Obstructive Sleep Apnea Syndrome: Links Betwen Pathophysiology and Cardiovascular Complications

The prevalence of obstructive sleep apnea syndrome (OSAS) is increasing, especially in the middle-aged population. OSAS is associated with an elevated risk of cardiovascular morbidity and mortality. Arterial hypertension is often the first consequence of OSAS, but the most severe complications are coronary artery disease, stroke and arrhythmias. The aim of this review was to analyze the several mechanisms involved in the development of the cardiovascular events, such as endothelial dysfunction accompanied by a pro-inflammatory and pro-oxidant status, hemorheological alterations, hypercoagulability and imbalance between matrix metalloproteases and their inhibitors.

A search on PubMed was carried out using the following terms: obstructive sleep apnea syndrome; endothelial dysfunction; oxidative stress; inflammation; rheology; matrix metalloproteases.

OSAS severity strongly influenced cardiovascular risk factors and, furthermore, it was correlated with the incidence of fatal and non-fatal events.

The treatment with continuous positive airways pressure (cPAP) is the gold standard for OSAS and was able to positively influence all the pathophysiological mechanisms responsible for cardiovascular diseases. Long-term cPAP improved endothelial function and hemorheology, reduced oxidative stress and inflammation, and decreased the levels of metalloproteases.