ArticleESC heart failure2025
Gastroesophageal reflux disease and risk of atrial fibrillation/flutter: Implications for heart failure progression.
Article in ESC heart failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Proteomic Signatures of Dental Enamel Hypomineralization: Divergent Molecular Pathways in Coal-Burning vs. Drinking-Water Fluorosis.Biological trace element research · 2026Article
- Gastroesophageal reflux disease and risk of atrial fibrillation/flutter: Implications for heart failure progression.ESC heart failure · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
aimsWhile observational studies suggest an association between gastroesophageal reflux disease (GERD) and atrial fibrillation/flutter (AF/AFL), the causal relationship and mechanisms remain undefined. This study employed Mendelian randomization (MR) to assess bidirectional causal relationships and explore potential implications for heart failure (HF) risk. METHODS AND
resultsA bidirectional two-sample MR analysis was conducted using genome-wide association study (GWAS) summary data from European populations (GERD: 129,080 cases and 473,524 controls; AF/AFL: 22,068 cases and 116,926 controls; Obesity: 4793 cases and 209,884 controls). Genetic instruments were selected for GERD and AF/AFL, with inverse variance weighting (IVW) as the primary analytical method to examine causality. Multivariable MR (MVMR) adjusted for obesity was performed to assess direct causal effects.
resultsIVW analysis demonstrated a significant causal effect of GERD on AF/AFL risk (OR = 1.373, 95% CI = 1.208-1.600, P = 0.017), which persisted after MVMR adjustment for obesity (OR = 1.303, 95% CI = 1.127-1.507, P < 0.001). Two-way analysis indicated no reverse causality. Sensitivity analyses supported result robustness with minimal pleiotropy.
conclusionsGenetic liability to GERD independently increases AF/AFL risk, unaffected by obesity pathways. Considering the well-established role of AF/AFL in the pathogenesis and progression of HF, our findings position GERD as a potential modifiable target within the causal pathway. Identification and management of GERD may therefore contribute to reducing atrial arrhythmia burden and subsequent HF risk.
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