2015
DOI: 10.1136/thoraxjnl-2015-207247
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Deleterious systemic effects of OSA: how much evidence do we need?

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Cited by 7 publications
(4 citation statements)
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“…The most prominent feature of this condition is chronic intermittent hypoxia, which stimulates chronic inflammatory processes, attenuates antioxidant mechanisms, and increases the production of reactive oxygen products during the reoxygenation phase (Vaccaro et al, 1992;Vakil et al, 2018;Ma et al, 2019). Patients with OSAHS have an increased risk of cardiovascular diseases (CVDs), like hypertension, heart failure, and coronary heart disease (Kohler, 2015;Stansbury and Strollo, 2015). Oxidative stress, sympathetic activity, and systemic inflammatory reactions are linked to chronic intermittent hypoxia that might impact the ocular vasculature (Kohler and Stradling, 2010).…”
Section: Introductionmentioning
confidence: 99%
“…The most prominent feature of this condition is chronic intermittent hypoxia, which stimulates chronic inflammatory processes, attenuates antioxidant mechanisms, and increases the production of reactive oxygen products during the reoxygenation phase (Vaccaro et al, 1992;Vakil et al, 2018;Ma et al, 2019). Patients with OSAHS have an increased risk of cardiovascular diseases (CVDs), like hypertension, heart failure, and coronary heart disease (Kohler, 2015;Stansbury and Strollo, 2015). Oxidative stress, sympathetic activity, and systemic inflammatory reactions are linked to chronic intermittent hypoxia that might impact the ocular vasculature (Kohler and Stradling, 2010).…”
Section: Introductionmentioning
confidence: 99%
“…Long-term intermittent hypoxia, hypercapnia, heightened sympathetic nervous system activity and increased catecholamine levels constitute the pathophysiological mechanism of OSAHS ( 4 ). The systemic hypertension, atheromatosis and autonomic nerve dysfunction caused by OSAHS may give rise to a series of complications, such as coronary atherosclerotic heart disease, diabetes mellitus, heart failure and even death ( 5 , 6 ). Ocular blood vessels are also affected by these mechanisms, including increased oxidative stress, systemic inflammation and sympathetic activity ( 4 ).…”
Section: Introductionmentioning
confidence: 99%
“…The cyclical desaturations, intermittent hypoxia, arousals and catecholamine surges of OSA have been well studied 2 . These pathophysiological features affect more than the sleep-wake cycle; impacts on hypertension, atherosclerosis, endothelial dysfunction, insulin resistance and autonomic dysfunction have been found 3,4 . There is clear potential for OSA to cause or worsen ocular disease through these mechanisms and interest in this area is increasing.…”
Section: Introductionmentioning
confidence: 99%