Obstructive sleep apnoea syndrome

Abstract

Obstructive sleep apnoea syndrome (OSAS) is a common clinical condition in which the throat narrows or collapses repeatedly during sleep, causing obstructive sleep apnoea events. The syndrome is particularly prevalent in middle-aged and older adults. The mechanism by which the upper airway collapses is not fully understood but is multifactorial and includes obesity, craniofacial changes, alteration in upper airway muscle function, pharyngeal neuropathy and fluid shift towards the neck. The direct consequences of the collapse are intermittent hypoxia and hypercapnia, recurrent arousals and increase in respiratory efforts, leading to secondary sympathetic activation, oxidative stress and systemic inflammation. Excessive daytime sleepiness is a burden for the majority of patients. OSAS is also associated with cardiovascular co-morbidities, including hypertension, arrhythmias, stroke, coronary heart disease, atherosclerosis and overall increased cardiovascular mortality, as well as metabolic dysfunction. Whether treating sleep apnoea can fully reverse its chronic consequences remains to be established in adequately designed studies. Continuous positive airway pressure (CPAP) is the primary treatment modality in patients with severe OSAS, whereas oral appliances are also widely used in mild to moderate forms. Finally, combining different treatment modalities such as CPAP and weight control is beneficial, but need to be evaluated in randomized controlled trials. For an illustrated summary of this Primer, visit: http://go.nature.com/Lwc6te.

Nonmuscle Myosin Light Chain Kinase: A Key Player in Intermittent Hypoxia‐Induced Vascular Alterations

“…OSA is recognized as an important and independent risk factor for hypertension, coronary heart diseases, and stroke. The deleterious effects of OSA on cardiovascular outcomes are mainly triggered by intermittent hypoxia (IH) severity and the subsequent oxidative stress, leading to activation of the autonomic nervous system 1, 2, 3. Vascular endothelial dysfunction is a major intermediate mechanism of cardiovascular complications in patients with OSA,4, 5, 6 preceding and predicting late cardiovascular events, such as hypertension, atherosclerosis, and coronary diseases 1.…”

Cell Death Biomarkers and Obstructive Sleep Apnea: Implications in the Acute Coronary Syndrome

“…When an MI takes place, the extensive cell lysis would induce remarkably higher concentrations of nucleosomes and dsDNA in blood than those seen in patients with OSA only. The aims of this study were (1) to assess the interrelationships between OSA and cell deathrelated biomarkers and (2) to evaluate their potential implication in the development and evolution of an ACS. To this end, serum nucleosomes and dsDNA were measured in four groups: individuals with no previous cardiovascular event (with and without OSA) and patients with ACS (with and without OSA).…”

“…1,2 During an apnea event (complete airway collapse) or a hypopnea (partial collapse), the airway is narrowed and oxygen saturation is reduced. The intermittent hypoxia could play an essential role in OSA pathophysiological consequences and comorbidities, such as an increased risk of cardiovascular disease and death of any cause.…”

Emerging co-morbidities of obstructive sleep apnea: cognition, kidney disease, and cancer

“…Despite progress in raising public awareness of OSA, it remains underdiagnosed in the general population (2,3). Episodes of intermittent hypoxia (IH) and sleep fragmentation occur during nocturnal cycles of pharyngeal collapse, leading to a cascade of adaptive and maladaptive processes, such as systemic inflammation, endothelial dysfunction, and oxidative stress (3)(4)(5). Whilst the association of OSA with cardiovascular and metabolic co-morbidities is well recognised and described (6,7), its potential role in brain injury, leading to or aggravating existent neurological/psychiatric and neurodegenerative disorders, has only recently started receiving significant attention (5,8).…”