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Angiotensin converting enzyme inhibition by captopril influences cardiac work in healthy hearts
I Derad1, A Dendorfer, P Dominiak
1Department of Internal Medicine, University of Lübeck, Germany. derad@kfg.mu-luebeck.de
Insights
Angiotensin converting enzyme (ACE) inhibition with captopril demonstrated beneficial effects in healthy hearts. Captopril reduced cardiac oxygen consumption and left ventricular pressure, suggesting a protective role in critical cardiac conditions.
Area of Science:
- Cardiovascular Pharmacology
- Cardiac Physiology
Background:
- Angiotensin converting enzyme (ACE) inhibitors are known to benefit diseased hearts.
- The effects of ACE inhibition on healthy hearts remain largely uncharacterized.
- Understanding these effects is crucial for managing hypertension and preventing cardiac disease progression.
Purpose of the Study:
- To investigate the effects of captopril, an ACE inhibitor, on the cardiac dynamics of healthy hearts.
- To assess the impact of varying captopril concentrations on cardiac work, metabolism, and coronary flow.
- To determine potential protective mechanisms of ACE inhibition in healthy cardiac tissue.
Main Methods:
- Utilized a refined working heart preparation to measure cardiac work, including atrial contribution and paracrine regulation.
- Administered captopril at concentrations ranging from 3 x 10(-8) to 3 x 10(-5) mol/L.
- Measured coronary overflow of bradykinin, norepinephrine, and lactate, alongside coronary flow, oxygen consumption, and left ventricular pressure.
Main Results:
- Captopril demonstrated a concentration-dependent decrease in cardiac oxygen consumption and maximal left ventricular pressure.
- Coronary flow was increased at the highest captopril concentration.
- Bradykinin outflow remained unaffected by captopril treatment.
Conclusions:
- Captopril exerts significant effects on healthy heart metabolism and workload.
- The observed reduction in oxygen consumption and pressure suggests a protective influence.
- Captopril may offer benefits in acute conditions involving cardiac malnourishment or overload in healthy hearts.
Abstract:
Although beneficial effects of angiotensin converting enzyme (ACE) inhibition have been demonstrated in ill (ischemic, failing) hearts, it has not been proved that ACE inhibition induces changes in healthy hearts. The question is of clinical relevance, as many hypertensive patients do not display cardiac damage at the onset of treatment with ACE inhibitors, and possible changes in cardiac work might turn out more or less advantageous in the development of hypertensive heart disease. In a refined working heart preparation allowing measurement of cardiac work, including the contribution of atrial work and paracrine cardiac regulation, effects of captopril on cardiac dynamics were assessed. Coronary overflow of bradykinin, norepinephrine, and lactate was measured. Hearts were perfused for 20 min with vehicle or captopril at 3 x 10(-8), 3 x 10(-7), 3 x 10(-6), and 3 x 10(-5) mol/L. At the highest concentration, captopril increased coronary flow. Extending previous studies, the present study demonstrates that, in a concentration-dependent manner, captopril decreased oxygen consumption and maximal left ventricular pressure although the bradykinin outflow was not affected. From these influences of the drug on cardiac work and metabolism in healthy hearts, a protective influence of captopril in acute, critical situations of cardiac malnourishment or cardiac overload may be derived.