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Study objectives: Chronic intermittent hypoxia (CIH), a hallmark feature of obstructive sleep apnea (OSA), induces accelerated atherogenesis as well as aorta vascular remodeling. Although the cyclooxygenase (COX) pathway has been proposed to contribute to the cardiovascular consequences of OSA, the potential benefits of a widely employed COX-inhibitor such (acetylsalicylic acid, ASA) on CIH-induced vascular pathology are unknown. Therefore, we hypothesized that a common non-selective COX inhibitor such as ASA would attenuate the aortic remodeling induced by CIH in mice.Methods: 40 wild-type C57/BL6 male mice were randomly allocated to CIH or normoxic exposures (N) and treated with daily doses of ASA or placebo for 6 weeks. At the end of the experiments, intima-media thickness (IMT), elastin disorganization (ED), elastin fragmentation (EF), length between fragmented fiber endpoints (LFF), aortic wall collagen abundance (AC) and mucoid deposition (MD) were assessed.Results: Compared to N, CIH promoted significant increases in IMT (52.58 ± 2.82 μm vs. 46.07 ± 4.18 μm, p < 0.003), ED (25.29 ± 14.60% vs. 4.74 ± 5.37%, p < 0.001), EF (5.80 ± 2.04 vs. 3.06 ± 0.58, p < 0.001), LFF (0.65 ± 0.34% vs. 0.14 ± 0.09%, p < 0.001), AC (3.43 ± 1.52% vs. 1.67 ± 0.67%, p < 0.001) and MD (3.40 ± 2.73 μm2 vs. 1.09 ± 0.72 μm2, p < 0.006). ASA treatment mitigated the CIH-induced alterations in IMT: 44.07 ± 2.73 μm; ED: 10.57 ± 12.89%; EF: 4.63 ± 0.88; LFF: 0.25 ± 0.17% and AC: 0.90 ± 0.13% (p

In all fields of medicine, major efforts are currently dedicated to improve the clinical, physiological and therapeutic understanding of disease, and obstructive sleep apnoea (OSA) is no exception. The personalised medicine approach is relevant for OSA, given its complex pathophysiology and variable clinical presentation, the interactions with comorbid conditions and its possible contribution to poor outcomes. Treatment with continuous positive airway pressure (CPAP) is effective, but CPAP is poorly tolerated or not accepted in a considerable proportion of OSA patients. This review summarises the available studies on the physiological phenotypes of upper airway response to obstruction during sleep, and the clinical presentations of OSA (phenotypes and clusters) with a special focus on our changing attitudes towards approaches to treatment. Such major efforts are likely to change and expand treatment options for OSA beyond the most common current choices (i.e. CPAP, mandibular advancement devices, positional treatment, lifestyle changes or upper airway surgery). More importantly, treatment for OSA may become more effective, being tailored to each patient's need.