心肌扩张型心脏病的病理形态特征及其临床意义

目的探讨单纯心壁病损造成的心脏扩张者的病理形态特征及其意义。方法收集2004年6月至2006年8月中国医学科学院北京协和医学院阜外心血管病医院60例心脏移植的受体心脏在离体后立即进行了肉眼观察、测量和摄影记录,并进行了全面的组织病理学观察。以其中40例单纯心壁病损造成的心脏扩张者进行临床-病理对照分析,并观察其形态特点。结果40例单纯心壁病损造成的心脏扩张者中21例（52．5％）为原发性扩张型心肌病,9例（22．5％）为致心律失常性右心室心肌病,6例（15．0％）为缺血性心肌病,其余的4例（10．0％）为局灶性心肌致密化不全、巨细胞性心肌炎和特异性心肌病中的酒精性心肌病和高血压性心肌病。40例中临床诊断与病理诊断不符15例（37．5％）,不相符率较高的依次为致心律失常性右心室心肌病（7／9）、缺血性心肌病（5／6）和巨细胞性心肌炎（1／1）。不相符的这几种病的原临床和影像学诊断都是扩张型心肌病。致心律失常性右心室心肌病、缺血性心肌病、心肌致密化不全和巨细胞性心肌炎都有特征性的病理形态表现,酒精性心肌病和高血压性心肌病等的病理诊断需要参考临床病史。该组病例没有观察到慢性心肌炎样病变发展成扩张型心肌病的形态学迹象。结论进行心脏移植病例受体心脏的病理学检查有利于提高心脏病的临床和影像诊断的正确率,病理形态检查是不可忽视的重要手段。     

不明原因猝死108例死因分析

本文对108例所谓原因不明猝死病例,进行病理尸检及其它检查,发现97.22％能找到猝死原因,其原因依次为潜在性心脏疾病47例11,占43.52％,消化系统疾病23例,占21.30％,主要是急性出血性胰腺炎。中枢系统疾病18例(16.66％),呼吸系统疾病7例(6.48％),其他原因13例(12.04％)。     

心源性猝死33例尸检临床病理分析

目的 分析心源性猝死的临床特点以及尸检病理学特征.方法 收集与医疗纠纷有关的不明原因死亡的87例尸体解剖资料进行病理组织学检查.结果 心源性猝死33例,其中,冠心病20例(占64%),主动脉夹层动脉瘤破裂4例,心肌炎5例,肥厚性心肌病2例,冠状动脉炎和肺动脉脂肪栓塞各1例.结论 正确、系统地进行尸体解剖,可以明确猝死原因,提高医疗质量,并为医疗纠纷鉴定提供可靠的鉴定依据.     

超声造影鉴别肝脏局灶性病变良恶性的临床价值

目的探讨超声造影对肝脏局灶性病变良恶性的鉴别能力.方法2004年7月至2005年9月间于深圳市人民医院进行超声造影的肝脏局灶性占位病变72例.所有患者均进行了增强CT或增强MRI检查,47例经病理证实及随访观察.结果72例肝脏局灶性病变,恶性病灶23例,包括肝细胞性肝癌17例、胆管细胞性肝癌2例、转移性肝癌4例;良性病灶49例,包括血管瘤18例、局灶性结节增生9例、局部脂肪缺失17例、肝脓肿3例、肝硬化增生结节3例、炎性假瘤1例、肝囊肿1例.肝脏恶性病灶和良性病灶的超声造影方式明显不同.结论超声造影对鉴别肝脏占位病变良恶性具有较大的价值,但对于一些不典型的病例仍需进一步检查.     

