Cocaine-Induced Myocardial Dysfunction

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Long-term cocaine abuse has been reported to cause left ventricular hypertrophy and systolic dysfunction. Several reports have described dilated cardiomyopathy in long-term cocaine abusers, as well as reversible, profound myocardial depression after binge cocaine use. Bertolet et al. found evidence of left ventricular systolic dysfunction (by radionuclide ventriculography) in 7 percent of asymptomatic long-term cocaine users. These and other reports provide evidence that repeated exposure to cocaine may induce left ventricular systolic dysfunction.

Cocaine may adversely affect left ventricular systolic function by means of several mechanisms. First, as described previously, cocaine may induce myocardial ischemia or infarction. Second, the profound repetitive sympathetic stimulation induced by cocaine is similar to that observed in patients with pheochromocytoma; both are associated with cardiomyopathy and characteristic microscopic changes of subendocardial contraction band necrosis.  Third, the concomitant administration of adulterants or infectious agents may cause myocarditis, which has been seen on occasion in postmortem studies of intravenous cocaine users. Fourth, studies in animals have shown that cocaine alters cytokine production in the endothelium and in circulating leukocytes, induces the transcription of genes responsible for changes in the composition of myocardial collagen and myosin, and induces myocyte apoptosis.

Aside from the effects of long-term cocaine use on myocardial performance, it may cause an acute deterioration of left ventricular systolic and diastolic function.

In some patients, this deterioration may be caused by metabolic disturbances, acid–base disturbances, or both that accompany cocaine intoxication, whereas in others it may be caused by a direct toxic effect of the drug. Pitts et al. demonstrated that an intracoronary infusion of cocaine (in an amount sufficient to yield a concentration in coronary-sinus blood similar in magnitude to the peripheral-blood concentration found in abusers who have died of cocaine intoxication) had a deleterious effect on left ventricular systolic and diastolic function. A possible mechanism for these effects is that cocaine or its metabolites alter the manner in which myocytes handle calcium.

Source Information

From the Cardiovascular Division, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas.

Address reprint requests to Dr. Hillis at the Department of Internal Medicine, Room CS7.102, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-9047.
References

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Richard A. Lange, M.D., and L. David Hillis, M.D.

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