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 β-blockade, nicardipine (5 or 10 mg i.v.) increased heart rate (+ 23 and + 15 beats/min after 5 and 10 mg, respectively; p < 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 < 0.005). Systemic vascular resistance decreased with both doses (−46 and −57%; p < 0.005), whereas mean aortic pressure decreased by 14 mm Hg after 5 mg and by 28 mm Hg after 10 mg (p < 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 < 0.008) and velocity of shortening. Peak (+) dP/dt and (dP/dt)/DP40(value of dPIdt at a developed pressure of 40 mm Hg) were unchanged, and Emax, the maximal left ventricular pressure/volume ratio, improved slightly (+8%; p < 0.05). After β-blockade, nicardipine (2.5 mg i.v.) still decreased mean aortic pressure (−16 mm Hg; p < 0.05) and systemic vascular resistance, and irnproved the ejection phase indices; cardiac output and ventricular relaxation, both depressed after propranolol administration, were also normalized after infusion of nicardipine. Further, after infusion of propranolol, nicardipine did not modify the isovolumic indexes of inotropic state or Emax. In conclusion, nicardipine is a powerful arteriodilator without detectable negative inotropic effects in vivo.