Post-mortem cardiac-specific troponin-I (cTnI) to determine the cause of non-traumatic hemopericardium.

Abstract

Hemopericardium is regularly seen at autopsy and post-mortem imaging. Once traumatic cases and resuscitation artefact are excluded, hemopericardium is almost always due to either ruptured myocardial infarction or aortic dissection. In this study, we explored whether post-mortem cardiac-specific troponin I (cTnI) can be helpful when autopsy is not feasible and post-mortem imaging findings are inconclusive. Post-mortem cTnI levels were compared between 46 cases with hemopericardium due to ruptured myocardial infarction (RMI), 38 cases of hemopericardium due to aortic dissection (AoD), and 44 cases of natural deaths without hemopericardium (controls). The results showed significantly higher cTnI levels in the RMI group (median 5,821 ng/L) compared to AoD (median 273 ng/L) and controls (median 95 ng/L). Receiver operating characteristic (ROC) analysis indicated that a cTnI threshold of 1,483 ng/L provided the best balance of sensitivity (87%) and specificity (90%) for distinguishing RMI from AoD. Levels of cTnI above 9688 ng/L were exclusively seen in RMI, whilst levels < 250 ng/L excluded this diagnosis. Calculated likelihood ratios demonstrated that higher levels of cTnI favour RMI over AoD, but substantial overlap between the cohorts limited the diagnostic value of intermediate cTnI values. Autopsy remains the gold standard for determining the cause of hemopericardium and cTnI testing is best reserved for cases in which an autopsy is not feasible.