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

Abstract

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.

The acute haemodynamic effects of intravenous enalaprilic acid (MK422) in patients with left ventricular dysfunction.

“…It is now well recognised that the ACE inhibitors taken orally for the first time may cause a marked drop in blood pressure in hypertensive patients, especially those already on diuretics (Hodsman et al, 1983). Profound hypotension has also been documented in patients with cardiac failure when started on captopril (Kramer et al, 1982) and enalapril (Cleland et al, 1985). Such 'first dose' .responses are thus of continuing concern as a cause of unpredictable morbidity following the use of ACE inhibitors.…”

Short-term improvement in submaximal exercise capacity by optimized therapy with ACE inhibitors and beta blockers in heart failure patients is associated with restoration of peripheral endothelial function

“…Evidence for the ability of neurohormonal blockade to reduce mortality and morbidity and to improve functional status is overwhelming [2]. In addition, it has been demonstrated that angiotensin-converting enzyme inhibitors (ACE inhibitors) and beta blockers increase exercise capacity in heart failure patients [3,4].…”

Antihypertensive effect of single doses of enalapril in hypertensive patients treated with bendrofluazide.

“…The addition of hydrochlorothiazide to enalapril increased the antihypertensive effect in both mild (Enalapril study group, 1984) and moderate to severe (Webster et al, 1986) hypertension, without evidence of severe symptomatic or postural hypotension. However, the reverse procedure-the addition of captopril to patients already on diuretic therapy-may cause profound hypotension (Hodsman et al, 1983;Kramer et al, 1982). Patients susceptible to profound hypotension may be salt depleted and highly dependent on activation of their renin-angiotensin-aldosterone system to maintain their electrolyte homeostasis and blood pressure.…”