Treatment of Primary Pulmonary Hypertension with Nifedipine

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Abstract
To evaluate the potential value of nifedipine treatment for primary pulmonary hypertension, hemodyanamic and scintigraphic mesurements were made before and 15-30 min after nifedipine, 10-20 mg, was given sublingually to 9 patients. Nifedipine treatment increased cardiac output (mean .+-. SD, 23.6 .+-. 1.7 to 5.3 .+-. 2.8 l/min, P < 0.001) and decreased mean aortic pressure (99 .+-. 19 to 85 .+-. 12 mm Hg, P < 0.001) and total pulmonary and total systemic resistances (1605 .+-. 787 to 1025 .+-. 540 dyn .cntdot. s .cntdot. cm-5 and 2761 .+-. 1557 to 1591 .+-. 823 dyn .cntdot. s .cntdot. cm-5, respectively; P < 0.005). Heart rate and mean pulmonary arterial pressure did not change significantly. Right ventricular end-diastolic volume decreased 10% (P = 0.01), end-systolic volume decreased 15% (P < 0.01), and right ventricular ejection fraction increased 18% (P < 0.05) in 8 patients. After 4-14 mo. (mean, 7.3 .+-. 3.8) of treatment with nifedipine, 40-120 mg/d [day], in 6 patients, cardiac output increased (3.6 .+-. 2.0 to 5.0 .+-. 1.8 l/min, P < 0.01) and total pulmonary resistance decreased (1572 .+-. 730 to 987 .+-. 586 dyn .cntdot. s .cntdot. cm-5, P = 0.025), whereas pulmonary arterial pressure remained unchanged (59 .+-. 23.2 to 55 .+-. 28.6 mm Hg, P > 0.05) compared with baseline values. Nifedipine therapy may be useful in the chronic management of patients with primary pulmonary hypertension.