Simpson Philippa J L, Hoyos Camilla M, Celermajer David, Liu Peter Y, Ng Martin K C
Translational Research Group, the Heart Research Institute, Sydney 2042, Australia; University of Sydney, Sydney 2006, Australia.
Int J Cardiol. 2013 Oct 3;168(3):2042-8. doi: 10.1016/j.ijcard.2013.01.166. Epub 2013 Feb 27.
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.
阻塞性睡眠呼吸暂停(OSA)的特征是反复出现呼吸暂停和呼吸浅慢,导致反复缺氧和复氧,并与内皮功能障碍和循环祖细胞(CPCs)水平降低有关。在一项假对照持续气道正压通气(CPAP)研究中,研究了通过CPAP预防缺氧发作来改善OSA患者内皮功能和CPC水平的可能性。
将未患糖尿病且未使用过CPAP的中度至重度OSA男性患者(平均±标准差:年龄=49±12岁,呼吸暂停低通气指数(AHI)=37.6±16.4次/小时,体重指数=31.5±5.7kg/m²)随机分为12周双盲假对照平行组研究,分别接受活性CPAP(n=25)或假CPAP(n=21)治疗。通过流式细胞术以及用乙酰化低密度脂蛋白(acLDL)和凝集素对培养细胞(7天)进行共染色来测量从血液中分离出的CPCs。通过外周动脉张力测定法(PAT)评估内皮功能。
与假治疗相比,CPAP治疗12周后显著降低了AHI(组间平均差异-36.0次/小时;95%CI,-49.7至-22.3,p<0.0001)。尽管AHI有改善,但与假治疗相比,CPAP对CPC水平的变化(包括CD34(+)/KDR(+)(565个细胞/mL;-977至2106,p=0.45)、CD34(+)/KDR(+)/CD45(-)(37.0个细胞/mL;-17.7至85.7,p=0.13)、acLDL(+)/凝集素(+)(-。43.1个细胞/视野,-247至161,p=0.67))或内皮功能变化(0.27;-0.14至0.67,p=0.19)均无影响。
尽管CPAP改善了OSA参数并消除了呼吸暂停事件,但与假对照相比,中度至重度OSA男性患者在接受12周治疗性CPAP后,CPC计数和内皮功能并未得到显著改善。