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Cocaine-induced Myocardial Infarction in Patients with Normal Coronary Arteries

Robert L. Minor Jr., MD; Brook D. Scott, MD; Donald D. Brown, MD; and Michael D. Winniford, MD
[+] Article, Author, and Disclosure Information

Grant Support: By grants HL-08357 and HL-32295 from the National Institutes of Health.

Requests for Reprints: Robert L. Minor Jr., MD, Department of Medicine, Cardiovascular Division, University of Iowa Hospitals and Clinics, Iowa City, IA 52242.

Current Author Addresses: Drs. Minor, Scott, Brown, and Winniford: Department of Medicine, Cardiovascular Division, University of Iowa Hospitals and Clinics, Iowa City, IA 52242.

© 1991 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1991;115(10):797-806. doi:10.7326/0003-4819-115-10-797
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Objective: To review the reported cases of myocardial infarction temporally related to recreational and topical anesthetic use of cocaine, with special regard for underlying etiologic factors in patients subsequently found to have normal coronary arteries.

Data Sources: Personal records of three cases and a comprehensive literature review using MEDLINE and supplemented by Index Medicus and the bibliographies of case reports.

Data Synthesis: A total of 114 cases of cocaine-induced myocardial infarction were identified. The coronary anatomy was defined by angiography or autopsy in 92 patients, 38% of whom had normal coronary arteries. In these 35 patients (average age, 32; range, 21 to 60 years), myocardial infarction typically involved the anterior left ventricular wall (77%). Moderate cigarette smoking with one or fewer associated coronary risk factors was prevalent (68%). Focal coronary vasospasm was shown convincingly in only two cases. Intracoronary thrombus was initially found on 9 of 11 angiograms (82%) done within 12 hours of the myocardial infarction. Experimental evidence suggests that cocaine has direct and indirect sympathomimetic effects on vascular smooth muscle, attenuates endothelium vasodilator capacity, exerts a potent depressant effect on cardiac myocytes, and promotes atherogenesis.

Conclusions: Cocaine-induced myocardial infarction in patients with normal coronary arteries probably involves adrenergically mediated increases in myocardial oxygen consumption, vasoconstriction of large epicardial arteries or small coronary resistance vessels, and coronary thrombosis. Accelerated atherosclerosis and impairment of endothelium vasodilator function may occur after chronic cocaine use.





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