• Bao-Li Zhu, Takaki Ishikawa, Tomomi Michiue, Dong-Ri Li, Dong Zhao, Yasunobu Kamikodai, Kohei Tsuda, Shuji Okazaki, and Hitoshi Maeda.
• Department of Legal Medicine, Osaka City University Medical School, Asahi-machi 1-4-3, Abeno, 545-8585 Osaka, Japan. baolizhu@med.osaka-cu.ac.jp
• Leg Med (Tokyo). 2006 Mar 1; 8 (2): 94-101.

AbstractAlthough previous forensic pathological studies have suggested the possible application of cardiac troponins in the diagnosis of myocardial infarction, there appears to be insufficient data with regard to its cardiac pathology. The present study analyzed the heart blood, peripheral blood and pericardial fluid levels of cardiac troponin T (cTnT) in sudden cardiac deaths (n = 96) within 48h postmortem in relation to pathological findings of acute myocardial infarction (AMI, n = 34), recurrent myocardial infarction (RMI, n = 23), ischemic heart disease without any pathological evidence of infarction (IHD, n = 24) and other heart diseases (OHD, n = 15). Control groups (n = 75, survival time <24 h) within 48 h postmortem consisted of asphyxiation (n = 35), drowning (n = 27) and cerebrovascular diseases (n = 13). There was a marked correlation in the cTnT levels between right and left heart blood samples. The pericardial level was usually higher than either heart blood level, and the external iliac venous blood level was the lowest. Although postmortem time-dependent increases in heart and pericardial blood cTnT levels were observed in most groups, they were most evident for AMI and asphyxiation. In the early postmortem period (<12 h) there was no significant difference between AMI or RMI and the other groups except for drowning. After 12 h postmortem, significantly elevated heart blood and pericardial cTnT levels were observed for AMI and RMI showing multiple interstitial hemorrhages and necrosis compared to those with localized eosinophilic changes or patchy interstitial hemorrhages, IHD and OHD. These differences were the smallest for peripheral blood. For sudden cardiac death cases, the difference in cTnT level at each site among the causes of death was independent of gender, age, heart or lung weight and pathologies of affected coronary artery and severity of coronary stenosis. These observations suggest that the elevation in postmortem blood and pericardial cTnT levels in sudden cardiac death may depend on the severity of ischemic myocardial damage including the size and intensity of myocardial lesions involving multiple interstitial hemorrhages and necrosis, and also the postmortem period for heart and pericardial levels.

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