Predictors and Early Outcome of Hemorrhagic Transformation after Acute Ischemic Stroke

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Abstract

Background: Hemorrhagic transformation (HT) after acute ischemic stroke is frequently detected using magnetic resonance imaging (MRI), in particular in patients treated with tissue plasminogen activator (tPA). Knowledge about causes and early clinical consequences of HT mostly arises from computed tomography-based studies. We analyzed potential predictors and early outcome of HT after stroke detected by MRI with T2*-weighted gradient echo sequences (T2*-MRI). Methods: 122 consecutive stroke patients (mean age 65.5 years, 41% women) who underwent T2*-MRI within 6–60 h after stroke onset were included. 25.4% of patients were treated with tPA; the overall detection rate of HT on T2*-MRI was 20.5%. Potential predictors of HT, such as age, sex, blood pressure, stroke etiology, prior antithrombotic medication, neurological deficit on admission, tPA treatment, and specific MRI findings, were analyzed. In addition, we evaluated the effect of HT on early outcome: a decrease of >4 points on the National Institute of Health Stroke Scale (NIHSS) on day 5 was considered early improvement, and an increase of >4 points was considered early deterioration. Results: The main predictor for occurrence of HT was tPA treatment (48.4 vs. 11.1%; odds ratio 7.50; 95% confidence interval 2.9–19.7; p < 0.001). Furthermore, the development of HT was associated with a severer neurological deficit on admission (mean NIHSS score 9.9 vs. 5.9; p = 0.003), and territorial infarction (88 vs. 58.8%; p = 0.007). 19 patients (15.6%) showed early improvement which was associated with the occurrence of HT (p = 0.011) and tPA treatment (p < 0.001). Conclusions: HT is a frequent finding on T2*-MRI in patients with acute ischemic stroke associated with tPA treatment, territorial infarction and severer neurological deficits on admission. However, HT does not cause clinical deterioration; it is rather related to a favorable early outcome likely reflecting early recanalization and better reperfusion in these patients.

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Most cited references 23

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Comparison of MRI and CT for detection of acute intracerebral hemorrhage.

Jeffrey L Saver, Nathaniel Davis, Margaret Tremwel … (2004)

Noncontrast computed tomography (CT) is the standard brain imaging study for the initial evaluation of patients with acute stroke symptoms. Multimodal magnetic resonance imaging (MRI) has been proposed as an alternative to CT in the emergency stroke setting. However, the accuracy of MRI relative to CT for the detection of hyperacute intracerebral hemorrhage has not been demonstrated. To compare the accuracy of MRI and CT for detection of acute intracerebral hemorrhage in patients presenting with acute focal stroke symptoms. A prospective, multicenter study was performed at 2 stroke centers (UCLA Medical Center and Suburban Hospital, Bethesda, Md), between October 2000 and February 2003. Patients presenting with focal stroke symptoms within 6 hours of onset underwent brain MRI followed by noncontrast CT. Acute intracerebral hemorrhage and any intracerebral hemorrhage diagnosed on gradient recalled echo (GRE) MRI and CT scans by a consensus of 4 blinded readers. The study was stopped early, after 200 patients were enrolled, when it became apparent at the time of an unplanned interim analysis that MRI was detecting cases of hemorrhagic transformation not detected by CT. For the diagnosis of any hemorrhage, MRI was positive in 71 patients with CT positive in 29 (P<.001). For the diagnosis of acute hemorrhage, MRI and CT were equivalent (96% concordance). Acute hemorrhage was diagnosed in 25 patients on both MRI and CT. In 4 other patients, acute hemorrhage was present on MRI but not on the corresponding CT--each of these 4 cases was interpreted as hemorrhagic transformation of an ischemic infarct. In 3 patients, regions interpreted as acute hemorrhage on CT were interpreted as chronic hemorrhage on MRI. In 1 patient, subarachnoid hemorrhage was diagnosed on CT but not on MRI. In 49 patients, chronic hemorrhage, most often microbleeds, was visualized on MRI but not on CT. MRI may be as accurate as CT for the detection of acute hemorrhage in patients presenting with acute focal stroke symptoms and is more accurate than CT for the detection of chronic intracerebral hemorrhage.

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Evidence of reperfusion injury, exacerbated by thrombolytic therapy, in human focal brain ischemia using a novel imaging marker of early blood-brain barrier disruption.

