title: Hyperglycemia during ischemia rapidly accelerates brain damage in stroke patients treated with tPA.
abstract: To evaluate impact of glucose burden on diffusion-weighted imaging (DWI)-lesion evolution according to ischemia duration in stroke. We studied 47 patients with transcranial Doppler (TCD)-documented artery occlusion treated with intravenous tissue plasminogen activator. Hyperglycemia (HG) was defined as glucose>140 mg/dL. A subcutaneous device continuously monitored glucose during 24 h. Magnetic resonance imaging was performed pretreatment (1) and at 24 to 36 h (2) in 30 patients. We measured initial PWI lesion (PW1) and DWI growth: DW2-DW1 (DWg). Serial TCD during 24 h determined occlusion time (OT). National Institutes of Health Stroke Scale (NIHSS) scores were obtained at baseline and 48 h. Poor short-term clinical course defined as <50% recovery of initial NIHSS. Baseline NIHSS was 18. On admission 10 patients (21.3%) were hyperglycemic and presented similar NIHSS, DW1, and PW1 lesion extension as those without HG. During monitoring 24 patients (51%) had HG, 21 (45%) of them during OT (median OT 12 h). Median 48 h-NIHSS was 10; 15 patients presented poor outcome. 48 h-NIHSS was higher in patients with HG during OT (15 versus 3; P<0.001). Patients with favorable outcome had shorter OT (8.4 versus 17.4 h; P<0.001). However, the only independent predictor of poor outcome was HG during OT (OR: 20.3; 95% CI: 3.77 to 108.8; P<0.001). At 24 h mean DWg was 52 cm(3). A receiver operating characteristic curve identified DWg>14 cm(3) best predictor of poor outcome (sensitivity, 85.7%; specificity, 75%). Total OT (P=0.007) and HG during OT (P=0.01) showed the strongest correlation with DWg. DWI lesion grew 2.7 times faster in patients with HG than without HG during OT (1.73 versus 4.63 cm(3)/h of occlusion; P=0.07). In a regression model the only independent predictor of DWg was HG during OT (OR: 10.83; 95% CI: 1.96 to 59.83; P=0.006). Hyperglycemia, especially during OT, has a powerful deleterious effect after stroke accelerating brain damage.
authors.affiliation: Unitat Neurovascular, Servei de Neurologia, Hospital Vall d'Hebron, Universitat Autónoma de Barcelona, Barcelona, Spain. marcriboj@hotmail.com
authors.forename: Marc
authors.initials: M
authors.lastname: Ribo
authors.forename: Carlos A
authors.initials: CA
authors.lastname: Molina
authors.forename: Pilar
authors.initials: P
authors.lastname: Delgado
authors.forename: Marta
authors.initials: M
authors.lastname: Rubiera
authors.forename: Raquel
authors.initials: R
authors.lastname: Delgado-Mederos
authors.forename: Alex
authors.initials: A
authors.lastname: Rovira
authors.forename: Josep
authors.initials: J
authors.lastname: Munuera
authors.forename: Jose
authors.initials: J
authors.lastname: Alvarez-Sabin
mesh_terms: D000368:Aged; D001786:Blood Glucose; D001921:Brain / Q000473:pathology*; D002545:Brain Ischemia / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D038524:Diffusion Magnetic Resonance Imaging; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D006943:Hyperglycemia / Q000150:complications*; D008297:Male; D012372:ROC Curve; D020127:Recovery of Function; D020521:Stroke / Q000150:complications* / Q000188:drug therapy / Q000473:pathology; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*; D017585:Ultrasonography, Doppler, Transcranial
chemical_list: D001786:Blood Glucose; D005343:Fibrinolytic Agents; D010959:Tissue Plasminogen Activator