Mechanisms of endothelial dysfunction in obstructive sleep apnea

Abstract

Endothelial activation and infl ammation are important mediators of accelerated atherogenesis and consequent increased cardiovascular morbidity in obstructive sleep apnea (OSA). Repetitive episodes of hypoxia/reoxygenation associated with transient cessation of breathing during sleep in OSA resemble ischemia/reperfusion injury and may be the main culprit underlying endothelial dysfunction in OSA. Additional factors such as repetitive arousals resulting in sleep fragmentation and deprivation and individual genetic suseptibility to vascular manifestations of OSA contribute to impaired endothelial function in OSA. The present review focuses on possible mechanisms that underlie endothelial activation and infl ammation in OSA.

Left ventricular subclinical dysfunction associated with myocardial deformation changes in obstructive sleep apnea patients estimated by real-time 3D speckle-tracking echocardiography

“…Moreover, one of the most important mechanisms involved in the development of cardiovascular disease in OSA patients is increased oxidative stress, resulting in the formation of hypoxia-related free radicals. The hypoxia-related free radical generation could cause an imbalance between myocardial oxidation and antioxidant activity, resulting in myocardial injury and increased susceptibility to myocardial ischemia [30,31]. Myocardial ischemia could lead to a shortage in ATP production, loss of cellular calcium, inorganic phosphate accumulation, and myocardial acidosis, making it difficult to induce the mechanism of excitementcontraction coupling and causing subtle regional ventricular systolic dysfunction in the early stages [32].…”

Reversibility of the endothelial dysfunction after CPAP therapy in OSAS patients

“…The pathogenesis of cardiovascular complications in OSAS is multi-factorial: it induces endothelial dysfunction [5,6], increases carotid artery intima-media thickness [7] (IMT) and arterial blood pressure [8][9][10]. There are also various different mechanisms involved in the pathogenesis of atherosclerosis in these patients [11]. A fundamental role is played by the apnoeainduced hypoxia.…”

Sleep Disorder as a Triggering Factor for Relapse in Multiple Sclerosis

“…Normal sleeping plays an important role in maintaining the normal function of the immune system. Various studies have shown that sleep disorders are associated with elevated serum levels of pro-inflammatory cytokines and markers of oxidative stress [19]. Since MS is considered an immune-mediated disease, the researchers of this study hypothesize that sleep disturbances may facilitate acute relapses via changes in the immune system function.…”