Acute effects of intravenous nisoldipine on left ventricular function and coronary hemodynamics

The hemodynamic effects of nisoldipine were investigated in 16 patients with suspected coronary artery disease who underwent routine cardiac catheterization. Nisoldipine was given intravenously in a dose of 6 μg/kg over 3 minutes and measurements made before and after drug administration during spontaneous and matched atrial paced heart rate. During sinus rhythm, nisoldipine produced a significant increase in heart rate (19%, p < 10^-5). Left ventricular systolic pressure decreased 28% (p < 10^-6) and left ventricular end-diastolic pressure did not change significantly (5%, difference not significant). Coronary sinus and great cardiac vein blood flow increased by 21% (p < 0.02) and 25% (p < 0.005), respectively, after nisoldipine administration. Simultaneously, mean aortic pressure decreased 33% (p < 10^-6); consequently, the global and regional coronary vascular resistances decreased by 50% (p < 10^-4). The decreases in global (-8%) and regional (-4%) myocardial oxygen consumption did not reach statistical significance. A 6% (not significant) increase in end-diastolic volume and an 11% (p < 0.002) decrease in end-systolic volume resulted in an increase of 21% in stroke volume (p < 10^-4) with a consistent increase in ejection fraction (+16%, p < 10^-5). Total systemic vascular resistance was reduced by 30% (p < 0.0002). During spontaneous heart rate and matched atrial pacing, the time constant of isovolumic relaxation as assessed by a biexponential model, was significantly shortened. The maximal velocity of isovolumic contraction after nisoldipine was administered remained higher (+12%, p < 0.02) at an identical paced heart rate. Thus, nisoldipine is a potent coronary and peripheral vasodilator. No negative inotropic effects were observed in the dosage used.