SARS病毒可感染心脏传导系统

为什么部分SARS患者会出现心律失常和心肌酶谱异常 ?重症SARS患者的肺脏为何会出现脱屑性肺泡炎性病理改变 ?解放军 30 2医院SARS病理研究组科研人员近日发现 ,SARS病毒可感染心脏及其传导系统 ;SARS病毒诱导的广泛且迅速的细胞凋亡 ,可能是SARS患者肺脏及免疫器官细胞死亡的主要方式。科研人员通过解剖SARS死亡患者的心脏及其传导系统 ,发现SARS病毒可感染患者的心脏及其传导系统 ,引起病毒性心肌炎性改变。此发现为临床部分SARS患者出现心律失常和心肌酶谱异常做出了合理的解释。此外 ,课题组采用原位末端标记法与单克隆抗…     

大鼠自身免疫性心肌炎模型的建立

目的: 建立Lewis大鼠实验性自身免疫性心肌炎模型。方法: 从猪心中获得心肌肌凝蛋白,以此蛋白免疫Lewis大鼠,建立自身免疫性心肌炎模型，于初次免疫后第18 d、30 d、49 d进行心脏超声及血流动力学检查，ELISA法检测血清细胞因子，取心肌组织进行组织病理学检查。结果: 心脏超声及血流动力学检查显示，免疫组鼠心功能明显低于正常对照组，以第18 d最明显。血清学检查显示IFN-γ和IL-2水平在急性期达到高峰，IL-6、IL-10水平则在恢复期达到高峰。心脏病理检查显示，初次免疫后18 d，免疫组鼠全部出现明显的心肌炎病理改变。HE染色显示初次免疫后21 d大量炎性细胞浸润，伴有心肌的坏死，第30 d炎性细胞有所减少，第49 d炎性细胞基本消失。Massine trichrome染色显示炎症区域逐渐由纤维组织代替。结论: 猪心肌肌凝蛋白可以诱导Lewis大鼠出现典型的自身免疫性心肌炎，炎症损伤在心肌炎的发生和发展中起重要作用，参与了心功能紊乱和心室重构过程。     

白细胞介素10基因修饰的树突状细胞对免疫炎症性心肌损伤的作用研究

心肌炎和特发性扩张型心肌病是以心室扩大伴收缩功能障碍为特征的原因不明性心肌疾病，是年轻患者发生心力衰竭、心律失常及猝死的主要原因。实验性自身免疫性心肌炎（experimental autoimmune myocarditis，EAM）是模拟心肌炎和心肌病等免疫炎症性心肌损伤的模型。     

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。     

重症病毒性心肌炎病人安装临时心脏起搏器的护理

病毒性心肌炎是指由嗜心肌性病毒感染引起的心肌非特异性间质性炎症为主要病变的心肌炎.□1□病情轻重变异很大,重症病毒性心肌炎病变程度广泛,症状危重,表现为严重的心律失常、心源性休克、心力衰竭、猝死等.     

重症乙型脑炎心肌损伤的形态学改变

重症乙型脑炎病人常合并心力衰竭。我们就尸检病人心脏标本作形态学观察,探讨其发病机制。 材料和方法 选择我院近年来死亡的生前有严重心力衰竭的重症乙型脑炎尸检病例10例,于左、右心室及心房、室间隔等5处取材,石蜡包埋,HE染色,光镜观察。 其中3例病人刚死亡即行心脏穿刺,取心室肌,戍二醛固定,常规透射电镜制样、切片,H-600透射电镜观察。 结果 光镜观察:心肌间质毛细血管扩张,淤血,并有红细胞渗出。有的病例有散在炎性细胞浸润,炎     

Cardiac sarcoidosis and sudden death. The heart may look normal or mimic other cardiomyopathies

Cardiac sarcoidosis has been known to give rise to heart failure, arrhythmias and sudden cardiac death. We have a large database of sudden cardiac death cases at the CRY Centre for Cardiac Pathology at Imperial College, London, UK in which we found 17 of 1,720 cases with a diagnosis of cardiac sarcoid. Macroscopic examination showed a variety of findings including left ventricular hypertrophy, a dilated thin-walled left ventricle ,areas of fibrosis, changes resembling arrhythmogenic right ventricular cardiomyopathy and in some cases, no gross abnormalities. Histological examination revealed large areas of fibrosis and focal lymphocytic inflammation mimicking infarction/myocarditis. Careful search had to be made for non-necrotizing granulomata, since the lymphocytic foci, fibrosis and granulation tissue often predominated throughout the heart. The conduction tissue is often not sampled at autopsy despite the history of heart block. The heterogeneous nature of the macroscopic appearance and histological findings means that widespread sampling of the heart and the conduction system is essential in cases of sudden death in order that a diagnosis of myocardial sarcoidosis is not missed.     

