OSA is a common disease that affects approximately 10% of the middle-aged population andbecomes more prevalent with age. It is caused by intermittent and repetitive collapse of theUA during sleep. The main acute physiological consequences of OSA are oxygendesaturation, intrathoracic pressure changes and arousals. OSA is associated with significantcardiovascular morbidity and mortality and is an independent risk factor for CVD. Thepathogenesis of CVD in OSA is not completely understood but is likely to be multifactorial,involving a diverse range of closely interrelated and detrimental intermediate mechanismsthat predispose patients to atherosclerosis, including oxidative stress, sympathetic activation,inflammation, hypercoagulability, endothelial dysfunction and metabolic dysregulation. IH isconsidered to lead to increased oxidative stress, systemic inflammation and sympatheticstimulation. Despite the existence of these detrimental mechanisms, there areepidemiological studies that suggest that some protective mechanisms could also be activatedin OSA patients. This chapter describes the underlying mechanisms linking OSA with CVD.
|Titolo della pubblicazione ospite||Sleep apnea|
|Numero di pagine||14|
|Stato di pubblicazione||Published - 2015|