Hemodynamic effects of captopril in patients with severe chronic heart failure.
The hemodynamic effects of captopril (SQ 14225), an oral inhibitor of angiotensin-converting enzyme, were measured in 10 patients with severe chronic heart failure poorly controlled by digitalis and diuretics. After administration of a 25 mg dose, the cardiac index increased from 1.82 +/- 0.14 to 2.28 +/- 0.30 liters/min/m2 (p less than 0.05) while pulmonary capillary wedge pressure decreased from 22.7 +/- 2.0 to 14.7 +/- 4.7 mm Hg (p less than 0.05). Mean blood pressure and systemic vascular resistance decreased from 85.7 +/- 6.7 to 71.2 +/- 12.0 mm Hg (p less than 0.001) and from 1,909 +/- 246 to 1,362 +/- 347 dynes-s-cm5 (p less than 0.001), respectively. Heart rate did not change significantly. There was an inverse relation between maximal augmentation in cardiac index and maximal reduction in pulmonary capillary wedge pressure (r = -0.82, p less than 0.01). While most patients demonstrated a constant hemodynamic benefit after repeated administration of captopril, some exhibited a triphasic response with attenuation of effects after the second dose and restoration of effects after the third dose. These hemodynamic benefits were observed in patients with stable chronic heart failure whose plasma renin activity was within normal range (1.1 to 7.3 ng/ml/hour).
D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000627:therapeutic use*; D002302:Cardiac Output / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D006333:Heart Failure / Q000188:drug therapy*; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D011392:Proline / Q000031:analogs & derivatives*; D012083:Renin / Q000097:blood; D014655:Vascular Resistance / Q000187:drug effects
D011392:Proline; D002216:Captopril; D012083:Renin