A case of sudden death due to spontaneous coronary artery dissection

Spontaneous dissection of the coronary arteries is an extremely rare event that occurs usually in middle-aged women and is mostly recognized at postmortem examination in victims of sudden death. It is a rare coronary pathologic finding whose precise incidence, etiology, pathogenesis, treatment, and evolution have not been clearly established. We present a sudden death case of a 53-year-old woman with spontaneous dissection of the left anterior descending coronary artery with eosinophilic coronary arteritis.     

Death from spontaneous coronary artery dissection in a healthy postmenopausal woman

Spontaneous dissection of the coronary arteries, in the absence of trauma, is an unusual but well-documented entity that occurs usually in middle-aged women. It is a rare cause of sudden death and myocardial infarction. Coronary eosinophilic arteritis is suggested to result in a predisposition to intimal disruption and dissection. We present the case of the sudden death of a previous healthy, 53-year-old postmenopausal female, while working, in a town of Thessalia in Greece. The cause of death was left anterior descending coronary dissection with histologic findings of eosinophilic arteritis and autoimmune thyroiditis.     

冠心病心肌线粒体DNA5.0kb缺失的检测

目的探讨冠心病心肌线粒体DNA5.0kb缺失的检测。方法120例心脏的左、右心室肌各1份,分为正常对照组、病例相关组和病例组,每组40例80个样本。用断裂点连接PCR分别扩增样本含线粒体DNA5.0kb缺失的片段,巢式PCR检测含5.0kb缺失片段的扩增产物的准确性,半定量PCR对该产物进行定量,聚丙稀酰胺凝胶电泳检测PCR产物。结果在对照片段扩增成功的样本中,正常对照组未检出线粒体DNA5.0kb缺失;病例相关组检出2例,占6.07%(2/33);病例组检出29例,占85.29%(29/34);左、右心室肌线粒体DNA5.0kb缺失量分别为0.0015%~0.7813%和0.0008%~0.3906%。病例组与其他两组缺失率经χ2检验,其差异具有极显著性意义(P<0.001);左、右心室肌的缺失量经t检验,其差异具有极显著性意义(P<0.001)。结论冠心病心肌多有线粒体DNA5.0kb缺失,缺血明显的区域其缺失量也较高。     

Sudden and unexpected death of a 6-month-old baby with silent heart failure due to anomalous origin of the left coronary artery from the pulmonary artery.

A 6-month-old girl died suddenly without any previous symptoms of heart failure. Autopsy examination showed cardiomegaly (97 g) with a severely fibrotized myocardium. The left coronary artery was originating from the pulmonary artery. Histologically, the myocardium showed myocardial infarcts of different ages, as well as grossly thickened arterial branches due to increased flow in left-right shunt. We suggest that rare anomalies of the coronary arteries should be considered in the autopsies of suspected sudden infant death syndrome cases.     

Sudden death in an adolescent four years after recovery from mucocutaneous lymph node syndrome (Kawasaki disease)

A case is presented of sudden death during physical activity in a 15-year-old boy with clinically inactive mucocutaneous lymph node syndrome (Kawasaki disease). At autopsy, the coronary arteries were involved by multiple aneurysms and obstructive thrombi, and the left ventricular myocardium was extensively scarred. Although Kawasaki disease most commonly occurs in infants and young children, it may be a cause of sudden death in adolescents.     

Multivascular atheromatous coronary microembolism

We report an unusual case of coronary-multivascular, small coronary artery embolism by atheromatous elements originating in a plaque in the main right coronary artery of a 52-year-old man who died of acute thrombotic occlusion of the severely stenotic left anterior descending vessel. The embolized arteries showed the characteristic multiphasic inflammatory changes of different ages previously described in arteries occluded by this material. The myocardium supplied by the involved channels showed ischemic damage of varying ages. Both these observations indicate that the multiple emboli had been discharged at different times, rather than as a single shower. Finally, we make a plea for the use of the correct term "erosion" rather than "ulcer" for the lesion that is the source of the invasive obstructions.     

Arrhythmogenesis and diagnosis of cardiac sarcoidosis. An immunohistochemical study in a sudden cardiac death

We present an uncommon case of sudden cardiac death in a 34-year-old white woman. She was found lifeless at home by her parents. Three months before death she was recovered at the Emergency Room for chest pain, palpitation and loss of consciousness. Subsequent cardiological evaluation with ECG showed sinusal rhythm, QRS deviation to the left, QS aspect, asymmetric and rounded T waves and slight length of QT. During hospitalization she presented some episodes of supraventricular paroxysmal tachycardia and non-sustained ventricular tachycardia. No echocardiography alterations were found. An anti-arrhythmic treatment was prescribed. Autopsy revealed some fibrotic scarring in the myocardium of left ventricle. The histological examination of the heart revealed diffuse and extensive fibrosis with non-caseating sarcoid granulomas. The lungs, kidneys and lymph node also showed the same non-caseating granulomas. The diagnosis of sarcoidosis with massive and extensive cardiac involvement was established as cause of death.     

