• John S Floras.
• University Health Network and Mount Sinai Hospital Division of Cardiology, University of Toronto, Toronto, Ontario, Canada. Electronic address: john.floras@utoronto.ca.
• Eur. J. Pharmacol. 2015 Sep 15; 763 (Pt A): 28-37.

AbstractObstructive sleep apnea (OSA), present in ~15% of the general population, increases the risks of stroke, heart failure, and premature death. Importantly, individuals with cardiovascular disease have a higher prevalence yet they often have few symptoms to alert clinicians to its presence. OSA with an apnea-hypopnea index (AHI) ≥15 events/hour is present in ≥30% of patients with primary hypertension and in up to 80% of those with drug resistant hypertension, suggesting that the neural, hormonal, inflammatory and vascular cascades triggered by OSA may elevate blood pressure chronically. The purpose of this review is to summarize: (1) the epidemiology of OSA and its relation to cardiovascular risk; (2) potential mechanisms by which OSA could promote conditions known to increase the risk of hypertension or contribute to its development and progression; (3) evidence for and against a pro-hypertensive effect of OSA; and, (4) the impact of treatment with continuous positive airway pressure (CPAP) on blood pressure and blood pressure-related morbidities. The prevailing view that the effect of treatment on blood pressure is modest arises from the inability of most contemporary technology to measure accurately the true impact of CPAP on OSA-entrained surges in nocturnal blood pressure. Moreover the exclusive focus on blood pressure, as if this is the principal determinant of cardiovascular event rates in this population, is naïve. The capacity to reduce cardiovascular risk by treating OSA with CPAP likely transcends a simple blood pressure effect; formal testing of this hypothesis will require adequately powered randomized clinical trials.Copyright © 2015 Elsevier B.V. All rights reserved.

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