Endothelial repair capacity and apoptosis are inversely related in obstructive sleep apnea

Original Research

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Authors: Sanja Jelic,  David J Lederer, Tessa Adams, et al.

Published Date November 2009 Volume 2009:5 Pages 909 - 920

DOI: http://dx.doi.org/10.2147/VHRM.S8123

Sanja Jelic¹,  David J Lederer¹, Tessa Adams¹, Margherita Padeletti¹, Paolo C Colombo², Phillip Factor¹, Thierry H Le Jemtel³

¹Division of Pulmonary, Allergy, and Critical Care Medicine, ²Division of Cardiology, Columbia University College of Physicians and Surgeons, New York, NY, USA; ³Division of Cardiology, Tulane University School of Medicine, New Orleans, LA, USA

Purpose: To investigate the impact of obstructive sleep apnea (OSA) on endothelial repair capacity and apoptosis in the absence of potentially confounding factors including obesity.

Patients and methods: Sixteen patients with a body mass index <30 and newly diagnosed OSA and 16 controls were studied. Circulating levels of endothelial progenitor cells, a marker of endothelial repair capacity, and endothelial microparticles, a marker of endothelial apoptosis, were quantified before and after four-week therapy with continuous positive airway pressure (CPAP). Endothelial cell apoptotic rate was also quantified in freshly harvested venous endothelial cells. Vascular reactivity was measured by flow-mediated dilation.

Results: Before treatment, endothelial microparticle levels were greater and endothelial progenitor cell levels were lower in patients with OSA than in controls (P < 0.001 for both). Levels of endothelial microparticles and progenitors cells were inversely related (r = -0.67, P < 0.001). Endothelial progenitor cell levels increased after effective treatment (P = 0.036).

Conclusions: In the absence of any co-morbid conditions including obesity, OSA alone impairs endothelial repair capacity and promotes endothelial apoptosis. These early endothelial alterations may underlie accelerated atherosclerosis and increased cardiovascular risk in OSA.

Keywords: sleep apnea, endothelium, apoptosis, endothelial repair capacity

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