Obstructive Sleep Apnea, Sleep Duration, and Associated Mediators With Carotid Intima-Media Thickness

Objective: To elucidate the independent associations of obstructive sleep apnea (OSA) and sleep duration (SD) as well as the potential inflammatory and metabolic mediators on carotid intima-media thickness (CIMT) in a large cohort of adults. Approach and Results: Consecutive participants from the ELSA-Brasil performed a clinical evaluation, sleep study, 1-week actigraphy for defining SD and CIMT using standard techniques. Gamma regression models were used to explore the association between OSA and SD with CIMT. Mediation analysis was performed using the mediation R package. A total of 2009 participants were included in the main analysis. As compared with no OSA (apnea-hypopnea index [AHI] <5 events/hour; n=613), patients with mild (AHI, 5–14.9; n=741), moderate (AHI, 15–29.9; n=389), and severe OSA (AHI ≥30 events/hour; n=266) presented a progressive CIMT increase (0.690 [0.610–0.790], 0.760 [0.650–0.890], 0.810 [0.700–0.940], and 0.820 [0.720–0.958] mm; P <0.001). In contrast, CIMTs were similar for those with SD <6 hours (0.760 [0.650–0.888]), 6 to 8 hours (0.750 [0.640–0.880]) and >8 hours (0.740 [0.670–0.900]). All forms of OSA were independently associated with CIMT (mild: β: 0.019, SE 0.008; P =0.022; moderate: β: 0.025, SE 0.011; P =0.022; severe OSA: β: 0.040, SE 0.013; P =0.002). Moreover, the association of AHI with CIMT was mediated by increased C-reactive protein and triglycerides ( P <0.01). SD did not interact with OSA in the association with CIMT. Conclusions: OSA is independently associated with increased CIMT in a dose-response relationship. This association is partially mediated by inflammation and dyslipidemia. In contrast, SD is not associated nor interacted with OSA to increase CIMT.