Cocaine and MI

Abstract

To the Editor: Myocardial infarction is being reported in alarming numbers as a consequence of cocaine abuse.1Cregler LL Mark H Medical complications of cocaine abuse.N Engl J Med. 1986; 315: 1495-1500Crossref PubMed Scopus (684) Google Scholar The pathogenesis of cocaine-induced myocardial infarction is as yet unknown, although coronary artery spasm may play a prominent role in some patients.2Simpson RW Edwards WD Pathogenesis of cocaine-induced ischemic heart disease.Arch Pathol Lab Med. 1986; 110: 479-484PubMed Google Scholar This mechanism is suggested particularly in those patients who have nonobstructive coronary artery disease. Recent investigations have noted, however, that the association between coronary spasm and cocaine must be considered a temporal rather than causal one because the effect of cocaine in these patients has not been confirmed by rechallenge with the drug.3Isner JM Estes M Thompson PD Costanzo-Norden MR Subramanian R Miller G et al.Acute cardiac events temporally related to cocaine abuse.N Engl J Med. 1986; 315: 1438-1443Crossref PubMed Scopus (513) Google Scholar We report an unusual patient with nonobstructive coronary artery disease who suffered two separate episodes of myocardial infarction related to abuse of cocaine. A previously healthy 31-year-old man developed severe chest discomfort after freebasing cocaine. He presented to the emergency room, where an initial electrocardiogram showed a right bundle branch block pattern with ST elevation in leads I, avL, and V1 through V5. Serial electrocardiograms and cardiac enzyme tests were diagnostic of an acute anterior wall myocardial infarction. Maximal serum creatine kinase level was 2,820 IU/L (normal 0 to 125) with an MB fraction of 9.3 percent (normal 0 to 3). Echocardiogram demonstrated extensive anterior wall akinesis with an apical aneurysm. Left ventricular thrombus was not present. Coronary arteriography performed 20 days after admission demonstrated a 30 percent lesion of the proximal left anterior descending artery. The patient was prescribed coumadin with strong advice against further cocaine abuse. Two weeks after discharge the patient again developed chest pain shortly after intranasal use of cocaine. Elevation of the ST segments in leads I, avL and V4 through V6 recurred, with new ST elevation in leads II, III, and avF. Additional myocardial necrosis was documented by cardiac enzyme levels. Peak creatine kinase was 588 IU/L with an MB fraction of 13.6 percent. Repeat echocardiogram showed the development of further segmental motion abnormalities of the inferior and posterior walls of the left ventricle. Diltiazem was added to the patient’s regimen and advice to abstain from cocaine use was reinforced. Recurrent myocardial infarction has been demonstrated in persons with significant coronary artery disease who repeatedly abuse cocaine.4Weiss RJ Recurrent myocardial infarction caused by cocaine abuse.Chest. 1986; 111: 793Google Scholar In such patients, myocardial ischemia may result from cocaine-induced elevation of heart rate and blood pressure. The mechanism of myocardial infarction in patients without critical coronary narrowing is less clear. We recently reported severe coronary artery spasm with superimposed thrombosis in a 29-year-old male with normal coronary arteries who suffered recurrent myocardial infarction after using cocaine.5Zimmerman FH Gustafson GM Kemp HG Recurrent myocardial infarction associated with cocaine abuse in a young man with normal coronary arteries: evidence for coronary artery spasm culminating in thrombosis.J Am Coll Cardiol. 1987; 9: 964-968Abstract Full Text PDF PubMed Scopus (148) Google Scholar The course of the patient described herein lends support to the hypothesis that use of cocaine may precipitate coronary vasospasm sufficient to produce myocardial infarction in patients with nonobstructive coronary artery disease.