Potentiation of Cocaine-Induced Coronary Vasoconstriction by Beta-Adrenergic Blockade

Abstract

Study Objective: To determine whether beta-adrenergic blockade augments cocaine-induced coronary artery vasoconstriction. Design: Randomized, double-blind, placebo-controlled trial. Setting: A cardiac catheterization laboratory in an urban teaching hospital. Patients: Thirty clinically stable patient volunteers referred for catheterization for evaluation of chest pain. Interventions: Heart rate, arterial pressure, coronary sinus blood flow (by thermodilution), and epicardial left coronary arterial dimensions were measured before and 15 minutes after intranasal salineo r cocaine administration (2 mg/kg body weight) and again after intracoronary propranolol administration (2 mg in 5 minutes). Measurements and Main Results: No variables changed after saline administration. After cocaine administration, arterial pressure and rate-pressure product increased; coronary sinus blood flow fell (139 .+-. 28 [mean .+-. SE] to 120 .+-. 20 mL/min); coronary vascular resistance (mean arterial pressure divided by coronary sinus blood flow) rose (0.87 .+-. 0.10 to 1.05 .+-. 0.10 mm Hg/mL .cntdot. min); and coronary arterial diameters decreased by between 6% and 9% (P < 0.05 for all variables). Subsequently, intracoronary propronolol administration caused no change in arterial pressure or rate-pressure product but further decreased coronary sinus blood flow (to 100 .+-. 14 mL/min) and increased coronary vascular resistance (to 1.20 .+-. 0.12 mm Hg/mL .cntdot. min) (P < 0.05 for both). Conclusions: Cocaine-induced coronary vasoconstriction is potentiated by beta-adrenergic blockade. Beta-adrenergic blocking agents probably should be avoided in patients with cocaine-associated myocardial ischemia or infarction.