Obstructive sleep apnea (OSA), a nightly respiratory condition, is characterized by recurrent upper airway collapse causing intermittent hypoxia (IH) resembling ischemia and reperfusion (I/R). Consequently, blood oxygenation levels are cyclically reduced; sleep fragmentation and sympathetic activation develop, thus invoking oxidative stress and inflammation. OSA is a major risk factor for cardio-/cerebrovascular morbidity and mortality. However, not all OSA patients develop cardio-/cerebrovascular disease, even if suffering from similar OSA severity. Possibly, this results from interindividual differences in responses to a given hypoxic stimulus involving gene polymorphism in oxygen-regulated transcription factors and downstream genes. The current review is aimed at highlighting potentially protective mechanisms induced by IH and OSA, rather than its well-established deleterious effects, while focusing on acute coronary syndromes. Therefore, protective mechanisms revealed in I/R biology and exhibited in vitro and in animal models utilizing IH followed by a severe ischemia are discussed and linked to acute myocardial infarction patients with concomitant OSA. The roles of endothelial progenitor cells, their proliferative and angiogenic properties, and collateral formation are emphasized in the clinical setting, as well as heterogenic interindividual responses to identical hypoxic stimuli. These findings might represent potential predictors to cardio-/cerebrovascular health, by identifying patients at higher or lower cardiovascular risk.
Part of the book: Atherosclerosis, Arteriosclerosis and Arteriolosclerosis