Captopril mediated decrease of aortic regurgitation.
The effect of captopril mediated afterload reduction on aortic regurgitation was investigated in 10 patients. Regurgitation was quantitated by means of the regurgitation fraction and the relation of regurgitant volume to end diastolic volume. These variables were derived from gated radionuclide ventriculography. After captopril treatment the blood concentration of angiotensin I rose whereas that of angiotensin II fell significantly. The conversion of angiotensin I to II was reduced to about 50% of the control value. Whereas blood pressure and heart rate did not change significantly, the regurgitation fraction and the regurgitant volume, normalised to end diastolic volume, were significantly reduced by captopril treatment. The ejection fraction remained essentially unchanged. These findings suggest that captopril reduces aortic regurgitation by reducing afterload.
D000803:Angiotensin I / Q000032:analysis; D000804:Angiotensin II / Q000032:analysis; D001022:Aortic Valve Insufficiency / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000627:therapeutic use*; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D011863:Radioimmunoassay; D013318:Stroke Volume / Q000187:drug effects
D000804:Angiotensin II; D000803:Angiotensin I; D002216:Captopril