JAPANESE CIRCULATION JOURNAL
Online ISSN : 1347-4839
Print ISSN : 0047-1828
ISSN-L : 0047-1828
Clinical Study
Determining the Optimum Dose for the Intravenous Administration of Nicardipine in the Treatment of Acute Heart Failure
A Multicenter Study
Yuzo HirotaChuichi KawaiRyohei HoriKatsuhiko OkumuraMasahiko KinoshitaToshiaki KumadaHiroshi OgawaKeishiro KawamuraReizo Kusukawafor the Nicardipine Heart Failure Study Group
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1997 年 61 巻 5 号 p. 367-374

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Nicardipine is a potent arteriolar vasodilator with a negligible negative inotropic effect. Although intravenous administration of this drug has been reported to be effective in the treatment of heart failure, the optimal dose by this route is not clear. This study was designed to determine the optimum dose for the intravenous infusion of nicardipine in the treatment of heart failure. In Trial 1, nicardipine was administered intravenously at a dose of 0.5 μg/kg per min to 14 patients with acute heart failure. The dose was increased to 1.0 μg/kg per min in 13 cases with marked improvement at 2 h. In Trial 2, nicardipine was administered in a double-blind manner to 53 patients at 3 different rates of infusion for 2 h: 1.0 (Group 1, n=19), 2.0 (Group 2, n=15), and 3.0 (Group 3, n=19)μg/kg per min. Neither heart rate nor mean right atrial pressure changed in any of the 3 groups. Favorable hemodynamic effects were evident in all groups beginning 30 min after the start of infusion, with an increase in cardiac index (control vs 2 h after infusion, L/min per m2)(Group 1: 2.2±0.4 vs 3.1±0.8, Group 2: 2.2±0.4 vs 2.9±0.5, Group 3: 2.3±0.3 vs 3.1±0.7, all p<0.01 compared to the control) and a decrease in diastolic pulmonary artery pressure (Group 1: 26±10 vs 19±7, Group 2: 27±10 vs 20±8, Group 3: 26±7 vs 18±5 mmHg, all p<0.01). The decrease in systolic pressure was greatest in Group 3 (Group 1: 141±31 vs 119±18, Group 2: 149±25 vs 118±17, Group 3; 147 ±27 vs 107±14 mmHg, all p<0.01 compared to control, and p<0.05 between Groups 1 and 3). The intravenous drip infusion of nicardipine is effective in the treatment of heart failure by inducing an increase in cardiac output and a decrease in pulmonary artery wedge pressure. The optimal dose in this study was 1.0 μg/kg per min. (Jpn Circ J 1997; 61: 367 - 374)

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© 1997 THE JAPANESE CIRCULATION SOCIETY
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