Abstract
BackgroundObstructive sleep apnea (OSA) is an independent risk factor for cardiovascular diseases (CVD) and vascular health. Peripheral blood-derived CD34+ progenitor cells have been used as biomarker for CVD risk and may play a similar role in OSA and CVD risk assessment. Although there are some controversial results in the literature, OSA patients may have a reduction in the number and function of CD34+ cells. The damages promoted by OSA in CD34+ cells may lead to an increase in endothelial oxidative stress and endothelial inflammation which may lead to a reduced endothelial repair capacity. In this study, we explored the effect of continuous positive airway pressure (CPAP) on peripheral blood-derived CD34+ cells and arterial stiffness (another predictor of endothelial health and CVD risk) in OSA patients.Methods and resultsNine overweight and obese subjects without prediabetes or diabetes were recruited. Eight out of nine subjects had moderate to severe degree of OSA. CD34+ cells were isolated from peripheral blood. Number and function of these cells were monitored before and after 3 months of treatment with CPAP. No significant changes were observed in the number of CD34+ cells, CFU-Hill’s colony formation unit (CFU) count or migratory response to the chemotactic factor SDF-1a after CPAP use. However, CXCR4 mRNA expression significantly increased by 2.2-fold indicating that CPAP may have a positive effect on SDF1a receptor (CXCR4), thereby improving migration of CD34+ cells mediated by SDF1a after the 3 month period. Interestingly, in clinical arena our results showed a reduction of pulse wave velocity (an established parameter of arterial stiffness) following CPAP therapy.ConclusionsOur findings suggest that 3-month CPAP intervention does not show statistical significant increase in CD34+ cell number and function, in mostly moderate to severe OSA subjects; however, it did demonstrate a positive trend. CPAP therapy, did help improve arterial stiffness parameter.
Highlights
Obstructive sleep apnea (OSA) is an independent risk factor for cardiovascular diseases (CVD) and vascular health
Blood biochemistry results showed no significant difference between visits for all the parameters except for blood urea nitrogen (BUN) that was reduced by approximately 13%
In our study, we demonstrated that continuous positive airway pressure (CPAP) has potential benefits in mostly moderate to severe OSA patients with 12 weeks of intervention but the improvement in the number and functionality of endothelial progenitor cells (EPCs) (CD34+) as well as in Arterial stiffness (AS) is limited according to the severity of the sleep apnea degree
Summary
Obstructive sleep apnea (OSA) is an independent risk factor for cardiovascular diseases (CVD) and vascular health. We explored the effect of continuous positive airway pressure (CPAP) on peripheral blood-derived CD34+ cells and arterial stiffness (another predictor of endothelial health and CVD risk) in OSA patients. The mechanisms between OSA and cardiovascular diseases (CVD) are not well understood; data suggest that OSA affects the endothelium adversely which might be contributing to the pathophysiology behind cardiovascular disease from OSA. This endothelial dysfunction is an early marker for vascular abnormalities preceding clinically overt CVD. OSA patients who are otherwise free of clinically apparent cardiovascular comorbidities have increased endothelial oxidative stress, inflammation, and reduced endothelial repair capability, thereby strongly suggesting that OSA independently impairs endothelial function [5]. The proposed mechanisms are believed to be due to intermittent hypoxia (similar to an ischemic-reperfusion injury), sleep fragmentation and deprivation (shown to have a 50% decline in endothelial dependent vasodilation), and genetics [6, 7]
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