Abstract

Debate persists as to whether obstructive sleep apnea (OSA) is an independent risk factor for subclinical atherosclerosis in the carotid arteries. Moreover, there is a lack of information on the effect of positive airway pressure (PAP) treatment on carotid wall thickness, an early sign of atherosclerosis, and existing results are conflicting. The purpose of this study was to compare carotid artery wall thickness between in obese and non-obese adults with and without OSA, as well as among OSA cases following PAP treatment. A total of 206 adults newly diagnosed with OSA with an apnea/hypopnea index (AHI) between 15 and 75 events/hour and 53 controls with AHI < 10 events/hour were enrolled. Waist circumference >107 centimeters in men and >96 centimeters in women was used to classify subjects as obese. Bilateral common carotid artery B-mode ultrasound was performed in all subjects at baseline to assess intima-media thickness (IMT) as a primary outcome and arterial-wall mass, diameter, and circumferential wall stress as secondary outcomes. Measurements were repeated in 117 OSA participants who completed 4-months of PAP treatment and had an average daily use over that period of ≥ 4 hours/day. No significant differences in carotid IMT, diameter, or arterial-wall mass were present at baseline between subjects with OSA and controls stratified by obesity status, after adjusting for other cardiovascular risk factors. In those subjects with OSA who had adequate PAP adherence over the 4 month treatment, carotid artery diameter significantly increased (mean change [95% CI] = 0.12 [0.05, 0.19] mm; p=0.002), but no significant changes in carotid IMT, arterial-wall mass, and circumferential stress were observed in either obese or non-obese subjects. Regardless of obesity status, carotid IMT was not increased in moderate to severe OSA versus controls and did not change in response to the PAP treatment. Only the diameter of carotid arteries significantly increased over the 4-month treatment period. This study was supported by National Institute of Health (NIH HL094307).

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