title: The Impact of Obstructive Sleep Apnea and Tobacco Smoking on Endothelial Function.
abstract: BACKGROUND
  Endothelial dysfunction has been recognized to occur in the context of obstructive sleep apnea (OSA) or tobacco smoking. However, the deleterious effect on vascular function with concurrence of both conditions is largely unknown.
  
  
  OBJECTIVE
  To investigate whether the concurrence of OSA and smoking poses an additive detriment to endothelial dysfunction.
  
  
  METHODS
  Chinese men without a history of chronic medical illness were invited to complete a questionnaire including smoking pack-year exposure, polysomnography and peripheral arterial tonometry (PAT) for endothelial function. Serum 8-isoprostane, advanced oxidation protein products (AOPP) and monocyte chemo-attractant protein-1 (MCP-1) were measured.
  
  
  RESULTS
  114 men were successfully enrolled. PAT ratio, adjusted for age and body mass index, correlated inversely with overall severity of OSA: apnea-hypopnea index (AHI), r = -0.160 (p = 0.092); oxygen desaturation index, r = -0.214 (p = 0.024); duration of oxygen saturation <90%, r = -0.219 (p = 0.020); and minimum oxygen saturation, r = 0.250 (p = 0.008). The PAT ratio decreased with increasing pack-year group (p = 0.018). It was lower with concurrent smoking history and moderate-severe OSA (AHI ≥15/h) compared to having one or neither factor (p = 0.011). Serum levels of 8-isoprostane and AOPP were positively related to severity of OSA, while MCP-1 correlated with smoking quantity. Multiple linear regression analyses showed that severity of intermittent hypoxia, MCP-1 and pack-year exposure were independent predictors of PAT ratio.
  
  
  CONCLUSIONS
  While OSA, in particular intermittent hypoxemia, and tobacco smoking were independent risk factors, the concurrence of moderate-severe OSA and smoking was associated with the most severe impairment in endothelial function.
authors.affiliation: Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, SAR, China.
authors.forename: Macy Mei Sze
authors.initials: MM
authors.lastname: Lui
authors.forename: Judith Choi Wo
authors.initials: JC
authors.lastname: Mak
authors.forename: Agnes Yuen Kwan
authors.initials: AY
authors.lastname: Lai
authors.forename: Christopher Kim Ming
authors.initials: CK
authors.lastname: Hui
authors.forename: Jamie Chung Mei
authors.initials: JC
authors.lastname: Lam
authors.forename: David Chi Leung
authors.initials: DC
authors.lastname: Lam
authors.forename: Mary Sau Man
authors.initials: MS
authors.lastname: Ip
mesh_terms: D000328:Adult; D062107:Advanced Oxidation Protein Products / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood; D015331:Cohort Studies; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D020181:Sleep Apnea, Obstructive / Q000097:blood / Q000503:physiopathology*; D012907:Smoking / Q000097:blood / Q000503:physiopathology*
chemical_list: D062107:Advanced Oxidation Protein Products; C111835:CCL2 protein, human; D018932:Chemokine CCL2; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost