中心纤维体。3.房室结可分为浅、深两部,浅部纤维纵行止于结的下端。1例深部又分为上、下两部。在结表面右心房心内膜隆起的标本上,结右侧的心房肌覆盖层止于心内膜。结的上缘、右侧面及后缘与房肌相连。4.成人房室束长5.7～7.9 mm,直径1.1～1.5 mm。房室束前部有7例在肌性室间隔顶部;3例在肌性室间隔左侧;2例在肌性室间隔肌肉内部。1例经行特殊,由肌性室间隔顶部至其左侧,最后至肌性室间隔内部偏右侧而终止。     

房室结区神经结构的组织化学研究

Wistar大白鼠20只,10例用于胆碱酯酶(AchE)组织化学反应.在房间隔内发现AchE阳性神经元,该神经元发出神经纤维延续至房室结及房室束.该结果证实房室结及房室束区副交感神经纤维来源于房间隔内的胆碱能神经元.另外10例行单磷酸硫胺素酶(TMPase)和抗氟酸性磷酸酶(FRAP)组织化学染色,观察到房室结周围区存在(TMPase)阳性神经细胞,室间隔上部近房室结区存在FRAP阳性神经细胞.该二类神经元可能系房室结区局部神经调制结构.     

大鼠房室交界区的组织化学研究

目的：比较大鼠房室交界区各部之间的糖代谢及神经分布的差异。方法：SD大鼠心脏冷冻切片;行糖原,乳酸脱氢酶,琥珀酸脱氢酶,单胺氧化酶和乙酰胆碱酯酶染色。结果：（1）糖原：房室结,中心纤维体＞房间隔,室间隔;乳酸脱氢酶：中心纤维体＞房室结,房间隔,室间隔;琥珀酸脱氢酶,单胺氧化酶：室间隔＞房间隔＞房室结＞中心纤维体;乙酰胆碱酯酶;房室结＞＞房间隔,室间隔,中心纤维体;（2）乙酰胆碱酯酶在房室束未分叉部光密度比其他部位高,其余染色在房室交界区各部无差异。结论：（1）房室交界区与心肌都具备有氧及无氧\代谢的能力,交界区糖原储备丰富;交界区各部间的代谢无差别;（2）副交感神经在房室束未分叉部的分布较其他部位多。     

KOCH三角的解剖

本实验解剖了110例人心标本(成人70、儿童40)的Koch三角区,观察和测量了房室结的形态、大小、毗邻和标志。房间隔及冠状窦口上、下方均有肌束连于房室结。Todaro腱在儿童多全部为腱性;在成人,其后部为肌性。三角区的深面为左、右心房壁和室间隔顶所构成的锥形间隙,其内为进入房室结区的血管和神经。根据构成不同,可将三角区分为5个区,即前上角的纤维支架区和房室结区,其余部分自上向下分别为房间隔区、右房壁区和室间隔区。本文还讨论了这些形态结构的功能及外科意义。     

心脏房室传导阻滞的分型与诊断

对心房与心室间激动传导的改变,传统认为只是房室结的问题,以后由于心内心电图(如希氏束电图等)和通过电生理学、微电极的应用以及电镜对微细的组织学观察等,首先对激动的产生,证实在房室结附近有起搏功能的细胞(即起搏细胞或称P细胞pacemaker cells)存在于心房与房室结的交界部(房-结区)、房室结与希氏束的交界部(结-希氏束区)、希氏束部以及冠状窦的附近区,而房室结本身并无起搏细胞,或只有很少的变异细胞.因此,将房-结区、结-希氏束区、希氏束及冠状赛区以及左心房后部(左房节律发生的部位)统称之为房室交界部或简称交界部,由此产生的心律,统称为交界部(或交界性)心律.     

房室结后延伸部形态学特征及与折返性心动过速的关系

目的：研究人房室结双径路，尤其是慢径的解剖学基础。方法：(1)取17例尸检心脏包括房室结在内的房室交界区的组织固定、脱水、包埋后切片，HE和Masson染色，光镜规察(2)由冠状窦151向房室结方向在心内膜下注射墨汁0．5ml，24h后光镜观察墨汁走向?结果：17例标本均可发现房室结，房室结前向形成房室束(His束)，发现47％(8例)有明确向后延伸一左后延伸和彳丁后延伸，35％(6例)仅有右后延伸，1例发现仅有左后延伸，2例未发现有向后延伸。向后延伸南房室结自然延伸而成，其有房室结自然延伸而成，左后延伸朝左行向房间隔，有后延伸行向有，与三尖瓣隔瓣近乎平行，纤维可达冠状窦口附近。结论：房室结后延伸部可能为慢径路，作为房室结折返性心动过速(AVNRT)的射频消融慢径的解剖学基础、     

