ArticleNature and science of sleep2025
Causal Effect of Obstructive Sleep Apnea on Sick Sinus Syndrome: A Bidirectional Mendelian Randomization Study.
Article in Nature and science of sleep, 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.
- Obstructive Sleep Apnea and Hypercoagulability: Combining Observational and Mendelian Randomization Analyses to Explore Causal Relationships.Nature and science of sleep · 2026Article
- Integrative clinical and molecular insights into the comorbidity between depression and sleep apnea syndrome.Frontiers in psychiatry · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Despite previous research establishing a connection between OSA and an increased risk of Bradyarrhythmias, the specific causal link between obstructive sleep apnea (OSA) and sick sinus syndrome (SSS) remains unexplored. This study aims to investigate the potential causal relationship between OSA and the development of SSS. Methods: To evaluate the association between OSA and SSS, we utilized a bidirectional two-sample Mendelian randomization (MR) method. Genetic variant OSA association data were sourced from FinnGens genome-wide association studies, comprising 410,385 individuals, while SSS association data were obtained from deCODE genetics, involving a dataset of 1, 000,187 individuals. Effect estimates were computed through the utilization of inverse-variance weighting (IVW), MR-Egger, weighted median, maximum likelihood techniques, and sensitivity analyses were conducted using the Mendelian Randomization Pleiotropy Residual Sum and Outlier (MR-PRESSO) approaches. Results: Our MR analyses utilizing IVW (fixed effects) revealed a heightened susceptibility to SSS among individuals with genetically predisposed OSA (OR= 1.493; 95% CI, 1.120-1.990; Conclusions: This MR analysis suggests a causal link between genetically predicted OSA and increased SSS risk. While finding no evidence for a causal relationship where SSS influences OSA.
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Registered trials
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