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on January 4, 2007

Stroke. 2007
Published online before print January 4, 2007, doi: 10.1161/01.STR.0000254565.51807.22
A more recent version of this article appeared on February 1, 2007
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Submitted on August 7, 2006
Revised on September 12, 2006
Accepted on September 18, 2006

Two Tales: Hemorrhagic Transformation but Not Parenchymal Hemorrhage After Thrombolysis Is Related to Severity and Duration of Ischemia. MRI Study of Acute Stroke Patients Treated With Intravenous Tissue Plasminogen Activator Within 6 Hours

Götz Thomalla MD*; Jan Sobesky MD; Martin Köhrmann MD; Jochen B. Fiebach MD; Jens Fiehler MD; Olivier Zaro Weber MD; Anna Kruetzelmann MD; Thomas Kucinski MD; Michael Rosenkranz MD; Joachim Röther MD; and Peter D. Schellinger MD, PhD

From Klinik und Poliklinik für Neurologie (G.T., A.K., M.R.), Neuro-Zentrum; Neuroradiologische Abteilung (J.F., T.K.), Klinik und Poliklinik für Radiologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany; Klinik und Poliklinik für Neurologie der Universität zu Köln (J.S., O.Z.W.), Köln, Germany; Neurologische Klinik (M.K., P.D.S.), Universitätsklinikum Erlangen, Erlangen, Germany; Klinik und Poliklinik für Neurologie, Charité- Universitätsmedizin Berlin, Berlin, Germany (J.B.F.); Neurologische Klinik (J.R.), Klinikum Minden, Minden, Germany.

* To whom correspondence should be addressed. E-mail: thomalla{at}uke.uni-hamburg.de.

Background and Purpose--Intracerebral hemorrhage represents the most feared complication of treatment with intravenous tissue plasminogen activator. We studied whether perfusion-weighted imaging and diffusion-weighted imaging has the potential to identify patients at risk of severe intracerebral hemorrhage after treatment with intravenous tissue plasminogen activator.

Methods--We analyzed data of prospectively studied MRI selected acute ischemic stroke patients treated with intravenous tissue plasminogen activator within 6 hours. All patients were examined by perfusion- and diffusion-weighted imaging ≤6 hours. Perfusion- and diffusion-weighted imaging lesion volumes were calculated. Hemorrhagic transformation was assessed on follow-up CT or MRI and diagnosed as hemorrhagic transformation, parenchymal hemorrhage, or symptomatic intracerebral hemorrhage according to ECASS II criteria.

Results--Of 152 patients, hemorrhagic transformation was seen in 60 (39.5%), parenchymal hemorrhage in 15 (9.9%), and symptomatic intracerebral hemorrhage in 4 (2.6%). Multiple logistic regression analysis identified onset to treatment time after 3 to 6 hours (P<0.001), a larger perfusion-weighted imaging lesion volume (P=0.002), and, as a tendency, a higher score on the National Institutes of Health Stroke Scale on admission (P=0.068) as independent predictors of hemorrhagic transformation. Neither MRI lesion volumes nor severity of symptoms, but rather only an older age tended to be associated with parenchymal hemorrhage (P=0.087).

Conclusion--Our results further support the concept of a different pathogenesis for hemorrhagic transformation and parenchymal hemorrhage. Whereas hemorrhagic transformation should be regarded as a clinically irrelevant epiphenomenon of ischemic damage and reperfusion, parenchymal hemorrhage appears to be related to biologic effects of tissue plasminogen activator and other pre-existing pathologic conditions, which deserve further investigation.


Key words: magnetic resonance imaging, diffusion-weighted • magnetic resonance imaging, perfusion-weighted • outcome • stroke, acute • thrombolytic therapy • tissue plasminogen activator


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