(Circulation. 1999;99:2737-2741.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Institute for Prevention of Cardiovascular Disease, Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Mass (M.A.M., D.M., G.H.T.); the Department of Epidemiology, Harvard School of Public Health, Boston, Mass (M.A.M., M.M.); the Department of Health and Social Behavior, Harvard School of Public Health, Boston, Mass (J.B.S.); and the Division of Cardiology, Department of Medicine, University of Kentucky Medical Center, Lexington, Ky (J.E.M.).
Correspondence to Murray A. Mittleman, MD, DrPH, Cardiovascular Division, Beth Israel Deaconess Medical Center, 1 Autumn St, Fifth Floor, Boston, MA 02215. E-mail mmittlem{at}hsph.harvard.edu
BackgroundCocaine has been implicated as a trigger of acute myocardial infarction in patients with and those without underlying coronary atherosclerosis. However, the magnitude of the increase in risk of acute myocardial infarction immediately after cocaine use remains unknown.
Methods and ResultsIn the Determinants of Myocardial Infarction Onset Study, we interviewed 3946 patients (1282 women) with acute myocardial infarction an average of 4 days after infarction onset. Data were collected on the use of cocaine and other potential triggers of myocardial infarction. We compared the reported use of cocaine in the hour preceding the onset of myocardial infarction symptoms with its expected frequency by using self-matched control data based on the case-crossover study design. Of the 3946 patients interviewed, 38 (1%) reported cocaine use in the prior year and 9 reported use within the 60 minutes preceding the onset of infarction symptoms. Compared with nonusers, cocaine users were more likely to be male (87% vs 67%, P=0.01), current cigarette smokers (84% vs 32%, P<0.001), younger (44±8 vs 61±13 years, P<0.001), and minority group members (63% vs 11%, P<0.001). The risk of myocardial infarction onset was elevated 23.7 times over baseline (95% CI 8.5 to 66.3) in the 60 minutes after cocaine use. The elevated risk rapidly decreased thereafter.
ConclusionsCocaine use is associated with a large abrupt and transient increase in the risk of acute myocardial infarction in patients who are otherwise at relatively low risk. This finding suggests that studying the pathophysiological changes produced by cocaine may provide insights into the mechanisms by which myocardial infarction is triggered by other stressors.
Key Words: cocaine myocardial infarction epidemiology
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