0
Correspondence |

Obstructive Sleep Apnea and Sodium IntakeObstructive Sleep Apnea and Sodium Intake: What Is the Mechanism? FREE TO VIEW

Aibek E. Mirrakhimov, MD; Erkin M. Mirrakhimov, MD, PHD
Author and Funding Information

From Saint Joseph Hospital (Dr A. E. Mirrakhimov); and Kyrgyz State Medical Academy (Dr E. M. Mirrakhimov).

Correspondence to: Aibek E. Mirrakhimov, MD, Saint Joseph Hospital, 2800 N Lake Shore Dr, Chicago, IL 60657: e-mail: amirrakhimov1@gmail.com


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

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


Chest. 2013;144(2):719-720. doi:10.1378/chest.13-0925
Text Size: A A A
Published online
To the Editor:

We read with keen interest the study by Pimenta et al1 in a recent issue of CHEST (April 2013). These researchers enrolled 97 patients with resistant hypertension (RHTN) and screened them with overnight polysomnography for the presence of obstructive sleep apnea (OSA). In addition, 24-h urinary sodium and aldosterone levels were measured. It was found that 77.3% of the patients with RHTN had OSA, which is much greater than the prevalence of OSA in the general population.2 On the other hand, 28.9% of the patients with RHTN were found to have hyperaldosteronism. It was found that the urinary sodium level was an independent marker for OSA severity in the patients with hyperaldosteronism (no such association was found in patients without hyperaldosteronism). We congratulate the authors, who contributed extensively to the topic of OSA and aldosterone metabolism. We would like to mention some of the possible mechanisms that may explain this association.

It is well known that patients with RHTN (including hyperaldosteronism), congestive heart failure, and advanced renal disease have a greater prevalence of OSA.3 Fluid overload associated with these conditions and rostral fluid shift may lead to narrowing of the upper airways, with resultant OSA. This hypothesis is bolstered by the fact that therapies aiming to remove excessive body fluid are associated with an improvement in OSA severity. Nevertheless, additional pathobiologic pathways may be implicated in the development or worsening of OSA severity. Research data point out that aldosterone may mediate multiple detrimental effects, such as tissue fibrosis, systemic inflammation, and oxidative stress.4 These mechanisms are believed to be responsible for an aldosterone-mediated increase in cardiovascular disease.4

It is possible that aldosterone may mediate upper airways inflammation and fibrosis. This, in turn, may contribute to the detrimental effects of fluid overload in patients with OSA and hyperaldosteronism. However, to our knowledge, there are no studies investigating this potential mechanism. It will be important to study this hypothesis in future research, which should provide more basic knowledge on the pathophysiology of both OSA and aldosterone excess.

References

Pimenta E, Stowasser M, Gordon RD, et al. Increased dietary sodium is related to severity of obstructive sleep apnea in patients with resistant hypertension and hyperaldosteronism. Chest. 2013;143(4):978-983. [CrossRef]
 
Mirrakhimov AE, Sooronbaev T, Mirrakhimov EM. Prevalence of obstructive sleep apnea in Asian adults: a systematic review of the literature. BMC Pulm Med. 2013;13:10. [CrossRef]
 
Mirrakhimov AE. Supine fluid redistribution: should we consider this as an important risk factor for obstructive sleep apnea? Sleep Breath. 2013;17(2):511-523. [CrossRef]
 
Nguyen Dinh Cat A, Jaisser F. Extrarenal effects of aldosterone. Curr Opin Nephrol Hypertens. 2012;21(2):147-156. [CrossRef]
 

Figures

Tables

References

Pimenta E, Stowasser M, Gordon RD, et al. Increased dietary sodium is related to severity of obstructive sleep apnea in patients with resistant hypertension and hyperaldosteronism. Chest. 2013;143(4):978-983. [CrossRef]
 
Mirrakhimov AE, Sooronbaev T, Mirrakhimov EM. Prevalence of obstructive sleep apnea in Asian adults: a systematic review of the literature. BMC Pulm Med. 2013;13:10. [CrossRef]
 
Mirrakhimov AE. Supine fluid redistribution: should we consider this as an important risk factor for obstructive sleep apnea? Sleep Breath. 2013;17(2):511-523. [CrossRef]
 
Nguyen Dinh Cat A, Jaisser F. Extrarenal effects of aldosterone. Curr Opin Nephrol Hypertens. 2012;21(2):147-156. [CrossRef]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543