ABSTRACT
A body of epidemiologic and clinical evidence dating back to the early 1960s establishes the relationships between sleep apnea and cardiovascular disease (CVD). Individuals with obstructive sleep apnea, the most common type of sleep-disordered breathing, are at increased risk for coronary artery disease, congestive heart failure, and stroke. Evidence that treatment of sleep apnea with continuous positive airway pressure reduces blood pressure, improves left ventricular systolic function, and diminishes platelet activation further supports linkage between obstructive sleep apnea and CVD. Notwithstanding, complex associations between these two conditions remain largely unexplained due to dearth of systematic experimental studies. Arguably, several intermediary mechanisms including sustained sympathetic activation, intrathoracic pressure changes, and oxidative stress might be involved. Other abnormalities such as dysfunctions in coagulation factors, endothelial damage, platelet activation, and increased systemic inflammation might also play a fundamental role. This review examines evidence for the associations between obstructive sleep apnea and CVD and suggested underlying anatomical and physiological mechanisms. Specific issues pertaining to definition, prevalence, diagnosis, and treatment of sleep apnea are also discussed. Consistent with rising interest in the potential role of the metabolic syndrome, this review explores the hypothesized mediating effects of each of the components of the metabolic syndrome.
