Decrease in pulmonary artery pressure with slow release nifedipine in Saudi patients with primary pulmonary hypertension

Abstract

We studied the acute and short-term hemodynamic effects of vasodilators in three Saudi patients with primary pulmonary hypertension. The study protocol included the measurement of pulmonary artery pressure, resistance and cardiac output at baseline and at 15, 30, 45 and 60 minutes after 10 mg sublingual nifedipine. These hemodynamic studies repeated at 3 and 6 months follow-up. A 24 hour profile of pulmonary artery and aortic pressures were recorded to evaluate the effect of 20 mg of slow release nifedipine, after 25 mg of captopril and 5 mg of sublingual isordil. After nifedipine there was a marked reduction in systolic pulmonary artery pressure from 85 +/- 18 to 55 +/- 8 mmHg and the pulmonary resistance decreased from 1422 +/- 367 to 954 +/- 69 dynes-sec/cm-5. The cardiac output increased from 2.9 +/- 0.2 to 0.2 to 4.0 +/- 0.4 l/min after nifedipine. The patients were discharged on nifedipine 10 mg qid, except for patient #3 who was a non-responder. At follow-up there was a symptomatic improvement and a favourable hemodynamic response was maintained, though patient #2 required a higher dose of nifedipine. The pulmonary artery 24 hour pressure profile revealed that 20 mg slow release adalat reduced pulmonary artery pressure for a 6 hour period. Whereas, regular nifedipine decreased pulmonary artery pressure for a period of less than 90 minutes. There was no favourable hemodynamic response to either captopril 25 mg oral of isordil 5 mg administered sublingually. We conclude that slow release nifedipine decreases the pulmonary artery pressure for longer periods compared to regular nifedipine in patients with primary pulmonary hypertension.