• Vol. 38 No. 5, 461–464
  • 15 May 2009

Endothelial Dysfunction in Patients With Obstructive Sleep Apnoea Independent of Metabolic Syndrome



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Introduction: Obstructive sleep apnoea syndrome (OSAS), characterised by intermittent hypoxia/re-oxygenation, has been identified as an independent risk factor for cardiovascular diseases and endothelial dysfunction. Our aim was to investigate flow-mediated dilatation (FMD) in patients with obstructive sleep apnoea with and without metabolic syndrome. Materials and Methods: Fifty-two subjects with OSAS diagnosed by polysomnography were classified into 2 groups according to the presence and absence of the metabolic syndrome and also according to the severity: mild to moderate OSAS group and severe OSAS group. Endothelial function of the brachial artery was evaluated by using high-resolution vascular ultrasound. Endothelial-dependent dilatation (EDD) was assessed by establishing reactive hyperaemia and endothelial-independent dilatation (EID) was determined by using sublingual isosorbide dinitrate. Spearman correlation and regression analysis were performed. Results: EDD was not significantly different in patients with OSAS and metabolic syndrome as compared with OSAS without metabolic syndrome (4.62 ± 0.69 versus 4.49 ± 0.93, P >0.05). Conclusions: Endothelial dysfunction in OSA may be independent of metabolic syndrome.

Obstructive sleep apnoea syndrome (OSAS) is a widely prevalent disorder characterised by recurrent partial or complete obstruction of upper airway during sleep. Compelling data from several large cross-sectional and longitudinal studies strongly suggest a role of OSAS in the development of cardiovascular disorders, including hypertension, coronary artery disease and stroke.1,2 However, the patho-physiologic mechanism by which OSAS contributes to the cardiovascular pathology remains unclear and awaits further elucidation.

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