Intravenous cocaine causes epicardial coronary vasoconstriction in the intact dog.

The effect of intravenous cocaine on coronary artery dynamics in 23 closed-chest dogs was examined. To determine dose-related effects, intravenous cocaine was administered in doses of 1, 3, 6, and 9 mg/kg; saline solution was used in control dogs. Heart rate, aortic pressure, and left anterior descending coronary artery cross-sectional area were measured before and for 60 minutes after each injection. Myocardial blood flow was measured with 15 microns radioactive microspheres at baseline and 30 minutes after administration of cocaine or saline solution. Plasma cocaine, benzoyl ecgonine, and norepinephrine concentrations were measured and correlated with physiologic changes. Cocaine caused sustained dose-dependent vasoconstriction of the left anterior descending coronary artery, which was significant at 15 minutes and maximum at 60 minutes (control = 2 +/- 10%; cocaine, 9 mg/kg = 46 +/- 10% cross-sectional area reduction). There was an immediate but transient reduction in aortic pressure and an elevation of heart rate after the 6 and 9 mg/kg doses and no hemodynamic changes with lower doses. Coronary blood flow was reduced 30 minutes after the 3, 6, and 9 mg/kg doses. Two dogs had refractory ventricular tachycardia after injection of cocaine and were not included in the analysis. Results of this investigation demonstrate angiographic evidence of dose-dependent, cocaine-induced epicardial coronary vasoconstriction and deleterious hemodynamic abnormalities at commonly used doses of cocaine. These results demonstrate a mechanism for the development of angina and myocardial infarction associated with cocaine use.