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

Richard A. Lange, MD; Ricardo G. Cigarroa, MD; Eduardo D. Flores, MD; Wade McBride, MD; Anatole S. Kim, MD; Peter J. Wells, MD; John B. Bedotto, MD; Robert S. Danziger, MD; and L. David Hillis, MD
[+] Article, Author, and Disclosure Information

Grant Support: By ischemic SCOR grant HL 17669 from the National Institutes of Health, Bethesda, Maryland, and a grant from the Texas Affiliate of the American Heart Association, Austin, Texas.

Requests for Reprints: Richard A. Lange, MD, Cardiology Division, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235.

Current Author Addresses: Drs. Lange, Cigarroa, Flores, McBride, Kim, Wells, Bedotto, Danziger, and Hillis: Cardiology Division, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235.

© 1990 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1990;112(12):897-903. doi:10.7326/0003-4819-112-12-897
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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.





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