Effects of nicardipine on left ventricular function and energetics in man

The effects of nicardipine, a new dihydropyridine calcium antagonist, on left ventricular function and energetics were studied in 13 patients. Nicardipine was administered as a 2 mg bolus (i.v.) followed by an infusion titrated to maintain a 10-20 mm Hg decrease in systolic pressure. Nicardipine increased heart rate 19% (P less than 0.001) while left ventricular end-diastolic pressure was not significantly changed and stroke volume (ml) increased 13% (P less than 0.01). Peak values for the first and second time derivatives of left ventricular pressure were increased by 26% (P less than 0.01) and 50% (P less than 0.02) respectively. Peak aortic blood flow, peak aortic blood acceleration, and the peak rate of change of ejection power were increased 86% (P less than 0.001), 123% (P less than 0.01), and 113% (P less than 0.001), respectively. Stroke work was not changed during nicardipine infusion. External power increased by 40% (P less than 0.01); however, the ratio of oscillatory to total power was not significantly different. Although the product of heart rate and systolic aortic pressure was not significantly altered with nicardipine, myocardial oxygen consumption increased 18% (P less than 0.02) with a disproportionate increase in coronary blood flow of 41% (P less than 0.001) and decrease in coronary resistance of 39% (P less than 0.001). The time constant for left ventricular isovolumic relaxation decreased 22% (P less than 0.001) during nicardipine infusion while the minimum value of dP/dt was unchanged. Thus, when administered intravenously in man, nicardipine is a potent coronary and systemic vasodilator producing reflex tachycardia, increased indices of myocardial contractile state, and improved isovolumic relaxation with an associated increase in myocardial oxygen consumption.