Apolipoprotein E gene polymorphisms and thrombosis and restenosis after coronary artery stenting

J Lipid Res. 2004 Dec;45(12):2221-6. doi: 10.1194/jlr.M400148-JLR200. Epub 2004 Oct 1.

Abstract

Experimental data support a protective function of apolipoprotein E (apoE) against restenosis, the main factor limiting the long-term benefit of percutaneous coronary interventions. We investigated the possibility that the single nucleotide polymorphisms (SNPs)--219G/T, 113G/C, 334T/C, and 472C/T of the gene encoding apoE (APOE) are associated with the incidence of death and myocardial infarction or restenosis after stenting in coronary arteries. In addition, we asked whether the apoE isotype-related epsilon2/epsilon3/epsilon4 polymorphism, defined by specific allele combinations (haplotypes) of the 334T/C and 472C/T polymorphism, and other APOE haplotypes, derived from all four SNPs investigated, are associated with adverse clinical and angiographic outcomes after stenting. Our study included 1,850 consecutive patients with symptomatic coronary artery disease (CAD) who underwent stent implantation. Follow-up angiography was performed in 1,556 patients (84.1%) at 6 months after the intervention. We found that none of the APOE SNPs is associated with death and myocardial infarction or restenosis after stenting. In addition, we observed no relationship between APOE haplotypes and adverse outcomes. In conclusion, the APOE -219G/T, 113G/C, 334T/C, and 472C/T polymorphisms, either alone or in combination, do not represent genetic markers of the risk of thrombotic and restenotic complications in patients with CAD treated with coronary stenting.

MeSH terms

  • Apolipoproteins E / genetics*
  • Apolipoproteins E / metabolism
  • Coronary Restenosis / genetics*
  • Coronary Restenosis / metabolism
  • Coronary Vessels*
  • Female
  • Humans
  • Male
  • Middle Aged
  • Myocardial Infarction / genetics
  • Myocardial Infarction / metabolism
  • Polymorphism, Genetic
  • Polymorphism, Single Nucleotide
  • Stents*
  • Thrombosis / genetics*
  • Thrombosis / metabolism

Substances

  • Apolipoproteins E