Hemodynamic and cardiac effects of nicardipine in patients with coronary artery disease.

The hemodynamic and cardiac effects of the calcium antagonist nicardipine, alone (n = 10 patients) or combined with propranolol (0.1 mg/kg i.v.; n = 9 patients), were assessed in patients with coronary artery disease. In the absence of beta-blockade, nicardipine (5 or 10 mg i.v.) increased heart rate (+23 and +15 beats/min after 5 and 10 mg, respectively; p less than 0.01) and cardiac output (from 4.7 +/- 1.1 to 7.4 +/- 1.3 L/min after 5 mg and from 5.1 +/- 1.1 to 8.6 +/- 1.6 L/min after 10 mg; p less than 0.005). Systemic vascular resistance decreased with both doses (-46 and -57%; p less than 0.005), whereas mean aortic pressure decreased by 14 mm Hg after 5 mg and by 28 mm Hg after 10 mg (p less than 0.004); left ventricular end-diastolic pressure was unchanged. Nicardipine also decreased significantly end-systolic left ventricular volume and increased ejection fraction (from 63 to 71% after 5 mg and from 54 to 63% after 10 mg; p less than 0.008) and velocity of shortening. Peak (+) dP/dt and (dP/dt)/DP40 (value of dP/dt at a developed pressure of 40 mm Hg) were unchanged, and Emax, the maximal left ventricular pressure/volume ratio, improved slightly (+8%; p less than 0.05). After beta-blockade, nicardipine (2.5 mg i.v.) still decreased mean aortic pressure (-16 mm Hg; p less than 0.05) and systemic vascular resistance, and improved the ejection phase indices; cardiac output and ventricular relaxation, both depressed after propranolol administration, were also normalized after infusion of nicardipine.(ABSTRACT TRUNCATED AT 250 WORDS)