右冠状动脉肌纤维结构不良一例

<正> 预激综合征合并三尖瓣轻度下移畸形和右冠状动脉肌纤维结构不良的病人手术中,心脏复苏困难治疗失败后,病检观察见:(1)于右侧房室沟和房室沟外侧的浅层脂肪组织中,有异常心肌细咆群,即Kent氏束10余支。(2)房室结呈裂隙状结构,形态不规则。经V·G—Et,PAS,     

家猪房室交界区的组织学观察

利用石蜡切片 ,HE和 Masson染色 ,光镜观测了 7例猪房室交界区的形态学和组织学特征。家猪房室结位于冠状窦口前方 ,大小为 7.0 2× 2 .6 5× 1.2 9mm3。传导细胞分两类 :1细胞短柱状 ,有时有分叉 ,细胞质内有横纹 ,核相对较大 ,此类细胞多位于结上部和前部 ;2典型的移行细胞 ,多位于结的后部和下部。有 2例存在副房室结。结上部和前部、房室束、右束支内的细胞在形态上介于 Purkinje细胞和心肌之间 ,未见典型的 P细胞。说明猪的传导细胞与其它哺乳动物有差异 ,但不同形式的传导细胞却在履行相同的传导功能     

婴幼儿和法洛氏四联症房室结和房室束的外科解剖及计算机三维重建Ⅰ.位置与毗邻

通过对15例人心(成人5例,婴幼儿5例,法四5例)房室结和房室束的连续切片观察和图像分析,表明:15例房室结均位于Koch三角内.与成人相比,婴幼儿房室结位置相对较高,法四房室结位置偏低,其结前部紧靠三尖瓣隔瓣根部.婴幼儿房室束多位子三尖瓣隔瓣附着缘以上的房室肌隔内或室嵴顶部,而法四房室束起始部紧邻三尖瓣隔瓣根部的深面,其余部份可位:室嵴左侧,室缺的后下缘;房室束可直接位于室缺游离缘的心内膜下,或距室缺游离缘(可为肌性或腱性)1.88-2.14mm处.为临床小儿心外科手术提供了直接的形态学依据.     

54例心源性猝死患者心传导系统病变的分析

目的 探讨心源性猝死的死亡原因。方法 采用本组建立的心脏传导系统检查法,对１２０例心源性猝死者进行常规组织学检查。结果 发现５４例猝死与ＣＣＳ病变有关。猝死者８５．２％为年青人,２０－３０岁为猝死高峰年龄,男性我于女性。病变以ＣＣＳ炎症最多见,其后顺序是脂肪浸润,肥厚性心肌病伴发ＣＣＳ病变,出血,发育异常,心脏神经组织病变,纤维化及肿瘤等。     

心脏传导系统部位肿瘤的形态观察

目的观察心脏传导系统部位的肿瘤发病率及其与猝死关系。方法采用本组建立的心脏传导系统检查法,对无心外原因猝死者１４９例及死于非心脏疾病者７３７例作组织学检查。结果发现１２例心脏传导系统有肿瘤,占１．３５％,加上会诊１例共１３例。其中原发性良性心脏肿瘤累及心脏传导系统１０例,转移性恶性肿瘤３例。１０例良性肿瘤主要为纤维瘤、血管瘤、心房间隔脂肪瘤样肥厚、房室结间皮瘤和横纹肌瘤,其中８例位于窦房结和房室结,转移瘤全部累及窦房结。１３例中３例引起猝死。结论心脏传导系统肿瘤是可致猝死的人体最小肿瘤。     

Histopathology of the cardiac conduction system in sudden intrauterine unexplained death

BACKGROUND: Sudden intrauterine unexplained death (SIUD) is one of the most heartbreaking tragedies that any parent can experience. It remains poorly understood and incompletely examined both morphologically and functionally. The aim of this work is to examine the likely role of cardiac conduction system in relation to sudden and unexplained fetal death. METHODS: We analyzed and compared the autopsy results in 15 cases of SIUD (6 males and 9 females, ranging in age from 35 to 40 weeks) and 11 cases of intrauterine explained death (IED). A complete autopsy was performed, focusing on the examination of the cardiac conduction system on serial sections. RESULTS: The following findings were observed: resorptive degeneration (33% of SIUD, 36% of IED), dispersion or septation of the atrioventricular (AV) junction (60% of SIUD, 64% of IED), islands of the conduction system in the central fibrous body (80% of SIUD, 73% of IED), Mahaim fibers (20% of SIUD), cartilaginous metahyperplasia (20% of SIUD, 18% of IED), an AV node (AVN) tongue (13% of SIUD), hemorrhage of the cardiac conduction system (7% of SIUD, 9% of IED), left-sided bifurcation (7% of SIUD), an intramural right bundle (7% of SIUD), central fibrous body hypoplasia (7% of SIUD), and thickening of the conduction system arteries (13% of SIUD). CONCLUSIONS: Most of the abnormal cardiac conduction findings were detected only in SIUD and were absent in controls, i.e., Mahaim fibers, AVN tongue, left-sided bifurcation, intramural right bundle, and central fibrous body hypoplasia. We are convinced that these cardiac conduction abnormalities, in association with altered neurovegetative stimuli, could underlie potentially malignant arrhythmias.     

