Sudden death and mitral valve prolapse

INTRODUCTION. The two presented cases of forensic interest demonstrate the important role of cardio-pathological examination in ascertaining cause of death. Case 1. A man of 25 was found dead inside his car, while changing a tyre. As there was reason to suspect third-party liability, a forensic autopsy was ordered, to identify the cause, means and dynamics of death. Case 2. A man of 43, stopped by police in a state of acute drunkenness, was detained in the police station and later underwent compulsory hospitalisation in a hospital. He was treated with psychoactive drugs, and died few hours later. A forensic autopsy was ordered to ascertain the professional liability of doctors or of police, regarding possible maltreatment in the police station. METHOD. In both cases, procedures for circumstantial-clinical-documentary and necroscopic ascertainments were applied, including external examination, autopsy, histopathological and chemico-toxicological analyses. RESULTS AND DISCUSSION. Neither necroscopic ascertainments revealed extra-cardiac pathologies which might have caused the deaths. Macroscopic examination of both hearts revealed floppy and thickened mitral valve leaflets. The chordae tendineae were elongated, thickened but not ruptured. Hystopathologic examination revealed thickening of both spongiosa and fibrosa layers due to myxomatous infiltration and patchy fibrosis of the papillary muscles and of subendocardium. Chemico-toxicological analysis was negative in case 1, and showed therapeutic concentrations of psychoactive drugs in case 2. Analysis of circumstantial and clinical records showed that arrhythmia was triggered by physical effort in case 1 and by a combination of physical effort and emotional stress in case 2. Comparative analysis of the clinical, autoptic and chemico-toxicological results, in both cases, revealed arrhythmia due to ventricular fibrillation. CONCLUSIONS. Sudden cardiac death is the result of interaction between pathological substrate and an acute functional change, or trigger, eligible to cause an autonomic imbalance with increased adrenergic tone. In these cases, the pathological substrate, consisting of patchy-fibrosis of the myocardium, typical of mitral valve prolapse, involved dispersion of ventricular repolarisation. The trigger, acting on this substrate, led to a delayed after-depolarization and inhomogeneus electric cardiac response, with ventricular fibrillation and sudden death. In the ascertained absence of data indicating natural extra-cardiac, traumatic and/or toxic pathologies, these two cases demonstrate the important role of cardio-pathological examination in defining cause of death. In these contexts, it is essential to recognise mitral valve prolapse as the substrate eligible to trigger a lethal arrhythmia and to identify the triggers, their interaction, and the possible correlation with criminal dynamics.