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已发表论文
阻塞性睡眠呼吸暂停与高凝状态：结合观察性研究和孟德尔随机化分析探索因果关系
Authors Su L, Wu L, Han T, Li Y , Zhang X
Received 21 October 2025
Accepted for publication 9 January 2026
Published 31 January 2026 Volume 2026:18 574439
DOI https://doi.org/10.2147/NSS.S574439
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Ahmed BaHammam
Linfan Su,1,* Lingwu Wu,1,2,* Teng Han,1 Yiming Li,1 Xiaolei Zhang1
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; 2China Japan Friendship Institute of Clinical Medicine Research, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xiaolei Zhang, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, 100029, People’s Republic of China, Email yutian728@sina.com
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.
Keywords: obstructive sleep apnea, hypercoagulability, Mendelian randomization, chronic intermittent hypoxia, obesity
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; 2China Japan Friendship Institute of Clinical Medicine Research, Beijing, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xiaolei Zhang, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, 100029, People’s Republic of China, Email yutian728@sina.com
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.
Keywords: obstructive sleep apnea, hypercoagulability, Mendelian randomization, chronic intermittent hypoxia, obesity