Obstructive sleep apnea (OSA) is a common disease with substantial health and economic impact [1][2][3]. During sleep, the upper airway collapses repeatedly leading to sleep fragmentation and oxyhemoglobin desaturation. Furthermore, there are compelling epidemiologic data implicating OSA in the development of myocardial infarction and cerebrovascular events. For example, Marin et al. [4] published data from a cohort of patients with varying degrees of sleep-disordered breathing (snorers, mild-severe OSA) and healthy participants who were followed for a mean of 10 years. Patients with severe untreated OSA had a much greater risk of developing fatal (odds ratio [OR] = 2.87, 95% CI = 1.17-2.51) and nonfatal cardiovascular disease (CVD) (OR = 3.17, 95% CI = 1.12-7.51) compared to healthy controls after adjustment for potential confounding factors. Patients with OSA who were treated with CPAP did not have an increased rate of events (OR = 1.05, 95% CI = 0.39-2.21 and OR = 1.42, 95% CI = 0.52-3.4, respectively) compared to healthy controls, suggesting that substantial benefits may be seen with therapy.In another study, Peker et al.[5] prospectively followed 182 middle-aged men with no hypertension or CVD at baseline who were referred for a sleep study. Incident CVD (i.e., hypertension, coronary artery disease, stroke, myocardial infarction, arrhythmias) over 7 years occurred in 37% of patients with OSA compared to 6.6% in those without OSA. In a study from the Sleep Heart Health Cohort, the prevalence of CVD, including myocardial infarction, angina, coronary revascularization, heart failure, and stroke was 1.42 times greater in patients with OSA (apnea-hypopnea index [AHI] [ 11 events/h) compared to those without OSA (AHI = 0-1.3 events/h) after controlling for potential confounders [6].