RT Journal Article
SR Electronic
T1 Amrinone in severe congestive heart failure: another look at an intriguing new cardioactive drug.
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 319
OP 326
VO 228
IS 2
A1 J B Hermiller
A1 M E Leithe
A1 R D Magorien
A1 D V Unverferth
A1 C V Leier
YR 1984
UL http://jpet.aspetjournals.org/content/228/2/319.abstract
AB Seven patients with severe congestive heart failure received amrinone i.v. (continuous infusions of 10, 20 and 40 micrograms/kg/min) and orally (1.5, 3.0 and 4.5 mg/kg) in order to determine the comprehensive acute hemodynamic response of this agent. Standard hemodynamic, echocardiographic and systolic time interval measurements were made before and sequentially after amrinone administration. Intravenous amrinone significantly increased cardiac index and stroke volume index, did not alter heart rate and significantly decreased pulmonary capillary wedge pressure, mean systemic blood pressure and systemic and pulmonary vascular resistances. The determinants of left ventricular inotropy, delta P/delta t, pre-ejection period index and velocity of circumferential fiber shortening were not affected by amrinone; dobutamine (5 and 10 micrograms/kg/min), used as an internal standard for inotropy, significantly improved these determinants. Except for a significant reduction in pulmonary capillary wedge pressure, first-dose oral amrinone effected little change in central hemodynamic variables and indices of ventricular inotropy; no additional changes occurred after the fifth dose. In the setting of severe chronic congestive heart failure, short-term iv infusions and oral administration of amrinone elicit only mild to moderate hemodynamic changes. Furthermore, these changes are a result of vasodilation (preload and afterload reduction) rather than positive inotropy.