Cathepsin-L在缺血心肌中的表达

目的检测cathepsin-L(CTSL)在大鼠早期缺血心肌中的表达变化,并探讨其法医学意义。方法建立大鼠早期心肌缺血模型,设置早期缺血组(early ischemic myocardium,EIM)、非缺血组(non-ischemic myocardium,NIM)、假手术组以及空白对照组,采用real-time PCR方法检测大鼠缺血后15min,30min,1h和2h CTSL mRNA的表达量,并进行组内和组间比较。收集心源性猝死者缺血心肌和机械性损伤致死者正常心肌样本,采用免疫组化染色方法观察心肌组织中CTSL蛋白表达。结果 EIM组CTSL mRNA表达量与NIM组、假手术组及空白组相比,在15min时无统计学意义(P>0.05),在30min、1h和2h时分别升高1.4、3.1和4.5倍(P<0.05);其余3组间差异无统计学意义(P>0.05)。观察10例冠脉狭窄程度Ⅲ～Ⅳ级的心源性猝死(SCD)者缺血心肌,CTSL表达增强。结论大鼠心肌缺血后早期即可检测到CTSL mRNA的升高,并在SCD冠脉狭窄死者缺血心肌中高表达,提示CTSL可作为心肌缺血与SCD的参考指标。     

Coronary arteritis diagnosed at autopsy: three case reports and review of the literature

Coronary arteritis is rare but can be fatal either by itself or in conjunction with other diseases. The authors report cases of three men in whom coronary arteritis was an interesting finding that may have caused or contributed to death. One 45-year-old man collapsed at work, another 56-year-old man was found dead in his parked car, and one 80-year-old man had a recent cerebrovascular accident. All three men had coronary arteritis, arteriosclerotic cardiovascular disease, some form of myocardial disease, and fatty liver change. Two had different lung diseases. The findings suggest that coronary arteritis may be an independent cause of death, part of a systemic disease, or, as these three cases illustrate, part of a constellation of cardiac and cardiovascular pathologies with a possible relation to other medical conditions. Coronary arteritis is an important finding in forensic pathology and merits consideration in a case of unexplained death.     

Fatal paradoxical air embolism diagnosed by postmortem imaging and autopsy

The recognition and visualization of an arterial gas embolism are difficult. We report a case of sudden death caused by paradoxical air embolism of coronary and cerebral arteries, diagnosed by the pre autopsy computed tomography (CT) scanning. A 54-year-old woman suddenly died after the self-removal of the jugular vein catheter. Postmortem imaging examination using CT scanning showed multiple gas embolisms in the cerebral arteries, pulmonary artery, right atrium and ventricle, left ventricle, aorta, and coronary arteries. These findings suggested that the occurrence of acute ischemia of the brain and heart caused by massive air inflow to the artery. Conventional autopsy revealed a patent foramen ovale of the heart. These results indicated that the patient died of paradoxical air embolization of the coronary and cerebral arteries through a patent foramen ovale because of right-to-left shunting. The use of postmortem imaging as an aid for conventional autopsy has proved to be of advantage in the case of gas embolism.     

急性心肌缺血早期血管内皮生长因子的免疫组织化学实验

对大鼠急性心肌缺血早期的不同时间、心脏不同部位的血管内皮生长因子（VEGF）的表达，运用免疫组织化学方法进行了研究。结果发现：缺血30min后在缺血心肌局部开始出现VEGF阳性表达，而缺血边缘区域和正常区域心肌在缺血1h后也开始出现VEGF阳性表达，并随着缺血时间的延长，VEGF的表达强度也越来越强。对照组未发现有阳性表达结果.表明运用免疫组化方法检测心肌缺血后心肌局部VEGF的表达，可望作为因心肌缺血导致心脏性猝死案例的诊断标准之一。     

Asymmetric septal hypertrophy of the heart. New findings concerning the possible etiology of sudden deaths in five males

This report describes certain interesting postmortem findings in the hearts of five subjects who died suddenly, silently, and unexpectedly, and in whom the only significant abnormality at autopsy was asymmetric septal hypertrophy (ASH) of the heart. Deep clefts, cystic faults, and dilated vascular channels were not only seen within the septal myocardium in all the hearts, but also within the left ventricular free walls of two hearts. The septal myocardium and the left ventricular free walls of two hearts and the A-V node and His bundle of one heart demonstrated mural and luminal thrombi of several dilated vascular channels. In another heart, foci of cardiocytic myofibrillar degeneration were seen, especially close to narrowed small coronary vessels. Fetal dispersion and fibrosis of the A-V node and His bundle were evident in one heart. These abnormalities in the conducting system and the ventricular myocardium suggest that the hearts of subjects with ASH are not only excellent anatomic substrates for lethal arrhythmias, but also are bound to be hemodynamically impaired. We believe that conditions such as hypoxia, increased oxygen demand by the heart or abnormal sympathetic stimulus may easily trigger fatal arrhythmias in such individuals, thereby causing sudden death.     

