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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
PubMed

Insights

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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