title: Effects of continuous positive airway pressure on coagulability in obstructive sleep apnoea: a randomised, placebo-controlled crossover study.
abstract: BACKGROUND
  Obstructive sleep apnoea (OSA) is associated with increased cardiovascular risk, however the mechanisms are not well established.
  
  
  OBJECTIVE
  This study aimed to determine whether treatment of OSA with nasal continuous positive airway pressure (CPAP) would favourably alter coagulability across the sleep-wake cycle.
  
  
  METHODS
  In a randomised crossover trial, 28 patients received therapeutic or placebo CPAP, each for 2 months with a 1 month washout between treatments. After each treatment period, a 24 h coagulation study was conducted in the laboratory. Plasminogen activator inhibitor-1 (PAI-1), D-dimer, fibrinogen, von Willebrand Factor (vWF), factor VIII (FVIII), factor VII (FVII) and factor V (FV) were determined at seven time points over the day and night.
  
  
  RESULTS
  At baseline, patients had severe OSA (Apnoea Hypopnoea Index 37.9 ± 23.9 events/h). Treatment of OSA with CPAP compared with placebo resulted in lower 24 h levels of vWF (-3.9%, p=0.013), FVIII (-6.2%, p=0.007) and FV (-4.2%, p<0.001). The greatest difference occurred during the nocturnal and early morning periods. In contrast, fibrinogen, D-dimer, FVII and PAI-1 did not differ between treatments, however all markers displayed diurnal variability independent of treatment.
  
  
  CONCLUSIONS
  In this randomised, placebo-controlled crossover trial, treatment of OSA with CPAP reduced the early morning level of vWF, and nocturnal levels of FVIII and FV. These findings suggest that CPAP may reduce cardiovascular risk in OSA, in part through reducing risk of thrombosis.
authors.affiliation: Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, St Leonards, New South Wales, Australia. craig.phillips@sydney.edu.au
authors.forename: Craig L
authors.initials: CL
authors.lastname: Phillips
authors.forename: Bradley J
authors.initials: BJ
authors.lastname: McEwen
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Morel-Kopp
authors.forename: Brendon J
authors.initials: BJ
authors.lastname: Yee
authors.forename: David R
authors.initials: DR
authors.lastname: Sullivan
authors.forename: Christopher M
authors.initials: CM
authors.lastname: Ward
authors.forename: Geoffrey H
authors.initials: GH
authors.lastname: Tofler
authors.forename: Ronald R
authors.initials: RR
authors.lastname: Grunstein
mesh_terms: D001777:Blood Coagulation; D045422:Continuous Positive Airway Pressure; D018592:Cross-Over Studies; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011446:Prospective Studies; D012307:Risk Factors; D020181:Sleep Apnea, Obstructive / Q000097:blood / Q000628:therapy*; D016896:Treatment Outcome; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; C036309:fibrin fragment D; D014841:von Willebrand Factor