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Editorials |

OSA and HypertensionOSA and Hypertension: Do We Know All the Answers?

Malcolm Kohler, MD; John R. Stradling, MD
Author and Funding Information

From the Division of Pulmonology, University Hospital Zurich (Prof Kohler); and NIHR Biomedical Research Centre (Prof Stradling).

Correspondence to: Malcolm Kohler, MD, Division of Pulmonology, University Hospital Zurich, Raemistrasse 100, 8091 Zurich, Switzerland; e-mail: Malcolm.Kohler@usz.ch


Financial/nonfinancial disclosures: Dr Stradling has received grants from ResMed Foundation and the British Heart Foundation and serves as a consultant to ResMed UK. Dr Kohler has no potential conflict of interests.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;144(5):1433-1435. doi:10.1378/chest.13-1096
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Extract

There is accumulating evidence from well-designed, randomized controlled trials suggesting that OSA syndrome (OSAS) independently adds to cardiovascular risk. One major mechanism underpinning the association between OSAS and cardiovascular disease is likely to be sustained arterial hypertension, and this association may possibly be enhanced by frequent nocturnal acute BP rises. The repetitive episodes of obstructive apneas and hypopneas are often associated with arousals and intermittent hypoxia, both of which lead to increased sympathetic nervous system activity and consequent considerable transient increases in arterial BP up to 80 mm Hg. The activation of the sympathetic nervous system is also associated with an augmented production of catecholamines during the night, which are released into the circulation and may thereby contribute to the development of sustained arterial hypertension.1 The nocturnal sympathetic nervous system activation, and consequently higher BP during sleep, may attenuate the advantageous physiologic dipping of BP normally seen at night. Augmented sympathetic activation in patients with OSAS has also been shown to be associated with impaired endothelial function, increased arterial stiffness, and blunted baroreflex sensitivity, which are contributing factors to the development of arterial hypertension.1,2

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