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Updated: Mar 27, 2026

Drug-Induced Sleep Endoscopy DISE with Target Controlled Infusion TCI and Bispectral Analysis in Obstructive Sleep Apnea
Published on: December 6, 2016
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.
Purpose:
The relationship between Obstructive sleep apnea (OSA) and hypercoagulability remains unclear. To address this uncertainty, the present study combined observational and Mendelian randomization (MR) analyses to assess the associations of OSA and coagulation markers.
Patients And Methods:
We conducted an observational study of 790 patients with OSA, evaluating associations between OSA severity and coagulation markers, including activated partial thromboplastin time (APTT), prothrombin time (PT), and fibrinogen (Fib). Multivariate linear regression adjusted for age, gender, body mass index (BMI), and comorbidities. Additionally, we performed a large-scale Mendelian randomization analysis using two East Asian OSA genome-wide association study (GWAS) datasets (Million Veteran Program [MVP], n=6550; Taiwan Precision Medicine Initiative [TPMI], n=316351) as exposures, and East Asian coagulation GWAS data from BioBank Japan (BBJ) as outcomes (APTT: n=37767; Fib: n=18348; PT: n=58110). Multivariable MR (MVMR) with body mass index (BMI)(TPMI GWAS, n=191458) was performed to assess residual direct effects of OSA.
Results:
Severe OSA showed higher Fib (p-value<0.01) and shorter PT (p-value<0.05) and APTT (p-value<0.05) than mild-moderate OSA. Multivariate regression analysis showed T90 (the percentage of time oxygen saturation is below 90%) and MSaO2 (mean oxygen saturation) were associated with Fib (β=-0.259; β=-0.224, p-value<0.001). While OSA severity is observationally associated with subclinical hypercoagulability, these significances vanished after adjusting for BMI and are not supported by genetic evidence since MR analyses provide no evidence for a moderate or clinically meaningful independent causal effect between genetic OSA liability and coagulation markers. MVMR confirmed no residual direct effect of OSA on coagulation after accounting for BMI.
Conclusion:
Severe OSA is associated with subclinical hypercoagulability, but this relationship is confounded by BMI. Genetic evidence does not support a moderate or clinically meaningful causal role for OSA in coagulation dysfunction, urging a paradigm shift toward obesity management as the primary strategy to reduce thrombotic risk in OSA patients.
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