Abstract
The belief that a depression of cardiac contractility is the fundamental defect in patients with chronic heart failure has led to the development during the past 20 years of nearly 100 new drugs with positive inotropic activity. Although all these agents exert favorable hemodynamic effects, none have produced consistent improvement in symptoms or exercise tolerance, and many have shortened the survival of patients with heart failure1,2. Questions about efficacy and safety have surfaced regardless of the drug's mechanism of action, but there has been particular concern about agents that act by inhibiting cyclic AMP phosphodiesterase (e.g., milrinone)2. . . .