Obstructive sleep apnoea in acute coronary syndrome

Abstract

Obstructive sleep apnoea (OSA) syndrome affects about 13% of the male and 7–9% of the female population. Hypoxia, oxidative stress and systemic inflammation link OSA and cardiovascular and metabolic consequences, including coronary artery disease. Current research has identified several clinical phenotypes, and the combination of breathing disturbances during sleep, systemic effects and end-organ damage might help to develop personalised therapeutic approaches. It is unclear whether OSA is a risk factor for acute coronary syndrome (ACS) and might affect its outcome. On the one hand, OSA in patients with ACS may worsen prognosis; on the other hand, OSA-related hypoxaemia could favour the development of coronary collaterals, thereby exerting a protective effect. It is unknown whether positive airway pressure treatment may influence adverse events and consequences of ACS. In non-sleepy patients with OSA and stable coronary artery disease, randomised controlled trials failed to show that continuous positive airway pressure (CPAP) treatment protected against cardiovascular events. Conversely, uncontrolled studies suggested positive effects of CPAP treatment in such patients. Fewer data are available in subjects with ACS and OSA, and results of randomised controlled studies on the effects of CPAP are expected shortly. Meanwhile, the search for reliable markers of risk continues. Recent studies suggest that daytime sleepiness may indicate a more severe OSA phenotype with regard to cardiovascular risk. Finally, some studies suggest sex-related differences. The picture is still incomplete, and the potential role of OSA in patients with ACS awaits confirmation, as well as clear definition of subgroups with different degrees of risk.