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  • Title: Acute and chronic effects of captopril therapy in patients with refractory heart failure.
    Author: Walsh WF, Lee CL.
    Journal: Br J Clin Pharmacol; 1982; 14 Suppl 2(Suppl 2):153S-159S. PubMed ID: 6753896.
    Abstract:
    1 The acute and chronic effects of the oral converting-enzyme inhibitor captopril were studied in 10 patients with refractory heart failure. Nine patients were in New York Heart Association functional class IV and one in class III. The acute haemodynamic and humoral effects were measured after the administration of 25-50 mg captopril. 2 Oral captopril reduced mean heart rate from 82 ± 13 (SD) to 76 ± 13 (p < 0.01), mean arterial pressure from 78 ± 8 to 61 ± 7 mm Hg (p < 0.01), mean pulmonary capillary wedge pressure from 29 ± 3 to 17 ± 4 mm Hg (p < 0.01), and systemic vascular resistance from 1667 ± 274 to 968 ± 152 dyne/s/cm-5 (p < 0.01). Cardiac index increased from 1.7 ± 0.2 to 2.5 ± 0.61/min/m2 (p < 0.01) and stroke volume index 22 ± 4 to 32 ± 7 ml/m2 (p < 0.01). Angiotensin II fell from a control of 85 ± 45 pg/ml to 27 ± 14 pg/ml (p < 0.01) measured at peak effect of captopril. 3 Captopril 25-50 mg every eight hours was continued long term. At mean follow-up 8 ± 5 months (maximum 17 months) seven patients had improved to NYHA functional class III and three to functional class II. Six of the 10 patients died, four suddenly. The one-year actuarial survival was 30%. 4 Haemodynamic and humoral effects were restudied on therapy in six patients after at least 6 months' treatment and their results compared with those in the short-term study. In the late study captopril reduced mean heart rate from 76 ± 7 to 71 ± 8 (p < 0.05), mean arterial pressure from 81 ± 4 to 72 ± 6 mm Hg (p < 0.05), pulmonary capillary wedge pressure from 27 ± 5 to 19 ± 2 (p < 0.05), systemic vascular resistance from 1812 ± 445 to 1234 ± 244 dyne/s/cm-5 (p < 0.05). Cardiac index increased from 1.9 ± 0.2 to 2.4 ± 0.2 l/min/m2 and stroke volume index from 25 ± 4 to 35 ± 6 ml/m2. There was no significant difference between the peak haemodynamic effect of captopril or the percentage change from control measured in the acute or the late study for the six patients. The acute reduction in angiotensin II concentrations was maintained at 6 months with a mean value of 5 ± 6 pg/ml. Mean plasma aldosterone concentration was reduced from 1412 ± 704 pmol/l before treatment to a mean of 387 ± 85 pmol/l at the 6 month study. 5 It is concluded that vasodilator therapy with captopril produces a beneficial acute clinical and haemodynamic response which is sustained at follow-up and that despite symptomatic and objective improvement in these patients with refractory heart failure survival remains poor.
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