Sleep-disordered breathing and cerebrovascular disease: A mechanistic approach

Patients who have obstructive sleep apnea have a higher prevalence of cardiovascular morbidity and stroke than the general population. The hallmark of sleep apnea is intermittent hypoxia and increased formation of reactive oxygen species, which may injure surrounding tissues and act as signaling molecules, activating hypoxia-adaptive and inflammatory pathways that affect cellular and molecular mechanisms. Activation of inflammatory responses results in increased expression of inflammatory cytokines and adhesion molecules, which facilitates endothelial cells/leukocytes/platelets interactions. These cellular interactions, which promote endothelial dysfunction and are a component of the mechanisms underlying atherosclerosis, can be amplified in patients who have sleep apnea, increasing cardiocerebrovascular events.