Sleep-Disordered Breathing and Coronary Artery Disease

Abstract

Coronary artery disease (CAD) is one of the most frequent diseases in industrial nations. Despite significant advances in diagnosis and therapy, CAD and its long-term consequences are important contributors to morbidity and mortality. Therefore, in addition to management of traditional CAD risk factors, there are continued efforts to evaluate other factors and comorbidities that might contribute to the development and progression of CAD. One such factor is sleep-disordered breathing (SDB), which is characterized by repetitive apneas, arousals from sleep, and intermittent hypoxia. There is increasing evidence that SDB is a risk factor for CAD. In the early phase after myocardial infarction (MI) the heart might be in a vulnerable state sensitive to the negative consequences of SDB, including increased cardiac workload and endothelial dysfunction, which might ultimately lead to a mismatch between oxygen demand and supply. Despite successful percutaneous coronary intervention, patients with acute MI and SDB have prolonged myocardial ischemia, less salvaged myocardium, and impaired left and right ventricular remodelling compared with those without SDB, all of which predispose to heart failure. Suppression of SDB with positive airway pressure therapy in the early phase after MI is feasible. However, whether treatment of SDB with positive airway pressure will be an effective nonpharmacological treatment approach that will prevent the development of heart failure after MI remains to be determined and is the subject of current investigations.