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.
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