title: Genetic inflammatory factors predict restenosis after percutaneous coronary interventions.
abstract: BACKGROUND
  Restenosis is a negative effect of percutaneous coronary intervention (PCI). No clinical factors are available that allow good risk stratification. However, evidence exists that genetic factors are important in the restenotic process as well as in the process of inflammation, a pivotal factor in restenosis. Association studies have identified genes that may predispose to restenosis, but confirmation by large prospective studies is lacking. Our aim was to identify polymorphisms and haplotypes in genes involved in inflammatory pathways that predispose to restenosis.
  
  
  RESULTS
  The GENetic DEterminants of Restenosis (GENDER) project is a multicenter prospective study, including 3104 consecutive patients after successful PCI. Forty-eight polymorphisms in 34 genes in pathways possibly involved in the inflammatory process were analyzed. The 16Gly variant of the beta2-adrenergic receptor gave an increased risk of target vessel revascularization (TVR). The rare alleles of the CD14 gene (-260T/T), colony-stimulating factor 2 gene (117Thr/Thr), and eotaxin gene (-1328A/A) were associated with decreased risk of TVR. However, through the use of multiple testing corrections with permutation analysis, the probability of finding 4 significant markers by chance was 12%.
  
  
  CONCLUSIONS
  Polymorphisms in 4 genes considered involved in the inflammatory reaction showed an association with TVR after PCI. Our results may contribute to the unraveling of the restenotic process. Given the explorative nature of this analysis, our results need to be replicated in other studies.
authors.affiliation: Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
authors.forename: Pascalle S
authors.initials: PS
authors.lastname: Monraats
authors.forename: Nuno M M
authors.initials: NM
authors.lastname: Pires
authors.forename: Willem R P
authors.initials: WR
authors.lastname: Agema
authors.forename: Aeilko H
authors.initials: AH
authors.lastname: Zwinderman
authors.forename: Abbey
authors.initials: A
authors.lastname: Schepers
authors.forename: Moniek P M
authors.initials: MP
authors.lastname: de Maat
authors.forename: Pieter A
authors.initials: PA
authors.lastname: Doevendans
authors.forename: Robbert J
authors.initials: RJ
authors.lastname: de Winter
authors.forename: René A
authors.initials: RA
authors.lastname: Tio
authors.forename: Johannes
authors.initials: J
authors.lastname: Waltenberger
authors.forename: Rune R
authors.initials: RR
authors.lastname: Frants
authors.forename: Paul H A
authors.initials: PH
authors.lastname: Quax
authors.forename: Bart J M
authors.initials: BJ
authors.lastname: van Vlijmen
authors.forename: Douwe E
authors.initials: DE
authors.lastname: Atsma
authors.forename: Arnoud
authors.initials: A
authors.lastname: van der Laarse
authors.forename: Ernst E
authors.initials: EE
authors.lastname: van der Wall
authors.forename: J Wouter
authors.initials: JW
authors.lastname: Jukema
mesh_terms: D019943:Amino Acid Substitution; D015906:Angioplasty, Balloon, Coronary; D023903:Coronary Restenosis / Q000235:genetics*; D006801:Humans; D007249:Inflammation / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D011446:Prospective Studies; D016896:Treatment Outcome