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The effect of ACE inhibition on myocardial energy metabolism
H P Schultheiss1, G Ullrich, M Schindler
1Medizinische Klinik and Poliklinik B, Universität Düsseldorf, F.R.G.
European Heart Journal
|April 1, 1990
Summary
Chronic heart failure impairs myocardial oxygen supply and demand, causing metabolic changes. ACE-inhibitor therapy improved the myocardial energy balance in patients, potentially interrupting heart failure progression.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Chronic heart failure (CHF) is characterized by an imbalance between myocardial oxygen supply and demand.
- This imbalance results from increased intramyocardial vascular resistance, elevated filling pressures, shortened diastolic perfusion time, and heightened myocardial oxygen demand.
- Metabolic adaptations in the myocardium, such as altered lactate dehydrogenase (LDH) isoenzyme patterns and changes in ADP/ATP-carrier concentration, are observed in severe CHF.
Purpose of the Study:
- To investigate the effects of ACE-inhibitor therapy on myocardial energy metabolism in patients with chronic heart failure.
- To determine if ACE-inhibitor treatment can reverse the observed metabolic changes associated with CHF.
Main Methods:
- Analysis of myocardial tissue from patients with chronic heart failure to assess LDH isoenzyme patterns (LDH 1 and LDH 5) and ADP/ATP-carrier concentration.
- Treatment of 33 CHF patients with ACE-inhibitors.
- Post-treatment assessment of LDH isoenzymes and ADP/ATP-carrier concentration.
Main Results:
- Baseline myocardial tissue showed increased LDH 5 and decreased LDH 1, along with elevated ADP/ATP-carrier concentration.
- ACE-inhibitor therapy led to a significant increase in LDH 1 and a decrease in LDH 5 (P < 0.005 and P < 0.001, respectively).
- ADP/ATP-carrier concentration significantly decreased, returning to normal ranges.
Conclusions:
- ACE-inhibitor therapy improves the myocardial energy balance in chronic heart failure patients.
- The observed shift in LDH isoenzymes and reduction in ADP/ATP-carrier concentration indicate enhanced myocardial energy metabolism.
- This improvement may help interrupt the self-perpetuation of chronic heart failure, possibly by addressing subendocardial perfusion deficits.
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