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Metabolic alterations in end-stage and less severe heart failure--myocardial carnitine decrease.

V Regitz1, C Bossaller, R Strasser

  • 1Clinic for Internal Medicine/Cardiology, German Heart Institute, Berlin.

Journal of Clinical Chemistry and Clinical Biochemistry. Zeitschrift Fur Klinische Chemie Und Klinische Biochemie
|September 1, 1990
PubMed
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Severe carnitine deficiency in the heart muscle impairs fatty acid oxidation. This study found significant carnitine reductions in heart failure patients, indicating it may be a non-specific marker for cardiac dysfunction.

Area of Science:

  • Biochemistry
  • Cardiology
  • Metabolic Diseases

Background:

  • Carnitine is crucial for fatty acid oxidation, a primary energy source for the heart.
  • Severe tissue carnitine deficiency is known to impair cardiac function.
  • Previous studies suggest altered carnitine levels in various heart conditions.

Purpose of the Study:

  • To quantify myocardial carnitine levels in patients with heart failure.
  • To compare carnitine levels between heart failure patients and healthy controls.
  • To determine if carnitine reduction is specific to certain heart diseases.

Main Methods:

  • Analysis of explanted hearts from end-stage heart failure patients and healthy donors.
  • Measurement of total and free carnitine in myocardial tissue.

Related Experiment Videos

  • Analysis of endomyocardial biopsies from patients with varying degrees of heart failure and controls.

    • Main Results:

    • Explanted hearts from heart failure patients showed a 57% decrease in carnitine compared to healthy donors.
    • Endomyocardial biopsies revealed a 42% decrease in total myocardial carnitine in heart failure patients.
    • Reductions in both total and free carnitine were observed across different types of heart failure, including dilated cardiomyopathy and coronary artery disease.

    Conclusions:

    • Myocardial carnitine levels are significantly decreased in patients with heart failure.
    • The observed decrease in carnitine is comparable across different etiologies of heart failure.
    • Alterations in myocardial carnitine content appear to be non-specific biochemical markers in heart failure, with their functional consequences yet to be fully elucidated.