Inflammation accelerates atherosclerotic processes in obstructive sleep apnea syndrome (OSAS).
Obstructive sleep apnea syndrome (OSAS) is an often underestimated sleep disorder that has been associated with cardiovascular disease. OSAS is characterized by cycles of apnea and/or hypopnea during sleep caused by the collapse of the upper airways. Intermittent hypoxia deriving from the cycles of apnea/arousals (to retrieve the ventilation) plays a pivotal role in the pathogenesis of the disease. Obesity is the most frequent predisposing condition of OSAS. Recent evidence suggests that OSAS could be considered as a pro-atherosclerotic disease, independently of visceral fat amount. Oxidative stress, cardiovascular inflammation, endothelial dysfunction, and metabolic abnormalities in OSAS could accelerate atherogenesis. The present review is focused on the possible pathophysiological mediators which could favor atherosclerosis in OSAS.
Quercioli
Alessandra
A
Division of Cardiology, Geneva University Hospital, Geneva, Switzerland. Alessandra.quercioli@hcuge.ch
Mach
François
F
Montecucco
Fabrizio
F
D050197:Atherosclerosis / Q000503:physiopathology*; D016207:Cytokines / Q000097:blood; D018450:Disease Progression; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology*; D020738:Leptin / Q000097:blood; D018384:Oxidative Stress / Q000502:physiology; D010974:Platelet Aggregation / Q000502:physiology; D012307:Risk Factors; D020181:Sleep Apnea, Obstructive / Q000503:physiopathology*
D016207:Cytokines; D020738:Leptin