Abstract
Obstructive sleep apnea (OSA) is a chronic and heterogeneous disorder that leads to early mortality, stroke, and cardiovascular disease (CVD). OSA is defined by the apnea–hypopnea index, which is an index of OSA severity that combines apneas (pauses in breathing) and hypopneas (partial obstructions in breathing) associated with hypoxemia. Yet, other sleep metrics (i.e., oxygen nadir, arousal frequency), along with clinical symptoms and molecular markers could be better predictors of stroke and CVD outcomes in OSA. The recent focus on personalized medical care introduces the possibility of a unique approach to the treatment of OSA based on its phenotypes, defined by pathophysiological mechanisms and/or clinical presentation. We summarized what is known about OSA and its phenotypes, and review the literature on factors or intermediate markers that could increase stroke risk and CVD in patients with OSA. The OSA phenotypes where divided across three different domains (1) clinical symptoms (i.e., daytime sleepiness), (2) genetic/molecular markers, and (3) experimental data-driven approach (e.g., cluster analysis). Finally, we further highlight gaps in the literature framing a research agenda.
Highlights
Obstructive sleep apnea (OSA) is a chronic disorder that leads to early mortality, stroke, and cardiovascular disease (CVD) (1–5)
The initial search was conducted with the terms “obstructive sleep apnea” or “sleep disordered breathing” and “phenotype” or “phenotypes.” articles were searched with the key word “obstructive sleep apnea phenotypes.”
The OSA-excessive daytime sleepiness (EDS) phenotype was associated with increased inflammatory markers, such as CRP and interleukin-6
Summary
Obstructive sleep apnea (OSA) is a chronic disorder that leads to early mortality, stroke, and cardiovascular disease (CVD) (1–5). OSA may lead to stroke through its associations with potent vascular risk factors, such as hypertension, diabetes mellitus, obesity, and atrial fibrillation. OSA may increase stroke and CVD risk through reduction in cerebral blood flow, altered cerebral autoregulation, impaired endothelial function, increased platelet activation, inflammation, and oxidative stress related to the intermittent hypoxemia–reoxygenation and arousals associated to increased sympathetic tone (10). The treatment of OSA has been considered an important intervention for reducing the morbidity and mortality associated with stroke and CVD (11). Treatment of OSA has not consistently reduced cardiovascular risk (12, 13); results partly explained by methodological limitations, such as suboptimal adherence to positive airway pressure therapy.
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