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Eduardo Pimenta, MD, PhD; David A. Calhoun, MD
Author and Funding Information

From the Endocrine Hypertension Research Centre and Clinical Centre of Research Excellence in Cardiovascular Disease and Metabolic Disorders (Dr Pimenta), The School of Medicine, The University of Queensland, Princess Alexandra and Greenslopes Private Hospitals; the Dante Pazzanese Institute of Cardiology (Dr Pimenta), São Paulo, Brazil; and the Sleep/Wake Disorders Center (Dr Calhoun), Division of Pulmonary, Allergy and Critical Care Medicine, and Vascular Biology and Hypertension Program (Dr Calhoun), The University of Alabama at Birmingham.

Correspondence to: David Calhoun, MD, The University of Alabama at Birmingham, 1530 3rd Ave S, Birmingham, AL, 35294-1150; e-mail: dcalhoun@uab.edu


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.

Funding/Support: This work was supported by National Institutes of Health National Center for Research Resources [Grant 5UL1 RR025777-04].

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):720. doi:10.1378/chest.13-0969
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We thank Drs Mirrakhimov and Mirrakhimov for their interest in our article1 and their comments. They point out that additional mechanisms other than fluid overload and rostral fluid shift may be associated with severity of obstructive sleep apnea (OSA) in patients with hyperaldosteronism and high dietary salt intake. Drs Mirrakhimov and Mirrakhimov are correct in hypothesizing that fibrosis and inflammation of the upper airway tissues may also contribute to the severity of OSA, although, as highlighted by them, there are no studies exploring this potential mechanism.

Experiments in animal models indicate that aldosterone excess, in addition to increasing BP, contributes directly to target-organ (heart, brain, and kidney) deterioration by inducing inflammation and perivascular fibrosis.2,3 These same studies have been consistent in demonstrating that the pressor, proinflammatory, and profibrotic effects of aldosterone are dependent on concomitant high dietary salt intake.

Clinical studies do suggest that aldosterone blockade reduces the severity of OSA. In a prospective, open-label study, 12 patients with resistant hypertension and moderate to severe OSA (apnea-hypopnea index ≥ 15) received spironolactone in addition to their previous antihypertensive medications for 8 weeks, after which overnight polysomnography was repeated.4 The apnea-hypopnea index was reduced by a mean of about 50% in all patients. This benefit occurred in the setting of increased diuresis, suggesting that aldosterone and sodium-mediated chronic fluid retention is an important mediator of OSA severity. This study is not able to distinguish diuretic vs antiinflammatory/fibrotic effect of mineralocorticoid blockade but does confirm aldosterone as an important mediator of OSA severity at least in patients with resistant hypertension.

In conclusion, we agree that additional mechanisms, other than fluid overload, may be involved in the development of OSA in these patients. Additional experimental and clinical studies are necessary to explore additional mechanisms involved in the development and maintenance of OSA in patients with resistant hypertension, hyperaldosteronism, or both to prospectively test management strategies of OSA.

Acknowledgments

Role of sponsors: The sponsors had no role in the design of the study, the collection and analysis of the data, or in the preparation of the manuscript.

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]
 
Brilla CG, Weber KT. Mineralocorticoid excess, dietary sodium, and myocardial fibrosis. J Lab Clin Med. 1992;120(6):893-901.
 
Rocha R, Rudolph AE, Frierdich GE, et al. Aldosterone induces a vascular inflammatory phenotype in the rat heart. Am J Physiol Heart Circ Physiol. 2002;283(5):H1802-H1810.
 
Gaddam K, Pimenta E, Thomas SJ, et al. Spironolactone reduces severity of obstructive sleep apnoea in patients with resistant hypertension: a preliminary report. J Hum Hypertens. 2010;24(8):532-537. [CrossRef]
 

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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]
 
Brilla CG, Weber KT. Mineralocorticoid excess, dietary sodium, and myocardial fibrosis. J Lab Clin Med. 1992;120(6):893-901.
 
Rocha R, Rudolph AE, Frierdich GE, et al. Aldosterone induces a vascular inflammatory phenotype in the rat heart. Am J Physiol Heart Circ Physiol. 2002;283(5):H1802-H1810.
 
Gaddam K, Pimenta E, Thomas SJ, et al. Spironolactone reduces severity of obstructive sleep apnoea in patients with resistant hypertension: a preliminary report. J Hum Hypertens. 2010;24(8):532-537. [CrossRef]
 
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