Transient elevation of pulmonary arterial pressure induced by sublingual angiotensin converting enzyme inhibitors

Twelve patients with ischemic heart disease had complete left and right catheterization before and after sublingual captopril. Hemodynamic measurements were ten (10) minutes apart and were monitored for thirty (30) minutes. The heart rate increased from 70 +/- 13 to 76 +/- 11 beats/minute (P = .04). There was no change in the arterial blood pressure, although the systemic vascular resistance decreased from 1500 +/- 400 to 1026 +/- 480 dynes-sec-cm-5 (P < .0001). The pulmonary artery pressure was increased 15 +/- 6 to 25 +/- 5mmHg (P = .005) and the pulmonary vascular resistance increased from 288 + 160 to 376 + 160 dynes-sec-cm-5 (P < .0001). The wedge pressure increased from 7 +/- 2 to 14 +/- 3 mmHg (P = .05). The cardiac output (CO) increased from 5.06 +/- 1.06 to 578 +/- 1.58 Lt/min. (P.05 =. The left ventricular end diastolic volume (LVEDV) increased from 128 +/- 40 to 145 +/- 37cc)P = .002), without change in the end systolic volume (ESV). The ejection fraction (EF) increased from 56 +/- 3 to 61 +/- 4% (P = .02). These pressure changes appeared at two (2) minutes and disappeared after thirty (30) minutes. The study shows that, sublingual captopril produces a transient elevation of the pulmonary artery pressure and resistance.