冠心病猝死193例尸检分析

本文对193例因冠心病而猝死的尸检材料进行以分析,并对冠状动脉粥样硬化好发部位,病理改变,心脏病理变化,以及冠心病猝死发生机理和诱因等进行讨论。     

浅析被监管人员猝死的预防工作

正1案例资料案例1喻某,2011年某日在某看守所,因冠心病急性发作猝死。相关就医资料记录:喻某有高血压病史,且在押期间一直服用珍菊降压片。法医学尸体解剖:冠状动脉内膜见粥样硬化斑块,管腔狭窄达IV级。案例2丁某,2012年某日在某监狱,因急性出血坏死性胰腺炎猝死。监狱门诊病历资料记录:丁某     

窦房结间质增生与年龄及右冠状动脉病变程度的关系

目的研究年龄及右冠状动脉粥样硬化病变程度对窦房结间质增生的影响。方法选择右冠状动脉有粥样硬化病变的心脏标本,登记年龄,复查并登记右冠状动脉病变,窦房结取材,常规制片,HE染色及Massom三色染色,用图像分析系统分析窦房结间质增生程度及右冠状动脉粥样硬化斑块病变的阻塞程度。结果右冠状动脉粥样硬化病变程度及年龄对窦房结间质增生的影响都有统计学意义(P0.001);右冠状动脉粥样硬化病变程度对窦房结间质增生的影响强度约为年龄的2.16倍。结论年龄及右冠状动脉粥样硬化病变程度均与窦房结间质增生有线性关系,右冠状动脉粥样硬化病变程度导致窦房结间质增生较年龄因素更为明显。     

胆囊收缩素(CCK)在冠状动脉粥样硬化斑块中的表达

目的揭示胆囊收缩素(CCK)在冠状动脉粥样硬化斑块中的表达情况,以进一步探讨CCK在动脉粥样硬化形成过程中的作用。方法选用100例35～92岁男性尸检冠状动脉粥样硬化标本,分为粥样硬化Ⅰ～Ⅱ级组和Ⅲ～Ⅳ级组,同时设正常对照组,用免疫组化技术进行检测。结果对照组CCK呈阴性表达,而冠状动脉粥样硬化组呈阳性表达(P0.01),Ⅰ～Ⅱ级组与Ⅲ～Ⅳ级组之间CCK表达无显著差异(P0.05)。结论 CCK在冠状动脉粥样硬化斑块中的有表达,但不随粥样硬化斑块程度的变化而变化。     

冠状动脉粥样斑块中C-反应蛋白的免疫组化研究

目的探讨冠状动脉粥样硬化斑块中C-反应蛋白(CRP)对冠心病猝死(SCD)的诊断意义。方法从本教研室2001~2004年尸检案例中挑选68例案例资料和心脏标本,分为3组A组SCD(27例);B组冠心病非猝死者(21例);C组无明显动脉粥样硬化病变的死者(20例);应用免疫组化染色(SABC法)和图像分析技术,检测每例冠状动脉左前降支和右主支粥样硬化斑块内的CRP染色情况,并对所得数据进行统计分析。结果A组有20例CRP免疫组化染色强阳性,6例呈较强阳性,1例为弱阳性;B组中3例呈较弱阳性,11例微弱阳性,7例为阴性;C组均未见阳性反应。结论检测冠状动脉粥样硬化斑块中的CRP对SCD的死后诊断具有一定意义。     

