We read with great interest the recent article in CHEST (September 2016) entitled “Hypertension Is Associated With Undiagnosed OSA During Rapid Eye Movement Sleep.” In their article, Appleton et al demonstrated that an apnea-hypopnea index during rapid eye movement sleep (REM AHI) > 30 events/h is independently related to the presence of hypertension (HTN). Interestingly, they also confirmed the relationship between REM OSA and HTN among patients without OSA (due to an AHI < 10 events/h). The authors remarked that the role of OSA in the development of HTN is due to its impact on endothelial damage. On the other hand, it is well known that HTN also is responsible for vascular dysfunction. In this regard, we would like to highlight the important impact of the simultaneous presence of OSA and HTN on the risk of atherosclerosis. Pathophysiologically, it is widely accepted that the role of both conditions in the development of endothelial damage is mediated by inflammation., Indeed, in patients with HTN, increased blood pressure stimulates inflammatory mechanisms, in which the vasoactive peptides angiotensin II and endothelin-1 have a key role. On the other hand, in patients with OSA, the hypoxia-reoxygenation cycle and sleep fragmentation trigger the generation of reactive oxygen species, and inflammation. Therefore, in patients with OSA and HTN, there is the possibility that all the aforesaid mechanisms operate simultaneously and/or synergistically. In this regard, Drager et al demonstrated additive effects of OSA and HTN on carotid intima-media thickness, diameter, and distensibility. Moreover, our group has recently evaluated the consequences of the coexistence of OSA and HTN on intima-media thickness, and on inflammatory markers of atherosclerosis (such as interleukin-6 and pentraxin-3). These early markers of atherosclerosis were significantly increased in hypertensive patients with OSA compared with normotensive patients with OSA, hypertensive patients without OSA, or control subjects.