Chen Jian-Hua, Inamori-Kawamoto Osamu, Michiue Tomomi, Ikeda Sayuko, Ishikawa Takaki, Maeda Hitoshi
Department of Legal Medicine, Osaka City University Medical School, Asahi-machi 1-4-3, Abeno, Osaka 545-8585, Japan; Forensic Autopsy Section, Medico-legal Consultation and Postmortem Investigation Support Center, Uehonmachi 7-1-16-1308, Tennoji, Osaka 543-0001, Japan.
Department of Legal Medicine, Osaka City University Medical School, Asahi-machi 1-4-3, Abeno, Osaka 545-8585, Japan; Forensic Autopsy Section, Medico-legal Consultation and Postmortem Investigation Support Center, Uehonmachi 7-1-16-1308, Tennoji, Osaka 543-0001, Japan.
Leg Med (Tokyo). 2015 Sep;17(5):343-50. doi: 10.1016/j.legalmed.2015.03.007. Epub 2015 Apr 30.
Previous studies suggested possible application of postmortem biochemistry of myocardial biomarkers to the investigation of sudden cardiac death; however, differences from clinical findings should be considered in autopsy materials. The present study involved a comprehensive investigation of cardiac troponin T and I (cTnT and cTnI), and creatine kinase MB (CK-MB) in cardiac and peripheral external iliac venous blood, pericardial fluid (PCF) and cerebrospinal fluid (CSF) for reassessment, with special regard to the estimated postmortem interval in relation to the cause of death, reviewing a large number of forensic autopsy cases (n=1923). These cardiac biomarkers showed cause-of-death- and postmortem-time-dependent differences: blood and PCF levels of each marker were higher in hyperthermia (heatstroke), bathwater drowning and chronic congestive heart disease in cases of postmortem interval (PMI) <12h. After 12h postmortem, these markers were also higher in fatal drug abuse, spontaneous cerebral/subarachnoid bleeding, electrocution and pulmonary embolism. In addition, most other causes of death, including ischemic heart disease, showed substantial elevations, while these markers remained low in acute hemorrhagic death from sharp instrument injury, hypothermia (cold exposure) and sea-/freshwater drowning during PMI of <48h. CSF cTnI and CK-MB showed similar findings. There was no difference between myocardial infarction and other causes of death to be discriminated, including asphyxiation, drowning and fire fatality. These findings are similar to clinical observations in critical ill patients, suggesting that elevated cardiac biomarkers cannot be a specific finding for death from acute ischemic heart disease, but indicate the severity of myocardial injury in postmortem investigation.
先前的研究表明,心肌生物标志物的死后生物化学可能应用于心脏性猝死的调查;然而,在尸检材料中应考虑与临床发现的差异。本研究对心脏和外周髂外静脉血、心包液(PCF)和脑脊液(CSF)中的心肌肌钙蛋白T和I(cTnT和cTnI)以及肌酸激酶MB(CK-MB)进行了全面调查,以进行重新评估,特别关注与死亡原因相关的估计死后间隔时间,回顾了大量法医尸检病例(n = 1923)。这些心脏生物标志物显示出与死亡原因和死后时间相关的差异:在死后间隔时间(PMI)<12小时的病例中,热射病(中暑)、洗澡水溺水和慢性充血性心力衰竭时,每种标志物的血液和PCF水平较高。死后12小时后,在致命药物滥用、自发性脑/蛛网膜下腔出血、触电和肺栓塞中,这些标志物也较高。此外,包括缺血性心脏病在内的大多数其他死亡原因也显示出大幅升高,而在PMI<48小时期间,锐器伤、低温(寒冷暴露)和海/淡水溺水导致的急性出血性死亡中,这些标志物仍然很低。脑脊液cTnI和CK-MB显示出类似的结果。心肌梗死与其他死亡原因(包括窒息、溺水和火灾致死)之间没有差异可区分。这些发现与重症患者的临床观察结果相似,表明心脏生物标志物升高并非急性缺血性心脏病死亡的特异性表现,但在尸检调查中表明心肌损伤的严重程度。