Administration of the angiotensin converting enzyme inhibitor SQ20,881 improved cardiac function in all 8 patients with congestive heart failure by decreasing afterload and total vascular resistance.
Observational (n=8)
The etiology of afterload elevation in congestive cardiac failure is unclear, but experimental evidence suggests a role for the renin-angiotensin system in maintaining elevated peripheral vascular resistance. The angiotensin converting enzyme inhibitor SQ20,881 was administered to eight patients with congestive cardiac failure (four hypertensives, four normotensives) during or one day after diagnostic cardiac catheterization. Various hemodynamic measurements performed before and during blockade indicate that this agent caused improvement in cardiac function in all patients by decreasing afterload. This improvement correlated with the decrease in total vascular resistance but was independent of the baseline blood pressure and plasma renin activity. These results suggest that inhibition of angiotensin converting enzyme is a worthwhile approach to the treatment of congestive heart failure, although its exact mechanism of action remains unclear.
Gavras et al. (Wed,) conducted a observational in Congestive heart failure (n=8). SQ20,881 (angiotensin converting enzyme inhibitor) was evaluated on Hemodynamic measurements including cardiac function and afterload. Administration of the angiotensin converting enzyme inhibitor SQ20,881 improved cardiac function in all 8 patients with congestive heart failure by decreasing afterload and total vascular resistance.
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