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  • Title: Effects of cocaine on the coronary arteries.
    Author: Benzaquen BS, Cohen V, Eisenberg MJ.
    Journal: Am Heart J; 2001 Sep; 142(3):402-10. PubMed ID: 11526352.
    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.
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