title: The effect of short-term withdrawal from continuous positive airway pressure therapy on sympathetic activity and markers of vascular inflammation in subjects with obstructive sleep apnoea.
abstract: Obstructive sleep apnoea (OSA) is commonly associated with cardiovascular disease and sympathetic activation. However, it is unclear whether this association is independent of obesity and to what extent treatment with nasal continuous positive airway pressure (CPAP) alleviates the vascular inflammation that underpins cardiovascular disease. We therefore evaluated whether short-term withdrawal from CPAP therapy in subjects with moderate-severe OSA would result in increased levels of sympathetic activity and circulating inflammatory cytokines independent of weight. Vascular inflammatory markers (hsCRP, hsIL-6 and hsTNF-alpha) were assessed in 20 subjects after one and seven nights of withdrawal from CPAP together with the hypoxia-responsive angiogenic marker VEGF and urinary catecholamines. Compared with baseline on CPAP, withdrawal from therapy resulted in an immediate return of OSA with an increase in RDI to 26.7 +/- 5.2 and 39.0 +/- 5.9 events per hour after one and seven nights without CPAP, respectively (both P < 0.0001). This was accompanied by a concomitant rise in daytime urinary noradrenaline (P < 0.0001) after seven nights CPAP withdrawal that was positively associated with the severity of hypoxaemia. In contrast, withdrawal from CPAP therapy was not accompanied by any change in measured cytokines or VEGF (all P > 0.1). In conclusion, 1 week of CPAP withdrawal was associated with a return of OSA and a marked increase in sympathetic activity without a concomitant elevation of vascular inflammatory markers.
authors.affiliation: Woolcock Institute of Medical Research, University of Sydney, Sydney, Australia. cphillips@mail.usyd.edu.au
authors.forename: Craig L
authors.initials: CL
authors.lastname: Phillips
authors.forename: Qiao
authors.initials: Q
authors.lastname: Yang
authors.forename: Andrew
authors.initials: A
authors.lastname: Williams
authors.forename: Michael
authors.initials: M
authors.lastname: Roth
authors.forename: Brendon J
authors.initials: BJ
authors.lastname: Yee
authors.forename: Jan A
authors.initials: JA
authors.lastname: Hedner
authors.forename: Norbert
authors.initials: N
authors.lastname: Berend
authors.forename: Ronald R
authors.initials: RR
authors.lastname: Grunstein
mesh_terms: D015415:Biomarkers; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism*; D002395:Catecholamines / Q000652:urine; D045422:Continuous Positive Airway Pressure / Q000379:methods*; D004797:Enzyme-Linked Immunosorbent Assay; D004837:Epinephrine / Q000652:urine; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000150:complications / Q000175:diagnosis / Q000378:metabolism; D007249:Inflammation / Q000209:etiology; D015850:Interleukin-6 / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000378:metabolism; D017286:Polysomnography; D012720:Severity of Illness Index; D020181:Sleep Apnea, Obstructive / Q000175:diagnosis / Q000378:metabolism* / Q000628:therapy*; D013997:Time Factors; D016312:Treatment Refusal / Q000706:statistics & numerical data*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D002395:Catecholamines; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D002097:C-Reactive Protein; D010100:Oxygen; D004837:Epinephrine