Abstract A quantification of different forms of acute myocardial necrosis, myocardial leukocytic infiltrates and myocardial fibrosis was accomplished in 26 chronic co- caine abusers who died of cocaine intoxication and com- pared to 45 normal subjects who died from head trauma and 38 who died of acquired immunodeficiency syndrome. The findings were: absence of infarct necrosis, a similar frequency and extent of coagulative myocytolysis (con- traction band necrosis) and leukocytic infiltrates in co- caine abusers and normal controls, and an absence of my- ocardial fibrosis in cocaine abusers. These findings ques- tion both the acute and chronic cardiotoxicity of cocaine. The infarct-like pattern in some predisposed subjects may be due to an excess of catecholamine release induced by the drug resulting in coagulative myocytolysis and plate- let thrombi. Key words Cocaine · Necrosis · Contraction band necrosis · Myocarditis Introduction The relationship between morphological background and cardiac disorders in cocaine abusers is still controversial. The present postmortem study has been carried out to de- fine the types and to quantify the frequency and extension of myocardial necrosis, inflammatory infiltrates and my- ocardial fibrosis in 26 chronic cocaine abusers who died of cocaine intoxication. The quantification of the morpho- logic background of cocaine cardiotoxicity should help in defining its functional significance. Materials and methods Study population The chronic cocaine abusers were 26 cases of cocaine-associated death; 16 from the Dade County Medical Examiner Department, Miami, USA, and 10 from the Department of Forensic Sciences, Faculty of Medicine, University of Siena, Italy. Of these 18 died out of hospital and 8 died in hospital. The controls subjects were 45 normal subjects who died almost instantaneously (26 cases) or after a survival time of 1–12 h fol- lowing head trauma (19 cases) without postmortem evidence of any disease and 38 subjects who died from documented acquired immunodeficiency syndrome (AIDS) after a long stay in hospital. This control group was selected since AIDS patients, irrespective of concurrent opportunistic diseases show contraction band necro- sis and lymphocytic myocarditis [1]. Toxicological tests were neg- ative for all subjects. Of the latter 29 had a history of intravenous drug abuse, mainly heroin. To avoid any possible interference between coronary athero- sclerosis and myocardial changes, only chronic cocaine abusers and controls with no or minor (≤ 50% lumen-diameter reduction) coronary atherosclerosis were included in this study. In all cases no resuscitation attempts were done. The method of heart examination has been reported previously [1]. In brief, in each case the heart was weighed, opened and in- spected and any gross changes examined histologically. The coro- nary arteries were cross-sectioned at 3 mm intervals and any seg- ment with luminal modification was processed for histology. My- ocardial samples of the left anterior wall (n = 2–4) were systemat- ically taken, fixed in 10% buffered formalin and embedded in paraffin. Histological sections were routinely stained with hema- toxylin-eosin. Quantitative analysis The myocardial area of each histological section was calculated in mm 2 by an image analysis system (Vidas, Zeiss). The slide image was digitized, the total myocardial area was measured in pixels and converted to mm 2 by a calibration procedure using a reference system. The following histological parameters were normalized to 100 mm 2 : V. Fineschi · C.V. Wetli · M. Di Paolo · G. Baroldi Myocardial necrosis and cocaine A quantitative morphologic study in 26 cocaine-associated deaths Int J Legal Med (1997) 110 : 193–198 © Springer-Verlag 1997 Received: 5 August 1996 / Received in revised form: 3 February 1997 ORIGINAL ARTICLE V. Fineschi () · M. Di Paolo Department of Forensic Sciences, University of Siena, Policlinico Le Scotte, Viale Bracci, I-53100 Siena, Italy C. V. Wetli Suffolk County Medical Examiner’s Office, Building 487/North County Complex, Hauppauge, NY 11787-4311, USA G. Baroldi Institute of Clinical Physiology, National Research Council, Department of Cardiology “De Gasperis”, Niguarda Hospital, Piazza Ospedale Maggiore 3, I-20162 Milano, Italy