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Published on: January 28, 2020

Role of inflammatory gene polymorphisms in left ventricular dysfunction (LVD) susceptibility in coronary artery

Avshesh Mishra1, Anshika Srivastava, T Mittal

  • 1Department of Genetics, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226 014 (UP), India.

Cytokine
|January 30, 2013
PubMed

Insights

The NFKB1 gene polymorphism is linked to left ventricular dysfunction (LVD) in coronary artery disease (CAD) patients. The ATTG/ATTG genotype increases LVD risk, impacting heart failure progression.

Area of Science:

  • Cardiology
  • Genetics
  • Molecular Biology

Background:

  • Inflammation significantly worsens heart conditions, particularly left ventricular dysfunction (LVD).
  • The NFKB1 gene, encoding the p50 subunit of NFkB, has a promoter polymorphism affecting anti-inflammatory protein levels.
  • NFkB transcription factor activation influences genes like IL6 and TNF-α, crucial in inflammatory pathways.

Purpose of the Study:

  • To investigate the association between polymorphisms in the NFKB1, IL6, and TNF-α genes and LVD in patients with coronary artery disease (CAD).

Main Methods:

  • A study involving 830 participants (600 CAD patients, 230 controls) across primary and replication cohorts.
  • Genotyping of NFKB1 -94 ATTG ins/del, IL6 -174 G/C, and TNF-α -308 G/A polymorphisms using PCR/ARMS-PCR.
  • Meta-analysis combining primary and replication cohort results using Fisher's and Mantel-Haenszel tests to validate findings.

Main Results:

  • The NFKB1 ATTG/ATTG genotype showed a significant association with LVD (p=0.007, OR=2.34).
  • This genotype also correlated with increased left ventricular end-diastole and end-systole dimensions, LV mass, and reduced LVEF (p<0.05).
  • A significant association was observed between the NFKB1 genotype and myocardial infarction (p=0.043).

Conclusions:

  • The NFKB1 -94 ATTG ins/del polymorphism is a significant risk factor for LVD susceptibility.
  • The ATTG/ATTG genotype may exacerbate heart failure risk by promoting ventricular remodeling and impairing LV function.
Abstract

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