BACKGROUND: Systemic low-grade inflammation is a prognostic risk factor of atrial fibrillation (AF). OBJECTIVE: We hypothesized that genetic polymorphisms, which determine the rate of inflammatory cytokines, are associated with the risk of AF, independently of comorbidity. METHODS AND RESULTS: We included 192 patients with so-called lone AF and age 40 years or below, and 188 healthy controls. All patients were genotyped for single nucleotide polymorphisms (SNPs) in inflammatory genes using fluorescence-based real-time polymerase chain reaction (PCR). A case-control analysis of the C/C, C/T and T/T genotypes on IL1A-889 revealed a significant difference in both the frequency of genotypes (p = 0.03) and in the allelic frequency (p = 0.015). These differences were not significant after Bonferroni corrections. For IL1B-511, IL10-592, IL10-1082, IL18-137, IL18-607 and TNF-308 there were no significant differences, neither in genotype frequency, nor in allelic frequency between the lone AF patients and the controls. CONCLUSION: Our study failed to show an association between polymorphisms in inflammatory genes and early onset of lone AF. It remains to be established whether polymorphisms in inflammatory genes play a causative role in the pathophysiology of AF.
BACKGROUND: Systemic low-grade inflammation is a prognostic risk factor of atrial fibrillation (AF). OBJECTIVE: We hypothesized that genetic polymorphisms, which determine the rate of inflammatory cytokines, are associated with the risk of AF, independently of comorbidity. METHODS AND RESULTS: We included 192 patients with so-called lone AF and age 40 years or below, and 188 healthy controls. All patients were genotyped for single nucleotide polymorphisms (SNPs) in inflammatory genes using fluorescence-based real-time polymerase chain reaction (PCR). A case-control analysis of the C/C, C/T and T/T genotypes on IL1A-889 revealed a significant difference in both the frequency of genotypes (p = 0.03) and in the allelic frequency (p = 0.015). These differences were not significant after Bonferroni corrections. For IL1B-511, IL10-592, IL10-1082, IL18-137, IL18-607 and TNF-308 there were no significant differences, neither in genotype frequency, nor in allelic frequency between the lone AFpatients and the controls. CONCLUSION: Our study failed to show an association between polymorphisms in inflammatory genes and early onset of lone AF. It remains to be established whether polymorphisms in inflammatory genes play a causative role in the pathophysiology of AF.
Authors: Y Du; R C Dodel; B J Eastwood; K R Bales; F Gao; F Lohmüller; U Müller; A Kurz; R Zimmer; R M Evans; A Hake; T Gasser; W H Oertel; W S Griffin; S M Paul; M R Farlow Journal: Neurology Date: 2000-08-22 Impact factor: 9.910
Authors: S L Kopecky; B J Gersh; M D McGoon; J P Whisnant; D R Holmes; D M Ilstrup; R L Frye Journal: N Engl J Med Date: 1987-09-10 Impact factor: 91.245
Authors: Seung Zhoo Yoon; In-Jin Jang; Yoon Ji Choi; Mae Hwa Kang; Hye Ja Lim; Young Jin Lim; Hye Won Lee; Seong Ho Chang; Suk Min Yoon Journal: J Cardiothorac Vasc Anesth Date: 2009-05-20 Impact factor: 2.628
Authors: Kristoffer M Henningsen; Morten S Olesen; Lasse S Ravn; Ulrik Dixen; Stig Haunsoe; Helle Bruunsgaard; Jesper H Svendsen Journal: Inflamm Res Date: 2010-12-04 Impact factor: 4.575