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There is accumulating evidence from well-designed observational cohort studies and randomised controlled trials suggesting that obstructive sleep apnoea syndrome (OSAS) may independently add to vascular risk and increased mortality. Major biological mechanisms underpinning the association between OSAS and systemic consequences such as cardiovascular disease are thought to include intermittent hypoxia leading to increased oxidative stress and sympathetic activity, intrathoracic pressure changes leading to excessive mechanical stress on the heart and large artery walls and arousal-induced reflex sympathetic activation with resultant repetitive large blood pressure rises.1 The nocturnal sympathetic nervous system activation and consequent elevation of blood pressure diminish its usual physiological nocturnal dipping. Augmented sympathetic activation in patients with OSAS has also been shown to be associated with blunted baroreflex sensitivity, increased arterial stiffness and impaired endothelial function, all of which contribute to the development of arterial hypertension and consecutive vascular disease.2 ,3
Treatment with CPAP and mandibular advancement devices (MAD) have been shown to effectively abolish apnoeas and oxygen desaturations, and to prevent arousals; thus, obviate acute blood pressure swings. More than 40 randomised controlled trials looking at the effect of CPAP or MAD therapy on blood pressure have been conducted in the past and the findings of these trials have established that CPAP treatment of patients with OSAS lowers blood pressure between 2 and 10 mm Hg after several weeks of CPAP therapy.2 ,4 ,5
What do the three papers published in the …
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