Abstract
Obstructive sleep apnea (OSA) is a common respiratory disorder characterized by partial obstruction of upper respiratory tract and repetitive cessation of breathing during sleep. The etiology behind OSA is associated with the occurrence of intermittent hypoxemia, recurrent arousals and intrathoracic pressure swings. These contributing factors may turn on various signaling mechanisms including elevated sympathetic tone, oxidative stress, inflammation, endothelial dysfunction, cardiovascular variability, abnormal coagulation and metabolic defect ( e.g., insulin resistance, leptin resistance and altered hepatic metabolism). Given its close tie with major cardiovascular risk factors, OSA is commonly linked to the pathogenesis of a wide array of cardiovascular diseases (CVDs) including hypertension, heart failure, arrhythmias, coronary artery disease, stroke, cerebrovascular disease and pulmonary hypertension (PH). The current standard treatment for OSA using adequate nasal continuous positive airway pressure (CPAP) confers a significant reduction in cardiovascular morbidity. Nonetheless, despite the availability of effective therapy, patients with CVDs are still deemed highly vulnerable to OSA and related adverse clinical outcomes. A better understanding of the etiology of OSA along with early diagnosis should be essential for this undertreated disorder in the clinical setting.