Sleep-disordered breathing (SDB) is a group of disorders defined by intermittent closure or narrowing of the upper airway, caused either by mechanical obstruction or dysregulation of the respiratory centers in the brainstem. The effects of SDB on cardiovascular and metabolic health and disease have been an area of growing interest. Many studies have shown mechanistic links between physiological changes seen in SDB and important cardiometabolic outcomes. In particular, SDB induces alterations in autonomic function, swings in intrathoracic pressure, systemic inflammation, sleep fragmentation, and oxidative stress, with diverse effectors including alterations in cellular gene expression, for example, through microRNA and hypoxia-inducible factor 1, changes in the gut microbiome, and many others. Ultimately, these mechanistic pathways have implications on vascular and myocardial dysfunction, hypertension, insulin sensitivity, lipid metabolism, and weight gain. Several treatment modalities exist for SDB, and are chosen based on the specific disease process and patient preference/tolerance. These therapies result in an improvement in symptoms related to SDB severity and varying levels of cardiometabolic disease risk mitigation. In this review, we will present some important mechanisms of SDB that increase the risk for cardiometabolic disease, and we will discuss therapies and their intended targets.
Gomez et al. (Thu,) studied this question.