死后CT血管造影对冠状动脉粥样硬化的诊断价值CSCD

目的探讨死后CT血管造影技术在冠状动脉粥样硬化血管狭窄程度诊断中的应用价值。方法基于前期实验研究结果,对人死后离体心脏CT造影装置进行改良,选取不同冠状动脉粥样硬化病变程度猝死的检案案例,于心脏解剖前完整取出心脏并立即行CT冠状动脉造影,并将CT血管造影结果与组织病理学所见进行比较;同时比较改良前后造影装置的优、缺点。结果改良的离体心脏造影装置可以获得更好的成像效果;死后CT血管造影技术在冠状动脉粥样硬化血管狭窄程度诊断上与解剖和组织病理学所见具有较高的一致性,同时还可以通过三维重建技术将冠状动脉病变更客观、形象地展现出来。但CT血管造影技术只能对病变血管进行检查,在死因的诊断上存在一定的局限性。结论死后CT血管造影技术在冠状动脉粥样硬化血管狭窄程度案件中可以作为传统尸体解剖的辅助手段。     

死后CT血管造影对冠状动脉粥样硬化的诊断价值

目的探讨死后CT血管造影技术在冠状动脉粥样硬化血管狭窄程度诊断中的应用价值。方法基于前期实验研究结果,对人死后离体心脏CT造影装置进行改良,选取不同冠状动脉粥样硬化病变程度猝死的检案案例,于心脏解剖前完整取出心脏并立即行CT冠状动脉造影,并将CT血管造影结果与组织病理学所见进行比较;同时比较改良前后造影装置的优、缺点。结果改良的离体心脏造影装置可以获得更好的成像效果;死后CT血管造影技术在冠状动脉粥样硬化血管狭窄程度诊断上与解剖和组织病理学所见具有较高的一致性,同时还可以通过三维重建技术将冠状动脉病变更客观、形象地展现出来。但CT血管造影技术只能对病变血管进行检查,在死因的诊断上存在一定的局限性。结论死后CT血管造影技术在冠状动脉粥样硬化血管狭窄程度案件中可以作为传统尸体解剖的辅助手段。     

冠心病猝死冠状动脉粥样硬化斑块病理形态学观察

目的观察冠心病猝死(SCD)和对照组心冠状动脉(CA)粥样硬化斑块的差异,探讨其在SCD中的意义。方法从本教研室2001年~2003年尸检档案中挑选64例有严重CA粥样硬化病变的病例及心脏标本,分SCD组(36例)和对照组(28例冠心病非猝死者)。除常规检查心脏外,重点检查CA左主干(LM)、左前降支(LAD)、左旋支(LC)和右主支(RM)的开口、类型、走向及粥样硬化斑块情况。每支CA分近、中、远3段,检测每个斑块距开口的距离、狭窄程度、长度、数目和形状(分偏心、环形、偏心+环形三种)。用SPSS11.5统计软件进行统计分析。结果SCD组中CA粥样硬化病变4级21例,3级15例;对照组4级12例,3级16例。两组斑块病变的严重程度无显著性差异(P>0.05)。SCD组粥样斑块长(x-2.0365 cm)、以CA近段较多、与CA开口或分支处的距离近(x-0.7457 cm);对照组斑块短(x-1.4283 cm)、以中段多见,与CA开口或分叉处的距离远(x-2.1942 cm);两组斑块的长度和距开口的距离均有非常显著性差异(P<0.01)。两组间斑块的形状在LAD和RM有显著性差异(P<0.05),而LM和LC则无(P>0.05)。结论SCD与冠心病非猝死者的CA粥样硬化斑块在部位、长度、形状和距CA开口的距离存在差异,而狭窄程度无差异。这对SCD的病理诊断和法医学鉴定具有十分重要的意义。     

心肌梗死和心脏传导系统病变在心源性猝死中的作用

心源性猝死(sudden cardiac death,SCD)是由心脏原因引起的突然死亡,最常见于冠心病,且很多合并心肌梗死。但某些SCD(包括早期心肌梗死)由于发生突然,在极短的时间内即可引起死亡,肉眼和镜下缺乏典型的形态学改变,是目前研究的重点及难点。心肌梗死与心脏传导系统(cardiac conduction system,CCS)异常引起SCD的原因都与冠状动脉粥样硬化密切相关,本文从形态学和分子生物学两个方面入手,对心肌梗死与CCS病变引起心脏功能障碍的相关研究进行综述,以进一步揭示两者之间的相关性,对今后心肌梗死引起猝死机制方面的研究提供线索,为SCD的法医学诊断提供帮助。     

