Cocaine-induced transmural myocardial infarction in a Yorkshire swine with normal coronary arteries: Evidence for microvascular and/or epicardial coronary artery spasm.

Cocaine-induced myocardial infarction with normal coronary arteries is well documented in humans. The exact mechanism of action remains speculative. We report one case of cocaine-induced myocardial infarction with normal coronaries in one swine. Systemic hemodynamics and angiographic, electrocardiographic, echocardiographic, and histopathologic data are presented. Intravenous cocaine (1, 3, 10 mg/kg) produced significant decreases in mean arterial pressure, heart rate, stroke volume, coronary blood flow, and coronary reserve, whereas pulmonary artery diastolic pressure and coronary vascular resistances increased. Left anterior descending and left circumflex coronary artery cross-sectional area decreased by 31% and 64%, respectively, without localized vasospasm. Electrocardiographic changes occurred (3 mm ST elevation in leads II, III, AVF). Peak creatine phosphokinase was 17,220 IU/L. The echocardiogram revealed severe hypokinesis of the inferior wall and normal ventricular function. The animal survived the acute phase of the infarction and the swine was restudied 12 weeks later. Upon rechallenge, systemic and coronary hemodynamics shoved changes similar to those in the previous study. The swine developed ventricular fibrillation and expired after the 10 mg/kg cocaine dose. Macroscopic examination of the external surface of the heart revealed marked diffuse fibrosis in the posteroinferior and lateral left ventricular wall. Our data suggest that the infarct induced by cocaine may have resulted from severe vasoconstriction or spasm at the level of the microcirculation, and/or the epicardial coronary arteries, which shoved slight but significant narrowing throughout their lengths.

Duke Scholars

Author Pamela Susan Douglas Medicine, Cardiology