Autonomic alterations and endothelial dysfunction in pediatric obstructive sleep apnea

The cardiovascular consequences of obstructive sleep apnea syndrome (OSAS) in children have started to emerge over the last decade. It is clear that the respiratory and sleep alterations that characterize this relatively prevalent condition induce substantial alterations in autonomic nervous system control, ultimately generating high sympathetic outflow and reactivity that reflect an imbalance between sympatho-excitatory and vagal inhibitory inputs. In addition to these important consequences, the constitutive elements of OSAS also elicit a rather extensive activation of systemic inflammatory pathways that in turn pose substantial risk to the integrity and functional homeostasis of the endothelial network. The complex interactions between the multiple injury-associated pathways recruited by OSAS are further compounded by the potential release of angiogenic factors and by the mobilization and homing of progenitor cells that have the potential to repair and restore the OSAS-disrupted vascular function. Improved characterization of the mechanisms involved in every one of these processes and identification of the determinants of susceptibility in pediatric populations along with the interactions with obesity will clearly modify our approaches to OSAS in the future.