Amrinone is an effective inotropic agent, but its electrophysiologic effects in humans have not been previously determined. Fifteen patients with congestive heart failure (CHF) New York Heart Association functional class II to IV, underwent an electrophysiologic study after withdrawal of all other cardioactive drugs before and after 10 to 20 μg/kg/min of intravenous amrinone (doses that increased cardiac index and decreased pulmonary capillary wedge pressure and systemic vascular resistance, p < 0.002). Amrinone caused no change in PR, QRS, QTc, AH or HV intervals or maximal corrected sinus node recovery time and had no significant effect on the ventricular effective refractory periods. Amrinone decreased the atrial effective refractory period from 256 ± 40 to 240 ± 38 ms (p = 0.015), and the atrioventricular (AV) nodal functional refractory period from 374 ± 65 to 356 ± 64 ms (p < 0.05), and enhanced maximal 1:1 AV nodal conduction from 371 ± 46 to 334 ± 47 ms (p = 0.006). Nine patients had baseline HV prolongation; this was not affected by amrinone. The frequency of inducible ventricular tachycardia was not significantly affected by amrinone. Holter recordings (24 to 48 hours) were obtained from 10 patients before and after acute oral amrinone dosing (75 to 150 mg every 8 hours). There was no change in the number of ventricular premature contractions per 24 hours (2,197 ± 3,305 vs 2,616 ± 2,436) or number of runs of ventricular tachycardia per 24 hours (10 ± 12 vs 12 ± 13); however, the number of ventricular couplets per 24 hours increased from 22 ± 34 to 52 ± 55 (p = 0.054). Thus, amrinone is safe to use in patients with intraventricular conduction disturbances. It shortens the atrial effective and AV nodal functional refractory period and enhances AV nodal conduction, and it has minimal effects on ventricular arrhythmogenesis during acute drug administration.
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine