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Haemodynamic and myocardial metabolic effects of captopril in chronic heart failure
Insights
Captopril, an oral angiotensin-converting enzyme inhibitor, improved cardiac function in patients with chronic heart failure. While generally reducing metabolic cost, it infrequently caused myocardial lactate production.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Chronic left ventricular failure due to ischemic heart disease presents significant challenges.
- Angiotensin-converting enzyme (ACE) inhibitors are crucial in managing heart failure.
Purpose of the Study:
- To evaluate the effects of captopril on cardiac function and myocardial metabolism in patients with chronic heart failure.
- To assess the impact of ACE inhibition on cardiac output, heart pressures, and myocardial oxygen consumption.
Main Methods:
- 15 patients with chronic left ventricular failure received increasing oral doses of captopril.
- Cardiac output, right heart pressures, coronary blood flow, myocardial oxygen extraction/consumption, and lactate extraction were measured before and after therapy.
Main Results:
- Captopril significantly increased cardiac index (25%) and stroke volume index (27%).
- Pulmonary capillary wedge pressure decreased by 27%, indicating improved left ventricular function.
- Rate-pressure product, coronary blood flow, and myocardial oxygen consumption decreased; one patient showed lactate production.
Conclusions:
- Captopril generally improves left ventricular function in chronic heart failure with a reduced metabolic cost.
- Deterioration of myocardial metabolic function during captopril therapy is infrequent.
Abstract:
In 15 patients with chronic left ventricular failure caused by ischaemic heart disease, cardiac output and right heart pressures were measured before and after the oral angiotensin-converting enzyme inhibitor, captopril, which was administered in increasing doses. In 12 of 15 patients, coronary blood flow, and in 11 patients myocardial oxygen extraction and consumption and lactate extraction were also determined before and after captopril therapy. Cardiac index and stroke volume index increased by an average of 25% and 27%, respectively. Pulmonary capillary wedge pressure also decreased in all patients (average 27%), suggesting improved left ventricular function. The rate-pressure product, coronary blood flow, and myocardial oxygen consumption decreased significantly; in one of 11 patients there was myocardial lactate production, despite decreased myocardial oxygen demand and consumption. These findings suggest that in patients with chronic heart failure, improved left ventricular function with captopril is generally associated with decreased metabolic cost and that deterioration of metabolic function occurs infrequently.