Abstract

Obstructive sleep apnoea (OSA) is characterised by reoccurring apnoeas and hypopneas, causing repetitive hypoxia and reoxygenation, and is associated with endothelial dysfunction and reduced levels of circulating progenitor cells (CPCs). The potential to improve endothelial function and CPC levels in people with OSA by preventing hypoxic episodes with Continuous Positive Airway Pressure (CPAP) was investigated in a sham-controlled CPAP study. Men with moderate-to-severe OSA (mean ± SD: age=49 ± 12 y, apnoea hypopnea index (AHI)=37.6 ± 16.4 events/h, body mass index=31.5 ± 5.7 kg/m(2)) who were CPAP naïve without diabetes mellitus were randomised in a 12-week double-blind sham-controlled parallel group study to receive either active (n=25) or sham (n=21) CPAP. CPCs, isolated from blood, were measured by flow cytometry and by co-staining cultured cells (7 days) with acetylated low-density lipoprotein (acLDL) and lectin. Endothelial function was assessed by peripheral arterial tonometry (PAT). Compared to sham, CPAP significantly decreased AHI (mean between-group difference -36.0 events/h; 95%CI, -49.7 to -22.3, p<0.0001) after 12 weeks. Despite this improvement in AHI, CPAP had no effect on change in CPC levels (including CD34(+)/KDR(+) (565 cells/mL; -977 to 2106, p=0.45), CD34(+)/KDR(+)/CD45(-) (37.0 cells/mL; -17.7 to 85.7, p=0.13), acLDL(+)/lectin(+) (-43.1 cells/field, -247 to 161, p=0.67)) or change in endothelial function (0.27; -0.14 to 0.67, p=0.19) compared to sham therapy. Despite the improvement in OSA parameters and ablation of apnoeic events by CPAP, CPC counts and endothelial function in men with moderate-to-severe OSA were not significantly improved after 12 weeks of therapeutic CPAP when compared to sham control.

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