troponin would be of significant value to provide further
insights into whether OSA severity is associated with a
lower rate of cardiovascular morbidity in patients with
OHS. Ultimately, if this association is confirmed in
future studies, there is a great interest to understand
the molecular mechanisms resulting in cardiovascular
protection and whether it has clinical implications.
Juan F. Masa, MD, PhD
Jaime Corral, MD
Javier Gómez-de-Terreros, MD, PhD
María-Ángeles Sánchez-Quiroga, MD
Cáceres, Spain
Babak Mokhlesi, MD, FCCP
Chicago, IL
AFFILIATIONS: From the Pulmonary Section (Drs Masa, Corral, and
Gómez-de-Terreros), San Pedro de Alcántara Hospital; Pulmonary
Section (Dr Sánchez-Quiroga), Virgen del Puerto Hospital, Plasencia;
Department of Medicine (Dr Mokhlesi), Section of Pulmonary and
Critical Care, University of Chicago; CIBER de enfermedades
respiratorias (CIBERES) (Drs Masa, Corral, and Gómez-deTerreros), Madrid, Spain.
FINANCIAL/NONFINANCIAL DISCLOSURES: See earlier cited article
for author conflicts of interest.
CORRESPONDENCE TO: Juan F. Masa, MD, PhD, Pulmonary
Section, San Pedro de Alcántara Hospital, Avda. Pablo Naranjo S/N,
10003 Cáceres, Spain; e-mail: [email protected]
Copyright Ó 2016 American College of Chest Physicians. Published
by Elsevier Inc. All rights reserved.
DOI: http://dx.doi.org/10.1016/j.chest.2016.08.1468
Reference
1. Masa JF, Corral J, Romero A, et al. Protective cardiovascular effect of
sleep apnea severity in obesity hypoventilation syndrome. Chest.
2016;150(1):68-79.
Cardiovascular Protection
From Severe OSA
The Pickwickian Paradox: Is Bigger
Really Better?
To the Editor:
We would like to congratulate Masa and colleagues1
(July 2016) for elaborating on a novel concept that
highlights the data and potential mechanisms of
cardiovascular protection in patients with severe OSA
and obesity hypoventilation syndrome. Of interest,
the authors found that patients with severe OSA (in the
third tertile) had the lowest prevalence of cardiovascular
morbidity. However, the ischemic preconditioning
hypothesis, as a plausible mechanism, may not be
generalizable for all conditions included in their
definition of cardiovascular morbidity.
1410 Correspondence
Even though the landmark Sleep Heart Health Study2
found a reduction in recurrent coronary events in
patients with severe OSA, the patient population was
free of any cardiovascular disease at the time of
enrollment, in contrast to the current study,1 in which
this crucial variable was not taken into consideration,
potentially adding to a significant selection bias in the
studied population. Further, the Sleep Heart Health
Study found OSA severity to be associated with
more “incident” heart failure in women but not in
men; in contrast, in the current study, it is not clear
whether there was a lower “prevalence” or lower
“incidence” of heart failure. This may be a major
limitation of this study’s findings in determining
causality.1
The possible selection biases that could explain the
greater prevalence of chronic heart failure in patients
with mild OSA1 vs severe OSA1 (based on tertiles) are:
(1) greater prevalence of atrial fibrillation, (2) overall
worse baseline left ventricular ejection fractions that
may have resulted in a greater proportion of patients
coming under medical care,3 and (3) lower compliance
to guideline-based medical therapy3 for heart failure,
resulting in more frequent symptoms and a greater
number of patients coming under clinical care, which is
a crucial variable because heart failure is a clinical
diagnosis.
From a pathophysiological perspective, heart failure
continues to be a cause of significant cardiovascular
burden in patients with severe OSA/obesity
hypoventilation syndrome, and the observations of the
current study should be interpreted with caution.
Yashasvi Chugh, MD
Robert T. Faillace, MD
Bronx, NY
AFFILIATIONS: From Jacobi Medical Center (Dr Chugh), Albert
Einstein College of Medicine, Bronx, NY; Department of Clinical
Medicine (Dr Faillace), Albert Einstein College of Medicine, Bronx,
NY; and North Bronx Healthcare Network (Dr Faillace), Jacobi
Medical Center and North Central Bronx Hospital, Bronx, NY.
