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. 2009 Oct;19(4):317-22.
doi: 10.1111/j.1552-6569.2008.00303.x. Epub 2008 Oct 21.

Impact of reperfusion after 3 hours of symptom onset on tissue fate in acute cerebral ischemia

Collaborators, Affiliations

Impact of reperfusion after 3 hours of symptom onset on tissue fate in acute cerebral ischemia

Oh Young Bang et al. J Neuroimaging. 2009 Oct.

Abstract

Background: Reperfusion of penumbral tissue is a promising strategy for treatment of acute cerebral ischemia more than 3 hours from symptom onset. However, there has been only sparse direct evidence that reperfusion after 3 hours prevents infarct growth.

Methods: We analyzed clinical and serial magnetic resonance imaging (MRI) data on patients who received endovascular recanalization therapy 3-12 hours after last known well time. Multimodal MRIs were acquired pretreatment, early (1-20 hours), and late (2-7 days) after treatment. Degree of recanalization was assessed on end of procedure catheter angiogram, degree of reperfusion on early posttreatment perfusion MRI, and infarct growth by analysis of diffusion lesion volumes on pretreatment and late MRIs.

Results: Twenty-seven (12 men, 15 women) underwent endovascular recanalization procedures at 6.0 +/- 2.1 hours (range, 3.0-11.5 hours) after last known well time. Immediate posttreatment perfusion lesion (Tmax > or =4 seconds) volume correlated strongly with infarct growth (r= .951, P < .001), exceeding the correlations of vessel recanalization score (r=-.198, P= .446) and pretreatment diffusion-perfusion mismatch volume (r= .518, P= .033). Without reperfusion, enlargement of DWI lesion volume was observed in all patients, and extent of enlargement depended on volume of immediate posttreatment perfusion defects.

Conclusion: Our data indicate that posttreatment reperfusion is the major determinant of threatened tissue outcome, and suggest reperfusion even after 3 hours of symptom onset can alter tissue fate over a wide range of mismatch volumes.

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Figures

Fig 1
Fig 1
Correlation between (A) pretreatment diffusion-perfusion mismatch volume and infarct growth, and (B) immediate posttreatment perfusion defect and infarct growth.
Fig 2
Fig 2
(A) Volume of initial and final DWI lesions and posttreatment perfusion defect. (B) MRI findings that show the DWI changes in patients (upper) without and (lower) with marked improvement in perfusion defect on immediate posttreatment PWI. Numbers in parenthesis represent time from last known well time to start of endovascular therapies. *Marked reperfusion. UKN = patient who developed symptoms during sleep.
Fig 3
Fig 3
Enlargement of DWI lesion volumes depending on (A) the presence and absence of definite diffusion-perfusion mismatch, and (B) the degree of recanalization.

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