Literature DB >> 18556588

Early disruption of the blood-brain barrier after thrombolytic therapy predicts hemorrhage in patients with acute stroke.

Andreas Kastrup, Klaus Gröschel, Thomas M Ringer, Christoph Redecker, Robert Cordesmeyer, Otto W Witte, Christoph Terborg.   

Abstract

BACKGROUND AND
PURPOSE: Leaks of the blood-brain barrier can be detected on postcontrast-enhanced T1-weighted MRIs. Although early disruptions of the blood-brain barrier appear to be an important risk factor for tissue plasminogen activator-related hemorrhages in rodents, little is known about their incidence and consequences in human stroke.
METHODS: This is a retrospective analysis of a prospectively collected stroke database over the past 6 years. In 52 patients, multimodal MRI (including diffusion-weighted, perfusion-weighted, and postcontrast-enhanced T1-weighted MRI to detect blood-brain barrier changes) had been performed immediately before systemic thrombolysis and in 48 patients within a median of 30 minutes (interquartile range: 30 to 60 minutes) after recombinant tissue plasminogen activator treatment. The incidence of symptomatic hemorrhage (SICH), defined as any parenchymal hemorrhage leading to deterioration in the patient's clinical condition, was related to several clinical and imaging variables, including early blood-brain barrier changes.
RESULTS: Overall, SICH was detected in 9 (9%) patients and among these, 2 died. Although no blood-brain barrier changes were detectable before thrombolysis, 3 of 48 patients (6.25%) had a parenchymal gadolinium enhancement in the areas of initial infarction after tissue plasminogen activator treatment. All 3 patients developed SICHs at sites corresponding to the areas of enhancement. The presence of a parenchymal enhancement was significantly associated with SICH (P<0.01), whereas other clinical and imaging variables did not predict SICH in this series.
CONCLUSIONS: Early parenchymal enhancement after intravenous tissue plasminogen activator is significantly associated with subsequent SICH and could therefore become a useful imaging sign for the rapid initiation of preventive strategies in the future.

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Year:  2008        PMID: 18556588     DOI: 10.1161/STROKEAHA.107.505420

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  46 in total

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3.  PI3Kγ (Phosphoinositide 3-Kinase-γ) Inhibition Attenuates Tissue-Type Plasminogen Activator-Induced Brain Hemorrhage and Improves Microvascular Patency After Embolic Stroke.

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Authors:  Mark Jrj Bouts; Ivo Acw Tiebosch; Umesh S Rudrapatna; Annette van der Toorn; Ona Wu; Rick M Dijkhuizen
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Authors:  Rong Jin; Adam Y Xiao; Shan Liu; Min Wang; Guohong Li
Journal:  Stroke       Date:  2018-05-29       Impact factor: 7.914

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8.  Hemorrhagic risk of recent silent cerebral infarct on prethrombolysis MR imaging in acute stroke.

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9.  Hydrogen Sulfide Attenuates Tissue Plasminogen Activator-Induced Cerebral Hemorrhage Following Experimental Stroke.

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Journal:  Transl Stroke Res       Date:  2016-03-28       Impact factor: 6.829

10.  Protective Effects of Autologous Bone Marrow Mononuclear Cells After Administering t-PA in an Embolic Stroke Model.

Authors:  Bing Yang; Weilang Li; Nikunj Satani; Duyen M Nghiem; XiaoPei Xi; Jaroslaw Aronowski; Sean I Savitz
Journal:  Transl Stroke Res       Date:  2017-08-23       Impact factor: 6.829

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