title: Optimal Tmax threshold for predicting penumbral tissue in acute stroke.
abstract: OBJECTIVE
  We sought to assess whether the volume of the ischemic penumbra can be estimated more accurately by altering the threshold selected for defining perfusion-weighting imaging (PWI) lesions.
  
  
  METHODS
  DEFUSE is a multicenter study in which consecutive acute stroke patients were treated with intravenous tissue-type plasminogen activator 3 to 6 hours after stroke onset. Magnetic resonance imaging scans were obtained before, 3 to 6 hours after, and 30 days after treatment. Baseline and posttreatment PWI volumes were defined according to increasing Tmax delay thresholds (>2, >4, >6, and >8 seconds). Penumbra salvage was defined as the difference between the baseline PWI lesion and the final infarct volume (30-day fluid-attenuated inversion recovery sequence). We hypothesized that the optimal PWI threshold would provide the strongest correlations between penumbra salvage volumes and various clinical and imaging-based outcomes.
  
  
  RESULTS
  Thirty-three patients met the inclusion criteria. The correlation between infarct growth and penumbra salvage volume was significantly better for PWI lesions defined by Tmax >6 seconds versus Tmax >2 seconds, as was the difference in median penumbra salvage volume in patients with a favorable versus an unfavorable clinical response. Among patients who did not experience early reperfusion, the Tmax >4 seconds threshold provided a more accurate prediction of final infarct volume than the >2 seconds threshold.
  
  
  CONCLUSIONS
  Defining PWI lesions based on a stricter Tmax threshold than the standard >2 seconds delay appears to provide more a reliable estimate of the volume of the ischemic penumbra in stroke patients imaged between 3 and 6 hours after symptom onset. A threshold between 4 and 6 seconds appears optimal for early identification of critically hypoperfused tissue.
authors.affiliation: Department of Neurology and Neurological Sciences and the Stanford Stroke Center, Stanford University Medical Center, Palo Alto, CA 94304, USA. jmolivot@stanford.edu
authors.forename: Jean-Marc
authors.initials: JM
authors.lastname: Olivot
authors.forename: Michael
authors.initials: M
authors.lastname: Mlynash
authors.forename: Vincent N
authors.initials: VN
authors.lastname: Thijs
authors.forename: Stephanie
authors.initials: S
authors.lastname: Kemp
authors.forename: Maarten G
authors.initials: MG
authors.lastname: Lansberg
authors.forename: Lawrence
authors.initials: L
authors.lastname: Wechsler
authors.forename: Roland
authors.initials: R
authors.lastname: Bammer
authors.forename: Michael P
authors.initials: MP
authors.lastname: Marks
authors.forename: Gregory W
authors.initials: GW
authors.lastname: Albers
mesh_terms: D000368:Aged; D001921:Brain / Q000473:pathology; D002545:Brain Ischemia / Q000175:diagnosis / Q000628:therapy; D002544:Cerebral Infarction / Q000473:pathology / Q000628:therapy; D017352:Echo-Planar Imaging; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging / Q000379:methods / Q000706:statistics & numerical data*; D008297:Male; D011237:Predictive Value of Tests; D018046:Protein C Inhibitor / Q000627:therapeutic use; D015427:Reperfusion Injury / Q000473:pathology / Q000628:therapy; D020521:Stroke / Q000175:diagnosis* / Q000628:therapy; D015912:Thrombolytic Therapy; D016896:Treatment Outcome
chemical_list: D018046:Protein C Inhibitor