Mahaim纤维七例形态学观察

目的 研究成人心传导系统的Mahaim纤维组织形态学特点并探讨其意义。方法 采用自行建立的心脏传导系统检查法,对无心外器官疾病猝死者165例、死于非心脏疾病者760例,作心传导系统的组织学检查,经连续切片确定有Mahaim纤维7例。结果 （1）7例具有心传导系统Ma-haim纤维,均为束室束型,检出率为0.76%(其中猝死组有5例,占3.0%,非心脏疾病者死亡组中有2例,占0.26%);（2）Mahaim纤维组织形态学特点是：胞体横径在10-35um左右;从房室束分出的Ma-haim纤维胞体呈细条状,核居中,而从左束支分出的Mahaim纤维胞体按其始发点不同自上而下逐渐变大,两种细胞皆胞质丰富,肌原纤维较少,Masson染色淡,与房室束或左束支细胞形态相似。纵切细胞未见分叉,但部分细胞周围见有一薄层结缔组织包围。结论 Mahaim纤维是一种成人房室传导系外的附加传导旁路。     

胎儿房室结的组织学和组织化学研究

利用光镜观察了２０例胎儿室房结、房室束和左、右束支的组织结构和组织化学特征。结果如下：１、胎儿房室结位于三尖瓣隔侧瓣上方，中心纤维体右侧。结石侧有普通心肌组成的覆盖层。房室结可分深浅两部。浅部纤维平行排列，垂直下行，止于结的下端。深部可分为上和下部。深部向后延伸与房间隔肌相连，向前延续为房室束。深部向右深入中心纤维体内形成许多细胞岛。２、房室束横断面大多为三角形，外包有疏松结缔组织鞘。房室束的前部     

Sudden Infant Death Syndrome (SIDS): a study of cardiac conduction system.

The theory that Sudden Infant Death Syndrome (SIDS) may be related to lethal cardiac arrhythmias or heart block due to structural abnormalities of the conduction system is attractive and still of particular interest. We analyze 69 autopsied cases of SIDS (46 males and 23 females, infants ranging in age from 3 to 365 days) and 24 age-matched cases of explained death (ED) as controls (16 males and 8 females), infants who died from extracardiac cause (cerebral and respiratory). SIDS and ED groups were divided into three subgroups according to the age: (A) from 3 to 60 days; (B) from 61 to 120 days; (C) from 121 to 365 days. Histological observations were focused on the cardiac conduction system (CCS) which was examined on serial sections with the technique devised by one of the present authors (L. Rossi). The following findings were observed: resorptive degeneration (97.10% of SIDS, 75% of ED), His bundle dispersion (33. 33% of SIDS, 16.66% of ED), Mahaim fibers (21.73% of SIDS, 8.3% of ED), cartilaginous meta-hyperplasia (5.79% of SIDS, 4.16% of ED), persistent fetal dispersion (24.63% of SIDS, 16.66% of ED), intramural right bundle (20.29% of SIDS, 25% of ED), left sided His bundle (20.29% of SIDS and 8.3% of ED), hemorrhage of the atrio-ventricular junction (15.94% of SIDS), septation of the bifurcation (13.04% of SIDS), atrio-ventricular node (AVN) dispersion (7.24% of SIDS), sino-atrial node hypoplasia (5.79% of SIDS), Zahn node (1.45% of SIDS), His bundle hypoplasia (1.45% of SIDS), intramural left bundle (1.45% of SIDS), AVN dualism (2.89% of SIDS), and His bundle dualism (2.89% of SIDS, 4.16% of ED). Only the presence of resorptive degeneration was significantly higher in SIDS than in ED cases (p = 0.004). Regarding the subgroups, the only significant difference was the higher presence of intramural right bundle in SIDS-A than in SIDS-B (p = 0.01). Despite the non-specificity of most of these findings, we believe that these changes, associated with particular conditions and/or neurovegetative stimuli, could cause potentially malignant arrhythmias. These data suggest the need for an accurate approach and examination of the cardiac conduction system in all cases of sudden death in infancy     

Anomalous coronary arteries arising from the aorta associated with sudden death in infancy and early childhood. An autopsy series

Anomalous coronary arteries arising from the aorta are a recognized cause of myocardial ischemia and sudden death. Death has been precipitated by exercise in most cases. We present the results of an autopsy study in which sudden and unexpected deaths associated with coronary anomalies were found in three children (less than 2 years of age). In two cases, death was not associated with exercise. In two case, the myocardium was morphologically normal, and in the third case, there was an extensive recent anterior myocardial infarct with a background of established fibrosis. Coronary artery anomalies may be easily overlooked in this age group because of small vessel size and difficulty in dissection; this is particularly so when there are normally placed ostia. One consequence of this is potential for confusion with sudden infant death syndrome.     

