Central and peripheral hemodynamic effects of angiotensin inhibition in patients with refractory congestive heart failure.

The central and peripheral hemodynamic responses to the angiotensin-converting enzyme inhibitor teprotide (SQ20881) were simultaneously determined in 10 patients with severe, refractory congestive heart failure using Swan-Ganz catheterization and venous-occlusion calf plethysmography. Significant declines in mean arterial pressure (82.5 ± 4.9 to 67.1 4 5.0 mm Hg [SEM], p < 0.001), systemic vascular resistance (1787 ± 130 to 1272 i 115 dyn-sec-cm-5, p < 0.001) and mean pulmonary capillary wedge pressure (26.8 ± 2.5 to 17.1 ± 2.5 mm Hg, p < 0.001) accompanied improvement in cardiac index (2.04 4 0.17 to 2.47 i 0.20 I/min/m2, p < 0.001). Reduction in mean right atrial pressure (9.8 4 2.0 to 5.2 : 1.8 mm Hg, p < 0.005) was not a result of limb venodilation, as calf venous capacitance did not change. The decrease in limb vascular resistance (76.6 ± 11.0 to 62.9 + 10.7 units, p < 0.05) did not parallel the fall in systemic vascular resistance in either magnitude or duration (p < 0.05). Pulmonary arteriolar resistance was not appreciably changed.Teprotide therefore reduces ventricular afterload and significantly improves cardiac function in patients with congestive heart failure. The greater change in systemic than in limb vascular resistance implies preferential redistribution of flow to other regions. These findings shed light upon the role of the renin-angiotensin system in the regulation of regional vasoconstriction in congestive heart failure and suggest that teprotide may act as a unique “vasoreleaser” of pathophysiologic arteriolar constriction.