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Trimetazidine: in vitro influence on heart mitochondrial function

L Demaison1, E Fantini, E Sentex

  • 1I.N.R.A., Unité de Nutrition Lipidique, Dijon, France.

The American Journal of Cardiology
|August 24, 1995
PubMed
Summary

Trimetazidine (TMZ) protects heart cells from hypoxia by preventing electromechanical damage and reducing cell death. However, it does not affect adenosine triphosphate (ATP) levels and inhibits fatty acid oxidation in mitochondria.

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Area of Science:

  • Cardiology
  • Cellular Electrophysiology
  • Mitochondrial Metabolism

Background:

  • The antianginal drug trimetazidine (TMZ) mechanism of action is not fully understood.
  • Hypoxia in cardiomyocytes leads to significant electromechanical alterations and cell damage.

Purpose of the Study:

  • To investigate the effects of trimetazidine (TMZ) on cardiac cell electrophysiology and energy metabolism under hypoxic conditions.
  • To elucidate the impact of TMZ on mitochondrial respiration and substrate oxidation.

Main Methods:

  • Cultured rat ventricular myocytes were subjected to hypoxia with and without TMZ treatment.
  • Electrophysiological parameters (action potential, resting membrane potential, contractility) and lactate dehydrogenase leakage were measured.
  • Mitochondrial respiration and substrate oxidation (pyruvate, palmitoylcarnitine, glutamate, citrate) were assessed in rats treated with TMZ.

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Main Results:

  • TMZ largely prevented hypoxia-induced electromechanical alterations and reduced lactate dehydrogenase leakage in cardiomyocytes.
  • TMZ did not prevent the decrease in adenosine triphosphate (ATP) content under hypoxia.
  • TMZ inhibited palmitoylcarnitine oxidation in heart mitochondria, with minor effects on pyruvate oxidation.

Conclusions:

  • Trimetazidine (TMZ) offers significant protection against hypoxic damage in cardiac cells.
  • TMZ's mechanism involves preserving cellular integrity rather than directly boosting ATP levels under hypoxia.
  • TMZ interferes with fatty acid oxidation pathways in cardiac mitochondria, suggesting a complex interplay with cellular energy metabolism.