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Acute and long-term effects of captopril on exercise cardiac performance and exercise capacity in congestive heart
Insights
Captopril (CPT) significantly improves heart function and exercise capacity in patients with severe congestive heart failure (CHF). Chronic CPT therapy enhances exercise duration and workload, offering substantial benefits for CHF patients.
Area of Science:
- Cardiology
- Pharmacology
- Exercise Physiology
Background:
- Severe congestive heart failure (CHF) significantly impairs cardiac function at rest and during exercise.
- Limited data exists on the effects of captopril (CPT) on exercise hemodynamics and tolerance in CHF patients.
Purpose of the Study:
- To evaluate the acute and chronic hemodynamic effects of captopril (CPT) in patients with stable severe congestive heart failure (CHF).
- To assess the impact of CPT on exercise tolerance and capacity in CHF patients.
Main Methods:
- 15 stable severe CHF patients underwent hemodynamic assessments at rest and during exercise before and after CPT administration (25-50 mg).
- Six patients with persistent beneficial hemodynamic changes after 3 months of chronic CPT therapy underwent repeat assessments.
Main Results:
- CPT acutely reduced resting heart rate, mean arterial pressure, and left ventricular filling pressure, while increasing cardiac and stroke indices.
- During exercise, CPT lowered heart rate, mean arterial pressure, and left ventricular filling pressure, with a trend towards increased peak exercise cardiac index.
- Chronic CPT therapy demonstrated sustained hemodynamic improvements and significantly increased peak exercise cardiac index, exercise duration, and workload.
Conclusions:
- Oral captopril (CPT) provides significant hemodynamic benefits at rest and during exercise in severe congestive heart failure (CHF) patients.
- Long-term captopril (CPT) therapy substantially improves exercise capacity and workload in severe CHF patients.
Abstract:
Although many studies have shown that captopril (CPT) provides acute hemodynamic improvement in patients with severe congestive heart failure (CHF) at rest, little information is available concerning exercise hemodynamic responses to CPT or the effect of this drug on exercise tolerance in CHF. Therefore, we evaluated the hemodynamic effects of CPT at rest and during upright bicycle exercise in 15 patients with stable CHF. CPT (25 to 50 mg) reduces both resting heart rate and mean arterial pressure (84 +/- 11 to 78 +/- 7 bpm, p less than 0.025 and 85 +/- 9 to 64 +/- mm Hg, p less than 0.001). Concomitantly, left ventricular filling pressure dropped dramatically (26 +/- 9 to 15 +/- 7 mm Hg, p less than 0.001), while cardiac and stroke indices rose (2.0 +/- 0.5 to 2.5 +/- 0.6 L/min/m2, p less than 0.001, and 25 +/- 8 to 33 +/- 7 ml/m2, p less than 0.001). Similar directional changes occurred during exercise, with heart rate, mean arterial pressure, and left ventricular filling pressure at maximum exercise being less (123 +/- 15 to 115 +/- 16 bpm, p less than 0.01; 93 +/- 17 to 86 +/- 14 mm Hg, p less than 0.05; and 35 +/- 10 to 30 11 mm Hg, p less than 0.001, respectively) after CPT ingestion. Peak exercise cardiac index rose slightly (3.6 +/- 0.7 to 3.9 +/- 0.6 L/min/m2) but not significantly. Six patients followed long term on CPT underwent elective recatheterization after 3 months. In these, the beneficial hemodynamic changes seen acutely persisted or further improvement was noted, both at rest and during exercise. Most impressively, peak exercise cardiac index rose from 3.6 +/- 0.7 to 4.6 +/- 1.0 L/min/m2 (p less than 0.05), and this was associated with an increase in exercise duration (8.0 +/- 2.2 to 11.5 +/- 1.4 minutes, p less than 0.05) and exercise work load (332 +/- 32 to 468 +/- 52 kp-m/min, p less than 0.05). These findings indicate that in patients with severe CHF, oral CPT provides markedly beneficial augmentation of cardiac function during activity as well as at rest; moreover, chronic CPT therapy substantially increases exercise capacity in this setting.