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Related Experiment Videos

Alcohol and the myocardium

P J Richardson1, V B Patel, V R Preedy

  • 1Department of Cardiology, King's College School of Medicine and Dentistry, London, UK.

Novartis Foundation Symposium
|February 9, 1999
PubMed
Summary

Alcoholic cardiomyopathy (ACM) involves structural and functional heart changes, distinct from dilated cardiomyopathy via morphometry. Ethanol and acetaldehyde disrupt cardiac protein synthesis and reduce protective heat shock proteins (HSPs) and desmin.

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Area of Science:

  • Cardiology
  • Toxicology
  • Biochemistry

Background:

  • Alcoholic cardiomyopathy (ACM) presents with structural and functional abnormalities.
  • Histological features of ACM closely resemble dilated cardiomyopathy, necessitating advanced differentiation methods.

Purpose of the Study:

  • To differentiate ACM from dilated cardiomyopathy using quantitative morphometry.
  • To investigate the molecular mechanisms underlying ACM, including enzyme activity, protein adducts, and protein synthesis alterations.

Main Methods:

  • Quantitative morphometry of myocardial biopsies.
  • Analysis of myocardial enzyme activities (e.g., alpha-hydroxybutyric dehydrogenase, creatine kinase).
  • Detection of serum antibodies against cardiac acetaldehyde-protein adducts.
  • Two-dimensional SDS-PAGE to assess cardiac muscle protein alterations in animal models.

Main Results:

  • Quantitative morphometry can distinguish ACM from dilated cardiomyopathy.
  • Increased myocardial enzyme activities in ACM correlate with alcohol intake patterns.
  • One-third of ACM patients exhibit antibodies against cardiac acetaldehyde-protein adducts.
  • Ethanol and acetaldehyde acutely reduce cardiac contractile protein synthesis.
  • Chronic alcohol exposure alters over 10% of heart muscle proteins, decreasing heat shock proteins (HSPs) Hsp60 and Hsp70, and desmin.

Conclusions:

  • ACM is a complex condition driven by altered protein synthesis, acetaldehyde adduct formation, and reduced cardiac HSPs and desmin.
  • Both alcohol and acetaldehyde act as myocardial perturbants, contributing to ACM pathogenesis.
  • Specific molecular changes, including protein alterations and adducts, offer targets for understanding and potentially treating ACM.

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