Cardiovascular mechanisms and consequences of obstructive sleep apnoea

Obstructive sleep apnoea (OSA) is considered as a risk factor for the development of arterial hypertension, coronary artery disease (CAD), myocardial infarction and stroke. These clinical manifestations are the consequences of elevated sympathetic activity, cardiovascular variability, intrathoracic pressure changes, inflammation, oxidative stress, endothelial dysfunction, insulin resistance and thrombosis provoked by OSA. As a result, OSA is often present in patients with cardiovascular disease (CVD) and the increased prevalence of CVD in OSA population raises both cardiovascular morbidity and mortality and the demand of healthcare resources. Observational cohort studies indicate that untreated patients with OSA have an increased risk of fatal and non-fatal cardiovascular events, an increased risk of sudden cardiac death during the sleeping hours and a higher risk of stroke or death from any cause. Continuous positive airway pressure (CPAP) and oral appliance therapy are the two treatments for OSA whose effects on cardiovascular endpoints have been assessed in randomised trials. There is increasing evidence that adequate CPAP therapy leads to a significant reduction in cardiovascular morbidity.