Immunostaining by complement C9: a tool for early diagnosis of myocardial infarction and application in forensic medicine

Before the first 12 hours, diagnosis of early myocardial infarctions is always difficult for forensic pathologists. We tested complement C9 expression in 121 formalin-fixed and paraffin-embedded heart samples by an immunohistochemical procedure. The heart specimens were separated into four groups: 33 cases in group 1 with typical ischemic damages histologically located, 20 cases in group 2 with death related to myocardial infarction on the basis of ischemic presentation on electrocardiogram but no obvious histological ischemic damage, 35 cases in group 3 with severe coronary disease without cause of death found at the autopsy, and 33 cases in group 4 without sign of myocardial infarction and without coronary disease. In the first group, all 33 heart samples showed a well-defined C9 expression in the necrotic areas. The second group in 17 of 20 cases showed positive areas for C9 expression. In the other three heart specimens, only few stained cells were observed whereas the painful symptoms had begun less than 1 h before death. The third group showed C9 immunopositive areas in six of 35 cases, few stained cells in 8 cases, and no C9 deposition in the 21 other cases. The last group showed no staining area. To avoid nonspecific C9 staining due to tissue autolysis, we studied C9 expression during a controlled putrefactive process in four cases included in group 1; staining was found only in infarcted myocardial areas, and was observed up to ten days. Specificity of C9 expression was evaluated to be 100% [89.4 to 100%] and sensitivity to be 85% [62.11 to 96.79%]. In conclusion, evaluation of immunohistochemical expression of C9 appears to be a highly sensitive and specific marker of early myocardial infarction, useful in forensic medicine if survival is more than 1 h after the beginning of myocyte damage.     

Detection of apoptosis in ischemic heart. Usefulness in the diagnosis of early myocardial injury

Myocardial samples of hearts with histologic findings of acute myocardial infarction (group A), sudden coronary deaths without histologic changes (group B), and chronic ischemic heart disease (group C) were analyzed to investigate the appearance of apoptosis in acute and chronic ischemic cardiac disorders. This analysis involved the morphologic detection of DNA strand breaks in myocyte nuclei by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay and the biochemical determination of DNA laddering in the myocardium using archival formalin-fixed, paraffin-embedded tissue sections of human myocardium. The authors demonstrated that apoptosis of myocardial cells could occur after ischemic myocardial cell injury. In all documented cases of acute myocardial infarction (group A), the infarcted area included extensive presence of both apoptosis and necrosis. In the tissue bordering on and away from the obviously infarcted areas, positive nuclei were intermingled with nonstained normal myocytes. The number of positive nuclei decreased with the distance from the infarction foci. In group B, myocardial samples showed focal or diffuse nuclear positivity of varying degrees for apoptosis, confirming the presence of myocardial ischemic cell death, whereas the histologic diagnosis remained inconclusive. This finding suggests that apoptosis could be used as a marker for acute ischemic injury. In group C, stained nuclei were dispersed with intermingled normal cardiomyocytes.     

青壮年猝死综合征心传导系统及心肌HHF35免疫组化研究

为了探讨青壮年猝死综合征（SMDS）的死亡原因与心性猝死之间的关系，作者对SMDS、冠心病、非心血管疾病死亡（正常对照）三组共23例心脏标本进行H．E和HHF35免疫组化观察．结果：9例SMDS中，8例心传导系统及心肌细胞出现小灶性HHF35阴性缺染区，而H．E染色未发现明显梗死灶；冠心病组7例均出现不同程度的心肌细胞缺染，呈广泛大面积分布；对照组心肌细胞、心传导系统及血管壁里均匀一致的阳性染色．表明部分SMDS死前已有早期心肌缺血或梗死等病变，其死亡原因应为急性心功能不全而致猝死．     

