Brugada syndrome risk loci seem protective against atrial fibrillation

Research output: Contribution to journalJournal articleResearchpeer-review

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Brugada syndrome risk loci seem protective against atrial fibrillation. / Andreasen, Laura; Nielsen, Jonas B; Darkner, Stine; Christophersen, Ingrid E; Jabbari, Javad; Refsgaard, Lena; Thiis, Jens J; Sajadieh, Ahmad; Tveit, Arnljot; Haunsø, Stig; Svendsen, Jesper H; Schmitt, Nicole; Olesen, Morten S.

In: European Journal of Human Genetics, Vol. 22, 26.03.2014, p. 1357-1361.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Andreasen, L, Nielsen, JB, Darkner, S, Christophersen, IE, Jabbari, J, Refsgaard, L, Thiis, JJ, Sajadieh, A, Tveit, A, Haunsø, S, Svendsen, JH, Schmitt, N & Olesen, MS 2014, 'Brugada syndrome risk loci seem protective against atrial fibrillation', European Journal of Human Genetics, vol. 22, pp. 1357-1361. https://doi.org/10.1038/ejhg.2014.46

APA

Andreasen, L., Nielsen, J. B., Darkner, S., Christophersen, I. E., Jabbari, J., Refsgaard, L., ... Olesen, M. S. (2014). Brugada syndrome risk loci seem protective against atrial fibrillation. European Journal of Human Genetics, 22, 1357-1361. https://doi.org/10.1038/ejhg.2014.46

Vancouver

Andreasen L, Nielsen JB, Darkner S, Christophersen IE, Jabbari J, Refsgaard L et al. Brugada syndrome risk loci seem protective against atrial fibrillation. European Journal of Human Genetics. 2014 Mar 26;22:1357-1361. https://doi.org/10.1038/ejhg.2014.46

Author

Andreasen, Laura ; Nielsen, Jonas B ; Darkner, Stine ; Christophersen, Ingrid E ; Jabbari, Javad ; Refsgaard, Lena ; Thiis, Jens J ; Sajadieh, Ahmad ; Tveit, Arnljot ; Haunsø, Stig ; Svendsen, Jesper H ; Schmitt, Nicole ; Olesen, Morten S. / Brugada syndrome risk loci seem protective against atrial fibrillation. In: European Journal of Human Genetics. 2014 ; Vol. 22. pp. 1357-1361.

Bibtex

@article{70b4517ebd4b4510a970ecfe2f0902cf,
title = "Brugada syndrome risk loci seem protective against atrial fibrillation",
abstract = "Several studies have shown an overlap between genes involved in the pathophysiological mechanisms of atrial fibrillation (AF) and Brugada Syndrome (BrS). We investigated whether three single-nucleotide polymorphisms (SNPs) (rs11708996; G>C located intronic to SCN5A, rs10428132; T>G located in SCN10A, and rs9388451; T>C located downstream to HEY2) at loci associated with BrS in a recent genome-wide association study (GWAS) also were associated with AF. A total of 657 patients diagnosed with AF and a control group comprising 741 individuals free of AF were included. The three SNPs were genotyped using TaqMan assays. The frequencies of risk alleles in the AF population and the control population were compared in two-by-two models. One variant, rs10428132 at SCN10A, was associated with a statistically significant decreased risk of AF (odds ratio (OR)=0.77, P=0.001). A meta-analysis was performed by enriching the control population with allele frequencies from controls in the recently published BrS GWAS (2230 alleles). In this meta-analysis, both rs10428132 at SCN10A (OR=0.73, P=5.7 × 10(-6)) and rs11708996 at SCN5A (OR=0.80, P=0.02) showed a statistically significant decreased risk of AF. When assessing the additive effect of the three loci, we found that the risk of AF decreased in a dose-responsive manner with increasing numbers of risk alleles (OR=0.50, P=0.001 for individuals carrying ≥4 risk alleles vs ≤1 allele). In conclusion, the prevalence of three risk alleles previously associated with BrS was lower in AF patients than in patients free of AF, suggesting a protective role of these loci in developing AF.European Journal of Human Genetics advance online publication, 26 March 2014; doi:10.1038/ejhg.2014.46.",
author = "Laura Andreasen and Nielsen, {Jonas B} and Stine Darkner and Christophersen, {Ingrid E} and Javad Jabbari and Lena Refsgaard and Thiis, {Jens J} and Ahmad Sajadieh and Arnljot Tveit and Stig Hauns{\o} and Svendsen, {Jesper H} and Nicole Schmitt and Olesen, {Morten S}",
year = "2014",
month = "3",
day = "26",
doi = "10.1038/ejhg.2014.46",
language = "English",
volume = "22",
pages = "1357--1361",
journal = "European Journal of Human Genetics",
issn = "1018-4813",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Brugada syndrome risk loci seem protective against atrial fibrillation

