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A Murine Model of Hyperlipidemia-Induced Heart Failure with Preserved Ejection Fraction
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Leptin, leptin gene and leptin receptor gene polymorphism in heart failure with preserved ejection fraction

Tarek A Abd El-Aziz1, Randa H Mohamed, Rasha H Mohamed

  • 1Cardiology Department, Faculty of Medicine, Zagazig University, 28-El-Galaa Street, Zagazig, Egypt. tarekaziz98@hotmail.com

Heart and Vessels
|May 18, 2011
PubMed

Insights

Heart failure with normal ejection fraction (HFNEF) is linked to higher leptin levels and specific gene variations. These factors significantly increase the risk of developing HFNEF in coronary artery disease patients.

Area of Science:

  • Cardiology
  • Genetics
  • Metabolic Syndrome

Background:

  • Heart failure with normal ejection fraction (HFNEF) is prevalent in patients with obesity and coronary artery disease (CAD).
  • Ischemia and reperfusion injury are known to affect leptin (LEP) and leptin receptor (LEPR) gene expression.
  • Understanding the role of leptin and its receptor in HFNEF is crucial for cardiovascular health.

Purpose of the Study:

  • To investigate the association between serum leptin levels, and leptin (LEP) and leptin receptor (LEPR) gene polymorphisms with HFNEF in Egyptian patients with CAD.
  • To determine if specific LEP and LEPR genotypes correlate with the severity of HFNEF.

Main Methods:

  • Genotyping for LEP and LEPR polymorphisms was performed on 100 Egyptian CAD patients with HFNEF and 100 healthy controls.
  • Serum leptin levels were quantified in both patient and control groups.
  • Association analysis was conducted between genotypes, leptin levels, and NYHA functional classes.

Main Results:

  • Serum leptin levels were significantly elevated in HFNEF patients compared to controls.
  • The leptin gene AA genotype and the leptin receptor gene RR genotype were significantly more frequent in HFNEF patients.
  • Leptin levels and the identified genotypes showed a stronger association with NYHA class III compared to NYHA classes I and II.

Conclusions:

  • Increased serum leptin levels are associated with HFNEF in CAD patients.
  • The LEP AA genotype and LEPR RR genotype represent significant risk factors, conferring at least a threefold increased risk for developing HFNEF.
  • Leptin and its receptor gene variations may play a critical role in the pathophysiology of HFNEF in the context of CAD.

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