Recurrent Coronary Vasoconstriction Caused by Intranasal Cocaine: Possible Role for Metabolites

Abstract

To define the temporal characteristics of cocaine-induced coronary vasoconstriction in humans and to assess the relation between cocaine-induced coronary vasoconstriction and the blood concentration of cocaine and its main metabolites. Randomized, double-blind, controlled clinical trial. Cardiac catheterization laboratory of a large teaching hospital. Eighteen patients (16 men and 2 women, 37 to 65 years of age) having catheterization for evaluation of chest pain. At catheterization, patients received intranasal saline (8 patients) or cocaine, 2 mg/kg body weight (10 patients). Cineangiographic examination of the left coronary artery and quantitation of the blood concentration of cocaine and its metabolites were done before (baseline) and 30, 60, and 90 minutes after administration of intranasal saline or cocaine. In response to cocaine, proximal coronary arterial diameter decreased from 2.4 +/- 1.6 mm (mean +/- SD) at baseline to 2.0 +/- 1.4 mm at 30 minutes (P less than 0.05). This change corresponded temporally to the peak blood concentration of cocaine. At 60 minutes, the cocaine concentration decreased and coronary artery diameter returned to baseline (2.3 +/- 1.6 mm) (P greater than 0.05 compared with baseline). At 90 minutes, all patients had recurrent vasoconstriction (1.9 +/- 1.4 mm, P less than 0.05) despite a further decrease in the blood cocaine concentration. This vasoconstriction corresponded temporally with an increasing blood concentration of cocaine's main metabolites, benzoylecgonine and ethyl methyl ecgonine. No changes were observed in the control group. Intranasal cocaine causes recurrent coronary vasoconstriction, which may be due to its metabolites.