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

  _{1. Office of Applied Studies. Year-end 1999 emergency department data from the Drug Abuse Warning Network. Rockville, Md.: Substance Abuse and Mental Health Services Administration, August 2000. (DHHS publication no. (SMA) 00-3462.)
  2. Office of Applied Studies. Summary of findings from the 1999 National Household Survey on Drug Abuse. Rockville, Md.: Substance Abuse and Mental Health Services Administration, August 2000. (DHHS publication no. (SMA) 00-3466.)
  3. Jeffcoat AR, Perez-Reyes M, Hill JM, Sadler BM, Cook CE. Cocaine disposition in humans after intravenous injection, nasal insufflation (snorting), or smoking. Drug Metab Dispos 1989;17:153-159.
  4. Ness RB, Grisso JA, Hirschinger N, et al. Cocaine and tobacco use and the risk of spontaneous abortion. N Engl J Med 1999;340:333-339.
  5. Kidwell DA, Blanco MA, Smith FP. Cocaine detection in a university population by hair analysis and skin swab testing. Forensic Sci Int 1997;84:75-86.
  6. Fendrich M, Johnson TP, Sudman S, Wislar JS, Spiehler V. Validity of drug use reporting in a high-risk community sample: a comparison of cocaine and heroin survey reports with hair tests. Am J Epidemiol 1999;149:955-962.
  7. Coleman DL, Ross TF, Naughton JL. Myocardial ischemia and infarction related to recreational cocaine use. West J Med 1982;136:444-446.
  8. Minor RL Jr, Scott BD, Brown DD, Winniford MD. Cocaine-induced myocardial infarction in patients with normal coronary arteries. Ann Intern Med 1991;115:797-806.
  9. Hollander JE, Hoffman RS. Cocaine-induced myocardial infarction: an analysis and review of the literature. J Emerg Med 1992;10:169-177.
  10. Pitts WR, Lange RA, Cigarroa JE, Hillis LD. Cocaine-induced myocardial ischemia and infarction: pathophysiology, recognition, and management. Prog Cardiovasc Dis 1997;40:65-76.
  11. Mittleman MA, Mintzer D, Maclure M, Tofler GH, Sherwood JB, Muller JE. Triggering of myocardial infarction by cocaine. Circulation 1999;99:2737-2741.
  12. Brody SL, Slovis CM, Wrenn KD. Cocaine-related medical problems: consecutive series of 233 patients. Am J Med 1990;88:325-331.
  13. Hollander JE, Todd KH, Green G, et al. Chest pain associated with cocaine: an assessment of prevalence in suburban and urban emergency departments. Ann Emerg Med 1995;26:671-676.
  14. Hollander JE, Hoffman RS, Gennis P, et al. Prospective multicenter evaluation of cocaine-associated chest pain. Acad Emerg Med 1994;1:330-339.
  15. Hollander JE, Hoffman RS, Burstein JL, Shih RD, Thode HC Jr. Cocaine-associated myocardial infarction: mortality and complications. Arch Intern Med 1995;155:1081-1086.
  16. Hollander JE, Hoffman RS, Gennis P, et al. Cocaine-associated chest pain: one-year follow-up. Acad Emerg Med 1995;2:179-184.
  17. Hollander JE, Vignona L, Burstein J. Predictors of underlying coronary artery disease in cocaine associated myocardial infarction: a meta-analysis of case reports. Vet Hum Toxicol 1997;39:276-280.
  18. Gitter MJ, Goldsmith SR, Dunbar DN, Sharkey SW. Cocaine and chest pain: clinical features and outcome of patients hospitalized to rule out myocardial infarction. Ann Intern Med 1991;115:277-282.
  19. Hollander JE, Levitt MA, Young GP, Briglia E, Wetli CV, Gawad Y. Effect of recent cocaine use on the specificity of cardiac markers for diagnosis of acute myocardial infarction. Am Heart J 1998;135:245-252.
  20. Lange RA, Cigarroa RG, Yancy CW Jr, et al. Cocaine-induced coronary-artery vasoconstriction. N Engl J Med 1989;321:1557-1562.
  21. Flores ED, Lange RA, Cigarroa RG, Hillis LD. Effect of cocaine on coronary artery dimensions in atherosclerotic coronary artery disease: enhanced vasoconstriction at sites of significant stenoses. J Am Coll Cardiol 1990;16:74-79.
  22. Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med 1990;112:897-903.
  23. Wilbert-Lampen U, Seliger C, Zilker T, Arendt RM. Cocaine increases the endothelial release of immunoreactive endothelin and its concentrations in human plasma and urine: reversal by coincubation with sigma-receptor antagonists. Circulation 1998;98:385-390.
  24. Mo W, Singh AK, Arruda JA, Dunea G. Role of nitric oxide in cocaine-induced acute hypertension. Am J Hypertens 1998;11:708-714.
  25. Amin M, Gabelman G, Karpel J, Buttrick P. Acute myocardial infarction and chest pain syndromes after cocaine use. Am J Cardiol 1990;66:1434-1437.
  26. Isner JM, Estes NAM III, Thompson PD, et al. Acute cardiac events temporally related to cocaine abuse. N Engl J Med 1986;315:1438-1443.
  27. Brogan WC, Lange RA, Glamann DB, Hillis LD. Recurrent coronary vasoconstriction caused by intranasal cocaine: possible role for metabolites. Ann Intern Med 1992;116:556-561.
  28. Stenberg RG, Winniford MD, Hillis LD, Dowling GP, Buja LM. Simultaneous acute thrombosis of two major coronary arteries following intravenous cocaine use. Arch Pathol Lab Med 1989;113:521-524.}

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