Relative contribution of inotropic and vasodilator effects to amrinone-induced hemodynamic improvement in congestive heart failure

Abstract

The relative contribution of inotropic and vasodilator effect to amrinone-induced hemodynamic improvement in congestive heart failure (CHF) is unknown. In 9 patients with CHF, the effects of amrinone and nitroprusside on hemodynamic and radionuclide measurements were compared to determine whether reduced afterload accounts for the anvinone-induced decrease in left ventricular end-systolic volume. In each patient, the end-systolic pressure-volume relation was derived using nitroprusside. After terminating nitroprusside treatment, intravenous amrinone (3 mg/kg) caused end-systolic volume to decrease from 148 ± 35 ml/m 2 (mean ± standard deviation) to 133 ± 32 ml/m 2 (p <0.05), causing an increase in cardiac index from 1.9 ± 0.8 to 2.7 ± 0.8 liters/min/m 2 (p <0.001). Arterial end-systolic pressure decreased in all patients during amrinone administration, from 96 ± 22 to 84 ± 19 mm Hg (p <0.005), as did systemic vascular resistance. Nitroprusside doses needed to match the decrease in LV end-systolic volume induced by amrinone caused significantly greater decreases in arterial end-systolic pressure than did amrinone (p <0.01). The amrinone-induced decrease in end-systolic volume exceeded that predicted for a pure vasodilator based on arterial end-systolic pressure and the nitroprusside-derived pressure-volume relation in 6 patients. In 3 patients, the decrease in ends-systolic volume did not exceed that expected for a pure vasodilator. In conclusion, after amrinone treatment, afterload reduction occurs in all patients with severe CHF and is the sole effect in some. However, the overall amrinone-induced improvement in LV end-systolic volume and cardiac index exceeds that expected for a pure vasodilator, indicating an inotropic contribution to the hemodynamic response.