Endothelial and Angiogenic Biomarkers in Obstructive Sleep Apnea: Longitudinal Associations With Continuous Positive
David Sanz-Rubio1, Carolina Cubillos-Zapata2, Marta Marín-Oto3
1Centro de Investigación Biomedica en Red, Instituto Carlos III, Ministry of Health, Madrid, Spain; Sleep Research Program, IIS-Aragón, Zaragoza, Spain.
Continuous positive airway pressure (CPAP) use in obstructive sleep apnea (OSA) patients reduces vascular endothelial growth factor (VEGF) over five years. Long-term CPAP therapy does not impact angiopoietin-2 (Ang-2) levels, suggesting non-hypoxic vascular risks in OSA.
Area of Science:
- Cardiovascular research
- Sleep medicine
- Biomarker analysis
Background:
- Obstructive sleep apnea (OSA) is linked to cardiovascular risks.
- Continuous positive airway pressure (CPAP) is a primary OSA treatment.
- Long-term effects of CPAP on vascular biomarkers in non-comorbid OSA patients are unclear.
Purpose of the Study:
- To investigate the longitudinal associations of CPAP use with endothelial and epithelial biomarkers in OSA patients without pre-existing cardiovascular disease.
- To assess the impact of CPAP therapy on vascular endothelial growth factor (VEGF) and angiopoietin-2 (Ang-2) levels over five years.
Main Methods:
- The EPIOSA study enrolled moderate-to-severe OSA patients and controls in a 5-year prospective cohort.
- Plasma levels of Ang-2, VEGF, Tie-2, and E-selectin were measured at baseline, 1 year, and 5 years.
- Multivariable regression models analyzed associations between biomarkers and clinical, sleep, and biochemical variables.
Main Results:
- CPAP-treated OSA patients exhibited sustained reductions in VEGF, linked to baseline VEGF and waist-to-hip ratio.
- Angiopoietin-2 (Ang-2) levels increased in both OSA and control groups, independent of CPAP.
- Tie-2 and E-selectin showed minimal changes; body weight and sST2 predicted baseline Ang-2.
Conclusions:
- Long-term CPAP therapy in OSA patients attenuates hypoxia-driven VEGF pathways.
- CPAP does not alter Ang-2 trajectories, indicating non-hypoxic vascular risks in OSA.
- Further research is needed to explore non-hypoxic mechanisms contributing to vascular risk in OSA.
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