title: Persistent poststroke hyperglycemia is independently associated with infarct expansion and worse clinical outcome.
abstract: OBJECTIVE
  Hyperglycemia at the time of ischemic stroke is associated with increased mortality and morbidity. Animal studies suggest that infarct expansion may be responsible. The influence of persisting hyperglycemia after stroke has not previously been examined. We measured the blood glucose profile after acute ischemic stroke and correlated it with infarct volume changes using T2- and diffusion-weighted MRI.
  
  
  METHODS
  We recruited 25 subjects within 24 hours of ischemic stroke symptoms. Continuous glucose monitoring was performed with a glucose monitoring device (CGMS), and 4-hour capillary glucose levels (BGL) were measured for 72 hours after admission. MRI and clinical assessments were performed at acute (median, 15 hours), subacute (median, 5 days), and outcome (median, 85 days) time points.
  
  
  RESULTS
  Mean CGMS glucose and mean BGL glucose correlated with infarct volume change between acute and subacute diffusion-weighted MRI (r>or=0.60, P<0.01), acute and outcome MRI (r=0.56, P=0.01), outcome National Institutes of Health Stroke Scale (NIHSS; r>or=0.53, P<0.02), and outcome modified Rankin Scale (mRS; r>or=0.53, P=0.02). Acute and final infarct volume change and outcome NIHSS and mRS were significantly higher in patients with mean CGMS or mean BGL glucose >or=7 mmol/L. Multiple regression analysis indicated that both mean CGMS and BGL glucose levels >or=7 mmol/L were independently associated with increased final infarct volume change.
  
  
  CONCLUSIONS
  Persistent hyperglycemia on serial glucose monitoring is an independent determinant of infarct expansion and is associated with worse functional outcome. There is an urgent need to study normalization of blood glucose after stroke.
authors.affiliation: Department of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australia.
authors.forename: Tracey A
authors.initials: TA
authors.lastname: Baird
authors.forename: Mark W
authors.initials: MW
authors.lastname: Parsons
authors.forename: Thanh
authors.initials: T
authors.lastname: Phan
authors.forename: Thanh
authors.initials: T
authors.lastname: Phanh
authors.forename: Ken S
authors.initials: KS
authors.lastname: Butcher
authors.forename: Patricia M
authors.initials: PM
authors.lastname: Desmond
authors.forename: Brian M
authors.initials: BM
authors.lastname: Tress
authors.forename: Peter G
authors.initials: PG
authors.lastname: Colman
authors.forename: Brian R
authors.initials: BR
authors.lastname: Chambers
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Davis
mesh_terms: D000208:Acute Disease; D000368:Aged; D001786:Blood Glucose; D002545:Brain Ischemia / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D002544:Cerebral Infarction / Q000175:diagnosis* / Q000209:etiology; D038524:Diffusion Magnetic Resonance Imaging; D018450:Disease Progression; D005343:Fibrinolytic Agents / Q000008:administration & dosage; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology* / Q000628:therapy; D008991:Monitoring, Physiologic; D011237:Predictive Value of Tests; D011446:Prospective Studies; D012044:Regression Analysis; D012720:Severity of Illness Index; D020521:Stroke / Q000150:complications / Q000503:physiopathology*; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage; D016896:Treatment Outcome
chemical_list: D001786:Blood Glucose; D005343:Fibrinolytic Agents; D006442:Glycated Hemoglobin; D010959:Tissue Plasminogen Activator