Hemodynamics of nicardipine in coronary artery disease

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 β 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 β blocker therapy.