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Original article
Distinct severity stages of obstructive sleep apnoea are correlated with unique dyslipidaemia: large-scale observational study
  1. Jian Guan1,2,
  2. Hongliang Yi1,2,
  3. Jianyin Zou2,
  4. Lili Meng1,
  5. Xulan Tang1,
  6. Huaming Zhu1,
  7. Dongzhen Yu1,2,
  8. Huiqun Zhou1,
  9. Kaiming Su1,2,
  10. Mingpo Yang3,
  11. Haoyan Chen4,
  12. Yongyong Shi5,
  13. Yue Wang6,
  14. Jian Wang7,
  15. Shankai Yin1,2
  16. for the Shanghai Sleep Health Study Research Group
  1. 1Department of Otolaryngology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China
  2. 2Department of Otolaryngology, Therapy Center for Obstructive Sleep Apnea, Otolaryngology Institute of Shanghai Jiao Tong University, Shanghai China
  3. 3Institute of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China
  4. 4Department of Gastroenterology and Hepatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
  5. 5Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Bio-X Institutes, Ministry of Education, Shanghai Jiao Tong University, Shanghai, China
  6. 6The Center for Disease Control and Prevention of China, Beijing, China
  7. 7School of Human Communication Disorders, Dalhousie University, Halifax, Canada
  1. Correspondence to Professor Shankai Yin, Department of Otolaryngology, Therapy Center for Obstructive Sleep Apnea, Otolaryngology Institute of Shanghai Jiao Tong University, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yishan Road, Shanghai 200233, China; skyin{at}sjtu.edu.cn

Abstract

Background Dyslipidaemia is an intermediary exacerbation factor for various diseases but the impact of obstructive sleep apnoea (OSA) on dyslipidaemia remains unclear.

Methods A total of 3582 subjects with suspected OSA consecutively admitted to our hospital sleep centre were screened and 2983 (2422 with OSA) were included in the Shanghai Sleep Health Study. OSA severity was quantified using the apnoea–hypopnea index (AHI), the oxygen desaturation index and the arousal index. Biochemical indicators and anthropometric data were also collected. The relationship between OSA severity and the risk of dyslipidaemia was evaluated via ordinal logistic regression, restricted cubic spline (RCS) analysis and multivariate linear regressions.

Results The RCS mapped a nonlinear dose–effect relationship between the risk of dyslipidaemia and OSA severity, and yielded knots of the AHI (9.4, 28.2, 54.4 and 80.2). After integrating the clinical definition and RCS-selected knots, all subjects were regrouped into four AHI severity stages. Following segmented multivariate linear modelling of each stage, distinguishable sets of OSA risk factors were quantified: low-density lipoprotein cholesterol (LDL-C), apolipoprotein E and high-density lipoprotein cholesterol (HDL-C); body mass index and/or waist to hip ratio; and HDL-C, LDL-C and triglycerides were specifically associated with stage I, stages II and III, and stages II–IV with different OSA indices.

Conclusions Our study revealed the multistage and non-monotonic relationships between OSA and dyslipidaemia and quantified the relationships between OSA severity indexes and distinct risk factors for specific OSA severity stages. Our study suggests that a new interpretive and predictive strategy for dynamic assessment of the risk progression over the clinical course of OSA should be adopted.

  • Sleep apnoea

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