Effects of the converting enzyme inhibitor (SQ 20881) on the pulmonary circulation in man

Abstract

The effects of the converting enzyme inhibitor (SQ 20881) on the pulmonary circulation were investigated in 13 patients in whom systemic hypertension developed following coronary artery bypass surgery. Pulmonary vascular resistance was decreased by the inhibitor, from 128 ± 19 to 92 ± 20 dynes sec cm −5 (or by 30 ± 7 per cent; P < 0.005), and this resulted in a decrease in mean pulmonary artery pressure from 17 ± 1 to 13 ± 1 mm Hg (or by 23 ± 3 per cent, P < 0.005). Consequently, right ventricular work was decreased by the inhibitor by 30 per cent (P < 0.01), despite an increase in cardiac output (increase in stroke volume) by 16 ± 6 per cent (P < 01). This increase occurred despite a 13 ± 3 per cent decrease in right ventricular filling pressure. The changes in pulmonary vascular resistance correlated with the pretreatment plasma renin activity (r = 0.74, P < 0.01), as did the decrease in mean pulmonary artery pressure (R = 0.82, P < 0.001), but neither change was related to the decrease in left ventricular filling pressure nor to changes in cardiac output or mean arterial pressure. These results indicate that blockade of the formation of angiotensin II by the converting enzyme inhibitor results in reductions in pulmonary vascular resistance and pulmonary artery pressure which are unrelated to alterations in left ventricular function. Thus, angiotensin inhibition may have therapeutic value in various clinical states characterized by pulmonary hypertension—especially if renin levels are high.