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Influence of Obstructive Sleep Apnea on Endothelial Function in Obese PatientsObstructive Sleep Apnea and Endothelial Function FREE TO VIEW

Mario Francesco Damiani, MD; Pierluigi Carratù, MD; Vitaliano Nicola Quaranta, MD; Onofrio Resta, MD
Author and Funding Information

From the Institute of Pulmonary Disease, University of Bari.

Correspondence to: Pierluigi Carratù, MD, PhD, Institute of Pulmonary Disease, University of Bari, Piazza G. Cesare 12, Bari 70124, Italy; e-mail: pierluigicarratu@yahoo.com


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.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


© 2012 American College of Chest Physicians


Chest. 2012;141(6):1639. doi:10.1378/chest.12-0144
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To the Editor:

We read with great interest the article by Ades et al1 in a recent issue of CHEST (December 2011). In their article, Ades et al1 demonstrated that weight loss is associated with improvement in endothelial-dependent flow-mediated dilatation (FMD) in overweight and obese patients with coronary heart disease. Moreover, the study pointed out that greater FMD is related to greater weight reduction in a dose-dependent way. The authors remarked on the causative relationship between several conditions and the impairment of FMD.

In this regard, we would like to highlight the important role of obstructive sleep apnea (OSA) in obese patients. Indeed, OSA can directly worsen endothelial function (EF), as reported by Kraiczi et al.2 Later, in 2005, Altin et al3 showed that OSA is responsible for increasing the intima-media thickness. More recently, Chung and colleagues4 demonstrated that the degree of nocturnal hypoxemia in OSA is positively correlated with both arterial stiffness and endothelial impairment. The primary mechanism underlying endothelial abnormalities in OSA is represented by repetitive episodes of hypoxia/reoxygenation associated with transient cessation of breathing during sleep. The hypoxia/reoxygenation cycle promotes the generation of reactive oxygen species and inflammation and leads to a reduction in nitric oxide availability. In addition, sleep fragmentation/deprivation and genetic susceptibility for vascular manifestations of OSA contribute to worsening EF.5 On the other hand, our group has recently evaluated the presence of changes in FMD among obese patients with OSA after treatment with CPAP. We showed significant improvement of FMD in patients treated with CPAP for >3 months vs patients not treated. It is important to underline that the two study groups had similar BMI. Besides, a noteworthy finding is that the FMD values in patients treated for >3 months are similar to those in healthy subjects without cardiovascular risk factors.6 In another article, published December 2011 in CHEST, Akinnusi and colleagues7 also demonstrated an improvement of EF in obese patients with OSA after CPAP. They found a reduced expression of lectin-like oxidized low-density lipoprotein receptor 1 together with apoptotic circulating endothelial cells in patients with OSA after 8 weeks of CPAP therapy. In this study, patients’ BMI at baseline was the same as post-CPAP. Taken together, these results suggest that, on one hand, weight loss can reduce the endothelial damage in obese patients; on the other hand, treatment with CPAP can improve EF among obese patients with OSA, regardless of weight reduction.

In conclusion, we would like to stimulate discussion about the need to consider sleep-disordered breathing in obese patients with cardiovascular complication. Moreover, given the well-established role of weight loss in the improvement of OSA,8 a polysomnographic examination performed both before and after weight loss may be helpful, to know the relative contribution of OSA in the improvement of EF.

Ades PA, Savage PD, Lischke S, et al. The effect of weight loss and exercise training on flow-mediated dilatation in coronary heart disease: a randomized trial. Chest. 2011;1406:1420-1427. [CrossRef] [PubMed]
 
Kraiczi H, Caidahl K, Samuelsson A, Peker Y, Hedner J. Impairment of vascular endothelial function and left ventricular filling: association with the severity of apnea-induced hypoxemia during sleep. Chest. 2001;1194:1085-1091. [CrossRef] [PubMed]
 
Altin R, Ozdemir H, Mahmutyazicioğlu K, et al. Evaluation of carotid artery wall thickness with high-resolution sonography in obstructive sleep apnea syndrome. J Clin Ultrasound. 2005;332:80-86. [CrossRef] [PubMed]
 
Chung S, Yoon IY, Lee CH, Kim JW. The association of nocturnal hypoxemia with arterial stiffness and endothelial dysfunction in male patients with obstructive sleep apnea syndrome. Respiration. 2010;795:363-369. [CrossRef] [PubMed]
 
Atkeson A, Jelic S. Mechanisms of endothelial dysfunction in obstructive sleep apnea. Vasc Health Risk Manag. 2008;46:1327-1335. [PubMed]
 
Ciccone MM, Favale S, Scicchitano P, et al. Reversibility of the endothelial dysfunction after CPAP therapy in OSAS patients [published online ahead of print February 24, 2011]. Int J Cardiol. doi:10.1016/j.ijcard.2011.01.065.
 
Akinnusi ME, Laporta R, El-Solh AA. Lectin-like oxidized low-density lipoprotein receptor-1 modulates endothelial apoptosis in obstructive sleep apnea. Chest. 2011;1406:1503-1510. [CrossRef] [PubMed]
 
Johansson K, Neovius M, Lagerros YT, et al. Effect of a very low energy diet on moderate and severe obstructive sleep apnoea in obese men: a randomised controlled trial. BMJ. 2009;339:b4609. [CrossRef] [PubMed]
 

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References

Ades PA, Savage PD, Lischke S, et al. The effect of weight loss and exercise training on flow-mediated dilatation in coronary heart disease: a randomized trial. Chest. 2011;1406:1420-1427. [CrossRef] [PubMed]
 
Kraiczi H, Caidahl K, Samuelsson A, Peker Y, Hedner J. Impairment of vascular endothelial function and left ventricular filling: association with the severity of apnea-induced hypoxemia during sleep. Chest. 2001;1194:1085-1091. [CrossRef] [PubMed]
 
Altin R, Ozdemir H, Mahmutyazicioğlu K, et al. Evaluation of carotid artery wall thickness with high-resolution sonography in obstructive sleep apnea syndrome. J Clin Ultrasound. 2005;332:80-86. [CrossRef] [PubMed]
 
Chung S, Yoon IY, Lee CH, Kim JW. The association of nocturnal hypoxemia with arterial stiffness and endothelial dysfunction in male patients with obstructive sleep apnea syndrome. Respiration. 2010;795:363-369. [CrossRef] [PubMed]
 
Atkeson A, Jelic S. Mechanisms of endothelial dysfunction in obstructive sleep apnea. Vasc Health Risk Manag. 2008;46:1327-1335. [PubMed]
 
Ciccone MM, Favale S, Scicchitano P, et al. Reversibility of the endothelial dysfunction after CPAP therapy in OSAS patients [published online ahead of print February 24, 2011]. Int J Cardiol. doi:10.1016/j.ijcard.2011.01.065.
 
Akinnusi ME, Laporta R, El-Solh AA. Lectin-like oxidized low-density lipoprotein receptor-1 modulates endothelial apoptosis in obstructive sleep apnea. Chest. 2011;1406:1503-1510. [CrossRef] [PubMed]
 
Johansson K, Neovius M, Lagerros YT, et al. Effect of a very low energy diet on moderate and severe obstructive sleep apnoea in obese men: a randomised controlled trial. BMJ. 2009;339:b4609. [CrossRef] [PubMed]
 
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