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Impact of pathogen burden in patients with coronary artery disease in relation to systemic inflammation and variation

Jean Louis Georges1, Hans J Rupprecht, Stefan Blankenberg

  • 1INSERM U525, Paris, France.

The American Journal of Cardiology
|August 29, 2003
PubMed

Insights

Increased pathogen burden is linked to coronary artery disease (CAD). Genetic factors, specifically interleukin-6 (IL-6) gene variations, influence this association, highlighting infection

Area of Science:

  • Immunology and Cardiovascular Medicine
  • Infectious Disease Epidemiology
  • Human Genetics and Genomics

Background:

  • Pathogen burden, the cumulative exposure to infectious agents, is associated with coronary artery disease (CAD) development and prognosis.
  • The interplay between host genetics, infectious agents, and CAD pathogenesis remains incompletely understood.
  • Inflammatory markers and specific gene polymorphisms may modulate the relationship between pathogen exposure and cardiovascular risk.

Purpose of the Study:

  • To investigate how serum inflammatory markers and polymorphisms in interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) genes modify the association between pathogen burden and CAD.
  • To determine the independent contribution of pathogen burden to CAD risk, controlling for traditional risk factors.

Main Methods:

  • Quantified immunoglobulin (Ig) G or IgA antibodies against 8 pathogens in 991 CAD patients and 333 controls.
  • Measured serum levels of high-sensitivity C-reactive protein, fibrinogen, IL-6, and TNF-alpha.
  • Genotyped subjects for IL-6/G-174C, TNF/C-851T, and TNF/G-308A polymorphisms.

Main Results:

  • A significant positive association was confirmed between increasing pathogen burden and CAD, even after adjusting for risk factors.
  • High pathogen burden (>/=4 pathogens) was observed in 50% of CAD patients versus 21% of controls (p <0.0001) and linked to lower HDL cholesterol.
  • The IL-6/G-174C polymorphism modulated the CAD-pathogen burden association, with heterozygotes showing a higher odds ratio, mediated by IL-6 serum levels. No interaction was found with TNF-alpha polymorphisms.

Conclusions:

  • Pathogen burden is a significant risk factor for coronary artery disease.
  • The genetic variation in the IL-6 gene influences the impact of pathogen burden on CAD risk, suggesting a role for IL-6 in mediating this interaction.
  • Further research into the combined effects of infectious agents and host genetics is warranted for understanding CAD.

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