致心律失常性右室心肌病心力衰竭期的病理特点分析

目的 通过分析致心律失常性右室心肌病(ARVC)心力衰竭期的病理改变,以进一步了解其临床分期与病理表型的关系.方法 从2004-2007 年在阜外心血管病医院接受心脏移植的心力衰竭病例中,收集病理诊断为ARVC的受体心脏8例,测量心脏重量,评价左右心室心腔扩张、心肌细胞肥大、脂肪浸润、纤维化、附壁血栓和伴发心肌炎等指标,注意左心室受累情况,并进行病理分型.结果 8例中的7例为经典型(即右心室改变为主),1例为左优势型(左心室改变为主),未见双室型病例.组织学均为纤维脂肪型,未见单纯脂肪型病例.经典型病例的右心室中、重度扩张,少数有室壁瘤形成,其中6例伴左心室受累,受累左心室轻、中度扩张,心肌广泛间质纤维化,部分病例伴替代性疤痕,而脂肪浸润量小,多局限于心外膜下.左心室心肌细胞肥大普遍.而左优势型的左心室重度扩张,弥漫间质纤维化和局部透壁性脂肪浸润.8例中3例左心室明显肥厚,3例查见双室附壁血栓,1例伴局灶性心肌炎.结论 ARVC心力衰竭期的左心室受累多见而严重,左心室间质纤维化突出,心肌细胞肥大明显,但脂肪替代少见和局限.左、右心室多扩张,可见附壁血栓,应注意与扩张型心肌病等鉴别.     

The cardiac conduction system in sudden infant death syndrome: a report on three cases.

The cardiac conduction systems in three cases of sudden infant death syndrome (SIDS) were compared with those in children dying from known causes. Foci of inflammatory cells and areas of necrosis were found in SIDS. Lymphocytes and eosinophils were counted in the adjacent myocardium and significantly larger numbers were present in SIDS. These parhological changes in the conduction systems may be capable of producing cardiac arrhythmia and sudden death.     

心源性猝死心肌细胞凋亡与c-jun基因蛋白的表达

目的 探讨心肌细胞凋亡和c-jun基因蛋白在心源性猝死(SCD)中的表达及其法医学意义. 方法 50例法医尸检案例,其中冠心病猝死组16例,病毒性心肌炎猝死组14例,扩张型心肌病猝死组10例及对照组(非SCD猝死病例)10例.通过TUNEL法和免疫组织化学法对各组心肌细胞凋亡指数、c-jan基因蛋白表达情况的吸光度进行半定量检测,并分析各组之间的差异. 结果 冠心病猝死组、病毒性心肌炎猝死组、扩张型心肌病猝死组的凋亡指数均显著高于对照组(P<0.01).病毒性心肌炎猝死组和扩张型心肌病猝死组的凋亡指数均高于冠心病猝死组(P<0.01),前两者之间差异无统计学意义(P>0.05).冠心病猝死组、病毒性心肌炎猝死组、扩张型心肌病猝死组的c-jan基因蛋白吸光度值均显著高于对照组(P<0.01).3组之间的吸光度值差异无统计学意义(P>0.05). 结论 应用TUNEL法检测心肌细胞凋亡和免疫组织化学法检测心肌细胞内c-jun基因蛋白的表达,可作为法医鉴定SCD的重要指标.     

Pl?tzlicher Herztod

Sudden cardiac death is one of the most common causes of death and a significant number of sudden deaths occurs especially in young people. Sudden cardiac death is also frequently represented in forensic autopsy practice. In such cases pathological findings in the heart can often explain the reason for the acute death. These pathological changes include not only myocardial infarction, coronary thrombosis and all forms of myocarditis/endocarditis but also rare diseases, such as hereditary structural or arrythmogenic anomalies, lesions of the cardiac conduction system or primary cardiac tumors.     

