Cocaine-induced coronary-artery vasoconstriction.

Area of Science:

• Cardiology
• Pharmacology
• Anesthesiology

Background:

• Intranasal cocaine is a common local anesthetic in rhinolaryngologic procedures.
• High-dose recreational cocaine use is linked to cardiac events, but its effects at anesthetic doses on human coronary vasculature are unknown.

Purpose of the Study:

• To investigate the impact of intranasal cocaine, at a dose used for local anesthesia, on coronary artery dimensions, blood flow, and myocardial oxygen demand in patients undergoing cardiac catheterization.

Main Methods:

• A study involving 45 patients undergoing cardiac catheterization.
• Measurements included heart rate, arterial pressure, coronary sinus blood flow (thermodilution), and left coronary artery dimensions (quantitative arteriography) before and after intranasal administration of saline or cocaine (10% cocaine hydrochloride, 2 mg/kg).

Main Results:

• Saline administration had no effect.
• Cocaine administration increased heart rate and arterial pressure, decreased coronary sinus blood flow (149 to 124 ml/min), and reduced left coronary artery diameter by 8-12% (P < 0.01).
• These cocaine-induced changes were reversed by phentolamine and were similar in patients with and without left coronary artery disease.

Conclusions:

• Intranasal cocaine at anesthetic doses induces coronary artery vasoconstriction and reduces coronary blood flow, mediated by alpha-adrenergic stimulation.
• These effects occur despite increased myocardial oxygen demand and are reversible.
• The findings suggest that these vascular effects may be more severe at higher, recreational doses of cocaine.