title: Association of clinical and aetiologic subtype of acute ischaemic stroke with inflammation, oxidative stress and vascular function: a cross-sectional observational study.
abstract: BACKGROUND
  The role of inflammation, vascular dysfunction and oxidative stress in the pathophysiology of different stroke subtypes is not well understood. We aimed to determine if the clinical and aetiologic subtype of acute ischaemic stroke influences systemic markers of vascular function, inflammation and oxidative stress.
  
  
  METHODS
  129 men and women were recruited within 10 days of acute ischaemic stroke or TIA at two tertiary hospitals in this cross-sectional observational study. Stroke severity (NIHSS score and S100B concentration); systemic markers of inflammation (high sensitivity C-reactive protein [hs-CRP] and fibrinogen), endothelial activation (E-selectin), endothelial cell damage (von Willebrand factor activity), and oxidative stress (F2-isoprostanes) were measured.
  
  
  RESULTS
  Hs-CRP concentrations were higher in total anterior (22.0 ± 24.1 mg/L) than partial anterior circulation (15.3 ± 32.4 mg/L) and lacunar (4.9 ± 4.3 mg/L) syndromes (p = 0.01). Hs-CRP concentrations correlated moderately with NIHSS score (r = 0.45, p < 0.01) and S100B (r = 0.48, p < 0.01). However aetiologic and clinical subtypes were not independently associated with hs-CRP when included with stroke severity in general linear models.
  
  
  CONCLUSIONS
  These data suggest that stroke aetiology and clinical syndrome may not be important independent determinants of the degree of systemic inflammation, oxidative stress or endothelial function in acute ischaemic stroke. Other factors, including stroke severity, pre-morbid inflammation and co-morbidity may explain variations among groups of participants with different subtypes of acute ischaemic stroke.
authors.affiliation: Western Australian Centre for Health and Ageing, University of Western Australia, Crawley, WA, Australia. christopher.beer@uwa.edu.au
authors.forename: Christopher
authors.initials: C
authors.lastname: Beer
authors.forename: David
authors.initials: D
authors.lastname: Blacker
authors.forename: Graeme J
authors.initials: GJ
authors.lastname: Hankey
authors.forename: Ian B
authors.initials: IB
authors.lastname: Puddey
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D002545:Brain Ischemia / Q000145:classification / Q000150:complications / Q000209:etiology* / Q000503:physiopathology*; D002097:C-Reactive Protein / Q000378:metabolism; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D016014:Linear Models; D008297:Male; D018384:Oxidative Stress; D020521:Stroke / Q000145:classification / Q000150:complications / Q000209:etiology* / Q000503:physiopathology*; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D015415:Biomarkers; D014841:von Willebrand Factor; D002097:C-Reactive Protein