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Correspondence |

Does Nocturnal Hypoventilation Have a Protective Effect on Cardiovascular Comorbidity in Obesity Hypoventilation Syndrome? FREE TO VIEW

Giorgio Castellana, MD; Pierluigi Carratù, MD, PhD; Silvano Dragonieri, MD, PhD; Lorenzo Marra, MD; Onofrio Resta, MD, FCCP
Author and Funding Information

FINANCIAL/NONFINANCIAL DISCLOSURES: None declared.

Institute of Respiratory Disease, University of Bari “Aldo Moro”, Bari, Italy

CORRESPONDENCE TO: Giorgio Castellana, MD, Institute of Respiratory Disease, University of Bari “Aldo Moro,” Piazza Giulio Cesare, 11, 70124 Bari, Italy


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


Chest. 2016;150(6):1407-1408. doi:10.1016/j.chest.2016.08.1469
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We recently read with great interest the article by Masa et al, published in CHEST (July 2016), in which the authors examined the association between OSA severity and cardiovascular morbidity in patients with obesity hypoventilation syndrome (OHS). Surprisingly, their results showed an inverse relationship between cardiovascular morbidity and severity of OSA, except for ischemic heart disease. As hypothesized by Lavie and Lavie, the cycles of apneic/hypopneic events in OSA that resemble cycles of ischemia/reperfusion could exert a protective effect from more severe ischemic and cardiovascular events, similar to ischemic preconditioning. There is the possibility that these factors may be a particular characteristic of OHS. Moreover, Cadby et al reported an independent association between the presence and severity of OSA and incident atrial fibrillation in a large clinic-based cohort group over a median 12-year follow-up period. What is the role of nocturnal hypoventilation and of tonic desaturation in the etiopathogenesis of cardiologic comorbidity?

It is known that patients with OHS often exhibit cycles of intermittent hypoxia and reoxygenation due to apneic/hypopneic events. Moreover, tonic desaturation caused by hypoventilation often co-exists. We previously demonstrated that nocturnal hypoventilation, defined as a period of persistent (≥ 2 min) reduction (two-thirds) of abdominal and rib cage excursion, associated with persistent sustained oxygen desaturation of 10% and a mean increase of transcutaneous CO2 > 7 mm Hg for at least 15% of the total sleep time, is present in approximately 50% of severely obese patients. These patients also have a high respiratory disturbance index score.

Ryan et al showed that intermittent hypoxia/reoxygenation in OSA may produce a selective and dose-dependent activation of the inflammatory pathway, whereas sustained hypoxia may lead to an adaptive effect with reduced expression of proatherogenic and proinflammatory factors such as tumor necrosis factor-α. The investigators hypothesized that these mechanisms may be an important underlying factor in the cardiovascular pathophysiology of OSA. Could these conclusions be extended to OHS?

To this extent, it would be interesting to examine the role of nocturnal hypoventilation in these patients with OHS described by Masa et al, particularly in those with severe OSA and high BMI who may remain mildly or severely hypoxemic between apneic events, resulting in a mild or severe degree of sustained hypoxia in addition to intermittent hypoxia.

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]
 
Lavie L. .Lavie P. . Ischemic preconditioning as a possible explanation for the age decline relative mortality in sleep apnea. Med Hypotheses. 2006;66:1069-1073 [PubMed]journal. [CrossRef] [PubMed]
 
Cadby G. .McArdle N. .Briffa T. .et al Severity of OSA is an independent predictor of incident atrial fibrillation hospitalization in a large sleep-clinic cohort. Chest. 2015;148:945-952 [PubMed]journal. [CrossRef] [PubMed]
 
Resta O. .Foschino-Barbaro M.P. .Legari G. .et al Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects. Int J Obes Relat Metab Disord. 2001;25:669-675 [PubMed]journal. [CrossRef] [PubMed]
 
Ryan S. .Taylor C.T. .McNicholas W.T. . Selective activation of inflammatory pathways by intermittent hypoxia in obstructive sleep apnea syndrome. Circulation. 2005;112:2660-2667 [PubMed]journal. [CrossRef] [PubMed]
 

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Tables

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]
 
Lavie L. .Lavie P. . Ischemic preconditioning as a possible explanation for the age decline relative mortality in sleep apnea. Med Hypotheses. 2006;66:1069-1073 [PubMed]journal. [CrossRef] [PubMed]
 
Cadby G. .McArdle N. .Briffa T. .et al Severity of OSA is an independent predictor of incident atrial fibrillation hospitalization in a large sleep-clinic cohort. Chest. 2015;148:945-952 [PubMed]journal. [CrossRef] [PubMed]
 
Resta O. .Foschino-Barbaro M.P. .Legari G. .et al Sleep-related breathing disorders, loud snoring and excessive daytime sleepiness in obese subjects. Int J Obes Relat Metab Disord. 2001;25:669-675 [PubMed]journal. [CrossRef] [PubMed]
 
Ryan S. .Taylor C.T. .McNicholas W.T. . Selective activation of inflammatory pathways by intermittent hypoxia in obstructive sleep apnea syndrome. Circulation. 2005;112:2660-2667 [PubMed]journal. [CrossRef] [PubMed]
 
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