Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Inflammation Research |
| Vol/bind | 59 |
| Udgave nummer | 11 |
| Sider (fra-til) | 965-9 |
| Antal sider | 5 |
| ISSN | 1023-3830 |
| DOI | |
| Status | Udgivet - 1 nov. 2010 |
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I: Inflammation Research, Bind 59, Nr. 11, 01.11.2010, s. 965-9.
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Single nucleotide polymorphisms in inflammatory genes and the risk of early onset of lone atrial fibrillation
AU - Henningsen, Kristoffer M A
AU - Olesen, Morten S
AU - Pedersen, Maria
AU - Nielsen, Lone
AU - Haunsø, Stig
AU - Bruunsgaard, Helle
AU - Svendsen, Jesper Hastrup
AU - Henningsen, Kristoffer M A
AU - Olesen, Morten S
AU - Pedersen, Maria
AU - Nielsen, Lone
AU - Haunsø, Stig
AU - Bruunsgaard, Helle
AU - Svendsen, Jesper Hastrup
PY - 2010/11/1
Y1 - 2010/11/1
N2 - 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.
AB - 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.
U2 - 10.1007/s00011-010-0210-8
DO - 10.1007/s00011-010-0210-8
M3 - Journal article
C2 - 20490891
SN - 1023-3830
VL - 59
SP - 965
EP - 969
JO - Inflammation Research
JF - Inflammation Research
IS - 11
ER -