M.B. B.S., F.R.A.C.P.

In a 33-year-old patient with severe primary pulmonary hypertension, the acute administration of the angio-tensin-converting-enzyme inhibitor captopril (SQ 14,225) induced a rise in cardiac output, and a fall in both pulmonary and systemic vascular resistance. Subsequent chronic oral administration of captopril induced only transient clinical improvement, and the patient died. Captopril may nevertheless be useful in the treatment of less advanced cases of this disease. Case report A 33-year-old married woman with 2 children was admitted to hospital in February, 1979 for manage-ment of right heart failure due to primary pulmonary hypertension. There was a past history of Raynaud's phenomenon and mild systemic hypertension. Oral contraceptives had last been used 18 months pre-viously. Exertional dyspnoea had been present for 15 months. Physical examination revealed signs of severe pulmonary hypertension with no evidence of intracardiac shunt. Pulmonary arteriography in September 1978 revealed no evidence of embolic disease. The pulmonary artery pressure was 70/32 mmHg (mean 50 mm). Pulmonary artery saturation was 53 %. The patient's course between April 1978 and February 1979 was marked by gradual clinical de-terioration with incapacitating dyspnoea on minimal exertion and stress