Key result
Obstructive sleep apnea and type 2 diabetes impaired brachial artery flow-mediated dilatation to a similar degree compared to normal-weight and obese controls (5.8% and 5.4% vs 9.1% and 8.3%, P<0.001).
Why the study?
Does obstructive sleep apnea impair vascular function to a similar degree as type 2 diabetes mellitus compared to healthy controls?
Cross-Sectional (n=153)
Does obstructive sleep apnea impair vascular function to a similar degree as type 2 diabetes mellitus compared to healthy controls?
Effect estimate: β = -2.45 for OSA
Absolute Event Rate: 5.8% vs 9.1%
p-value: p=<0.001
Obstructive sleep apnea impairs endothelial function in the brachial artery to a similar degree as type 2 diabetes, suggesting treatment of OSA may improve macrovascular outcomes.
OSA-associated endothelial dysfunction comparable to T2DM; leaves open whether OSA treatment improves macrovascular outcomes.
Despite the high prevalence of obstructive sleep apnea (OSA) in type 2 diabetes mellitus (DM), the attributable vascular risk from each condition is unknown. We hypothesize that OSA may have a similar effect on vascular function as type 2 diabetes does. Healthy normal-weight subjects, healthy obese subjects, subjects with type 2 diabetes, and obese subjects with OSA were enrolled. Vascular function was assessed with brachial artery ultrasound for flow-mediated dilatation (FMD) and in skin microcirculation by laser Doppler flowmetry. One hundred fifty-three subjects were studied: healthy normal-weight controls (NCs) (n = 14), healthy obese controls (OCs) (n = 33), subjects with DM (n = 68), and obese subjects with OSA (n = 38). The DM group did not undergo sleep study and thus may have had subclinical OSA. The OSA and type 2 diabetes groups had impaired FMD as compared to both the normal-weight and OC groups (5.8 ± 3.8%, 5.4 ± 1.6% vs. 9.1 ± 2.5%, 8.3 ± 5.1%, respectively, P < 0.001, post hoc Fischer test). When referenced to the NC group, a multiple linear regression model adjusting for covariates found that baseline brachial artery diameter (β = -3.75, P < 0.001), OSA (β = -2.45, P = 0.02) and type 2 diabetes status (β = -2.31, P = 0.02), negatively predicted % FMD. OSA status did not seem to affect nitroglycerin-induced vasodilation (endothelium-independent) of the brachial artery or vascular function in the skin microcirculation. OSA impairs endothelial function in the brachial artery to a similar degree as type 2 diabetes does. OSA, however, does not appear to affect brachial endothelium-independent vasodilation or skin microcirculatory function. Treatment of OSA in patients with concomitant type 2 diabetes, therefore, may be a potential therapeutic option to improve macro-, but not microvascular outcomes.
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Yim‐Yeh et al. (2010) conducted a cross-sectional in Obstructive sleep apnea and Type 2 diabetes mellitus (n=153). Obstructive sleep apnea and Type 2 diabetes vs. Healthy normal-weight and obese controls was evaluated on Flow-mediated dilatation (FMD) (β = -2.45 for OSA, p=<0.001). Obstructive sleep apnea and type 2 diabetes impaired brachial artery flow-mediated dilatation to a similar degree compared to normal-weight and obese controls (5.8% and 5.4% vs 9.1% and 8.3%, P<0.001).
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