Digitalis: Reappraisal of its Use after Acute Myocardial Infarction

Digitalis is a potent inhibitor of sarcolemmal sodium (Na+), potassium (K+)-ATPase, and, through this property, effects net movement of calcium (Ca++) into the myocardial cell. Augmented contractility probably directly results from increased concentrations of activator Ca++ available to the contractile elements. The clinical manifestations of digitalis toxicity are due to intracellular K+ depletion, which is an obligatory consequence of Na+, K+-ATPase inhibition.Digitalis, as a positive inotropic agent, also augments myocardial energy consumption in the nonfailing heart. However, when digitalis is employed in the enlarged, failing heart, a simultaneous reduction in the intramyocardial tension leaves net myocardial oxygen balance unchanged or improved. Digitalis has no unique effect on myocardial energy metabolism. Digitalis acutely increases peripheral vascular resistance in man. Through sympathetically mediated responses, digitalis dilates peripheral blood vessels in patients with heart failure. The direct action of digitalis on the coronary vascular bed is uncertain. In ischemic heart muscle, digitalis can improve contractility, but at a metabolic price. The extent to which myoca