Efficacy of oral angiotensin-converting enzyme inhibition with captopril therapy in severe chronic normotensive congestive heart failure

Awan, Najam A.; Evenson, Mark K.; Needham, Kathleen E.; Win, Aung Ko; Mason, Dean T.

doi:10.1016/0002-8703(81)90379-3

Cited by 114 publications

(27 citation statements)

References 42 publications

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“…Other groups have reported small numbers of patients with chronic heart failure who increased their exercise tolerance after 1-20 weeks of therapy. 13, 13 15 …”

Section: Calculations and Statistical Analysismentioning

confidence: 99%

Controlled trial of captopril in chronic heart failure: a rest and exercise hemodynamic study.

Kramer¹,

Massie²,

Topic³

1983

Circulation

220

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“…Other groups have reported small numbers of patients with chronic heart failure who increased their exercise tolerance after 1-20 weeks of therapy. 13, 13 15 …”

Section: Calculations and Statistical Analysismentioning

confidence: 99%

Controlled trial of captopril in chronic heart failure: a rest and exercise hemodynamic study.

Kramer¹,

Massie²,

Topic³

1983

Circulation

220

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“…Captopril, the first orally active inhibitor of the angiotensin I converting enzyme available, has been found to be effective in the treatment of renovascular and essential hypertension and of congestive heart failure (Heel et al, 1980;Horovitz, 1981;Awan et al, 1981). Since captopril is mainly eliminated by urinary excretion (Kripalani et al, 1980;Duchin et al, 1982) and since impairment of renal function is often associated with severe hypertension, this study was designed to investigate in three groups of hypertensive patients with various degrees of renal dysfunction the influence of renal impairment on (a) the pharmacokinetics of plasma unchanged captopril after administration of a single oral dose, (b) the kinetics of the induced plasma converting enzyme blockade and related biological modifications and (c) the kinetics of the acute antihypertensive effect of the drug.…”

Section: Introductionmentioning

confidence: 99%

Influence of chronic renal failure on captopril pharmacokinetics and clinical and biological effects in hypertensive patients.

Jf¹,

Chaignon²,

Richer³

et al. 1984

Brit J Clinical Pharma

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The pharmacokinetic parameters of unchanged plasma captopril and the kinetics of the drug effects on plasma converting enzyme activity (PCEA), plasma renin activity (PRA), plasma aldosterone (PA) and mean blood pressure (MBP) were studied over 24 h after oral administration in three groups of hypertensive patients: with normal renal function (group 1, plasma creatinine less than 110 mumol/l, n = 10), with moderate chronic renal failure (group 2, 135 less than plasma creatinine less than 450 mumol/l, n = 10) and with severe chronic renal failure (group 3, plasma creatinine greater than 500 mumol/l, n = 10). Renal impairment had no effect on plasma captopril Cmax, CLtot and relative bioavailability (AUC). In contrast, captopril kel decreased while T1/2 increased progressively from group 1 to group 3. PCEA blockade (T1/2 and AUC) was increased significantly and proportionally to the degree of renal impairment. However, there were no differences between the three groups regarding captopril‐induced modifications of PRA and PA. Although the maximal reduction in MBP was identical in the three groups, the overall antihypertensive effect (AUC) of captopril increased significantly and progressively from group 1 to group 3, especially in duration. There was no correlation between basal plasma creatinine values and unchanged captopril relative bioavailability (AUC) and between unchanged captopril relative bioavailability (AUC) and the drug effects (AUC) on PCEA, PRA, PA and MBP. However there was a correlation between basal plasma creatinine values and plasma captopril T1/2, PCEA blockade (AUC) and overall antihypertensive effect (AUC). The apparent discrepancy between the lack of effects of chronic renal failure on plasma unchanged captopril bioavailability and its potentiating effects on PCEA blockade and MBP reduction may be accounted for by the renal impairment‐induced accumulation of captopril metabolites.

