Abstract
A patient with sustained ventricular tachycardia was operated on after an unsuccessful trial of amiodarone. Profound myocardial depression and low cardiac output became evident as he was weaned from cardiopulmonary bypass. Despite inotropic support, use of the intra-aortic balloon pump and left heart assist device, he died. Because of this experience, the authors developed a canine model to determine the effects on left ventricular function of amiodarone given orally. Left ventricular stroke work, cardiac output, ventricular contractility (maximum dP/dt) and peripheral vascular resistance were measured in 12 mongrel dogs at a heart rate of 150 beats/min and at a constant preload of 10 mm Hg. Six animals received the drug orally and the remaining animals were used as sham-operated controls. Maximum dP/dt decreased from 2855 mm Hg/s to 1291 mm Hg/s (p less than 0.01) and left ventricular stroke work was reduced from 48.7 g-m/beat to 21.8 g-m/beat (p less than 0.05) after the administration of amiodarone. Cardiac output and peripheral vascular resistance did not differ significantly. Amiodarone severely depressed left ventricular function in this experiment. The prolonged half-life of this antiarrhythmic combined with its adverse effect on myocardial function suggests that it should not be used in patients with refractory life-threatening ventricular tachycardia who are good candidates for electrophysiologic evaluation and endocardial resection.