Acute haemodynamic effects of nifedipine at rest and during maximal exercise in patients with chronic cor pulmonale.

The pulmonary hypertension of cor pulmonale can be reversed by sustained correction of hypoxia but continuous oxygen treatment poses problems in clinical practice. Alternative methods of relieving pulmonary vasoconstriction have therefore been explored. Eight patients with chronic cor pulmonale (five of them men) were studied to measure the haemodynamic effects of the calcium antagonist nifedipine, both at rest and on maximal, symptom limited exercise. The mean duration of exercise was unchanged by nifedipine (7.8 (SD 3.3) compared with 7.3(3.1) min). Cardiac output rose from 5.2(1.5) l min-1 to 8.6(3.3) 1 min-1 on exercise. Nifedipine increased resting cardiac output by 26%, but did not influence maximal exercise output. It did not significantly alter resting mean pulmonary artery pressure but reduced the level during exercise from 67(15) to 52(11) mm Hg. Nifedipine lowered resting pulmonary vascular resistance (PVR) by 32% and exercise PVR by 28%. It reduced supine mean systemic arterial pressure by 17%, standing pressure by 22%, and pressure at the maximal exercise level by 20%. Nifedipine lowered supine systemic vascular resistance (SVR) by 35%, standing SVR by 28%, and exercise SVR by 20%. Haemodynamic changes were achieved without adverse symptoms, alteration in arterial PO2, or impairment of calculated oxygen delivery. Nifedipine therefore reduced both pulmonary and systemic vasomotor tone at rest and during exercise. It did not alter exercise tolerance, which is probably limited by underlying respiratory disease. It seems possible therefore that nifedipine could delay the development of cor pulmonale, although this hypothesis remains to be tested.