Related Experiment Videos
Hemodynamics of nicardipine in coronary artery disease
Insights
Nicardipine, a calcium antagonist, effectively reduces vascular resistance and improves cardiac output. It demonstrates minimal impact on myocardial contractility, even in heart failure patients on beta blockers.
Area of Science:
- Cardiovascular Pharmacology
- Clinical Cardiology
Background:
- Calcium antagonists modulate cardiovascular hemodynamics through peripheral and coronary arterial vasodilation, and negative inotropic effects.
- The net hemodynamic impact of calcium antagonists depends on the balance of these individual actions.
Purpose of the Study:
- To evaluate the hemodynamic effects of intravenous nicardipine, a novel dihydropyridine calcium antagonist.
- To assess nicardipine's efficacy in patients with and without beta-blockade, including those with chronic heart failure and compromised left ventricular function.
Main Methods:
- Intravenous administration of nicardipine.
- Hemodynamic monitoring including systemic vascular resistance, cardiac output, left ventricular ejection fraction, and pressures.
- Assessment during rest, exercise, and intracoronary administration compared to nifedipine.
Main Results:
- Intravenous nicardipine significantly reduced systemic vascular resistance and increased cardiac output and left ventricular ejection fraction.
- Nicardipine prevented increases in end-diastolic pressure during exercise and augmented ejection fraction in heart failure.
- Intracoronary nicardipine showed minimal effects on left ventricular contractility and end-diastolic pressure compared to nifedipine.
Conclusions:
- Nicardipine is a potent systemic vasodilator with minimal negative inotropic effects.
- Its favorable hemodynamic profile is maintained even in patients with compromised cardiac function or on beta-blocker therapy.
Abstract:
Calcium antagonists influence cardiovascular hemodynamics by 3 actions: peripheral arterial dilatation, coronary arterial dilatation and negative inotropic effect. The net hemodynamic effects vary depending on the relative strength of each action. Intravenous administration of the new compound nicardipine, a dihydropyridine derivative with calcium antagonist activity that is chemically related to nifedipine, induced a marked reduction of systemic vascular resistance in patients with and without beta blockade. This was accompanied by an increase in cardiac output and left ventricular ejection fraction. In addition, end-diastolic pressure, peak (+) dP/dt and dP/dt measured at a developed pressure of 40 mm Hg and normalized for this pressure remained unchanged. The time constant of isovolumetric pressure drop during the first 40 ms also decreased. Intravenous administration of nicardipine prevented a marked increase in end-diastolic pressure during exercise, and augmented left ventricular ejection fraction in chronic heart failure. At doses producing similar increases in coronary sinus blood flow, intracoronary administration of nicardipine, unlike nifedipine, has little effect on left ventricular contractility and end-diastolic pressure. Nicardipine is a powerful systemic vasodilator with minimal effects on myocardial inotropic state, even in patients with compromised left ventricular function and patients receiving beta blocker therapy.