AU - Andreasen, Laura

AU - Nielsen, Jonas B

AU - Darkner, Stine

AU - Christophersen, Ingrid E

AU - Jabbari, Javad

AU - Refsgaard, Lena

AU - Thiis, Jens J

AU - Sajadieh, Ahmad

AU - Tveit, Arnljot

AU - Haunsø, Stig

AU - Svendsen, Jesper H

AU - Schmitt, Nicole

AU - Olesen, Morten S

PY - 2014/3/26

Y1 - 2014/3/26

N2 - Several studies have shown an overlap between genes involved in the pathophysiological mechanisms of atrial fibrillation (AF) and Brugada Syndrome (BrS). We investigated whether three single-nucleotide polymorphisms (SNPs) (rs11708996; G>C located intronic to SCN5A, rs10428132; T>G located in SCN10A, and rs9388451; T>C located downstream to HEY2) at loci associated with BrS in a recent genome-wide association study (GWAS) also were associated with AF. A total of 657 patients diagnosed with AF and a control group comprising 741 individuals free of AF were included. The three SNPs were genotyped using TaqMan assays. The frequencies of risk alleles in the AF population and the control population were compared in two-by-two models. One variant, rs10428132 at SCN10A, was associated with a statistically significant decreased risk of AF (odds ratio (OR)=0.77, P=0.001). A meta-analysis was performed by enriching the control population with allele frequencies from controls in the recently published BrS GWAS (2230 alleles). In this meta-analysis, both rs10428132 at SCN10A (OR=0.73, P=5.7 × 10(-6)) and rs11708996 at SCN5A (OR=0.80, P=0.02) showed a statistically significant decreased risk of AF. When assessing the additive effect of the three loci, we found that the risk of AF decreased in a dose-responsive manner with increasing numbers of risk alleles (OR=0.50, P=0.001 for individuals carrying ≥4 risk alleles vs ≤1 allele). In conclusion, the prevalence of three risk alleles previously associated with BrS was lower in AF patients than in patients free of AF, suggesting a protective role of these loci in developing AF.European Journal of Human Genetics advance online publication, 26 March 2014; doi:10.1038/ejhg.2014.46.

AB - Several studies have shown an overlap between genes involved in the pathophysiological mechanisms of atrial fibrillation (AF) and Brugada Syndrome (BrS). We investigated whether three single-nucleotide polymorphisms (SNPs) (rs11708996; G>C located intronic to SCN5A, rs10428132; T>G located in SCN10A, and rs9388451; T>C located downstream to HEY2) at loci associated with BrS in a recent genome-wide association study (GWAS) also were associated with AF. A total of 657 patients diagnosed with AF and a control group comprising 741 individuals free of AF were included. The three SNPs were genotyped using TaqMan assays. The frequencies of risk alleles in the AF population and the control population were compared in two-by-two models. One variant, rs10428132 at SCN10A, was associated with a statistically significant decreased risk of AF (odds ratio (OR)=0.77, P=0.001). A meta-analysis was performed by enriching the control population with allele frequencies from controls in the recently published BrS GWAS (2230 alleles). In this meta-analysis, both rs10428132 at SCN10A (OR=0.73, P=5.7 × 10(-6)) and rs11708996 at SCN5A (OR=0.80, P=0.02) showed a statistically significant decreased risk of AF. When assessing the additive effect of the three loci, we found that the risk of AF decreased in a dose-responsive manner with increasing numbers of risk alleles (OR=0.50, P=0.001 for individuals carrying ≥4 risk alleles vs ≤1 allele). In conclusion, the prevalence of three risk alleles previously associated with BrS was lower in AF patients than in patients free of AF, suggesting a protective role of these loci in developing AF.European Journal of Human Genetics advance online publication, 26 March 2014; doi:10.1038/ejhg.2014.46.

U2 - 10.1038/ejhg.2014.46

DO - 10.1038/ejhg.2014.46

M3 - Journal article

C2 - 24667784

VL - 22

SP - 1357

EP - 1361

JO - European Journal of Human Genetics

JF - European Journal of Human Genetics

SN - 1018-4813

ER -

ID: 108549486