Early changes of tissue perfusion after tissue plasminogen activator in hyperacute ischemic stroke.

Journal Article (Clinical Trial;Journal Article;Multicenter Study)

BACKGROUND AND PURPOSE: it is hypothesized that tissue plasminogen activator rescues brain tissue by improving perfusion. In this study, we aimed to examine acute regional perfusion changes and how they influence infarction and clinical outcome. METHODS: three sequential MR scans were performed in 15 tissue plasminogen activator-treated patients within 3.5 (tp1), at 6 hours (tp2), and at 1 month (tp3) after stroke onset. "Hypoperfusion" was defined if mean transit time prolongation was more than a threshold (4 thresholds: 3, 4, 5, and 6 seconds). Four regions of interest were classified: (1) "reperfusion"-hypoperfused at tp1, normal at tp2; (2) "nonreperfusion"-hypoperfused at tp1 and tp2; (3) "normal perfusion"-normal at tp1 and tp2; and (4) "new hypoperfusion"-normal at tp1 and hypoperfused at tp2. Risk of infarction was calculated within each region of interest. Associations between tissue perfusion changes and clinical variables were evaluated using stepwise multiple linear regressions. Moreover, the association between National Institutes of Health Stroke Scale changes and perfusion alterations was assessed using linear mixed effect models. RESULTS: regardless of the mean transit time threshold chosen, the risk of infarction in nonreperfused regions (40% to 68%, thresholds 3 to 6 seconds) was higher than reperfused regions (9% to 30%, P<0.05), and it was higher in new hypoperfusion regions (9% to 33%) than normal perfusion regions (3% to 4%, P<0.05). Volume of new hypoperfusion was significantly associated with onset-to-treatment time and initial hypoperfused volume. Overall relative reperfusion was significantly associated with National Institutes of Health Stroke Scale improvement. CONCLUSIONS: early tissue perfusion changes influenced final tissue fate. The development of new hypoperfusion may result from delay in tissue plasminogen activator and a large initial lesion.

Full Text

Duke Authors

Cited Authors

  • An, H; Ford, AL; Vo, K; Eldeniz, C; Ponisio, R; Zhu, H; Li, Y; Chen, Y; Powers, WJ; Lee, J-M; Lin, W

Published Date

  • January 2011

Published In

Volume / Issue

  • 42 / 1

Start / End Page

  • 65 - 72

PubMed ID

  • 21148444

Pubmed Central ID

  • PMC3082770

Electronic International Standard Serial Number (EISSN)

  • 1524-4628

Digital Object Identifier (DOI)

  • 10.1161/STROKEAHA.110.590323


  • eng

Conference Location

  • United States