TY - JOUR
T1 - Intravenous fenoldopam in heart failure
T2 - Comparing the hemodynamic effects of dopamine1 receptor agonism with nitroprusside
AU - Young, James B.
AU - Leon, Carlos A.
AU - Pratt, Craig
AU - Kingry, Connie
AU - Taylor, Addison A.
AU - Roberts, Robert
N1 - Funding Information:
From the Sections of Cardiology, gy and The Multi Organ Transplant Baylor College of Medicine. Computational assistance provided by the CLINFO Grant RR-00350, Division of Research Resources, Health, Bethesda, Md. This project was partially grant from Smith, Kline & French Laboratories,
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 1988/2
Y1 - 1988/2
N2 - Dopamine1 receptors mediate hemodynamic effects that may be beneficial in patients with congestive heart failure. We infused the selective dopamine1 receptor agonist, fenoldopam mesylate (SKF 82526 J), to evaluate hemodynamic and neurohumoral changes during continuous intravenous infusion in patients with congestive heart failure and compared them with the effects of nitroprusside, a traditional vasodilator that works by a distinctly different mechanism. In 15 patients with a mean radionuclide ejection fraction of 17%, the agents were infused in a random-ordered, double-blinded, crossover, active drug-controlled protocol after optimal dosing was determined during a titration period. Hemodynamic changes were induced in minutes with both drugs during a mean (±standard deviation) infusion dose of 1.45 ± 1.66 μg/kg/min for fenoldopam and 2.99 ± 1.59 μg/kg/min for nitroprusside. At 1 hour, mean blood pressure decreased and cardiac index rose with both drugs, and the effect lasted throughout the 6-hour infusion period. Nitroprusside, but not fenoldopam, reduced right heart filling pressures (including mean pulmonary capillary wedge, mean right atrial, and mean pulmonary artery pressures) during the infusion period. Both drugs caused significant reduction in systemic vascular and pulmonary arteriolar resistances. No significant change occurred in plasma norepinephrine levels. Fenoldopam ameliorates some of the adverse hemodynamic changes that occur during heart failure but does not reduce right heart filling pressures as does nitroprusside. Because of fenoldopam's unique characteristics, it may benefit certain patients with heart failure.
AB - Dopamine1 receptors mediate hemodynamic effects that may be beneficial in patients with congestive heart failure. We infused the selective dopamine1 receptor agonist, fenoldopam mesylate (SKF 82526 J), to evaluate hemodynamic and neurohumoral changes during continuous intravenous infusion in patients with congestive heart failure and compared them with the effects of nitroprusside, a traditional vasodilator that works by a distinctly different mechanism. In 15 patients with a mean radionuclide ejection fraction of 17%, the agents were infused in a random-ordered, double-blinded, crossover, active drug-controlled protocol after optimal dosing was determined during a titration period. Hemodynamic changes were induced in minutes with both drugs during a mean (±standard deviation) infusion dose of 1.45 ± 1.66 μg/kg/min for fenoldopam and 2.99 ± 1.59 μg/kg/min for nitroprusside. At 1 hour, mean blood pressure decreased and cardiac index rose with both drugs, and the effect lasted throughout the 6-hour infusion period. Nitroprusside, but not fenoldopam, reduced right heart filling pressures (including mean pulmonary capillary wedge, mean right atrial, and mean pulmonary artery pressures) during the infusion period. Both drugs caused significant reduction in systemic vascular and pulmonary arteriolar resistances. No significant change occurred in plasma norepinephrine levels. Fenoldopam ameliorates some of the adverse hemodynamic changes that occur during heart failure but does not reduce right heart filling pressures as does nitroprusside. Because of fenoldopam's unique characteristics, it may benefit certain patients with heart failure.
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U2 - 10.1016/0002-8703(88)90485-1
DO - 10.1016/0002-8703(88)90485-1
M3 - Article
C2 - 2893527
AN - SCOPUS:0023846722
SN - 0002-8703
VL - 115
SP - 378
EP - 384
JO - American Heart Journal
JF - American Heart Journal
IS - 2
ER -