Hemodynamic effects of nifedipine versus hydralazine in primary pulmonary hypertension

Abstract

The acute hemodynamic effects of both sublingual nifedipine (N) and intravenous hydralazine (Hy) were studied in 5 patients with primary pulmonary hypertension to ascertain whether the capacity for pulmonary vasodilatation was generalized or drug-specific, and to determine which of the 2 agents had preferential pulmonary vasodilatory effects. For the group as a whole, neither N nor Hy produced changes in heart rate, mean pulmonary capillary wedge or right atrial pressures. Both N and Hy reduced mean systemic arterial pressure (before N 90 ± 8 mm Hg, after N 76 ± 7 mm Hg, p < 0.01; before Hy 92 ± 11 mm Hg, after Hy 68 ± 8 mm Hg, p < 0.05), and decreased systemic vascular resistance (before N 1,558 ± 645 dynes s cm −5, after N 1,192 ± 430 dynes s cm −5, p < 0.05; before Hy 1,700 ± 415 dynes s cm −5, after Hy 957 ± 285 dynes s cm −5, p < 0.05). In addition, N administration resulted in an increased cardiac output (before N 4.5 ± 2.0 liters/min, after N 4.8 ± 2.0 liters/min, p < 0.01); Hy administration was associated with a more varied effect on cardiac output (before Hy 4.0 ± 1.0 liters/min, after Hy 5.3 ± 1.8 liters/min, p < 0.10, difference not significant [NS]). Although for the group neither agent decreased mean pulmonary artery pressure (PAP) (before N 51 ± 13 mm Hg, after N 44 ± 13 mm Hg, NS; before Hy 50 ± 15 mm Hg, after Hy 51 ± 15 mm Hg, NS) or pulmonary vascular resistance (before N 873 ± 458 dynes s cm −5, after N 680 ± 450 dynes s cm −5, NS; before Hy 945 ± 454 dynes s cm −5, after Hy 715 ± 309 dynes s cm −5, NS), 4 of 5 patients had a decrease in PAP after N and 1 had no change, and only 1 of 5 patients had a decreased PAP after Hy administration. Moreover, compared with the changes after Hy administration, PAP declined after N administration (δPAP after Hy 0.2 ± 9 mm Hg, after N −7 ± 9 mm Hg, p < 0.05). The PA diastolic to mean PA wedge pressure gradient tended to decrease after N administration (after N −5.0 ± 10 mm Hg, after Hy +4.7 ± 7 mm Hg, NS), suggesting more pulmonary vasodilatation after N administration. Moreover, the ratio of pulmonary to systemic vascular resistances was unchanged after N but increased after Hy administration (before N 0.55 ± 0.2, after N 0.53 ± 0.2, NS; before Hy 0.55 ± 0.2, after Hy 0.74 ± 0.3, p < 0.02), indicating the more balanced vasodilatory effect of N. Two patients were treated chronically with Hy but had intolerable adverse effects; 1 was subsequently treated successfully with N. A third patient had pulmonary edema (presumably neurogenic) 30 minutes after Hy administration; this patient later died. Another patient has symptomatically improved with chronic N therapy. Thus, N appears to be a more specific pulmonary arterial vasodilator than Hy in acute drug testing; in this small group of patients with primary pulmonary hypertension, N appears to be more efficacious when administered chronically.