Author + information
- Received August 6, 1992
- Revision received June 25, 1993
- Accepted June 25, 1993
- Published online November 15, 1993.
- Mark J. Eisenberg, MD, MPH∗,
- John Mendelson, MD,
- G.Thomas Evans Jr., MD,
- John Jue, MD, FRCP(C) FACC,
- Resse T. Jones, MD and
- Nelson B. Schiller, MD, FACC
- ↵∗Address for correspondence: Dr. Mark J. Eisenberg, Moffitt 1186/Box 0124; University of California, 505 Parnassus Avenue, San Francisco, California 94143.
Objectives. We tested the hypothesis that intravenous cocaine, in doses commonly self-administered in nonmedical settings, causes acute myocardial ischemia and left ventricular dysfunction.
Background. Cocaine-induced cardiac complications are responsible for a growing number of deaths in young people, but the mechanism by which cocaine induces complications is unclear.
Methods. We performed 12-lead electrocardiography and quantitative two-dimensional echocardiography in 20 subjects before and after single intravenous doses of high dose cocaine (1.2 mg/kg body weight), low dose cocaine (0.6 mg/kg) and placebo.
Results. At 2 to 7 min after cocaine administration, the rate-pressure product was increased significantly from baseline (high dose 73%, low dose 63%, placebo 8%, p < 0.001 for either dose vs. placebo). During this time, electrocardiography demonstrated dose-related nonspecific changes (high dose in 14 of 20 subjects, low dose in 9 of 20 subjects, placebo in 2 of 20 subjects, p < 0.002 for either dose vs. placebo). In contrast, echocardiography showed that the frequency of hyperdynamic left ventricular wall segmented doubled after high dose cocaine compared with placebo (34% [108 of 318] vs. 16% [51 of 319], respectively, p = 0.0001) but that there was no change in either left ventricular ejection fraction (high dose 66 ± 9%, placebo 67 ± 6%, p = NS) or wall motion score index (high dose 0.67 ± 0.44, placebo 0.85 ±0.30, p = NS).
Conclusions. We concluded that cocaine, in doses commonly self-administered in nonmedical settings, does not cause acute myocardial ischemia or left ventricular dysfunction. We speculate that cocaine-induced cardiac complications are caused by idiosyncratic coronary artery vasospasm, by exceptionally high dosages or by cocaine-induced coronary artery thrombosis.
☆ This study was supported in part by Grants DA02829, DA010696 and DA00053 from the National Institutes of Health, Bethesda, Maryland and Contract 90-IJ-CX-0012, from the Department of Justice, Washington, D.C. Dr. Eisenberg was supported by an Institutional National Research Service Award (HL07192), Training Program in Heart and Vascular Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
☆☆ All editorial decisions for this article, including selection of referees, were made by a Guest Editor. This policy applies to all articles with authors from the University of California, San Francisco.
- Received August 6, 1992.
- Revision received June 25, 1993.
- Accepted June 25, 1993.