The temporal relationship between cocaine use and myocardial infarction is well documented. Several mechanisms have been proposed to explain this relationship. An increase in double product as a result of cocaine use seems logical but should not be a problem in patients who have normal coronary arteries. Coronary spasm has also been invoked but has not been duplicated in the catheterization laboratory using ergonovine. Coronary thrombi are found in many but not all of the patients. Furthermore, the role of cocaine in coronary thrombus formation has not been clarified. Clearly there is a need for more studies.
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