[Pathophysiology of obstructive sleep apnea syndrome and its cardiometabolic consequences]

Obstructive sleep apnoea syndrome (OSAS) is characterized by recurrent partial or complete pharyngeal collapses during sleep. The pathophysiology of OSAS is complex and multifactorial. Factors influencing upper airway patency include a reduction in upper airway dimensions that can result from both anatomical and functional alterations (obesity, fluid shift or maxillo-facial structural changes), and increased pharyngeal collapsibility owing to reduced neuromuscular compensation and lack of the pharyngeal protective reflex during sleep. Severe OSAS is associated with a high cardiometabolic risk. Obstructive apnoeic events incorporate a range of stressors that activate mechanisms contributing to the initiation and progression of cardiac, vascular and metabolic diseases. Obstructed breathing induces markedly negative intrathoracic pressure and also provokes hypoxia and hypercapnia. The hypoxaemic stress is further amplified by the subsequent reoxygenation (intermittent hypoxia), resulting in the generation of reactive oxygen species (ROS), sympathetic activation and inflammation. OSAS is able to increase the number of fatal and non-fatal cardiovascular events, including arrhythmias, myocardial infarction and stroke. OSAS is associated with dyslipidemia, type 2 diabetes, its poor control and non-alcoholic fatty liver disease. Screening, diagnosis and integrated care of OSAS should be included in an aggressive management of risk reduction in chronic cardiovascular and metabolic diseases.