"Spontaneous" coronary artery dissection. The challenge of detection, the enigma of cause

Sudden death secondary to acute dissection of a coronary artery is a rare, but increasingly recognized, cause of sudden, unexpected death in apparently healthy persons. It has been reported more frequently in women and has been associated with sudden death during the puerperium. It has also been reported that these involved coronary vessels contain increased numbers of eosinophils and often show areas of cystic medial necrosis. In this article, we report a case of sudden death in a 47-year-old white woman due to dissection of the distal segment of her left anterior descending coronary artery. There was marked involvement of the coronary arterial walls with cystic degeneration of the media with accumulation of glycosaminoglycans as demonstrated by Alcian blue staining. There was no eosinophilic infiltrate within the arterial walls. This case is unusual in that this woman's mother and brother both have had aneurysms, which stresses the importance of not only searching carefully for these lesions, but also of obtaining family history in such cases.     

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.     

Sudden infant death with anomalous origin of the left coronary artery.

Autopsy of a 3-month-old girl, an apparent case of sudden infant death syndrome, revealed anomalous origin of the left coronary artery from the right aortic sinus. Acute angulation of the left coronary artery along the aortic root, as well as a focal intramyocardial course within the ventricular septum, may have contributed to episodic luminal narrowing. Anomalous coronary origins of similar type have been associated with sudden death in children, teenagers, and young adults, but have not necessarily been associated with sudden death in older adults. Somewhat similar malformations have been reported in sudden infant death; two cases involved the left coronary artery and six involved the right.     

Dissecting coronary artery aneurysm: a report of two cases

Two cases of sudden, unexpected death resulting from coronary artery dissection have been reported. Since sudden and unexpected death falls within medical examiners' jurisdiction, the systematic autopsy examination of such cases offers an opportunity to evaluate this entity as well as other rare causes of natural death. A review of the literature concerning the subject has been presented.     

Association of right coronary artery hypoplasia with sudden death in an eleven-year-old child

Congenital coronary artery abnormalities are a rare but well-documented cause of sudden and unexpected death in the pediatric age group. Most reported cases involve both an aberrant origin and course of the abnormal vessel. A case of unexpected death occurring in an otherwise healthy eleven-year-old boy, who had been previously investigated for sudden collapse, is described. The major finding at autopsy was marked disparity in diameter between the coronary arteries due to diffuse hypoplasia of the right coronary artery. This case demonstrates the importance of meticulous examination of the coronary artery system in cases of sudden death in childhood so that significant reduction in luminal cross section will be adequately documented. The possible role played by this finding in the etiology of sudden death is discussed.     

Sudden Cardiac Death in a Young Man with Migraine-associated Arrhythmia

A 31-year-old man with migraine-induced syncope and bradycardia with subsequent pacemaker implantation died unexpectedly. Clinically unsuspected cardiac anomalies were found at autopsy including myocardial bridging of the left anterior descending artery and shelf-like coronary artery ostia. Nortriptyline was identified by toxicologic analysis. A review of the autopsy findings, the historical information, and the effects of the possible arrhythmogenic circumstances is undertaken and the potential contributions to the death are discussed. Cardiac arrhythmias have been documented during migraines. Coronary artery bridging has been known to lead to ischemia and infarction, ventricular tachycardia, and sudden death; however, these are very rare sequelae. Congenital coronary artery anomalies have been linked to sudden cardiac death, but only rarely cause death in people younger than 31 years. Migraines and the autopsy findings described have been associated with cardiac arrhythmia and sudden death. Altogether, they led to the unexpected death of this young man.     

