Related Experiment Videos
Influence of labetalol on cocaine-induced coronary vasoconstriction in humans
J D Boehrer1, D J Moliterno, J E Willard
1Department of Internal Medicine (Cardiovascular Division), University of Texas Southwestern Medical Center, Dallas 75235.
Insights
Labetalol does not alleviate cocaine-induced coronary vasoconstriction in patients with chest pain, though it does lower blood pressure. This study investigated labetalol
Area of Science:
- Cardiology
- Pharmacology
- Toxicology
Background:
- Cocaine use is associated with chest pain and cardiovascular events.
- Labetalol is sometimes used for cocaine-associated chest pain.
- The effect of labetalol on cocaine-induced coronary vasoconstriction is not well understood.
Purpose of the Study:
- To determine if labetalol alleviates cocaine-induced coronary vasoconstriction.
- To assess the impact of labetalol on hemodynamic parameters in patients with cocaine-associated chest pain.
Main Methods:
- A study involving 15 patients undergoing cardiac catheterization for chest pain.
- Measurements included heart rate, mean arterial pressure, and coronary arterial area via quantitative angiography.
- Patients received intranasal cocaine (2 mg/kg) followed by intravenous saline or labetalol (0.25 mg/kg).
Main Results:
- Cocaine significantly decreased coronary arterial area by 13% in most analyzed segments.
- Saline administration did not alter any measured variables.
- Labetalol reduced mean arterial pressure but did not affect coronary arterial area.
Conclusions:
- Labetalol effectively lowers cocaine-induced increases in mean arterial pressure.
- Labetalol does not mitigate cocaine-induced coronary vasoconstriction.
- These findings suggest alternative strategies may be needed for managing cocaine-associated coronary vasospasm.
Purpose:
Although labetalol is sometimes given to patients with cocaine-associated chest pain, its influence on cocaine-induced coronary vasoconstriction is unknown.
Patients And Methods:
In 15 patients (7 men, 8 women, aged 40 to 79 years) undergoing catheterization for chest pain, heart rate, mean arterial pressure, and coronary arterial area (by computer-assisted quantitative angiography) were measured (1) at baseline, (2) 15 minutes after intranasal cocaine, 2 mg/kg, then (3) 5 minutes after intravenous saline (n = 6) or labetalol, 0.25 mg/kg (n = 9).
Results:
Of 40 coronary arterial segments analyzed, cocaine induced a 13% +/- 10% (mean +/- standard deviation) decrease in coronary arterial area in 32. Subsequently, no variable changed after saline administration. Although labetalol reduced mean arterial pressure (117 +/- 14 mm Hg after cocaine, 110 +/- 11 mm Hg after labetalol; p < 0.05), it induced no change in the coronary arterial area (3.47 +/- 1.37 mm2 after cocaine, 3.37 +/- 1.32 mm2 after labetalol; p = NS).
Conclusion:
Labetalol reverses the cocaine-induced rise in mean arterial pressure, but does not alleviate cocaine-induced coronary vasoconstriction.