ArticleScientific reports2025
Impact of gene-environment interactions on atrial fibrillation and cardiac structure.
Article in Scientific reports, 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Temporal trends of atrial fibrillation and atrial flutter burden across the BRICS: An observational study analysis for the GBD 2021.Medicine · 2026Observational
- The joint effects of multiple air pollutants, genetic susceptibility, and their interactions on incident cardiovascular disease, arrhythmia, and mortality.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
Environmental pollution is a major burden of cardiovascular disease. The aim of the study was to investigate the interactions between combined environmental factors and genetic susceptibility on atrial fibrillation (AF) and cardiac structures. The study included 374,495 participants from the UK Biobank, utilizing genetic data and environmental variables (including air pollution, noise, greenspace and water quality). Polygenic risk score (PRS) was calculated to estimate individual genetic risk. Cox proportional hazard model was applied to estimate the impact of exposure factors on the risk of AF occurrence. The mediation analysis was applied to assess the relationship among environmental scores, AF and cardiac structures. Population attributable fraction (PAF) was employed to assess potential influence of mitigating unfavorable environment characteristics on AF. The results showed that the highest group of four domain scores exhibited 3.38-16.83% higher AF risk than the lowest. Individuals with higher scores in four domains and high PRS had hazard ratio (95%CI) of 2.76 (2.62, 2.91), 2.61 (2.47, 2.75), 2.86 (2.71, 3.02) and 2.84 (2.66, 3.02). Environmental factors could indirectly affect cardiac structures through AF. Up to 7.37% of AF cases could be preventable through environmental interventions. Our findings pointed that gene-environment interaction can increase AF risk, which further affect cardiac structures.
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Registered trials
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