病毒性心肌炎心肌碱性成纤维生长因子的实验研究

用 8只小鼠接种柯萨奇 B3病毒（ Coxsackie B3 viral CVB3）,形成病毒性心肌炎动物模型。用免疫组织化学方法对心肌碱性成纤维生长因子（ basic Fibroblast Growth Factor:bFGF）的变化进行了研究。目的是观察 CVB3对心肌的损害。结果发现小鼠感染病毒第 3天病变心肌中即有 bFGF阳性表达,并且随病程的延长其阳性程度随之增加。常规 HE染色通常在感染病毒 5天后才出现明显的镜下改变。本研究提示 bFGF可以为病毒性心肌炎早期轻微病变的判定提供帮助。     

心肌炎猝死案例的法医病理学研究

从法医尸检案例中取心肌炎猝死17例进行分析及病理学观察，对心肌炎的分关、心肌炎导致猝死机制进行探讨，认为诱发急性心力衰竭是心肌炎猝死的主要原因。     

病毒性心肌炎和扩张性心肌病心肌中β-sarcoglycan的免疫组化染色观察

目的探讨病毒性心肌炎(viralmyocarditis,VCM)和扩张型心肌病(dilatedcardiomyopathy,DCM)的发病机制及相互关系,从而提高心性猝死法医学鉴定的可靠性和准确性。方法对17例对照组(包括冠心病、高血压性心脏病和正常心脏等),25例VCM和28例DCM的心肌组织进行改良的β-sarcoglycan免疫组织化学染色观察,并对其阳性反应率进行χ2检验及相关分析。结果β-SG蛋白在对照组,VCM组和DCM组中阳性反应率分别为100%,80%,46.4%。经χ2检验,3组阳性反应率差异有显著性意义(P<0.05);用χ2分割法分析,VCM和DCM组间差异有显著意义(P<0.05),且Spearman等级相关分析呈显著负相关(rs=-0.605)。结论病毒性心肌炎和扩张性心肌病病变与β-SG的被破坏有关;随着VCM病变程度的加重,其可能发展为DCM。     

病毒性心肌炎和扩张性心肌病中Dystrophin蛋白的表达

目的探讨病毒性心肌炎和扩张性心肌病的发病机制及相互关系,从而提高心性猝死法医学鉴定的可靠性和准确性。方法对17例对照(包括正常心脏、冠心病、高血压性心脏病等),25例病毒性心肌炎和28例扩张性心肌病的心肌组织进行改良的病理学dystrophin免疫组织化学研究。结果dystrophin蛋白在对照组,病毒性心肌炎组和扩张性心肌病组中阳性表达率分别为100%,88%,57%,三组表达差异有显著性(P<0.05),且在病毒性心肌炎和扩张性心肌病组间表达有显著差异(P<0.05),经Spearman等级相关分析呈显著负相关(r=-0.526)。结论病毒性心肌炎和扩张性心肌病心肌中细胞骨架蛋白均有破坏,且随着由病毒性心肌炎进展为扩张性心肌病,dystrophin蛋白表达逐渐降低,说明在病毒性心肌炎和扩张性心肌病的发病机制中可能与dystrophin的被破坏有关,病毒感染并破坏心肌细胞骨架蛋白并最终导致心肌细胞坏死,心功能受损,从而使病毒性心肌炎进展为扩张性心肌病。     

Influenza A/H1N1 (2009) Infection as a Cause of Unexpected Out‐of‐Hospital Death in the Young*

Abstract: In March 2009, a new strain of influenza A/H1N1 virus was identified in Mexico, responsible for a pandemic. Worldwide, more than 13,500 patients died, most often from acute respiratory distress syndrome. Because sudden death cases were rare, involving mostly young apparently healthy persons, influenza A/H1N1 (2009)‐related deaths may be misdiagnosed, which can raise medico‐legal issues. Case history: we report on an unexpected out‐of‐hospital death involving a young male with no past medical history and no vaccination. Fever was his only symptom. Laboratory tests: histology showed patchy necrotic foci with mononuclear inflammation in the lungs. The heart was histologically normal, but virological analyses using molecular biology on frozen myocardial samples showed high virus load. In conclusion, this case report shows that influenza A/H1N1 (2009) virus can be a cause of sudden cardiac death in the young and demonstrates the importance of quantitative virological analyses for the diagnosis of myocarditis.     

