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The Assessment of Endothelial Dysfunction among OSA Patients after CPAP Treatment

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MEDICINA-LITHUANIA
卷 57, 期 4, 页码 -

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MDPI
DOI: 10.3390/medicina57040310

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obstructive sleep apnea; CPAP; microcirculation; endothelial dysfunction

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Patients with obstructive sleep apnea (OSA) exhibit microcirculation dysfunction due to oxidative stress and impaired nitric oxide secretion. Continuous positive airway pressure (CPAP) treatment significantly improves endothelial function and microvascular blood flow, reducing inflammatory mediator levels.
Background and Objectives: Microcirculation dysfunction is present in patients with obstructive sleep apnea (OSA). Intermittent hypoxia generates oxidative stress, which contributes to chronic inflammation. The secretion of nitric oxide (NO), which is responsible for adequate regulation of the endothelium, is impaired due to a decrease in endothelial nitric oxide synthetase (eNOS) expression and an increase in endogenous eNOS inhibitors. Furthermore, nocturnal awakenings lead to the dysregulation of cortisol release and increased stimulation of the sympathetic nervous system. The non-invasive method of choice in OSA treatment is continuous positive airway pressure (CPAP). Materials and Methods: PubMed, Scopus, and Google Scholar databases were searched, and only papers published in the last 15 years were subsequently analyzed. For this purpose, we searched for keywords in article titles or contents such as obstructive sleep apnea, microcirculation, and CPAP. In our review, we only studied English articles that reported systemic reviews and meta-analyses, clinical studies, and case reports. Results: Endothelial dysfunction can be assessed by methods based on reactive hyperemia, such as flow-mediated dilation (FMD) measured by ultrasonography, laser-Doppler flowmetry (LDF), or capillaroscopy. In invasive techniques, intravenous administration of vasodilator substances takes place. Some surveys detected impaired microcirculation in OSA patients compared with healthy individuals. The level of dysfunction depended on the severity of OSA. CPAP treatment significantly improved endothelial function and microvascular blood flow and lowered the inflammatory mediator level. Conclusions: The first-choice treatment-CPAP-reduces the number of apneas and hypopneas during the night, induces the reversal of hypopnea and the chronic inflammatory state, and enhances activation of the sympathetic nervous system. Changes are visible as improved blood flow in both macro- and microcirculation, increased arterial elasticity, and decreased stiffness. Thus, early implementation of adequate treatment could be essential to reduce high cardiovascular risk in patients with OSA.

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