title: Severity of leukoaraiosis and susceptibility to infarct growth in acute stroke.
abstract: OBJECTIVE
  Leukoaraiosis (LA) is associated with structural and functional vascular changes that may compromise tissue perfusion at the microvascular level. We hypothesized that the volume of LA correlated with the proportion of initially ischemic but eventually infarcted tissue in acute human stroke.
  
  
  METHODS
  We studied 61 consecutive patients with diffusion-weighted imaging-mean transit time mismatch. All patients were scanned twice within 12 hours of symptom onset and between days 4 and 30. We explored the relationship between the volume of white matter regions with LA on acute images and the proportion of diffusion-weighted imaging-mean transit time mismatch tissue that progressed to infarction (percentage mismatch lost).
  
  
  RESULTS
  Bivariate analyses showed a statistically significant correlation between percentage mismatch lost and LA volume (r=0.33, P<0.01). A linear regression model with percentage mismatch lost as response and LA volume, acute diffusion-weighted imaging and mean transit time volumes, age, admission blood glucose level, admission mean arterial blood pressure, etiologic stroke subtype, time to acute MRI, and time between acute and follow-up imaging as covariates revealed that LA volume was an independent predictor of infarct growth (P=0.04). The adjusted percentage mismatch lost in the highest quartile of LA volume was 1.9-fold (95% CI: 1.2 to 3.1) greater than the percentage mismatch lost in the lowest quartile.
  
  
  CONCLUSIONS
  LA volume at the time of acute ischemic stroke is a predictor infarct growth. Because LA is associated with factors that modulate tissue perfusion as well as tissue capacity for handling of ischemia, LA volume appears to be a composite predictive marker for the fate of acutely ischemic tissue.
authors.affiliation: A.A. Martinos Center for Biomedical Imaging and Stroke Service, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Room 2301, Charlestown, MA 02129, USA. hay@partners.org
authors.forename: Hakan
authors.initials: H
authors.lastname: Ay
authors.forename: E Murat
authors.initials: EM
authors.lastname: Arsava
authors.forename: Jonathan
authors.initials: J
authors.lastname: Rosand
authors.forename: Karen L
authors.initials: KL
authors.lastname: Furie
authors.forename: Aneesh B
authors.initials: AB
authors.lastname: Singhal
authors.forename: Pamela W
authors.initials: PW
authors.lastname: Schaefer
authors.forename: Ona
authors.initials: O
authors.lastname: Wu
authors.forename: R Gilberto
authors.initials: RG
authors.lastname: Gonzalez
authors.forename: Walter J
authors.initials: WJ
authors.lastname: Koroshetz
authors.forename: A Gregory
authors.initials: AG
authors.lastname: Sorensen
mesh_terms: D000208:Acute Disease / Q000453:epidemiology; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000473:pathology; D015415:Biomarkers / Q000032:analysis; D001921:Brain / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D020520:Brain Infarction / Q000453:epidemiology* / Q000473:pathology* / Q000503:physiopathology; D002545:Brain Ischemia / Q000453:epidemiology* / Q000473:pathology* / Q000503:physiopathology; D002536:Cerebral Arteries / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D015897:Comorbidity; D018450:Disease Progression; D005260:Female; D006801:Humans; D049292:Leukoaraiosis / Q000453:epidemiology* / Q000473:pathology* / Q000503:physiopathology; D008279:Magnetic Resonance Imaging; D008297:Male; D008833:Microcirculation / Q000503:physiopathology; D008875:Middle Aged; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D011237:Predictive Value of Tests; D015995:Prevalence; D011379:Prognosis; D012189:Retrospective Studies
chemical_list: D015415:Biomarkers