P物质在过敏性休克家兔胃肠道内的表达

目的观察P物质在过敏性休克家兔胃肠道组织中随时间变化的规律,探讨其在过敏性休克中的作用。方法 30只家兔随机分为实验组(24只)和对照组(6只)。实验组采用多人混合血清致敏家兔,建立过敏性休克模型。休克不同时间段(猝死即刻、休克0.5h、休克1h、休克2h)提取家兔胃、小肠、圆小囊。冰冻切片,应用免疫组化(IHC)SP法和原位杂交(ISH)方法进行P物质染色,BI-2000计算机图像分析系统进行图像分析,计算阳性积分光密度值(IOD),用SPSS11.5统计软件进行方差分析,SNK检验。结果与对照组相比,实验组各小组胃、肠、圆小囊P物质蛋白和mRNA表达明显增加,且随着休克时间的变化逐渐减弱(P0.001)。IHC方差分析结果为:胃组织F=198.008,肠组织F=56.796,圆小囊组织F=67.231;ISH统计学分析方差分析结果为:胃组织F=67.506,肠组织F=72.117,圆小囊组织F=216.798。结论家兔胃肠道P物质在过敏性休克后一段时间内(2h)均表达增高,随休克时间的延长逐渐下降。     

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.     

A study of various morphologic variables and troponin I in pericardial fluid as possible discriminators of sudden cardiac death

Pathologists frequently examine victims of sudden cardiac death. In some cases, a firm diagnosis of cardiac-related death can be made based on conclusive gross and histologic findings. In many other cases, we find evidence supportive of, but not diagnostic of, cardiac death (e.g., atherosclerotic coronary artery disease, cardiomegaly, myocardial scarring). A final cohort consists of cases of sudden death with minimal to mild cardiac disease, no other significant pathology, and negative toxicologic studies. This prospective study compared 38 cardiac-related deaths with 52 control cases with respect to concentrations of pericardial cardiac troponin I (cTnI), heart weight, evidence of old and/or recent myocardial injury, and presence of significant coronary artery disease. The influence of documented chest trauma and/or perimortem cardiopulmonary resuscitation (CPR) on levels of cTnI was also analyzed. Even though median cTnI levels were significantly higher in cardiac deaths than in controls (p = .003), cTnI was not found to be a significant predictor of cardiac deaths, as determined by discriminant analysis (p = .52). Heart weight >500 g, evidence of old and recent myocardial injury, and significant coronary artery disease were seen statistically more often in cardiac deaths than in controls (p < or = .005 in each case), and median age was significantly higher in cardiac deaths than in controls (p = .001). Based on a stepwise logistic regression model, significant coronary artery disease, old and recent myocardial injury, and heart weight >500 g were found to contribute significantly to the prediction of cardiac death. Finally, neither chest injury nor CPR significantly affected concentrations of cTnI in pericardial fluid. These data confirm that the presence of acute and remote myocardial injury, significant coronary artery disease, and cardiomegaly (heart weight >500 g) strongly supports the diagnosis of a cardiac-related death. In contrast to a recently published report, we do not find that elevated concentrations of cTnI in pericardial fluid are strong indicators of cardiac-related deaths using our methodology.     

Left Ventricular Aneurysm: Sudden Unexpected Deaths in a 29‐Year‐Old Man

Left ventricular aneurysm (LVA) is an abnormal dilated heart structure, either congenital or acquired. LVA is a rare cardiac condition with no symptoms in most cases, thus occasionally diagnosed during investigations of other diseases. Its association with certain cardiac complications and sudden cardiac deaths has been reported. However, its role as a cause of sudden unexpected death is rare. The author reported a sudden cardiac death in a 29‐year‐old man with LVA. Without a significant coronary artery disease and known etiologies of LVA, such an abnormal heart structure in the present case was considered congenital LVA. As no other possible mechanisms of death could be identified other than LVA with its associated pathologic lesions, mural thrombi, and dilated cardiomegaly, his death was attributable to fatal cardiac arrhythmia (most commonly ventricular tachycardia) secondary to LVA.