The immediate and sustained haemodynamic effects of Captopril (CPT), an oral inhibitor of angiotensin converting enzyme, were studied in six patients (pts) with severe pulmonary hypertension (PH) (pulmonary artery pressure: mean +/- SD value = 57 +/- 20 mmHg). Two pts had primary PH, 2 embolic PH and 2 Eisenmenger Physiology (EP). Administration of 100 mg of CPT in a single oral dose produced a significant decrease only in systemic arterial pressure (SAP) (p less than 0.025) and systemic vascular resistance (SVR) (p less than 0.05) in 5 of 6 pts. Heart rate (HR), cardiac index (CI), pulmonary vascular resistance (PVR), pulmonary arterial (PAP), pulmonary wedge (PWP) and right atrial pressure (RAP) did not change significantly. These results were confirmed in a repeat haemodynamic study after 4 months of long-term treatment with 50 or 100 mg of CPT 3 times daily. In 1 pt with EP and severe congestive heart failure (CHF) the same chronic treatment produced a marked decrease in HR (from 114 to 88 b/min), RAP (from 10 to 1 mmHg), PWP (from 15 to 6 mmHg), PVR (from 41 to 30 UR), SVR (from 58 to 43 UR). Systemic CI increased from 1.68 to 2.60 l/min/m2 and pulmonary CI from 1.64 to 2.5 l/min/m2; no changes were seen in PAP and SAP. These data suggest that CPT is not effective on pulmonary haemodynamics in pts with precapillary PH and normal CI whereas the drug seems to influence favourably the pulmonary circulation in pts with PH secondary to or associated with left ventricular failure. The necessity of evaluating not only PVR but PAP as well, in studying the effect of vasodilators especially in pts with precapillary PH and normal CI, is discussed. In fact a reduction of PAR without decrease of PAP, as frequently seen in previous reports, is probably due to a primary increase of CI induced by the drug.
Adolescent Adult