ArticleFrontiers in endocrinology2024
Causal association between gastrointestinal diseases and coronary artery disease: a bidirectional Mendelian randomization study.
Article in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Recent Advances in Material Basis for Co-treatment of Cardiovascular and Gastrointestinal Disorders.Chinese journal of integrative medicine · 2026Review
- Causal Relationships Between Gastroesophageal Reflux Disease and Myocardial Infarction: Insights From Univariable and Multivariable Mendelian Randomization Analyses.Annals of human genetics · 2026Article
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4 authors.
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Abstract
Background: Coronary artery disease (CAD) has been a dominating reason of mortality globally due to its complexity of etiology. A variety of gastrointestinal disorders (GDs) have been accounted to be related to CAD. Thus, this study aims to determine their causal relationship by two-sample Mendelian randomization (MR) analysis. Methods: Single-nucleotide polymorphisms (SNPs) relevant to 22 GDs were employed as instrumental variables from the genome-wide association summary (GWAS) datasets. Genetic associations with CAD and HF were acquired from UK Biobank, FinnGen, and other GWAS studies. We conducted a univariable MR (UVMR) analysis followed by a meta-analysis. A multivariable MR (MVMR) analysis was then performed with smoking and body mass index (BMI) as justifications. Also, a bi-directional MR analysis was leveraged to verify the reverse causal correlations. Results: Generally, UVMR analyses separately observed the causal effects of GDs on CAD and HF. Genetic liability to gastroesophageal reflux disease displayed a positive association with both CAD (OR=1.19; 95%CI: 1.01-1.41) and HF (OR=1.22; 95%CI: 1.00-1.49) risk; genetic liability to celiac disease separately attributed to CAD (OR=1.02; 95%CI: 1.01-1.03) and HF (OR=1.01; 95%CI: 1.00-1.02), which also maintained after MVMR analysis. Besides, we observed mutually causal associations between CAD and celiac disease. Conclusion: Our work suggested that genetic susceptibility to some GDs might causally increase the risk of CAD and HF, emphasizing the importance of preventing CAD in patients with GDs.
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