Looking back reveals how the direction of therapy for heart failure has changed since the inception of the first large clinical trial of vesnarinone, an inotropic agent, in April 1990. At that time, many investigators remained interested in the concept of heart failure as a defect that could be remedied by drugs that enhanced cardiac contractility.¹ Intravenous dopamine and dobutamine were widely used to increase cardiac output with less chronotropy and fewer arrhythmias than the more potent adrenergic agonists isoproterenol, epinephrine, and norepinephrine. Even though excess mortality was found with long-term outpatient infusions of dobutamine and the oral sympathomimetic amines . . .