Document Type

Article

Rights

Available under a Creative Commons Attribution Non-Commercial Share Alike 4.0 International Licence

Publication Details

Journal of hypertension, Apr. 34:4, 808-810, 2016.

https://journals.lww.com/jhypertension/pages/default.aspx

Abstract

Obstructive sleep apnoea syndrome (OSAS) is a consequence of repetitive oropharyngeal airway narrowing/closure during sleep resulting in chronic intermittent hypoxaemia [1]. OSAS is regarded as an independent risk factor for hypertension (HTN) development [2] and is associated with decreased cerebral blood flow [3], leading to daytime neuropsychological sequelae [1]. Blood pressure (BP) follows a circadian rhythm termed dipping and the absence of nocturnal BP dipping is associated with target-organ damage, cerebrovascular disease, myocardial remodelling and increased cardiovascular events/mortality [4]. Abnormal BP in OSAS typically manifests as reduced nocturnal BP dipping [5]. Although continuous positive airway pressure therapy (CPAP) represents the current gold standard treatment of OSAS, its antihyper- tensive effect is limited

DOI

10.1097/HJH.0000000000000858

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