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

TLDR

The study aimed to assess whether beta‑adrenergic blockade increases cocaine‑induced coronary vasoconstriction. In a randomized, double‑blind, placebo‑controlled trial at an urban teaching hospital, 30 stable chest‑pain patients underwent cardiac catheterization, with measurements taken before and after intranasal saline or cocaine (2 mg/kg) and after intracoronary propranolol (2 mg). Cocaine raised arterial pressure, reduced coronary flow, and narrowed vessels, and intracoronary propranolol further worsened flow and resistance, demonstrating that beta‑adrenergic blockade potentiates cocaine‑induced coronary vasoconstriction.

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 saline or 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 · min); and coronary arterial diameters decreased by between 6% and 9% (P < 0.05 for all variables). Subsequently, intracoronary propranolol 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 · 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.