Abstract
For many years digitalis and diuretic agents have been the cornerstones of pharmacologic treatment for patients with heart failure. A potential therapeutic role for vasodilators was first suggested in 1956, when Eichna and coworkers showed that an infusion of the ganglionic blocking agent trimethaphan increased cardiac output and reduced pulmonary-artery wedge pressure in such patients.1 Several years later, the use of intraarterial counterpulsation represented the first step toward deliberately reducing ventricular after-load to alleviate heart failure.2 This intervention was soon followed by the use of intravenous phentolamine3 and then sodium nitroprusside.By 1977, when I was first asked to comment . . .