Elsevier

American Heart Journal

Volume 142, Issue 3, September 2001, Pages 402-410
American Heart Journal

Curriculum in Cardiology
Effects of cocaine on the coronary arteries,☆☆

https://doi.org/10.1067/mhj.2001.117607Get rights and content

Abstract

Background A number of studies have documented myocardial ischemia and infarction associated with cocaine use. Mismatch between myocardial oxygen supply and demand from cocaine-induced vasoconstriction and increased myocardial workload are often invoked as the major postulated mechanism by which cocaine induces myocardial ischemia. This article reviews the literature studying the effects produced by cocaine on the coronary arteries to provide insight into the various pathophysiologic mechanisms by which cocaine triggers acute cardiac ischemia or infarction. Methods We reviewed the published literature describing the effects of cocaine on the coronary arteries. A MEDLINE search of English language articles published between 1985 and 2000 was performed. Key words included coronary arteries, coronary vasoconstriction, vasospasm, coronary vasodilation, cardiac vasculature, myocardial ischemia, platelets, thrombosis, and cocaine. Both animal and human studies were included. The bibliographies of identified articles were also explored for additional sources of information. Results A recreational dose of cocaine increases the heart rate by approximately 30 beats/min. It also increases the blood pressure by 20/10 mm Hg. These increases are modest, are equivalent to mild exercise, and are not believed to be sufficient to result in myocardial ischemia in the majority of cases. Animal and human studies have documented cocaine-induced early coronary artery vasodilation as shown by a decrease in coronary perfusion pressure ranging from 13% to 68%. This was followed by a more sustained vasoconstriction demonstrated by a decrease in epicardial coronary artery diameter ranging from 5% to 30% with various doses of cocaine by various methods of administration. These changes alone are also an unlikely explanation for cocaine-induced myocardial ischemia. Therefore neither increases in myocardial workload nor hemodynamic changes are sufficient to explain cocaine-induced myocardial ischemia. However, evidence also exists that cocaine activates platelets and promotes thrombosis, resulting in intracoronary thrombus formation. Cocaine may also promote premature and more severe coronary atherosclerosis. Conclusion The etiology of cocaine-induced myocardial ischemia is complex and is likely to be multifactorial. It appears to be the result of coronary artery vasoconstriction, intracoronary thrombosis, and accelerated atherosclerosis. (Am Heart J 2001;142:402-10.)

Section snippets

Methods

We reviewed the published literature describing the effects of cocaine on the coronary arteries. This was accomplished through a MEDLINE search of English Language articles published between 1985 and 2000. Subject headings used were coronary arteries, coronary vasoconstriction, coronary vasospasm, coronary vasodilation, cardiac vasculature, myocardial ischemia, platelets, thrombosis, and cocaine. The bibliographies of identified articles were also evaluated for additional sources of

Normal physiologic features

The caliber of the coronary arteries is controlled by a complex interplay between local metabolic factors and neural input. This interplay results in an appropriate coronary blood flow to supply the demands of the working myocardium. Oxygen delivery to the myocardium is achieved through changes in coronary artery caliber. Important mediators of coronary caliber include adenosine, endothelial-derived relaxing factor,13 angiotensin II,14 and vasopressin.15 Neural control of coronary caliber is

Conclusion

Cocaine-induced myocardial ischemia and infarction involves multiple and distinct pathogenic mechanisms likely acting in combination. Cocaine increases myocardial oxygen demand by increasing heart rate and systemic blood pressure along with concurrent decreases in coronary artery diameter. Experimental and clinical evidence suggest that this mismatch between oxygen supply and demand is, by itself, not enough to result in myocardial ischemia and infarction in doses used recreationally. However,

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    M. J. E. is a research scholar of the Heart and Stroke Foundation of Canada.

    ☆☆

    Reprint requests: Mark J. Eisenberg, MD, MPH, Jewish General Hospital, Suite A-118, 3755 Cote St-Catherine Road, Montreal, Quebec H3T 1E2, Canada. E-mail: [email protected]

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