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Obstructive Sleep Apnea and Hypercoagulability: Combining Observational and Mendelian Randomization Analyses to
Linfan Su1, Lingwu Wu1,2, Teng Han1
1National Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Department of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing, People's Republic of China.
Nature and Science of Sleep
|March 25, 2026
Summary
Obstructive sleep apnea (OSA) is linked to hypercoagulability, but this association is confounded by BMI. Genetic studies show no causal link, suggesting obesity management is key for reducing thrombotic risk in OSA patients.
Area of Science:
- Cardiovascular Medicine
- Sleep Medicine
- Genetics
Background:
- Obstructive sleep apnea (OSA) is a prevalent condition associated with cardiovascular complications.
- The link between OSA and hypercoagulability, a state of increased clotting tendency, requires further investigation.
- Understanding this relationship is crucial for managing thrombotic risk in OSA patients.
Purpose of the Study:
- To investigate the association between Obstructive Sleep Apnea (OSA) and hypercoagulability.
- To differentiate between observational associations and potential causal effects using Mendelian randomization (MR).
- To assess the influence of Body Mass Index (BMI) as a potential confounder.
Main Methods:
- Combined observational analysis of 790 OSA patients with coagulation markers (APTT, PT, Fibrinogen).
- Multivariate linear regression adjusted for age, gender, BMI, and comorbidities.
- Large-scale Mendelian randomization (MR) analyses using GWAS data for OSA and coagulation markers, including multivariable MR (MVMR) to account for BMI.
Main Results:
- Severe OSA showed higher fibrinogen and shorter PT/APTT compared to mild-moderate OSA observationally.
- T90 and MSaO2 were associated with fibrinogen in regression analyses.
- MR analyses found no significant evidence of a causal effect of OSA on coagulation markers, with associations disappearing after adjusting for BMI.
Conclusions:
- While severe OSA is observationally linked to subclinical hypercoagulability, this association is confounded by BMI.
- Genetic evidence does not support a causal role for OSA in coagulation dysfunction.
- Obesity management should be prioritized to mitigate thrombotic risk in OSA patients.
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