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Hemodynamic and clinical effects of captopril in patients with severe congestive heart failure
Insights
Captopril (CPT) acutely improved hemodynamics in severe congestive heart failure (CHF) patients, with sustained benefits for weeks. While quality of life improved, CPT did not significantly impact long-term life expectancy in this cohort.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Severe congestive heart failure (CHF) poses significant challenges.
- Ischemic heart disease and dilatative cardiomyopathy are common etiologies of CHF.
Purpose of the Study:
- To evaluate the acute and chronic hemodynamic and clinical response to captopril (CPT) in patients with severe CHF.
- To assess the long-term effects of CPT on quality of life and survival.
Main Methods:
- Acute hemodynamic response to a single 50 mg oral dose of CPT was measured in 10 severe CHF patients.
- CPT was initiated orally and titrated over 2-3 days.
- Hemodynamic re-evaluations were performed after 20 days and 1 year.
- Clinical follow-up occurred every 3 months for up to 3 years.
Main Results:
- CPT acutely decreased pulmonary wedge pressure and increased cardiac index (p < 0.01).
- Systemic and pulmonary resistances decreased significantly post-CPT.
- Favorable hemodynamic changes persisted for at least 20 days.
- Chronic CPT treatment led to gradual clinical improvement and stabilization within 2-3 weeks.
- Mortality rates were 30% (1 year), 50% (2 years), and 60% (3 years).
- Quality of life improved, but life expectancy was not significantly affected.
Conclusions:
- CPT demonstrates acute and short-term hemodynamic benefits in severe CHF.
- Chronic CPT improves quality of life in CHF patients.
- CPT's impact on long-term survival in this severe CHF cohort appears limited.
Abstract:
In a group of 10 patients (9 male, 1 female, aged 16 to 56, mean 43 years) with severe congestive heart failure (CHF), due to ischemic heart disease (8 cases) or dilatative cardiomyopathy (2 cases), the acute hemodynamic response to captopril (CPT) (90 min after 50 mg po) was evaluated. CPT was then given starting with 15 mg q 8 hr, gradually increased within 2 or 3 days to 50 or 75 mg q 8 hr. A hemodynamic re-evaluation was performed after 20 days, and, in 5 patients, after 1 year of CPT treatment. The clinical follow-up done every 3 months in the outpatient clinic. CPT acutely produced a decrease in mean pulmonary wedge pressure: 23.8 +/- 8.9 to 18.6 +/- 8.6 mmHg, p less than 0.01, and an increase in cardiac index: 2.43 +/- 0.73 to 2.91 +/- 0.85 l/min/m2, p less than 0.01; systemic and pulmonary resistances decreased significantly, with no significant changes in heart rate and in mean brachial artery pressure. This favourable hemodynamic response persisted after 20 days of CPT treatment. In the group of 5 patients, who underwent a third hemodynamic evaluation, no statistically significant differences were demonstrated in respect to the previous control values. All patients on chronic CPT treatment experienced a gradual clinical improvement, reaching a steady state after 2 to 3 weeks; the surviving patients remained stable in the improved functional class for at least 6 months. The mortality rate was 30% in the first year, increasing to 50% in the second and to 60% in the third year of treatment. After a mean follow-up 35.7 months (range 33 to 39) the 4 surviving patients remained in the same functional class as after the first year for therapy. In our CHF patients CPT improved the quality of life, with the best clinical and hemodynamic results the first few months of treatment; life expectancy probably was not affected.