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Juan F. Masa, MD, PhD; Jaime Corral, MD; Javier Gómez-de-Terreros, MD, PhD; María-Ángeles Sánchez-Quiroga, MD; Babak Mokhlesi, MD, FCCP
Author and Funding Information

FINANCIAL/NONFINANCIAL DISCLOSURES: None declared.

FUNDING/SUPPORT: See earlier cited article for author conflicts of interest.

aPulmonary Section, San Pedro de Alcántara Hospital, Cáceres, Spain

bPulmonary Section, Virgen del Puerto Hospital, Plasencia, Spain

cDepartment of Medicine, Section of Pulmonary and Critical Care, University of Chicago, Chicago, IL

dCIBER de enfermedades respiratorias (CIBERES), Madrid, Spain

CORRESPONDENCE TO: Juan F. Masa, MD, PhD, Pulmonary Section, San Pedro de Alcántara Hospital, Avda. Pablo Naranjo S/N, 10003 Cáceres, Spain


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(6):1411. doi:10.1016/j.chest.2016.09.019
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We are grateful to Dr Chugh and colleagues for their interest in our article.

In contrast to the Sleep Heart Health Study (a prospective cohort study to determine the cardiovascular and other consequences of sleep-disordered breathing), our study (clinicaltrial.gov identifier: NCT01405976) published in CHEST was a cross-sectional analysis using baseline variables from the randomized clinical trial (RCT) assessing the efficacy of different treatment strategies in patients with obesity hypoventilation syndrome (OHS). With a cross-sectional design, we can only determine prevalence, not incidence, of cardiovascular events.

Additionally, the aim of the RCT was not to enroll patients for a primary prevention trial of cardiovascular events in those with OHS. We enrolled patients from a clinical population referred for suspicion of OHS. We agree that there is a risk for selection bias and we have acknowledged this limitation in our article. However, patients in our study were sequentially screened; therefore, we believe our sample is representative of the overall population of patients with OHS. Moreover, we tried to minimize bias by adjusting for various confounders in our regression models. Our results should be considered as hypothesis generating and would need to be tested more rigorously in either prospective longitudinal studies or RCTs of patients with OHS and various degrees of sleep apnea severity.

References

Masa J.F. .Corral J. .Romero A. .et al Protective cardiovascular effect of sleep apnea severity in obesity hypoventilation syndrome. Chest. 2016;150:68-79 [PubMed]journal. [CrossRef] [PubMed]
 
Roca G.Q. .Redline S. .Claggett B. .et al Sex-specific association of sleep apnea severity with subclinical myocardial injury, ventricular hypertrophy, and heart failure risk in a community-dwelling cohort: the Atherosclerosis Risk in Communities-Sleep Heart Health Study. Circulation. 2015;132:1329-1337 [PubMed]journal. [CrossRef] [PubMed]
 

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References

Masa J.F. .Corral J. .Romero A. .et al Protective cardiovascular effect of sleep apnea severity in obesity hypoventilation syndrome. Chest. 2016;150:68-79 [PubMed]journal. [CrossRef] [PubMed]
 
Roca G.Q. .Redline S. .Claggett B. .et al Sex-specific association of sleep apnea severity with subclinical myocardial injury, ventricular hypertrophy, and heart failure risk in a community-dwelling cohort: the Atherosclerosis Risk in Communities-Sleep Heart Health Study. Circulation. 2015;132:1329-1337 [PubMed]journal. [CrossRef] [PubMed]
 
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