FINANCIAL/NONFINANCIAL DISCLOSURES: None declared.
CORRESPONDENCE TO: Yashasvi Chugh, MD, Jacobi Medical
Center, 1400 Pelham Parkway, S Bldg 1, Room 3N21, Bronx, NY
10461-1197; e-mail: [email protected]
Copyright Ó 2016 American College of Chest Physicians. Published
by Elsevier Inc. All rights reserved.
DOI: http://dx.doi.org/10.1016/j.chest.2016.08.1475
References
1. Masa JF, Corral J, Romero A, Caballero C, et al. Protective
cardiovascular effect of sleep apnea severity in obesity hypoventilation
syndrome. Chest. 2016;150(1):68-79.
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2. Roca GQ, 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(14):1329-1337.
3. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA Guideline
for the Management of Heart Failure: a report of the American
College of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):
e147-e239.
Response
To the Editor:
We are grateful to Dr Chugh and colleagues for their
interest in our article.1
In contrast to the Sleep Heart Health Study
(a prospective cohort study to determine the
cardiovascular and other consequences of sleepdisordered breathing2), our study (clinicaltrial.gov
identifier: NCT01405976) published in CHEST1 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.
AFFILIATIONS: From the Pulmonary Section (Drs Masa, Corral, and
Gómez-de-Terreros), San Pedro de Alcántara Hospital; Pulmonary
Section (Dr Sánchez-Quiroga), Virgen del Puerto Hospital, Plasencia;
Department of Medicine (Dr Mokhlesi), Section of Pulmonary and
Critical Care, University of Chicago; and CIBER de enfermedades
respiratorias (CIBERES) (Drs Masa, Corral, and Gómez-deTerreros), Madrid, Spain.
FINANCIAL/NONFINANCIAL DISCLOSURES: None declared.
FUNDING/SUPPORT: See earlier cited article for author conflicts of
interest.
CORRESPONDENCE TO: Juan F. Masa, MD, PhD, Pulmonary
Section, San Pedro de Alcántara Hospital, Avda. Pablo Naranjo S/N,
10003 Cáceres, Spain; e-mail: [email protected]
Copyright Ó 2016 American College of Chest Physicians. Published
by Elsevier Inc. All rights reserved.
DOI: http://dx.doi.org/10.1016/j.chest.2016.09.019
References
1. Masa JF, Corral J, Romero A, et al. Protective cardiovascular effect
of sleep apnea severity in obesity hypoventilation syndrome. Chest.
2016;150(1):68-79.
2. Roca GQ, 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(14):1329-1337.
Cancer and OSA
Beyond Hypoxia
To the Editor:
I have read with great interest and pleasure the excellent
review by Martínez-García et al1 entitled “Cancer and
OSA: Current Evidence from Human Studies” published
in CHEST (August 2016). The authors shed light on
this important and aporetical topic.
I was concerned about one issue not addressed
adequately in the analysis: the role of sleep
fragmentation on the innate and adaptive immune
systems. In the literature, there are old and new data
showing the impact of poor sleep and OSA in decreasing
not only circulating monocytes but also natural killer
cells, which play a key role in cancer biology and in
other conditions such as autoimmune diseases.2-4
Furthermore, there is evidence that poorer global sleep
quality is associated with shorter telomere length in
CD8þ and CD4þ lymphocytes.5
Maurizio Marvisi, MD
Cremona, Italy
Juan F. Masa, MD, PhD
Jaime Corral, MD
Javier Gómez-de-Terreros, MD, PhD
María-Ángeles Sánchez-Quiroga, MD
Cáceres, Spain
Babak Mokhlesi, MD, FCCP
Chicago, IL
AFFILIATIONS: From the Department of Internal Medicine and
Respiratory Diseases, Istituto Figlie di San Camillo.
FINANCIAL/NONFINANCIAL DISCLOSURES: None declared.
CORRESPONDENCE TO: Maurizio Marvisi, MD, Via Filzi 56,
Cremona, Italy, 26100; e-mail: [email protected]
Copyright Ó 2016 American College of Chest Physicians. Published
by Elsevier Inc. All rights reserved.
DOI: http://dx.doi.org/10.1016/j.chest.2016.08.1472
journal.publications.chestnet.org
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