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.     

Adipositas cordis sudden death: a series of 79 patients

Background: The principal aim of this study was to investigate the clinical, epidemiological and pathologic features for a series of 79 cases of adipositas cordis sudden death. Methods: We analyzed clinical and autopsy pathological features of 79 patients (43 females and 36 males) with adipositas cordis who died suddenly between 1975 and 2010. Data were extracted from China National Knowledge Infrastructure and Wan Fang Database. Results: The average age of the 79 cases was 36.6±1.4 years old ranging from 13 to 68, and 82.3% of them were between 20 to 50 years old. Sudden death was the first symptom in 62 (78.5%) of the cases, only 17 (21.5%) had a history of chest distress or dyspnea. More than 4/5 (87.3%) of the cases had no any past medical history. At autopsy, the subjects’ heart weight was mild or moderately increased, and a large amount of fatty tissues but not fibrous or fibro fatty was accumulated underneath the epicardium and infiltrated toward the right ventricle walls, and even infiltrated to all layers of the cardiac walls. Regional epidemiological data showed that about 80% of cases were living north and only 20% were living south of the Yangzi River, but not any familial heredity. Conclusion: Adipositas cordis sudden death is a very severe disease, it occurs mostly in youth and middle-aged and sudden death is often the first symptom. There is a significant regional difference, but not any genetic correlation. The pathogenesis of adipositas cordis sudden death should to be further explored.     

Heart lesions associated with anabolic steroid abuse: Comparison of post-mortem findings in athletes and norethandrolone-induced lesions in rabbits

Among 15,000 forensic post-mortem examinations performed on the coroner's order over a 24-year period (January 1981–December 2004) in the area of Lyon, France (population: 2,000,000), 2250 cases of unexpected cardiac sudden death were identified retrospectively according to WHO criteria. Of these, 108 occurred during recreational sport and 12 occurred in athletes. In the latter category, a history of anabolic steroid abuse was found in 6 cases, whereas pre-existing ordinary cardiac lesions were observed in the 6 remaining cases. To shed light on the possible role of anabolic steroids in the induction of cardiac lesions, an experimental study was conducted in rabbits that were treated orally with norethandrolone 8 mg/kg/day for 60 days, and sacrificed at day 90. The histopathological examination of the heart from treated animals showed coronary thrombosis associated with left ventricle hypertrophy in 3 cases, and lesions analogous to toxic or adrenergic myocarditis in all other treated animals. These findings were very similar to those observed after cardiac sudden death in the 6 athletes with a history of anabolic steroid abuse. In addition, elevated caspase-3 activity in the heart of treated rabbits as compared to controls suggests that apoptosis is involved in the induction of norethandrolone-induced cardiac lesions. These results confirm the cardiotoxic potential of anabolic steroid abuse.     

Cooperation of Th1 and Th17 cells determines transition from autoimmune myocarditis to dilated cardiomyopathy

Myocarditis is a potentially lethal inflammatory heart disease of children and young adults that frequently leads to dilated cardiomyopathy (DCM). Since diagnostic procedures and efficient therapies are lacking, it is important to characterize the critical immune effector pathways underlying the initial cardiac inflammation and the transition from myocarditis to DCM. We describe here a T-cell receptor (TCR) transgenic mouse model with spontaneously developing autoimmune myocarditis that progresses to lethal DCM. Cardiac magnetic resonance imaging revealed early inflammation-associated changes in the ventricle wall including transient thickening of the left ventricle wall. Furthermore, we found that IFN-γ was a major effector cytokine driving the initial inflammatory process and that the cooperation of IFN-γ and IL-17A was essential for the development of the progressive disease. This novel TCR transgenic mouse model permits the identification of the central pathophysiological and immunological processes involved in the transition from autoimmune myocarditis to DCM.