Author + information
- Received February 7, 1993
- Accepted March 8, 1993
- Published online October 1, 1993.
- Jay N. Cohn, MD, FACC∗
- ↵∗Address for correspondence: Jay N. Cohn, MD, Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Box 488 UMHC, 420 Delaware Street SE, Minneapolis, Minnesota 55455.
Vasodilator drugs have been undergoing evaluation as therapy for heart failure for > 20 years. It has become clear that hemodynamic benefits, short-term improvement in exercise tolerance and long-term alteration in mortality are independent end points for efficacy of these drugs. Differing hemodynamic responses, variable effects on exercise capacity and differential effect on mortality of various vasodilator compounds raise the likelihood that vascular smooth muscle relaxation is not the sole mechanism of action of these drugs. Neurohormonal and aitiproliferative effects of these agents may play a key rote in the long-term response. Data from trials indicate that the vasodilator combinatiom of hydralazine and isosorbide dinitrate as well as converting enzyme inhibitors can favorably affect all end points. The global efficacy of other vasodilators, such as calcium antagonists, has not yet been fully evaluated.
Milton Packer, MD, FACC, Chairman
- Received February 7, 1993.
- Accepted March 8, 1993.