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Published on: August 21, 2010
Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade
R A Lange1, R G Cigarroa, E D Flores
1University of Texas Southwestern Medical Center, Parkland Memorial Hospital, Dallas.
Insights
Beta-adrenergic blockade potentiates cocaine-induced coronary artery vasoconstriction. These findings suggest that beta-adrenergic blocking agents should be avoided in patients experiencing cocaine-associated myocardial ischemia or infarction.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Cocaine use is associated with cardiovascular complications, including myocardial infarction.
- The role of beta-adrenergic blockade in cocaine-induced coronary vasoconstriction is not fully understood.
Purpose of the Study:
- To investigate whether beta-adrenergic blockade exacerbates cocaine-induced coronary artery vasoconstriction.
Main Methods:
- A randomized, double-blind, placebo-controlled trial was conducted in a cardiac catheterization laboratory.
- Thirty patients undergoing evaluation for chest pain received intranasal cocaine (2 mg/kg) or saline, followed by intracoronary propranolol.
- Measurements included heart rate, arterial pressure, coronary sinus blood flow, and coronary arterial dimensions.
Main Results:
- Cocaine administration increased arterial pressure and rate-pressure product, decreased coronary sinus blood flow, and reduced coronary arterial diameters.
- Subsequent intracoronary propranolol administration further decreased coronary sinus blood flow and increased coronary vascular resistance.
- These changes indicate potentiation of cocaine-induced vasoconstriction by beta-adrenergic blockade.
Conclusions:
- Beta-adrenergic blockade potentiates cocaine-induced coronary vasoconstriction.
- Beta-adrenergic blocking agents should likely be avoided in patients with cocaine-associated myocardial ischemia or infarction.
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 less than 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 less than 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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