Abstract Rationale Sleep disorders have a well-established link with chronic pain, with emerging evidence of associations with obstructive sleep apnea (OSA). Arousals and desaturations are two distinct aspects of OSA; the degree to which different patients experience these components (i. e. , OSA endotypes) may influence the impact of OSA on pain. Methods We examined the effect of sleep apnea on bodily pain in the SHHS study cohort, where subjects underwent baseline and 5-year follow-up polysomnography and pain questionnaires, among other study procedures. OSA severity was quantified by the apnea-hypopnea index AHI3A (AASM recommended scoring) ; pain was assessed using the pain domain of the SF-36 questionnaire (0-100 scale, lower scores = worsened pain). Two related analyses were performed: (1) cross-sectional and (2) longitudinal. For analysis 1, the relationship between AHI and pain was assessed using a linear model with all participants at baseline. In analysis 2, individuals without baseline OSA were included, with baseline-to-follow-up ΔAHI3A compared to Δpain. Effect modification of hypoxemia (%sleep with SpO290%; T90) was explored in additional models. Results For analysis 1, participants (n = 5804) were median (IQR) age 63 (55, 72) years, 52% female, BMI of 27. 5 (24. 7, 30. 8), and AHI of 13 (7, 24). There was a significant association between OSA severity and pain intensity: as AHI3A increased, pain scores worsened (βstdᵤnadjusted = -0. 12 95%CI: -0. 18, -0. 05; p 0. 001). There was no effect modification by T90 (p = 0. 50). For analysis 2, participants without baseline OSA with available follow-up (n = 711) were age 57 (51, 66) years, 77% female, and BMI 26 (23, 28) kg/m2. AHI3A was 3 (2, 4) at baseline and 5 (2, 9) at follow-up, with incident OSA severity consisting of 41% mild, 7. 7% moderate, and 1. 3% severe. There was a significant association between ΔAHI and Δpain, with increasing AHI linked to worsened pain (β stdᵤnadjusted = -0. 12 95%CI: -0. 22, -0. 03; p = 0. 009). While there was no significant interaction between ΔAHI3A and ΔT90 (p = 0. 23), ΔAHI had a significant inverse association with Δpain in individuals without increased hypoxemia (quartiles 1-3) but not those with increased T90 (quartile 4; Figure). Conclusions OSA is linked with pain in both cross-sectional and longitudinal analyses of new-onset OSA. These findings suggest OSA treatment as an avenue for chronic pain management, though its effect may depend on the OSA endotype. Sleep hypoxia may have a mitigating effect on pain. This abstract is funded by: None
Scroggie et al. (Fri,) studied this question.
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