急性心肌缺血再灌注HSP70及c-Fos的免疫组织化学研究

运用免疫组织化学方法 ,观察心肌缺血后不同时间再灌注HSP70及Fos蛋白在心肌组织不同区域表达的规律 ,为心肌缺血 /再灌注损伤所致心性猝死的法医学诊断提供形态学依据。结扎大鼠左冠状动脉前降支建立急性心肌缺血 /再灌注模型 ,取缺血区域 (左冠脉前降支供血区 )及非缺血区 (右心室 )心肌组织。结果显示 :对照组正常心肌组织无Fos蛋白及HSP70表达。Fos蛋白在心肌缺血 15min再灌注 0 5h后即在缺血区域表达 ,随着再灌注时间延长其表达增强 ;非缺血区域 1h始有表达 ,缺血区域表达明显强于非缺血区域。HSP70在心肌缺血区域再灌注 1h后始有表达 ,随着再灌注时间延长其表达增强 ;非缺血区域心肌 2h始有表达 ,且明显弱于缺血区域。同时发现再灌注早期HSP70及Fos均先于心肌内层表达 ,随着时间延长其表达向心肌外层扩展。Fos在再灌注 0 5h时主要在心肌内层表达 ,1h时已扩展到心肌全层 ,4h时其心肌外层表达明显强于心肌内层。HSP70在再灌注 1、 2h时主要在心肌内层表达 ,4、 6h时表达扩展至全层心肌。心肌缺血 /再灌注早期不同时间HSP70及Fos表达有不同的区域性及强度 ,此可为心肌缺血 /再灌注的早期诊断提供一项新的辅助诊断依据     

Sudden Death After Myocardial Infarction in a High‐School Athlete

Abstract: This is an unusual case of ischemic heart disease occurring in a young female athlete, aged 14 years, in whom almost the entire posterior wall of the left ventricle was affected. The patient collapsed and died suddenly after a vigorous physical activity while resting at home. The ischemic lesion was apparently owing to right orifice stenosis in association with a small hypoplastic right coronary artery.     

Sudden death in infancy due to bicuspid aortic valve

Symptoms of bicuspid aortic valve usually occur in the age group of 50-70 years, but rarely, it can also lead to sudden unexpected death in infancy and early childhood. The autopsy of a 2-month-old baby boy, found dead in his cot, revealed the heart weight as 25 g, and the macroscopic examination showed the circumference of the aortic valve consisting of two leaflets as 8 mm. The thickness of the left ventricle, right ventricle, and septum was measured as 8, 7, and 10 mm, respectively. Microscopically, the heart revealed hypertrophic changes of myocytes. Subendocardial areas displayed necrosis of myocytes, and severe and diffuse ischemic changes characterized by loss of myofibers and vacuolization. Interstitial pneumonia was identified in the lungs. Death occurred as a result of a congenital bicuspid aortic valve obstructing the left ventricular outflow tract complicated by lung infection. As there are only a few reported cases in infancy, and congenital bicuspid aortic valve can lead to sudden unexpected death, this case is presented to the forensic community.     

Giant cell myocarditis with cardiac tamponade: a rare combination

Giant cell myocarditis (GCM) is a rare but fatal disease of idiopathic origin. It results in focal necrosis of myocardium. This is a case report of middle aged Malaysian Indian female who died due to cardiac tamponade due to rupture myocardium and tear in the root of aorta. On naked eye examination, it simply resembled as recent as well as old fibrotic areas of myocardial infarction. She was clinically diagnosed as a case of obstructive cardiomyopathy with atrioventricular block, and was on pace maker. There was subendocardial fibrosis and left ventricular transmural infarction in the left ventricle. On histopathology, this was diagnosed as GCM, there were widespread areas of inflammatory cellular infiltration within the myocardium with multinucleated giant cells and granulomas interspersed with lymphocytes. Microscopic field showed up to 10 multinucleated giant cells. In this case, there were focal areas at multiple locations and caused uneven thickness in the left ventricle wall. Idiopathic GCM is very rare and causation of hemopericardium is the unique feature of this case. In this case the direct link of GCM with aortitis and rupture of left ventricle wall resulting in hemopericardium is shown. This case is documented through macroscopic as well as microscopic photographs in H&E, Ziel-Nelson, and GMS staining.     

VEGF在家兔缺血心肌中的表达及其死后稳定性研究

目的观察心肌中VEGF在死后一定时间的稳定性及表达的变化规律，评价其对死后诊断机体早期心肌缺血的作用。方法用冠状动脉结扎法建立家兔急性心肌缺血模型，应用SP法染色、图像分析和统计学处理系统，检测缺血心肌细胞内VEGF阳性表达面积和强度，并对VEGF在死后不同时间的稳定性进行比较。结果VEGF在缺血心肌组织中，见灶性或成片心肌细胞强阳性表达，部分细胞呈阴性或弱阳性表达，血管内皮及平滑肌细胞表达弱阳性，间质表达阴性；在4℃放置，随时间延长，缺血心肌组织VEGF阳性表达有减弱趋势，至10d时缺血心肌组织仍可见VEGF在少许心肌细胞胞浆内呈弱阳性表达。在4℃放置10d以内，缺血心肌和正常心肌标本之间VEGF阳性表达具有极显著性差异。结论VEGF能耐受一定程度自溶及腐败的影响，其免疫组化检测对于判断死后4℃放置10d以内的尸体是否出现过心肌缺血具有一定意义。