Author + information
- Received February 9, 1988
- Revision received July 27, 1988
- Accepted July 29, 1988
- Published online January 1, 1989.
- Mihai Gheorghiade, MD, FACC∗,
- Veronica Hall, RN,
- Jeffrey B. Lakier, MD, FACC and
- Sidney Goldstein, MD, FACC
- ↵∗Address for reprints: Mihai Gheorghiade, MD, Heart and Vascular Institute, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, Michigan 48202.
The effects of intravenous captopril and intravenous digoxin given separately and in combination on rest and exercise hemodynamics were studied in 16 patients with severe heart failure and sinus rhythm. When given separately, both captopril and digoxin decreased the pulmonary capillary wedge pressure by, respectively, 24% (p = 0.003) and 34% (p = 0.004) and systemic vascular resistance by 23% (p = 0.09) and 20% (p = 0.03). Only digoxin increased cardiac index by 23 % (p = 0.03) and stroke work index by 52% (p = 0.01).
During maximal exercise, captopril alone decreased systemic vascular resistance by 28% (p = 0.0002) and increased cardiac index by 33% (p = 0.02). Digoxin alone decreased pulmonary capillary wedge pressure by 11 % (p = 0.04) and increased stroke work index by 44% (p = 0.01). The combination of captopril and digoxin resulted in a decrease in pulmonary capillary wedge pressure and systemic vascular resistance and an increase in cardiac index and stroke work index both at rest and during exercise that was greater than values observed with either drug given alone.
Cardiac index response to the combination of captopril and digoxin correlated with baseline serum aldosterone concentration (r = 0.81, p < 0.001) and plasma renin activity (r = 0.74, p < 0.0002). A significant decrease in norepinephrine concentration was noted after digoxin was administered alone or added to captopril.
These findings demonstrate that in patients with severe heart failure, the acute administration of captopril and digoxin has an independent salutary hemodynamic effect. The combination of these agents, however, has an adjunctive effect on cardiac function at rest and during exercise.
☆ This study was presented in part at the 36th Annual Scientific Session of the American College of Cardiology, New Orleans, Louisiana, March 8 to 12, 1987.
- Received February 9, 1988.
- Revision received July 27, 1988.
- Accepted July 29, 1988.