Post-hoc analysis on the CD14 C(-260)T promoter polymorphism and coronary heart disease

Physiol Res. 2007;56(6):727-733. doi: 10.33549/physiolres.930964. Epub 2006 Nov 6.

Abstract

Functional C(-260)--> T polymorphism in the promoter of the CD14 gene has been reported to be associated with coronary heart disease (CHD). The functional role of the polymorphism, however, is still a matter of debate, since several studies have not proved its effect on clinical outcomes associated with atherosclerosis. Cardiovascular-related morbidity and mortality was assessed in a post-hoc approach four years after baseline characterization of patients (male/female n = 36/32) with angiographically proven coronary heart disease. CD14 C(-260)--> T promoter genotype was determined at baseline. Seventeen out of 20 CHD patients with non-lethal cardiovascular events carried at least one T-allele. CD14 T-260 allele carriers have a 3.59-fold (95 % confidence interval: 1.11-6.75) increased risk for non-lethal cardiovascular events (Kaplan-Meier plot: log rank test p = 0.029). All patients with lethal outcomes (n = 6) were also T-allele carriers. Multivariate logistic regression analysis among CHD patients including age, established risk factors and the C(-260)--> T polymorphism as covariates and non-lethal events as a dependent variable confirmed the independent prospective effect of the T-allele on cardiovascular outcomes in this subset. Further evidence is provided for the role of CD14 C(-260)--> T promoter polymorphism as a genetic susceptibility marker of atherosclerosis in patients with an advanced clinical course of the disease. Due to the small sample size and post-hoc character of the study large-scale prospective studies that monitor patients with proven CHD are needed to confirm these findings.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Biomarkers
  • Coronary Disease / epidemiology
  • Coronary Disease / genetics*
  • DNA / biosynthesis
  • DNA / genetics
  • Female
  • Genetics
  • Genotype
  • Humans
  • Lipids / blood
  • Lipopolysaccharide Receptors / genetics*
  • Logistic Models
  • Male
  • Middle Aged
  • Polymorphism, Genetic / genetics
  • Promoter Regions, Genetic / genetics*
  • Risk

Substances

  • Biomarkers
  • Lipids
  • Lipopolysaccharide Receptors
  • DNA