Acute hemodynamic effects of nitrendipine in chronic congestive heart failure

The acute hemodynamic response to a single oral dose of nitrendipine (10-20 mg) was evaluated in eight subjects with severe chronic congestive heart failure during right heart catheterization. A hemodynamic effect began within 1 h. At peak effect (1-2 h after drug administration), mean arterial pressure fell from 84.0 ± 9.2 to 76.0 ± 9.2 mm Hg (mean ± SD), right arterial pressure from 10.6 ± 5.9 to 8.0 ± 7.1 mm Hg, mean pulmonary arterial pressure from 35.5 ± 9.2 to 30.1 ± 9.4 mm Hg, pulmonary wedge pressure from 23.6 ± 6.7 to 17.7 ± 6.3 mm Hg, and cardiac index rose from 1.91 ± 0.38 to 2.45 ± 0.34 L/min/m². Heart rate did not change (85 ± 18 to 82 ± 18 beats/min) despite the significant fall in arterial pressure. Systemic and pulmonary vascular resistances fell significantly. Whereas forearm blood flow increased from 1.44 ±0.52 to 2.06 ± 0.41 ml/min/100g (p < 0.05), hepatic and renal blood flows were unchanged. This study demonstrates the acute effectiveness of nitrendipine in reducing ventricular preload and impedance in heart failure and in increasing cardiac output that appears to be preferentially directed to the skeletal bed. The left-upward shift of the Frank-Starling curve suggests the absence of any clinically important negative inotropic effect of nitrendipine. Nitrendipine therefore may be a useful agent for vasodilator therapy of heart failure.