title: Risk factors of symptomatic intracerebral hemorrhage after tPA therapy for acute stroke.
abstract: BACKGROUND
  Studies evaluating predictors of tPA-associated symptomatic intracerebral hemorrhage (SICH) have typically focused on clinical and CT-based variables. MRI-based variables have generally not been included in predictive models, and little is known about the influence of reperfusion on SICH risk.
  
  
  METHODS
  Seventy-four patients were prospectively enrolled in an open-label study of intravenous tPA administered between 3 and 6 hours after symptom onset. An MRI was obtained before and 3 to 6 hours after tPA administration. The association between several clinical and MRI-based variables and tPA-associated SICH was determined using multivariate logistic regression analysis. SICH was defined as a > or = 2 point change in National Institutes of Health Stroke Scale Score (NIHSSS) associated with any degree of hemorrhage on CT or MRI. Reperfusion was defined as a decrease in PWI lesion volume of at least 30% between baseline and the early follow-up MRI.
  
  
  RESULTS
  SICH occurred in 7 of 74 (9.5%) patients. In univariate analysis, NIHSSS, DWI lesion volume, PWI lesion volume, and reperfusion status were associated with an increased risk of SICH (P<0.05). In multivariate analysis, DWI lesion volume was the single independent baseline predictor of SICH (odds ratio 1.42; 95% CI 1.13 to 1.78 per 10 mL increase in DWI lesion volume). When early reperfusion status was included in the predictive model, the interaction between DWI lesion volume and reperfusion status was the only independent predictor of SICH (odds ratio 1.77; 95% CI 1.25 to 2.50 per 10 mL increase in DWI lesion volume).
  
  
  CONCLUSIONS
  Patients with large baseline DWI lesion volumes who achieve early reperfusion appear to be at greatest risk of SICH after tPA therapy.
authors.affiliation: Stanford University, Stanford Stroke Center, Palo Alto, California 94304, USA. Lansberg@stanford.edu
authors.forename: Maarten G
authors.initials: MG
authors.lastname: Lansberg
authors.forename: Vincent N
authors.initials: VN
authors.lastname: Thijs
authors.forename: Roland
authors.initials: R
authors.lastname: Bammer
authors.forename: Stephanie
authors.initials: S
authors.lastname: Kemp
authors.forename: Christine A C
authors.initials: CA
authors.lastname: Wijman
authors.forename: Michael P
authors.initials: MP
authors.lastname: Marks
authors.forename: Gregory W
authors.initials: GW
authors.lastname: Albers
mesh_terms: D000208:Acute Disease; D000368:Aged; D000369:Aged, 80 and over; D001921:Brain / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology; D002536:Cerebral Arteries / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D002543:Cerebral Hemorrhage / Q000139:chemically induced* / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology; D005260:Female; D006801:Humans; D007049:Iatrogenic Disease / Q000517:prevention & control; D008279:Magnetic Resonance Imaging; D008297:Male; D011237:Predictive Value of Tests; D011446:Prospective Studies; D012044:Regression Analysis; D015427:Reperfusion Injury / Q000139:chemically induced* / Q000503:physiopathology / Q000517:prevention & control; D012307:Risk Factors; D020521:Stroke / Q000188:drug therapy*; D015912:Thrombolytic Therapy / Q000009:adverse effects*; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage / Q000009:adverse effects*
chemical_list: D010959:Tissue Plasminogen Activator