title: Elevated hematocrit is associated with reduced reperfusion and tissue survival in acute stroke.
abstract: BACKGROUND
  Elevated hematocrit (Hct) contributes to blood viscosity and has an adverse effect in acute stroke. The authors investigated the influence of Hct on tissue fate using serial MRI in acute stroke patients.
  
  
  METHODS
  The effects of Hct on reperfusion, penumbral salvage, and infarct expansion in 64 patients presenting within 24 hours of stroke onset were measured. MRI was performed at baseline (< 24 hours), days 3 to 5, and 90 days from stroke onset.
  
  
  RESULTS
  Median Hct was 42% with a bimodal distribution. There was a strong inverse relationship between Hct and reperfusion (Spearman rho = -0.74, p < 0.0001). The odds of major reperfusion (> 50% resolution of the baseline perfusion-weighted imaging deficit) were significantly lower with increasing Hct (odds ratio [OR] = 0.53; 95% CI = 0.97 to 1.00), independent of age, perfusion, and diffusion lesion volumes and recombinant tissue plasminogen activator (rtPA) administration. There was a trend toward reduced penumbral salvage at days 3 to 5 with increasing Hct (p = 0.06, 95% CI = -4.76 to 0.14). An increasing Hct was a significant predictor of infarct growth (OR = 1.26, 95% CI = 1.00 to 1.59), independent of baseline perfusion and diffusion volumes and glucose. The effect of Hct on reperfusion and infarct expansion was similar irrespective of rtPA administration (p = 0.31) and independent of smoking status.
  
  
  CONCLUSIONS
  Higher hematocrit (Hct) values have a significant independent association with reduced reperfusion and greater infarct size after ischemic stroke. An elevated Hct may also be a potential physiologic determinant of reduced penumbral salvage.
authors.affiliation: Department of Neurology, Royal Melbourne Hospital, University of Melbourne, Parkville Victoria, Australia.
authors.forename: L E
authors.initials: LE
authors.lastname: Allport
authors.forename: M W
authors.initials: MW
authors.lastname: Parsons
authors.forename: K S
authors.initials: KS
authors.lastname: Butcher
authors.forename: L
authors.initials: L
authors.lastname: MacGregor
authors.forename: P M
authors.initials: PM
authors.lastname: Desmond
authors.forename: B M
authors.initials: BM
authors.lastname: Tress
authors.forename: S M
authors.initials: SM
authors.lastname: Davis
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001809:Blood Viscosity; D001921:Brain / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000503:physiopathology*; D015984:Causality; D002536:Cerebral Arteries / Q000503:physiopathology; D002544:Cerebral Infarction / Q000175:diagnosis / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D018450:Disease Progression; D006400:Hematocrit; D006801:Humans; D016015:Logistic Models; D008279:Magnetic Resonance Imaging; D008875:Middle Aged; D011086:Polycythemia / Q000150:complications*; D011237:Predictive Value of Tests; D015427:Reperfusion Injury / Q000503:physiopathology*; D020521:Stroke / Q000175:diagnosis / Q000503:physiopathology*