PDF(Pubmed)
Abstract：
UNASSIGNED: The risk of atrial fibrillation (AF) is increased in individuals with gastroesophageal reflux disease (GERD), according to observational research. The causal significance of this association is still unclear. This study sought to assess GERD\'s role as a potential contributing factor in AF.
UNASSIGNED: With the use of a two-sample Mendelian randomization (MR) technique, we assessed the causal relationship between GERD and AF. The association of genetic variants with GERD was examined using data from a recent genome-wide association study (GWAS) that included 602,604 people. Data on the association between genetic variations and AF was obtained from a second GWAS with 1,030,836 participants. The effect sizes were examined based on the inverse-variance weighted method. Additional statistical techniques, including MR-Egger, simple mode, weighted mode, MR Pleiotropy Residual Sum, outlier, and weighted median were used in the sensitivity analysis.
UNASSIGNED: MR analyses in inverse-variance weighted models, using 76 single nucleotide polymorphisms (SNPs) as markers, revealed a relationship between genetically predicted GERD and a greater AF incidence [odds ratio (OR): 1.165, 95% CI 1.102-1.231; P = 7.637 × 10-8]. According to MR-Egger, there was no evidence of gene pleiotropy that could be found (intercept = 0.003, P = 0.581). The findings of the sensitivity study, which used several MR methods, were found to be reliable.
UNASSIGNED: The MR analysis revealed a correlation between GERD and increased AF incidence, supporting the idea that treating patients with GERD as early as possible might reduce their chance of developing AF.
UNASSIGNED: With the use of a two-sample Mendelian randomization (MR) technique, we assessed the causal relationship between GERD and AF. The association of genetic variants with GERD was examined using data from a recent genome-wide association study (GWAS) that included 602,604 people. Data on the association between genetic variations and AF was obtained from a second GWAS with 1,030,836 participants. The effect sizes were examined based on the inverse-variance weighted method. Additional statistical techniques, including MR-Egger, simple mode, weighted mode, MR Pleiotropy Residual Sum, outlier, and weighted median were used in the sensitivity analysis.
UNASSIGNED: MR analyses in inverse-variance weighted models, using 76 single nucleotide polymorphisms (SNPs) as markers, revealed a relationship between genetically predicted GERD and a greater AF incidence [odds ratio (OR): 1.165, 95% CI 1.102-1.231; P = 7.637 × 10-8]. According to MR-Egger, there was no evidence of gene pleiotropy that could be found (intercept = 0.003, P = 0.581). The findings of the sensitivity study, which used several MR methods, were found to be reliable.
UNASSIGNED: The MR analysis revealed a correlation between GERD and increased AF incidence, supporting the idea that treating patients with GERD as early as possible might reduce their chance of developing AF.
摘要：
■患有胃食管反流病（GERD）的个体发生房颤（AF）的风险增加，根据观察研究。这种关联的因果意义尚不清楚。本研究旨在评估GERD作为房颤潜在影响因素的作用。
■使用双样本孟德尔随机化（MR）技术，我们评估了GERD与AF之间的因果关系.使用最近的全基因组关联研究（GWAS）的数据检查了遗传变异与GERD的关联，该研究包括602,604人。关于遗传变异和AF之间的关联的数据是从第二个GWAS获得的，有1,030,836名参与者。基于逆方差加权方法检查了效应大小。其他统计技术，包括MR-Egger,简单模式，加权模式，MR辉变剩余和,离群值,和加权中位数用于敏感性分析。
■逆方差加权模型中的MR分析，使用76个单核苷酸多态性（SNP）作为标记，揭示了遗传预测的GERD与更高的AF发生率之间的关系[比值比（OR）：1.165，95％CI1.102-1.231；P=7.637×10-8]。根据MR-Egger的说法,没有发现基因多效性的证据(截距=0.003,P=0.581).敏感性研究的结果，使用了几种MR方法，被发现是可靠的。
■MR分析显示GERD与房颤发生率增加之间存在相关性，支持尽早治疗GERD患者可能会减少他们发生房颤的机会。
■使用双样本孟德尔随机化（MR）技术，我们评估了GERD与AF之间的因果关系.使用最近的全基因组关联研究（GWAS）的数据检查了遗传变异与GERD的关联，该研究包括602,604人。关于遗传变异和AF之间的关联的数据是从第二个GWAS获得的，有1,030,836名参与者。基于逆方差加权方法检查了效应大小。其他统计技术，包括MR-Egger,简单模式，加权模式，MR辉变剩余和,离群值,和加权中位数用于敏感性分析。
■逆方差加权模型中的MR分析，使用76个单核苷酸多态性（SNP）作为标记，揭示了遗传预测的GERD与更高的AF发生率之间的关系[比值比（OR）：1.165，95％CI1.102-1.231；P=7.637×10-8]。根据MR-Egger的说法,没有发现基因多效性的证据(截距=0.003,P=0.581).敏感性研究的结果，使用了几种MR方法，被发现是可靠的。
■MR分析显示GERD与房颤发生率增加之间存在相关性，支持尽早治疗GERD患者可能会减少他们发生房颤的机会。
