Pavel Šiarnik1, Lucia Krížová1, Branislav Kollár1, Marek Sýkora1,2, Peter Turčáni1
Obstructive sleep apnea syndrome is form of a sleep-related breathing disorder. It is characterised by repetitive upper airways obstruction. Intermittent changes of the oxygen desaturation of the blood and subsequent oxygen resaturation play a significant role in the pathophysiology of the obstructive sleep apnea syndrome. Intermittent hypoxia in sleep apnea syndrome restricts the availability of endothelial nitric oxide, causes consequent worsening of the vascular endothelium-dependent dilation and has thus a key importance for the development of the endothelial dysfunction. Endothelial dysfunction represents an initial step in the process of atherogenesis, which leads to the well-known clinical complications, including cerebrovascular diseases.