Chest

Chest

Volume 131, Issue 2, February 2007, Pages 453-459
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Original Research: Sleep Medicine
Plasma Aldosterone Is Related to Severity of Obstructive Sleep Apnea in Subjects With Resistant Hypertension

https://doi.org/10.1378/chest.06-1442Get rights and content

Abstract

Objective:Obstructive sleep apnea (OSA) and primary aldosteronism are common in subjects with resistant hypertension; it is unknown, however, if the two disorders are causally related. This study relates plasma aldosterone and renin levels to OSA severity in subjects with resistant hypertension, and in those with equally severe OSA but without resistant hypertension serving as control subjects.

Methods:Seventy-one consecutive subjects referred to the University of Alabama at Birmingham (UAB) for resistant hypertension (BP uncontrolled on three medications) and 29 control subjects referred to UAB Sleep Disorders Center for suspected OSA were prospectively evaluated by an early morning plasma aldosterone concentration (PAC) and renin level, and by overnight, attended polysomnography.

Results:OSA (apnea-hypopnea index [AHI] ≥ 5/h) was present in 85% of subjects with resistant hypertension. In these subjects, PAC correlated with AHI (ρ = 0.44, p = 0.0002) but not renin concentration. Median PAC was significantly lower in control subjects compared to subjects with resistant hypertension (5.5 ng/dL vs 11.0 ng/dL, p < 0.05) and not related to AHI. In male subjects compared to female subjects with resistant hypertension, OSA was more common (90% vs 77%) and more severe (median AHI, 20.8/h vs 10.8/h; p = 0.01), and median PAC was significantly higher (12.0 ng/dL vs 8.8 ng/dL, p = 0.006).

Conclusion:OSA is extremely common in subjects with resistant hypertension. A significant correlation between PAC and OSA severity is observed in subjects with resistant hypertension but not in control subjects. While cause and effect cannot be inferred, the data suggest that aldosterone excess may contribute to OSA severity.

Section snippets

Subjects

Consecutive subjects referred to the University of Alabama at Birmingham (UAB) Hypertension Clinic for resistant hypertension were enrolled. Resistant hypertension was defined as uncontrolled BP (> 140/90 mm Hg) in spite of use of three or more antihypertensive agents of different classes.9Consecutive subjects referred to the UAB Sleep/Wake Disorders Center for suspicion of OSA and without resistant hypertension (normotensive or BP controlled on two or fewer antihypertensive medications) were

Resistant Hypertension Subjects

Biochemical assessment and overnight polysomnography were completed in 71 subjects with resistant hypertension. The demographic, biochemical, and polysomnographic values are listed inTable 1. Forty-five percent of subjects were African American. The majority of subjects were receiving a thiazide diuretic (83%), an angiotensin-converting enzyme inhibitor (67%), a calcium-channel antagonist (72%), and a β-adrenergic antagonist (68%). Subjects with resistant hypertension had a higher prevalence of

Discussion

This study is novel in demonstrating a strong positive correlation between plasma aldosterone and OSA severity in subjects with resistant hypertension. In contrast, there was no correlation noted between OSA and aldosterone levels in control subjects with equally severe OSA as defined by AHI. These results do not prove causality but are consistent with the hypothesis that hyperaldosteronism induces and/or exacerbates OSA. Less likely, although not excluded, is the possibility that aldosterone

Clinical Implications

The results of the current study confirm that patients with resistant hypertension are at extremely high risk of having OSA. These results and those of Logan et al3support aggressively screening all patients with resistant hypertension for OSA. The current results further indicate that patients with resistant hypertension and OSA have elevated aldosterone levels consistent with an increased likelihood of having PA. Whether treatment of OSA will reduce aldosterone levels or whether preferential

Acknowledgments

We thank David Moore, RPSGT, and S. Justin Thomas, BS, RPSGT, for assistance in conducting and scoring the overnight sleep studies.

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    • Cited by (0)

    This work was supported by American Heart Association Grant-in-Aid 0355302B received by Dr. Calhoun, and National Heart, Lung, and Blood Institute grants HL075614 and SCCOR P50HL077100 received by Dr. Calhoun, HL007457 received by Dr. Pratt-Ubunama, and National Institutes of Health grant M01-RR00032 received by the General Clinical Research Center. Drs. Pratt-Ubunama, Nishizaka, Boedefeld, and Cofield have no conflicts of interest to disclose. Dr. Calhoun has received research support from Novartis and AstraZeneca LLP and has participated in an advisory board for AstraZeneca LLP. Dr. Harding has received research support, honoraria, and consultant payments from AstraZeneca LLP. There was no off-label or investigational drug use.

    Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml)

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    Copyright © 2007 The American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.