Myocardial findings in fatal carbon monoxide poisoning: a human and experimental morphometric study

Abstract

The aim of this study was to define the status of the myocardium in selected human cases of acute, fatal carbon monoxide intoxication and the myocardial changes in rats exposed to carbon monoxide in relation to the type of cardiac arrest and the effects of reoxygenation following pre-fatal CO intoxication. The human study consisted of 26 cases (17 accidental and 9 suicide) of acute, fatal CO intoxication, without evidence of obstructive coronary atherosclerosis or history of ischemic heart disease which were compared with 45 cases of fatal head trauma in subjects who died instantaneously (26 cases) or within 1-12 h (19 cases). Inhalation of a lethal dose of CO in rats was compared with sub-lethal doses plus reoxygenation with and without pre-treatment by a betablocker. In all human and experimental histological sections, changes were normalised per mm2 area. In the human cases the myocardium did not show any ischemic types of changes or other lesions. Only in "three accidental" cases a few, small foci of coagulative myocytolysis were detected. In the case of spontaneous death in 31 rats following CO intoxication, no pathological myocardial changes were seen. Of the 15 "reoxygenated" rats, 2 of the 7 spontaneous deaths presented coagulative myocytolysis with 15 +/- 6 foci and 381 +/- 255 necrotic myocells. All the eight rats sacrificed at 3 h had coagulative myocytolysis with 5 +/- 4 foci and 60 +/- 47 myocells. Of the 24 reoxygenated rats pre-treated with a betablocker, 5 died spontaneously after a short survival and 2 of these showed 11 +/- 9 foci and 21 +/- 20 myocells. The 19 rats sacrificed after 3 h all presented coagulative myocytolysis with figures of 75 +/- 43 and 356 +/- 301 with 0.5 mg/kg of propranolol hydrochloride and 55 +/- 45 and 253 +/- 216 with 2 mg/kg, respectively.

Markers of cardiac oxidative stress and altered morphology after intraperitoneal cocaine injection in a rat model

“…In the present study, the only myocardial lesion found corresponded to "contraction band necrosis" or "coagulative myocytolysis" or "Zenker necrosis": the two latter terms prove to be more precise due to the presence of different types of contraction bands and they indicate a necrosis of the myocardial cells in a hypercontracted state (tetanic death) characterised by rhexis of the myofibrillar apparatus, anomalous hypereosinophilic cross-bands formed by segments of hypercontracted sarcomeres with extremely thickened Z lines, as shown ultrastructurally [32,33,34,35]. Within chronological limits, the present findings confirm the conclusions of the previous human study [7]: a. Cocaine-related adrenergic overactivity does not induce extensive myocardial necrosis and thus per se is unable to explain the cardiac arrest.…”

Effect of Melatonin and Atenolol on Carbon Monoxide Cardiotoxicity: An Experimental Study in Rats

“…The incidence of non-lethal CO poisoning is not well established nor is that of unrecognized CO poisoning (subacute poisoning). Also, there are some reports on myocardial morphologic changes in acute CO poisoning, especially stressing the importance of contraction bands (Fineschi et al 2000;Baroldi et al 2001).Melatonin is a pineal hormone, and also commercially available as over-the-counter for use in hope of rejuvenation. Melatonin affects the heart by direct and indirect ways (Pang et al 2000;Sewerynek 2002).…”

“…The incidence of non-lethal CO poisoning is not well established nor is that of unrecognized CO poisoning (subacute poisoning). Also, there are some reports on myocardial morphologic changes in acute CO poisoning, especially stressing the importance of contraction bands (Fineschi et al 2000;Baroldi et al 2001).…”

A Forensic Pathological Approach to Sudden Cardiac Death

“…For instance, contraction band necrosis is absent in carbon monoxide intoxication, whether accidental or suicidal, suggesting an antiadrenergic effect of lethal anoxia despite a longer survival period. Only if reoxygenation is restored, contraction bands lacking interstitial hemorrhage will be present (30). In other words, we need to know the frequency, extent, and stages of this lesion to interpret both the natural history of a disease and the mode of death.…”