Association between high risk of obstructive sleep apnea and inflammatory markers in a population sample of young and middle-aged adults in the Miami Heart Study

Study Objectives: There are limited data depicting the association between high risk of obstructive sleep apnea (OSA) and the levels of inflammatory markers in a population-based sample free from cardiovascular disease (CVD). In a large US cohort enriched with a Hispanic population and free of CVD, we aimed to assess the association between high risk of OSA and inflammatory markers. Methods: We analyzed data for 2,359 clinical CVD-free participants from the Miami Heart Study, aged 40–65 years (May 2015–September 2018). High risk of OSA included those with a high risk using the Berlin Questionnaire. Poisson regression analyses were used to examine the associations between high risk of OSA (reference: low risk of OSA) and high-sensitivity C-reactive protein (hs-CRP), interleukin 6, and tumor necrosis factor alpha levels (continuous) in univariate and multivariate models (adjusting for age, sex, race/ethnicity, and body mass index, diabetes, hypertension, high cholesterol, and smoking). Results: A total of 552 (28%) participants were categorized as having a high risk of OSA. Patients with a high risk of OSA had higher median values of hs-CRP (2.3 vs 1.0), interleukin 6 (1.9 vs 1.4), and tumor necrosis factor alpha (1.2 vs 1.1) compared with those with a low risk of OSA (all P < .001). When adjusting for age, sex, and race/ethnicity, the mean difference between patients with high and low risk of OSA in hs-CRP was 2.04 (95% confidence interval, 1.85, 2.23) and 0.73 (95% confidence interval, 0.57, 0.89) in interleukin 6. These differences were attenuated when further adjusting for CVD risk factors but remained statistically significant for hs-CRP (0.38; 95% confidence interval, 0.21, 0.55). Conclusions: After accounting for CVD risk factors, individuals at high risk of OSA had significantly higher levels of hs-CRP, suggesting that OSA screening identified subclinical inflammation in this population sample of individuals free of CVD.