title: Assessment of interleukin-1 gene cluster polymorphisms in lone atrial fibrillation: new insight into the role of inflammation in atrial fibrillation.
abstract: BACKGROUND
  Systemic inflammation is accepted as one of the pathophysiological mechanisms of atrial fibrillation (AF). The role of inflammation has been shown previously. Interleukin (IL) system is the main modulator of the inflammatory responses and genetic polymorphisms of IL-1 cluster genes are associated with increased risk for inflammatory diseases.
  
  
  OBJECTIVE
  To investigate the association between polymorphisms of IL-1 cluster genes and lone AF.
  
  
  METHODS
  DNA samples were collected from 70 proven lone AF patients and 70 healthy subjects. Genomic DNA was typed for the variable number of the tandem repeat (VNTR) IL-1 receptor antagonist (RN) gene polymorphism, IL-1B -511 C > T(rs16944) promoter polymorphism, and +3953 C > T(rs1143634) polymorphism in exon 5 by polymerase chain reaction.
  
  
  RESULTS
  In lone AF group the frequency of IL-1RN2/2 and IL-1RN1/2 genotypes were higher than in the control group (7.2% vs 4.3% and 48.5% vs 22.8%, respectively; χ(2) = 14.1; P = 0.028). The frequency of allele 2 was significantly higher in the lone AF group (32.1% vs 15.7%; χ(2) = 10.7; P = 0.005). Allele and genotype distribution of IL-1B -511 C > T and +3953 C > T polymorphisms were not statistically different between the groups. C-reactive protein (CRP) levels were higher in lone AF patients compared to the control group (median = 1.25, interquartile range [IQR] = 0.85 vs median = 1.08, IQR 0.46 mg/L, respectively; P = 0.02). In multivariate regression analysis, presence of allele 2 of IL-1 VNTR polymorphism and elevated plasma high-sensitive-CRP levels were the independent predictors of lone AF.
  
  
  CONCLUSIONS
  Presence of allele 2 of VNTR polymorphism of IL-1RN gene may cause increased risk for lone AF probably due to the inadequate limitation of inflammatory reactions.
authors.affiliation: Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital, Istanbul, Turkey.
authors.forename: Baris
authors.initials: B
authors.lastname: Gungor
authors.forename: Ahmet
authors.initials: A
authors.lastname: Ekmekci
authors.forename: Ahmet
authors.initials: A
authors.lastname: Arman
authors.forename: Kazim S
authors.initials: KS
authors.lastname: Ozcan
authors.forename: Ekrem
authors.initials: E
authors.lastname: Ucer
authors.forename: Ahmet T
authors.initials: AT
authors.lastname: Alper
authors.forename: Nazmi
authors.initials: N
authors.lastname: Calik
authors.forename: Hale
authors.initials: H
authors.lastname: Yilmaz
authors.forename: Tuna
authors.initials: T
authors.lastname: Tezel
authors.forename: Ajda
authors.initials: A
authors.lastname: Coker
authors.forename: Osman
authors.initials: O
authors.lastname: Bolca
mesh_terms: D000328:Adult; D001281:Atrial Fibrillation / Q000453:epidemiology* / Q000235:genetics*; D001483:Base Sequence; D015897:Comorbidity; D005260:Female; D005819:Genetic Markers / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000453:epidemiology* / Q000235:genetics*; D006801:Humans; D007249:Inflammation / Q000453:epidemiology* / Q000235:genetics*; D008297:Male; D008969:Molecular Sequence Data; D005810:Multigene Family / Q000235:genetics; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D015995:Prevalence; D012307:Risk Factors; D014421:Turkey / Q000453:epidemiology
chemical_list: D005819:Genetic Markers
keywords: CRP; interleukin polymorphism; lone atrial fibrillation