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“…Captopril is unique among the currently available oral vasodilating agents in that it specifically inhibits the converting-enzyme responsible for the production of angiotensin II (Peach, 1977 (Davis et al, 1979;Tarazi et al, 1979;Ader et al, 1980;Levine et al, 1980;Awan et al, 1981b;Dzau et al, 1980;Faxon et al, 1981;Awan et al, 1982). Additionally, we and other investigators have shown that captopril has a significant beneficial effect on left ventricular filling pressure that is not adequately explained by its effect on angiotensin II levels (Rose etal., 1962;Davis etal., 1979;Tarazi et al, 1979;Ader et al, 1980;Levine et al, 1980;Awan et al, 1981;Dzau et al, 1980;Awan et al, 1982).…”

Section: Discussionmentioning

confidence: 95%

“…In several recent studies captopril, an angiotensin-converting-enzyme inhibitor, produces 0306-5251/82/100143-09 $01.00 acute haemodynamic improvement in patients with chronic congestive heart failure. In a few patients, follow-up measurements have shown that this beneficial effect has been maintained during chronic treatment (Davis et al, 1979;Tarazi et al, 1979;Ader et al, 1980;Levine et al, 1980;Awan et al, 1981b;Dzau et al, 1980;Faxon et al, 1981;Awan et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Acute and long‐term effects of captopril on exercise cardiac performance and exercise capacity in congestive heart failure.

Kramer¹,

Topic²,

Massie³

1982

Brit J Clinical Pharma

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1 Although in many studies patients in heart failure treated with captopril have shown acute haemodynamic improvement at rest, little information is available about the haemodynamic response to captopril during exercise or about its effect on exercise tolerance. 2 Haemodynamic measurements were taken at rest and during upright bicycle exercise before and during the first two days of captopril treatment in 15 patients with stable congestive heart failure. At rest, the heart rate and mean arterial pressure both declined (84 + 11 to 78 + 7 beats/min (p < 0.25) and 85 + 9 to 64 + 8 torr (p<0.001), the left ventricular filling pressure dropped dramatically (26 ± 9 to 15 ±7 torr (p < 0.001) while cardiac and stroke indices rose (2.0 ± 0.5 to 2.5 ± 0.61/min/m2 (p < 0.001) and 25 ± 8 to 33 ± 7 ml/min2 (p < 0.001). Similar directional changes occurred during exercise, with heart rate, mean arterial pressure, and left ventricular filling pressure at maximum exercise all falling (123 ± 15 to 115 ± 16beats/min(p<0.01);93 ± 17to86± 14torr(p<0.05);and35 + 10to330 lltorr(p< 0.001) respectively). Maximum cardiac index rose slightly, from 3.6 ± 0.7 to 3.9 ± 0.6 1/min/m2, acutely, but the change was not significant. 3 Six patients studied taking captopril long term underwent elective recatheterisation after 3 months. In these, either the beneficial haemodynamic changes seen with short-term treatment persisted or further improvement was noted, both at rest and during exercise. Most impressively, maximum exercise index rose from 3.6 ± 0.7 to 4.6 ± 1.01/min/m2 (p < 0.05) and this was associated with an increase in exercise duration (8.0 ± 2.2 to 11.5 ± 1.4 minutes (p < 0.05), exercise work load (332 ± 32 to 468 ± 52 kilopond-metres min, (p<0.05) and maximum oxygen consumption (11.8 ± 2.6 to 15.6 ± 2.7 ml/min/kg, (p < 0.05). These findings indicate that captopril is beneficial during activity as well as at rest and that chronic treatment increases exercise capacity.

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Efficacy of oral angiotensin-converting enzyme inhibition with captopril therapy in severe chronic normotensive congestive heart failure

Cited by 114 publications

References 42 publications

Controlled trial of captopril in chronic heart failure: a rest and exercise hemodynamic study.

Controlled trial of captopril in chronic heart failure: a rest and exercise hemodynamic study.

Influence of chronic renal failure on captopril pharmacokinetics and clinical and biological effects in hypertensive patients.

Acute and long‐term effects of captopril on exercise cardiac performance and exercise capacity in congestive heart failure.

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