Eosinophilic myocarditis from a forensic histopathological perspective

Eosinophilic myocarditis (EM) is a rare and potentially fatal form of myocarditis characterized by infiltration of the myocardium with eosinophil leukocytes, often accompanied by eosinophilia. Although the exact underlying cause remains unknown, it has been shown to be associated with hypersensitivity reactions, immune-mediated disorders, infections, or cancer. Due to the differences in symptomatology, it is often diagnosed by postmortem histopathological examination. We aimed to retrospectively examine the histopathological findings of rare cases of EM and to detect accompanying cardiac and other organ pathologies. The histopathological findings of the cases that underwent autopsies between 2012 and 2020 and were diagnosed with EM were assessed. Demographic features, symptoms, causes of death, macroscopical findings at autopsy, toxicologic and microbiological analysis results, accompanying cardiac pathologies, and histopathological findings in other organs were evaluated. Myocarditis was detected on histopathologic examination in 558 (1.1%) of 49,612 forensic autopsies. There were 12 (2.3%) EM cases. There were nine males and four females. The mean age was 42.3 (3–83) years. Heart weights ranged from 82 to 564 g. The most common finding on macroscopic examination was the mottled discoloration and scarring in the myocardium. Microscopic examination revealed perivascular and interstitial infiltration of eosinophils in all of the cases accompanied by myocyte necrosis in four of them. EM was reported as the cause of death in four cases. EM remains a challenging heart disease with its obscure etiopathogenesis and varying clinical presentation and a rare entity diagnosed by postmortem histopathological examination in sudden and unexpected deaths.     

Lethal manifestations of systemic lupus erythematosus in a forensic context

Systemic lupus erythematosus is an autoimmune connective tissue disorder that affects multiple organs. While the clinical manifestations may vary in intensity over time and be associated with chronic disease, occasional cases occur where sudden and unexpected death has occurred. Cardiovascular disease is common, with accelerated atherosclerosis, intravascular thrombosis associated with antiphospholipid syndrome, and hypertensive cardiomegaly. Vasculitis with superimposed thrombosis may result in critical reduction in blood to vital organs, such as the heart and brain with infarction. Mesenteric ischemia may be caused by vasculitis, thrombosis, and accelerated atherosclerosis and may result in lethal intestinal infarction. Other diverse causes of sudden death include myocarditis, epilepsy, pulmonary hypertension, pulmonary thromboembolism, and sepsis. The autopsy evaluation of such cases requires careful examination of all organs with extensive histological sampling to include blood vessels, and microbiological sampling for bacteria, viruses, and fungi.     

病毒性心肌炎肌动蛋白的免疫组化观察

对１０例尸检心脏标本进行了肌动蛋白（Ａｃｔｉｎ,Ａｔ）的免疫组化观察。依据Ｄａｌｓ标准的明确或界限性病毒性心肌炎５例,心肌组织内Ａｔ含量减损,呈局灶性或弥漫性淡染,偶见小灶性单个心肌细胞内Ａｔ缺失。心肌梗死２例,心肌组织内Ａｔ大片缺失;非心性死亡对照组３例,心肌组织内Ａｔ呈均匀一致的强阳性染色。结果表明,心肌组织内Ａｔ的免疫组化观察可望提高对不典型病毒性心肌炎诊断的敏感性,同时对区分轻度缺血性与炎症性心肌细胞损伤有参考价值     

单用口服中药治疗成人病毒性心肌炎随机对照试验的Meta分析

目的 对单用口服中药治疗成人病毒性心肌炎的疗效进行评价。方法 在中国期刊全文数据库（CNKI）、中文科技期刊数据库（VIP）和万方数据库中检索2000年1月至2016年4月发表的单用口服中药治疗成人病毒性心肌炎的随机对照试验文献，对文献进行二次筛选并进行Jadad评分，采用RevMan 5.2软件进行Meta分析。结果 口服中药治疗在改善成人病毒性心肌炎临床症状方面具有明显疗效（OR值为3.32，OR值的95% CI为2.42～4.57, P<0.000 01，I2=0%）；在治疗心电图（或动态心电图）异常方面较单独西医常规疗法无明显优势（OR值为1.94，OR值的95% CI为0.98～3.85，P=0.06, I2=71%）。结论 单用口服中药治疗成人病毒性心肌炎可能具有一定的疗效。     

A Case of Sudden Infant Death Due to Incomplete Kawasaki Disease

Although Kawasaki disease (KD) is a self‐limiting disease, it may cause sudden cardiac death. Diagnosis of KD is principally based on clinical signs; however, some infant cases do not meet the criteria. Such cases are identified as incomplete KD. The sudden death risk in incomplete KD cases is similar to conventional KD. In our 5‐month‐old case, he had been admitted to a hospital for a fever and suppuration at the site of Bacille de Calmette et Guerin (BCG) vaccination. However, after discharge from the hospital, his C‐reactive protein (CRP) levels declined, he got indisposed and died suddenly. A medico‐legal autopsy revealed myocarditis, coronaritis, platelet‐aggregated emboli in coronary arteries, and myocardial degeneration, suggesting that the fatal myocardial infarction was due to thrombus emboli in the coronary arteries. Forensic pathologists therefore should pay attention to the cardiac pathology originated from incomplete KD as a potential cause in cases of sudden infant death.