The effects of amrinone, dobutamine, and a combination of the two drugs on peak positive left ventricular dP/dt and left ventricular performance were evaluated in 11 patients with chronic congestive heart failure. When administered alone, both dobutamine (10.9 gg/kg/min) and intravenous amrinone (1.9 mg/kg/min) significantly increased left ventricular dP/dt and performance. When compared with dobutamine alone, the addition of amrinone resulted in further increases in left ventricular dP/dt and cardiac index (to 1319 ± 419 from 1202 ± 376 mm Hg/sec, p < .002, and to 3.56 ± 0.78 from 3.04 ± 0.67 liters/min/m2, p < .01, respectively). The combination also induced a further reduction in left ventricular end-diastolic pressure (to 15.3 ± 11.3 from 18.2 ± 10.3 mm Hg, p < .05) when compared with amrinone alone. The combination of dobutamine and amrinone increased heart rate slightly when compared with either drug alone, but did not further reduce systemic arterial pressure when compared with amrinone alone. The dose-response curve of left ventricular dP/dt and performance during titration of dobutamine with and without the addition of intravenous amrinone was evaluated in seven patients. The addition of amrinone to any dose of dobutamine produced higher cardiac index and lower systemic vascular resistance than dobutamine or amrinone alone. Thus, when compared with dobutamine alone in patients with chronic congestive heart failure, the addition of intravenous amrinone to dobutamine results in an additive improvement in left ventricular performance throughout the dose range. Circulation 74, No. 2, 367-373, 1986. DOBUTAMINE is a synthetic catecholamine that directly stimulates myocardial /,-adrenergic receptors.It has been used extensively to improve myocardial contractility and ventricular performance in patients with acute left ventricular dysfunction or decompensated congestive heart failure.", 2 Dobutamine is usually well tolerated. Through its effects on cardiac mechanics and hemodynamics, it has the potential to alter myocardial oxygen utilization (MVO2) in several different ways. By increasing contractility and heart rate, it may increase MVO2, but the simultaneous reduction in wall tension tends to lower oxygen use. In some situations the stimulation of contractility and heart rate may outweigh the reduction in wall tension to