Association between obstructive sleep apnea severity and endothelial dysfunction in patients with

type 2 diabetes

Cardiovasc Diabetol. 2017 Mar 21;16(1):39. doi: 10.1186/s12933-017-0521-y.

Association between obstructive sleep apnea severity and endothelial dysfunction in patients with type 2 diabetes.

Bironneau V1, Goupil F2, Ducluzeau PH3, Le Vaillant M4, Abraham P5, Henni S5, Dubois S6, Paris A2, Priou P1,7, Meslier N1,7, Sanguin C8, Trzépizur W1,7, Andriantsitohaina R1, Martinez MC1, Gagnadoux F9,10.

Author information 1Université Bretagne Loire, INSERM UMR 1063, Angers, France.2Service de Pneumologie, Centre Hospitalier, Le Mans, France.3Unité d’Endocrinologie-Diabétologie-Nutrition, Pole de Médecine, CHRU de Tours, Tours, France.4Centre de Recherche Médecine, Sciences, Santé, Santé mentale, Société, CNRS UMR 8211, INSERM UMR U988-EHESS, Villejuif, France.5Département de Médecine du Sport et Explorations Fonctionnelles Vasculaires, Université Bretagne Loire, CHU d’Angers, Angers, France.6Département d’Endocrinologie, Diabétologie, Nutrition, Université Bretagne Loire, CHU d’Angers, Angers, France.7Département de Pneumologie, Université Bretagne Loire, CHU d’Angers, 4 Rue Larrey, 49100, Angers, France.8Service d’Endocrinologie, Diabétologie, Centre Hospitalier, Le Mans, France.9Université Bretagne Loire, INSERM UMR 1063, Angers, France.10Département de Pneumologie, Université Bretagne Loire, CHU d’Angers, 4 Rue Larrey, 49100, Angers, France. frgagnadoux@chu-angers.fr.

Abstract BACKGROUND: Obstructive sleep apnea (OSA) and type 2 diabetes (T2D) are associated with endothelial dysfunction a main predictor of late cardiovascular (CV) events. Despite the high prevalence of OSA in patients with T2D, the impact of OSA severity on endothelial function has not been clearly elucidated. The aim of this cross-sectional study was to determine whether increasing OSA severity is associated with poorer endothelial function in patients with T2D.

METHODS: 140 patients with T2D and no overt CV disease underwent polysomnography, peripheral arterial tonometry, clinic blood pressure (BP) measurement, biological assessment for CV risk factors, daytime sleepiness and health related quality of life (HRQL) questionnaires. The following commonly used cut-offs for apnea-hypopnea index (AHI) were used to define 3 categories of disease severity: AHI below 15 (no OSA or mild OSA), 15 AHI 30 (moderate OSA), and AHI over 30 (severe OSA). The primary outcome was the reactive hyperemia index (RHI), a validated assessment of endothelial function.

RESULTS: 21.4% of patients had moderate OSA and 47.6% had severe OSA. Increasing OSA severity and nocturnal hypoxemia were not associated with a significant decrease in RHI. Endothelial dysfunction (RHI below 1.67) was found in 47.1, 44.4 and 39.2% of patients with no OSA or mild OSA, moderate OSA and severe OSA, respectively (p = 0.76). After adjustment for confounders including body mass index, increasing OSA severity was associated with higher systolic BP (p = 0.03), lower circulating levels of adiponectin (p = 0.0009), higher levels of sP-selectin (p = 0.03), lower scores in 3 domains of HRQL including energy/vitality (p = 0.02), role functioning (p = 0.01), and social functioning (p = 0.04).

CONCLUSIONS: Moderate to severe OSA is very common but has no impact on digital micro-vascular endothelial function in patients with T2D.