What is the pathophysiology of cocaine-induced MI?

Updated: Dec 31, 2020
  • Author: Lynn Barkley Burnett, MD, EdD, JD; Chief Editor: Sage W Wiener, MD  more...
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A nationally representative study of 10,085 US adults aged 18-45 years found that regular use of cocaine was associated with an increased likelihood of MI. Approximately 1 of every 4 nonfatal MIs was attributable to frequent use of cocaine (defined in this study as >10 uses in a lifetime). [12]

Patients with cocaine-related MI often have fixed atherosclerotic lesions. Cocaine can induce increased heart rate and BP, resulting in increased myocardial oxygen demand. The additional metabolic requirements may convert an asymptomatic obstruction into one of clinical significance.

Substantial evidence indicates that cocaine use causes accelerated coronary atherosclerosis. According to a 1995 study of trauma fatalities among men with a mean age of 34 years and an incidental finding of cocaine metabolites, 25% had lesions in 2 or more vessels, and 19% had disease in 3-4 vessels. Of the control subjects, only 6% had 2-vessel disease, and none had 3- or 4-vessel disease. In another study of 22 long-term cocaine users with a mean age of 32 years, all of whom died suddenly with detectable serum cocaine levels, severe narrowing of more than 75% cross-sectional area was found in 1 or more coronary arteries in 36% of patients. [10]

Hollander and Hoffman reviewed and analyzed the literature of 91 patients with cocaine-induced MI. Cardiac catheterization in 54 patients demonstrated that 31% had significant coronary atherosclerosis. Autopsy studies of patients with cocaine-related MI revealed atherosclerotic lesions in more than one half of patients. [13]

In another review of medical examiners' records, 495 deceased patients had positive toxicologic findings of cocaine; 6 of them, whose mean age was 29 years, had MI with total thrombotic occlusion primarily involving the left anterior descending coronary artery. All of the patients had significant coronary atherosclerosis, with 83% having lesions that caused luminal stenosis of more than 75% cross-sectional area in 1 or more vessels.

Of the patients reviewed by Hollander and Hoffman, 24% had a thrombotic occlusion in the absence of clinically significant coronary disease. [13] Cocaine's effect of increasing levels of plasma plasminogen activator enhances clot formation. In addition, cocaine activates platelets both directly and indirectly by means of an alpha-adrenergic–mediated increase in platelet aggregation.

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