Cocaine-induced acute myocardial infarction in young individuals with otherwise normal coronary risk profile: Is coronary microvascular dysfunction one of the underlying mechanisms?

Abstract

Recently, Raddino et al. [1] have reported a 19-year-old woman with acute anterior myocardial infarction (MI) giving a history of cocaine abuse with last exposure 4 days before symptom onset. Her coronary angiographic evaluation has revealed the thrombotic occlusion of anterior descending coronary artery without atherosclerotic plaques, and complete recanalization of the vessel after anticoagulation with enoxaparine. She has been normotensive, nondiabetic, non-smoker, with normal lipid profile and normal body mass index, without familial history of coronary artery disease. Laboratory analysis has shown the presence of antiphospholipid antibodies. Raddino at al. [1] have suggested that cocaine-induced endothelial activation and synergic prothrombotic activity of cocaine and antiphospholipid antibodies may be the possible factors in the development of acute MI in this patient. Cocaine has been shown to be associated with myocardial ischemia and MI independently of the administration route, the amount ingested and the frequency of use [2,3]. Most patients with cocaine-related acute MI are young and male and have a low coronary risk factor profile for atherosclerosis and have previously normal epicardial coronary arteries [3,4]. The pathogenesis of cocaine-related MI has been reported to be multifactorial including increased myocardial oxygen demand, marked vasoconstriction of the coronary arteries, enhanced platelet aggregation and thrombus formation and accelerated atherosclerosis [2–5]. Cocaine-related acute MI due to