This project was supported by a Haas Foundation Grant from the Mount Sinai Medical Center and a grant from the Department of Emergency Medicine of MetroHealth Medical Center.
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Cocaine and Ethanol: Combined Effects on Coronary Artery Blood Flow and Myocardial Function in Dogs
Article first published online: 22 JUN 2009
DOI: 10.1111/j.1553-2712.2009.00443.x
© 2009 by the Society for Academic Emergency Medicine
Additional Information
How to Cite
Wilson, L. D., Malik, M. and Willson, H. (2009), Cocaine and Ethanol: Combined Effects on Coronary Artery Blood Flow and Myocardial Function in Dogs. Academic Emergency Medicine, 16: 646–655. doi: 10.1111/j.1553-2712.2009.00443.x
Presented at the Society for Academic Emergency Medicine Annual Meeting, Atlanta, GA, May 2001.
Publication History
- Issue published online: 1 JUL 2009
- Article first published online: 22 JUN 2009
- Received December 15, 2008; revision received February 12, 2009; accepted March 18, 2009.
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Keywords:
- cocaine;
- ethanol;
- coronary blood flow;
- cocaethylene;
- cardiac arrhythmia;
- myocardial depression
Abstract
Objectives: In combination, cocaine and ethanol are more cardiotoxic than is either substance alone. These substances together constitute a drug abuse combination that commonly results in fatality. Previously the authors have demonstrated that cardiotoxicity of cocaine and ethanol is in part due to synergistic myocardial-depressant effects. However, it remains unclear whether this myocardial depression is associated with concomitant adverse effects on coronary blood flow in relation to these substances. The aim of this study was to investigate combined effects of cocaine and ethanol on myocardial blood flow, in relation to indices of myocardial function.
Methods: Anesthetized dogs were instrumented for hemodynamic monitoring with Doppler flow probes placed on the circumflex and left anterior descending (LAD) coronary arteries. Dogs were randomized to three groups (each n = 6): ethanol (E, 1.5 g/kg followed by placebo), cocaine (C, placebo followed by cocaine, 7.5 mg/kg IV), or cocaine plus ethanol (C + E). All measurements were made at control, after placebo or ethanol, and then at fixed time intervals after cocaine or placebo bolus over 3 hours.
Results: In both the C + E and the C groups, circumflex blood flow (CBF) decreased by 71% (95% confidence interval [CI] = 56% to 85%) and 57% (95% CI = 43% to 72%, both p < 0.04 vs. baseline) immediately after cocaine bolus. This was associated with transient depression of cardiac output, myocardial contractile function, and rate-pressure product (RPP), all indices of myocardial oxygen demand. A subsequent rebound increase of coronary sinus blood flow (CSBF) of 56% (95% CI = 26% to 137%, p < 0.03) compared to baseline occurred only in the C group and was associated with increases of myocardial contractile function and RPP. In the C + E group, 2 hours after drug administration, there was a decrease in CSBF of 49% (95% CI = 32% to 67%; p < 0.01) compared to baseline, which was associated with concomitant numerical decreases of the indices of myocardial oxygen demand and accumulation of cocaethylene.
Conclusions: Acute decreases in myocardial flow secondary to cocaine, and cocaine and ethanol in combination, were similar and temporally associated with cocaine’s direct myocardial-depressant effects. Rebound increases in myocardial function and blood flow due to cocaine were attenuated by ethanol. Delayed myocardial depression and decreases in myocardial blood flow were observed only with coadministration of cocaine and ethanol.