Obstructive sleep apnea, hypertension, and fibrin clot properties: a novel pathogenetic link with cardiovascular disease?

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Obstructive sleep apnea (OSA) is a relatively common syndrome that affects approximately 3–7% of the middle-aged individuals and becomes more prevalent with aging [1]. Over recent decades, the prevalence of the syndrome has been rising, potentially because of the increasing prevalence of obesity. OSA patients are in increased risk for hypertension (especially in a nondipping pattern) and drug-resistant hypertension, metabolic disorders, cardiovascular morbidity and mortality, cancer-related, and all-cause mortality [2–4]. Respiratory abnormalities during the night-time, including recurrent events of upper airways obstruction during sleep seem to be the predominant pathogenetic mechanism. Subsequent hypoxia leads to sympathetic stimulation, inflammation, and oxidative stress. These disorders are the major contributors of increased blood pressure (BP) and cardiovascular damage in OSA patients. Continuous positive airway pressure (CPAP) is presented as the first-line therapy for OSA via reversing upper airway obstruction and hypoxia [5]. Meta-analytic data also suggests that CPAP use could significantly reduce BP levels and the effect is more pronounced in higher adherence [6,7]. However, CPAP impact on attenuation of cardiovascular disorders in OSA stays inconclusive and several aspects such as duration and time of use is under consideration [5].

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