Some possibilities in the diagnosis of early acute ischaemic changes in the heart muscle in sudden death.

INTRODUCTION

Ischaemic heart disease is the leading cause of death in industrialised countries. Sudden death accounts for approximately 2/3 of autopsies in forensic medicine, which is why the accurate diagnosis of IHD and first of all acute myocardial ischaemia is so important. On certain occasions in forensic medical practice it is difficult to diagnose AMI from morphological observation alone. In such cases, complementary diagnostic techniques, such as the determination of biochemical markers of the necrosis of the heart muscle (myoglobin, troponin I and creatine kinase) in cadaver fluids, take on special importance, so we decided to test the diagnostic evaluation of postmortem cTnl, myoglobin and creatine kinase determination in serum and pericardial fluid. Recently, cardiac troponins have gained attention as very specific markers of myocardial cell injury, and the European Society of Cardiology and the American College of Cardiology have suggested that these proteins should be preferred markers for the diagnosis of the necrosis of heart muscle.

METHODS

We studied 71 cadavers, which were divided into 2 groups. The first group (38 cases) consisted of people where the acute myocardial infarction was the only cause of death (the myocardial lesion could be easily detected by macroscopic examination or by formazan test, other causes of death were excluded and the constriction or obturation of the coronary arteries was detected). The second group (non-AMI deaths) was formed by 4 cases of cardiac failure, 6 cases of intracerebral haemorrhage, 5 cases of pulmonary embolism, 7 cases of asphyxia (4 hangings, 1 traumatic asphyxia, 2 drownings), 3 cases of brain contusion, 2 cases of carbon monoxide poisoning, 1 case of cyanide poisoning, 1 case of alcohol poisoning, 1 case of epilepsy, 1 case of bronchopneumonia, 1 case of hyperglycaemic coma and 1 case of exsanguination.

RESULTS

The values of creatine kinase and myoglobin were increased in all cases (100%) of AMI-deaths and non-AMI deaths in blood and pericardial fluid and there was no statistically significant difference between these groups. Troponin I was increased in all cases of both groups in pericardial fluid, and again there was no significant difference in concentration between both groups. In blood, troponin I was increased by 87% in the group of AMI deaths and in 91% of non-AMI deaths. There was no significant statistical difference between the groups and there was no difference in concentration either.

CONCLUSION

We did not find a statistically significant difference in pericardial fluid or in serum for cTnl, CK-MB and myoglobin between the group of AMI deaths and the group of non-AMI deaths and we cannot confirm the diagnostic efficacy of these biochemical markers in the postmortem diagnosis of acute myocardial infarction.