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Cocaine-Induced Acute Myocardial Infarction

Shereif H. Rezkalla, MD, Department of Cardiology, Marshfield Clinic, 1000 North Oak Avenue, Marshfield, Wisconsin
Robert A. Kloner, MD, PhD, The Heart Institute, Good Samaritan Hospital, Division of Cardiovascular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California

Reprint Requests: Shereif H. Rezkalla, MD, Department of Cardiology, Marshfield Clinic, 1000 North Oak Avenue, Marshfield, WI 54449, Tel: 715-387-5845, Fax: 715389-3808, Email: rezkalla.shereif{at}marshfieldclinic.org

Acute myocardial infarction may occur following cocaine use. Cocaine-induced infarction is particularly common in younger patients aged 18 to 45 years old. Patients may or may not have angiographic evidence of coronary artery disease at the time of their acute event. Previous studies have shown that coronary artery spasm occurs with cocaine use, and perhaps platelet activation, both contributing to a process that may culminate in coronary artery occlusion. Primary coronary intervention should be the preferred revascularization modality by an experienced team. Thrombolytic therapy needs to be instituted if this intervention is unavailable. Beta blockers should be utilized with caution since they may increase coronary spasm or cause a paradoxical rise in blood pressure. They should be avoided in the early hours of the infarction, but be instituted prior to patient discharge. Interruption of cocaine abuse is the cornerstone of secondary prevention in cocaine-related myocardial infarction.

Key Words: Acute myocardial infarction • Cocaine • Heart disease • Coronary artery disease • Coronary spasm • Platelet aggregation • Platelet function • Thrombosis