Persistent hemodynamic and clinical improvement after captopril in patients with pulmonary hypertension.
Ten patients with primary or secondary pulmonary hypertension who had normal left ventricular function (group I) and nine patients with pulmonary hypertension in response to impaired left ventricular function (group II) were given captopril. At peak effect (1.5 hours after administration) pulmonary vascular resistance fell from 935 to 717 dyn X s X cm-5 in group I and from 554 to 355 dyn X s X cm-5 in group II in association with a decrease in pulmonary arterial pressure by 8 and 12 mmHg, respectively (p less than 0.01). Systemic vascular resistance declined by 26 and 29 per cent, and cardiac index increased by 17 and 20 per cent, respectively (p less than 0.01). On re-catheterization four to 15 months later, seven chronically treated patients (five of group I; two of group II) showed additional reductions in pulmonary vascular resistance (25 per cent) and pulmonary arterial pressure (20 per cent), whereas systemic hemodynamics had almost reached pre-treatment values. All patients reported symptomatic improvement. The hemodynamic changes did not correlate with concomitant alterations in circulating renin or angiotensin II levels. These data suggest that captopril can produce sustained hemodynamic and clinical benefits in patients with pulmonary hypertension of various causes and may be useful for the chronic treatment of this disorder.
D000293:Adolescent; D000328:Adult; D000368:Aged; D000804:Angiotensin II / Q000097:blood; D002216:Captopril / Q000627:therapeutic use*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood / Q000188:drug therapy*; D008134:Long-Term Care; D008297:Male; D008875:Middle Aged; D011652:Pulmonary Circulation / Q000187:drug effects*; D012083:Renin / Q000097:blood
D000804:Angiotensin II; D002216:Captopril; D012083:Renin