Differences in hemodynamic response to vasodilation due to calcium channel antagonism with nifedipine and direct-acting agonism with hydralazine in chronic refractory congestive heart failure

• Published in: The American journal of cardiology Vol. 54; no. 1; pp. 126 - 131
• Main Authors: Elkayam, Uri, Weber, Laura, McKay, Charles R., Rahimtoola, Shahbudin H.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01-07-1984; Elsevier
• Subjects: Adult; Aged; Biological and medical sciences; Blood Pressure - drug effects; Cardiovascular system; Female; Heart Failure - drug therapy; Heart Rate - drug effects; Hemodynamics - drug effects; Humans; Hydralazine - therapeutic use; Male; Medical sciences; Middle Aged; Nifedipine - therapeutic use; Pharmacology. Drug treatments; Pulmonary Wedge Pressure - drug effects; Random Allocation; Stroke Volume - drug effects; Vascular Resistance - drug effects; Vasodilator agents. Cerebral vasodilators; Human; Heart failure; Chemotherapy; Randomization; Treatment; Vasodilator agent; Heart disease; Calcium antagonist; Cardiovascular disease; Hemodynamics; Comparative study
• ISSN: 0002-9149; 1879-1913
• DOI: 10.1016/0002-9149(84)90316-3

The hemodynamic response to a similar reduction of systemic vascular resistance after nifedipine and hydralazine administration was compared in a randomized crossover protocol in patients with severe chronic congestive heart failure (CHF). All 15 patients showed a 25% or greater reduction in vascular resistance with intravenous hydralazine (5 to 30 mg) and 11 patients showed a similar response with oral nifedipine (20 to 50 mg). In the latter 11 patients, despite similar reductions in systemic vascular resistance (35 ± 2% with nifedipine and 36 ± 4% with hydralazine, difference not significant), nifedipine resulted in a smaller increase in stroke volume index (from 23 ± 2 to 30 ± 2 ml/m
2 and from 24 ± 2 to 34 ± 2 ml/m
2 with hydralazine, p <0.05), cardiac index (from 2.0 ± 0.1 to 2.6 ± 0.2 liters/min/m
2 with nifedipine and from 2.0 ± 0.1 to 2.8 ± 0.2 liters/min/m
2 with hydralazine, p <0.05) and stroke work index (from 25 ± 3 to 27 ± 3 gm/m
2 with nifedipine and from 26 ± 2 to 32 ± 2 gm/m
2 with hydralazine, p <0.05). The decrease in blood pressure after nifedipine was slightly but not significantly larger than that with hydralazine (13 ± 3% vs 8 ± 2%). The changes in right atrial pressure, pulmonary artery wedge pressure and pulmonary vascular resistance were similar. The 4 patients who did not reduce their systemic vascular resistance by at least 25% with nifedipine had a worsening of their hemodynamic state as evidenced by 1 or more of the following findings: elevation of vascular resistance, decrease in cardiac index and increase in pulmonary artery wedge pressure. These results suggest that nifedipine exerts a clinically important negative inotropic effect in patients with severe chronic CHF that is only partially offset by its strong arteriolar dilatory effect. Hydralazine appears to be better than nifedipine when left ventricular afterload-reducing therapy is indicated in patients with severe CHF.