The additive effects of OSA and nondipping status on early markers of subclinical atherosclerosis in normotensive patients: a cross-sectional study.

The additive effect of hypertension on carotid atherosclerosis in patients with obstructive sleep apnea (OSA) is well-established; however, the effect of the nondipping pattern has not yet been evaluated. In this study, we aim to assess the effect of the nondipping pattern on carotid atherosclerosis, which is quantified as carotid intima-media thickness (CIMT), and on the high-risk carotid profile in normotensive patients with OSA. We included 189 patients with OSA in this cross-sectional study. We followed a 2 × 2 factorial design to create groups according to the presence of OSA and nondipping pattern. All patients underwent carotid ultrasonography to quantify their CIMT and presence of plaques. Patients who had CIMT ≥ 0.9 mm and/or carotid plaques were classified as having a high-risk carotid profile. Patients in the OSA/nondipper group had a 26% higher CIMT and five times the prevalence of a high-risk carotid profile compared to patients in the non-OSA/dipper group. CIMT was correlated with age, the apnea-hypopnea index (AHI), minimum oxygen saturation, and nighttime systolic blood pressure (SBP). Independent of age, diabetes, and AHI, a one mmHg increase in nighttime SBP was associated with a 0.22 mm increase in CIMT and a 4% increase in odds for the high-risk carotid profile. Similarly, independent of age and diabetes, being in the OSA/nondipper group was associated with 6.7 times increased odds for a high-risk carotid profile than being in the non-OSA/dipper group. Modeling with both the nondipping status and presence of OSA produced an 8% higher discriminative value than modeling with neither of these parameters. We found an additive effect of the nondipping pattern on carotid atherosclerosis in normotensive patients with OSA. Our findings suggested that in addition to having established hypertension, a nondipping pattern in normotensive patients with OSA may aggravate atherosclerosis.