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Controlled Clinical Trial
. 2009:5:909-20.
doi: 10.2147/vhrm.s8123. Epub 2009 Nov 16.

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

Affiliations
Controlled Clinical Trial

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

Sanja Jelic et al. Vasc Health Risk Manag. 2009.

Abstract

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: apoptosis; endothelial repair capacity; endothelium; sleep apnea.

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Figures

Figure 1
Figure 1
Levels of circulating endothelial progenitor cells (EPC) and apoptotic microparticles (EMP) in healthy controls and patients with obstructive sleep apnea (OSA) before and after treatment with continuous positive airway pressure (CPAP). Baseline levels of EPC were lower in OSA patients (n = 16) than in controls (n = 16) A) while levels of EMP were greater B). Levels of EPC increased significantly C) while levels of EMP tended to decreased D) when patients adhered with CPAP ≥ 4 hours daily (n = 7).
Figure 2
Figure 2
Relation between endothelial apoptotic rate and endothelial repair capacity in obstructive sleep apnea (OSA). Levels of circulating endothelial progenitor cells (EPC) and microparticles (EMP) are inversely related at baseline (Spearman correlation coefficient r = −0.67, P < 0.001). OSA patients (closed circles), healthy controls (open circles).
Figure 3
Figure 3
Relation between endothelial apoptotic rate and flow-mediated dilation in obstructive sleep apnea (OSA). Levels of circulating apoptotic microparticles correlate inversely with flow-mediated dilation in OSA (Spearman correlation coefficient adjusted for body mass index r = −0.43, P = 0.02). OSA patients (closed circles), healthy controls (open circles).

References

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