Arterial Stiffness in Patients with Obstructive Sleep Apnea and Hypertension: A Narrative Review

Arterial stiffness is a determinant of cardiovascular risk and has been increasingly associated with obstructive sleep apnea (OSA), although its independent contribution remains unclear due to the presence of comorbidities, the most important of which is hypertension. This narrative review synthesizes current evidence on the relationship between OSA, hypertension, and arterial stiffness, with a particular focus on the mediating role of hypertension and its clinical phenotypes. Evidence from observational and longitudinal studies indicates that OSA is generally associated with increased arterial stiffness, particularly in younger and normotensive individuals. A stepwise increase in pulse wave velocity (PWV) is consistently observed across control, OSA, hypertension, and combined OSA–hypertension groups, supporting an additive vascular burden. Hypertension emerges as a central correlate and amplifier of vascular remodeling, with its presence attenuating the independent association between OSA and arterial stiffness. Findings regarding masked hypertension are heterogeneous, with some studies showing increased PWV in OSA while others demonstrate minimal differences after adjustment. In contrast, resistant hypertension is consistently associated with high-risk hemodynamic and metabolic profiles, although the independent contribution of OSA to arterial stiffness in this group is often limited after multivariable adjustment. Large cohort evidence further suggests that associations between OSA and arterial stiffness surrogates are largely explained by age, blood pressure status, and cardiometabolic comorbidities. Because the evidence base is predominantly cross-sectional, these findings should be interpreted as showing that OSA’s association with arterial stiffening is closely intertwined with the presence and development of hypertension, rather than establishing a causal or temporal sequence. Future longitudinal and interventional studies are needed to clarify causal pathways and therapeutic implications.