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Effects of intravenous and intracoronary nicardipine
1Department of Medicine, University of Florida, Gainesville.
Insights
Nicardipine, a calcium antagonist, significantly increases coronary blood flow and cardiac output in patients. While it causes mild, temporary effects on heart function, its primary action is vasodilation with minimal myocardial depression.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Calcium antagonists are crucial in managing cardiovascular conditions.
- Understanding the specific hemodynamic effects of nicardipine is essential for its clinical application.
Purpose of the Study:
- To investigate the systemic and coronary hemodynamic effects of nicardipine.
- To differentiate between direct myocardial and peripheral vasodilatory effects of nicardipine.
Main Methods:
- Intravenous and intracoronary administration of nicardipine in 30 patients.
- Hemodynamic parameters including coronary blood flow, heart rate, cardiac output, and vascular resistance were measured.
Main Results:
- Intravenous nicardipine increased coronary blood flow, heart rate, stroke volume, and cardiac output, while decreasing systemic and coronary resistance.
- Intracoronary nicardipine showed mild, transient depression of left ventricular function and relaxation.
- Coronary blood flow increase persisted longer than myocardial effects.
Conclusions:
- Nicardipine acts as a relatively selective vasodilator.
- The drug exhibits minimal direct myocardial depressant activity in humans.
Abstract:
The systemic and coronary hemodynamic effects of nicardipine, a calcium antagonist, were studied in 30 patients. Increased coronary blood flow (from 102 +/- 9 to 147 +/- 13 ml/min; p less than 0.001), heart rate (from 69 +/- 3 to 81 +/- 3 beats/min; p less than 0.001), stroke volume (108 +/- 6 to 123 +/- 6 ml; p less than 0.001) and cardiac output (from 7.3 +/- 0.5 to 9.9 +/- 0.5 liters/min; p less than 0.001) were demonstrated in 15 patients administered intravenous nicardipine (2 mg bolus given over 1 minute, followed by infusion of 50 micrograms/min to maintain 10 to 20 mm Hg decrease in systolic blood pressure). Systemic vascular resistance decreased (from 1,183 +/- 70 to 733 +/- 33 dynes s cm-5) as did coronary resistance (from 1.47 +/- 0.1 to 0.7 +/- 0.1 mm Hg/ml/min; p less than 0.001). Other hemodynamic parameters such as left ventricular end-diastolic pressure, stroke volume and work, aortic blood flow and acceleration, ejection and external power, myocardial oxygen consumption and time constant for left ventricular isovolumic relaxation also were evaluated. To distinguish between direct myocardial effects of nicardipine and peripheral effects, 15 patients were given intracoronary nicardipine (0.1 or 0.2 mg) during cardiac catheterization. Nicardipine produced slight depression of left ventricular contractile function and impairment of left ventricular relaxation; but these changes were mild and transient compared with the marked and sustained increase in coronary blood flow that persisted 7 minutes after administration. Thus, nicardipine is a relatively selective vasodilator with minimal direct myocardial depressant activity n humans.