Vascular Dysfunction in Sleep Apnea

Abstract

See related article, pp 417–424 Cardiovascular disease remains one of the leading causes of morbidity and mortality. Obstructive sleep apnea (OSA) has been increasingly implicated in a breadth of cardiovascular diseases, including systemic hypertension, heart failure, stroke, arrhythmias, myocardial ischemia, and pulmonary arterial hypertension.1 The importance of this association, especially in the context of OSA as an etiologic factor, is compellingly relevant to disease management strategies, given the high prevalence of OSA and its likely rising trajectory secondary to the ongoing obesity epidemic.2 OSA may be present in approximately 20% of American adults, only a minority of whom have ever been diagnosed; this is true even for patients with established cardiovascular disease3 and despite the widespread availability of several effective treatment modalities (including continuous positive airway pressure [CPAP]). It is only over the past 2 decades that serious investigative interest has been paid to the interactions between OSA and cardiac and vascular disease and dysfunction. Deciphering the mechanisms, causal relationships, and potential therapeutic targets in the links between OSA and cardiovascular morbidity has not been an easy task, in part because of the constellation of comorbidities that characterize a large proportion of sleep apnea patients. OSA leads to multiple sources of cardiovascular stress, including nocturnal hypoxemia and hypercapnia, precipitous intrathoracic pressure changes, repetitive arousals, and poor sleep quality with consequent sleep deprivation. These, in turn, have been linked to endothelial dysfunction,4 systemic inflammation, sympathetic activation,5 metabolic dysregulation, hypercoagulability, and atrial enlargement, the combination of which may contribute to the initiation and progression of a range of cardiovascular diseases. Of these, endothelial dysfunction …