Pavol Joppa, Ivana Paraničová, Pavol Pobeha, Ružena Tkáčová
Presence of obstructive sleep apnoea (OSA) is an established independent risk factor of cardiovascular disease, in particular arterial hypertension, coronary artery disease, cerebrovascular disease, heart failure and arrhytmias. In patients with OSA repeated increases of sympathetic nerve system occur due to acute haemodynamic changes during the episodes of obstruction. These in turn lead into persistent autonomic dysfunction and impaired regulation of blood pressure. Episodes of hypoxia and re-oxygenation provoke endothelial dysfunction and with accelerated development of atherosclerosis as a result. Although elimination of apnoeic episodes by continuous positive pressure (CPAP) treatment ameliorates the above pathological mechanisms, there was no substantial benefit on overall cardiometabolic risk unless other risk factors (in particular obesity) were tackled.