title: Biomarkers of inflammation and endothelial dysfunction in stroke with and without sleep apnea.
abstract: OBJECTIVE
  Although sleep apnea (SA) is a risk factor for ischemic stroke and an important prognostic factor in affected patients, the exact pathophysiological link between SA and stroke is unknown. We investigated whether the plasma concentration of biomarkers of inflammation and endothelial dysfunction, including soluble tumor necrosis factor receptor-1 and -2 (sTNF-R1 and sTNF-R2), tumor necrosis factor-β (TNF-β), soluble intercellular cell adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) are increased in patients with acute stroke and SA compared with stroke patients without SA.
  
  
  METHODS
  In total, 76 patients with ischemic stroke admitted to the stroke unit were included in this study. Plasma concentrations of biomarkers were determined after CT scans on admission. All patients received cardiorespiratory polygraphy within the first 72 h after admission. In all patients, demographic data, National Institutes of Health Stroke Scale scores and cerebrovascular risk factors were assessed.
  
  
  RESULTS
  An apnea-hypopnea index (AHI) ≥10/h was found in 37 of our patients (48.7%). In these patients with SA, sTNF-R1 and sTNF-R2 levels were significantly higher than in patients with an AHI lower than 10/h. TNF-β, however, showed no significant difference between both groups, just like the soluble intercellular and vascular cell adhesion molecules sICAM-1 and sVCAM-1.
  
  
  CONCLUSIONS
  SA is associated with raised levels of sTNF-R1 and sTNF-R2 in patients with acute ischemic stroke. Taking into account the established impact of these two markers on the causation and course of cerebrovascular disease, these proteins may be part of the pathophysiological pathway linking SA to stroke.
authors.affiliation: Paracelsus Medical University and Salzburger Landeskliniken, Christian-Doppler-Klinik, Department of Neurology, Salzburg, Austria.
authors.forename: Alexander Baden
authors.initials: AB
authors.lastname: Kunz
authors.forename: Jörg
authors.initials: J
authors.lastname: Kraus
authors.forename: Peter
authors.initials: P
authors.lastname: Young
authors.forename: Reinhard
authors.initials: R
authors.lastname: Reuss
authors.forename: Peter
authors.initials: P
authors.lastname: Wipfler
authors.forename: Patrick
authors.initials: P
authors.lastname: Oschmann
authors.forename: Franz
authors.initials: F
authors.lastname: Blaes
authors.forename: Rainer
authors.initials: R
authors.lastname: Dziewas
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers; D004730:Endothelium, Vascular / Q000473:pathology*; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008233:Lymphotoxin-alpha / Q000097:blood; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination; D017286:Polysomnography; D019948:Receptors, Interleukin-4 / Q000097:blood; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood; D012307:Risk Factors; D012891:Sleep Apnea Syndromes / Q000097:blood* / Q000150:complications / Q000175:diagnosis; D020521:Stroke / Q000097:blood* / Q000150:complications / Q000175:diagnosis; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014652:Vascular Diseases / Q000097:blood* / Q000473:pathology
chemical_list: D015415:Biomarkers; D008233:Lymphotoxin-alpha; D019948:Receptors, Interleukin-4; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D005340:Fibrinogen