The anatomical basis of complete atrioventricular block in cats with hypertrophic cardiomyopathy

The cardiac conduction system was examined histologically in 13 feline cases of hypertrophic cardiomyopathy (HCM) with complete atrioventricular (AV) block. Marked degeneration and fibrous replacement of the AV conduction system were consistently observed in the combined regions of the branching portion of the AV bundle and the upper portion of the left bundle branch. These changes were associated with extensive fibrosis of the central fibrous body and endocardial and myocardial fibrosis in the upper border of the ventricular septum. Chondrometaplastic lesions or osseous lesions, or both, present in the base of the central fibrous body, compressed the underlying penetrating or branching (or both) portions of the AV bundle, causing apparent reduction of the conduction fibres. The pathological process and the nature and predilection sites of the lesions resembled those associated with ageing in human patients with complete AV block. It is possible that the pathological process in the cats was fundamentally related to the normal ageing phenomenon and may have been exacerbated by mechanical forces created by the cardiac hypertrophy associated with HCM.     

Sudden cardiac death: an 11-year postmortem analysis in the region of Epirus, Greece

The aim of the study was to determine the rate of sudden cardiac death in people aged between 1 and 80 years, and to investigate its etiology. All autopsies performed during an 11-year period were reviewed. Circumstances of death, individual's information, and post-mortem findings were determined. Among 1254 sudden death autopsies performed during the study period, 688 cases were recognized as sudden cardiac death (79.8% males). The estimated annual frequency of sudden cardiac death in the region of Epirus was 18.6/100,000. The major cause of death was ischemic heart disease (82%), and in 2.6%, death was unexplained. Among our study's total population, 4.1% were <35 years old. The estimated annual rate of sudden cardiac death in the population 1-35 years old was 1.78/100,000. The most common etiology in that age group was atherosclerosis (17.8%), myocarditis (10.7%), and cardiomyopathies (10.7%), whereas 39.3% exhibited structurally normal heart. Although ischemic heart disease accounts for most of sudden cardiac death episodes, many other causes contribute. Most sudden deaths in the young were "unascertained". The likely cause of death in these cases might be a primary arrhythmogenic disorder. Correct identification of such cases at autopsy will enable an appropriate clinical screening of surviving relatives.     

Sudden cardiac death.

The rate of cardiac deaths that are sudden is approximately 50%, and decreases with age. The causes of sudden cardiac death are diverse, and are a function of age. In children and adolescents, coronary anomalies, hypertrophic cardiomyopathy and myocarditis are frequent substrates for lethal arrhythmias; in adults, coronary atherosclerosis and acquired forms of cardiomyopathy are the most common findings at autopsies of sudden cardiac death. This review focuses on coronary causes of sudden cardiac death, especially congenital coronary artery anomalies, which result in sudden death almost exclusively in adults younger than age 35, and coronary thrombosis. The most lethal coronary artery anomaly is the left coronary artery arising from the right sinus of Valsalva; this anomaly often results in fatal arrhythmias, often with exercise. The right coronary artery arising from the left sinus of Valsalva may also be lethal in adolescents and young adults, but, unlike the anomalous left, is more often an incidental finding at autopsy. Approximately 60% of sudden coronary death is caused by coronary thrombosis, the rest die with severe coronary disease in the absence of thrombosis. The two major substrates of coronary thrombosis are plaque rupture and plaque erosion, and are not only different pathologically, but are seen in patients with divergent risk factor profiles. Plaque rupture is the most common cause of fatal coronary thrombus, and is characterized by necrotic core with a thin fibrous cap, infiltrated by macrophages. The factors that result in plaque instability and rupture are largely unknown, and are under intense scrutiny; morphologic studies have identified serum lipid abnormalities as a key risk factor in the development of plaque rupture. Plaque erosion, in contrast to plaque rupture, is seen in younger men and women, is not associated with lipid abnormalities, and does not result from exposure of the lipid core to the lumen. The heterogeneity of the atherosclerotic plaque and the diverse mechanics of plaque progression and thrombosis have only been relatively recently explored, and are largely elucidated by autopsy studies of victims of sudden coronary death.