Lawrence Latour, Steven Warach (2004)

Loss of integrity of the blood-brain barrier (BBB) resulting from ischemia and reperfusion is a hypothesized precursor to hemorrhagic transformation (HT) and worse clinical outcome than would be expected from the beneficial effects of reperfusion. We used a novel magnetic resonance imaging marker to characterize early BBB disruption in acute focal brain ischemia and tested associations with reperfusion, HT, and poor outcome (modified Rankin score >2). The BBB disruption was evident as delayed gadolinium enhancement of cerebrospinal fluid space on fluid-attenuated inversion recovery (FLAIR) images and, for convenience, has been termed hyperintense acute reperfusion marker (HARM). HARM was found in 47 of 144 (33%) ischemic stroke patients. Reperfusion was found to be the strongest independent predictor of early BBB disruption (P=0.018) in multivariate analysis. HARM was associated with HT and worse clinical outcome (after adjustment for initial severity). It was also associated with more severe strokes at onset and greater age. Because the timing of the disruption was early enough (median estimate 3.8 hours from onset) to make it relevant to acute thrombolytic therapy, early BBB disruption as defined by HARM may be a promising target for adjunctive therapy to reduce the complications associated with thrombolytic therapy, broaden the therapeutic window, and improve clinical outcome.

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New Approach to Stroke Subtyping: The A-S-C-O (Phenotypic) Classification of Stroke

P Amarenco, J Bogousslavsky, L.R. Caplan … (2009)

We now propose a new approach to stroke subtyping. The concept is to introduce a complete ‘stroke phenotyping’ classification (i.e. stroke etiology and the presence of all underlying diseases, divided by grade of severity) as distinguished from past classifications that subtype strokes by characterizing only the most likely cause(s) of stroke. In this phenotype-based classification, every patient is characterized by A-S-C-O: A for atherosclerosis, S for small vessel disease, C for cardiac source, O for other cause. Each of the 4 phenotypes is graded 1, 2, or 3. One for ‘definitely a potential cause of the index stroke’, 2 for ‘causality uncertain’, 3 for ‘unlikely a direct cause of the index stroke (but disease is present)’. When the disease is completely absent, the grade is 0; when grading is not possible due to insufficient work-up, the grade is 9. For example, a patient with a 70% ipsilateral symptomatic stenosis, leukoaraiosis, atrial fibrillation, and platelet count of 700,000/mm 3 would be classified as A1-S3-C1-O3. The same patient with a 70% ipsilateral stenosis, no brain imaging, normal ECG, and normal cardiac imaging would be identified as A1-S9-C0-O3. By introducing the ‘level of diagnostic evidence’, this classification recognizes the completeness, the quality, and the timing of the evaluation to grade the underlying diseases. Diagnostic evidence is graded in levels A, B, or C: A for direct demonstration by gold-standard diagnostic tests or criteria, B for indirect evidence or less sensitive or specific tests or criteria, and C for weak evidence in the absence of specific tests or criteria. With this new way of classifying patients, no information is neglected when the diagnosis is made, treatment can be adapted to the observed phenotypes and the most likely etiology (e.g. grade 1 in 1 of the 4 A-S-C-O phenotypes), and analyses in clinical research can be based on 1 of the 4 phenotypes (e.g. for genetic analysis purpose), while clinical trials can focus on 1 or several of these 4 phenotypes (e.g. focus on patients A1-A2-A3).

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Author and article information

Journal

Journal ID (publisher-id): CED

Journal ID (nlm-ta): Cerebrovasc Dis

Journal ID (doi): 10.1159/issn.1015-9770

Title: Cerebrovascular Diseases

Publisher: S. Karger AG

ISSN (Print): 1015-9770

ISSN (Electronic): 1421-9786

Publication date Subscription-year: 2011

Publication date (Print): October 2011

Publication date (Electronic): 15 September 2011

Volume: 32

Issue: 4

Pages: 334-341

Affiliations

^aDepartment of Neurology, UniversitätsMedizin Mannheim, University of Heidelberg, Mannheim, ^bDepartment of Psychiatry and Psychotherapy Bethel, Evangelisches Krankenhaus Bielefeld, Bielefeld, and ^cAOK-Klinik Stöckenhöfe, Wittnau, Germany

Author notes

*Micha Kablau, MD, Department of Neurology, UniversitätsMedizin Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1–3, DE–68167 Mannheim (Germany), Tel. +49 621 383 2885, E-Mail kablau@neuro.ma.uni-heidelberg.de

Article

Publisher ID: 331702 Other ID: Cerebrovasc Dis 2011;32:334–341

DOI: 10.1159/000331702

PubMed ID: 21921596

SO-VID: 44ace9f0-12af-4466-a230-9cd149df45da

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 11 April 2011

Date accepted : 10 August 2011

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Figures: 1, Tables: 3, Pages: 8

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Predictors and Early Outcome of Hemorrhagic Transformation after Acute Ischemic Stroke

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Karger: Neurology and Neuroscience

Most cited references 23

Comparison of MRI and CT for detection of acute intracerebral hemorrhage.

Evidence of reperfusion injury, exacerbated by thrombolytic therapy, in human focal brain ischemia using a novel imaging marker of early blood-brain barrier disruption.

New Approach to Stroke Subtyping: The A-S-C-O (Phenotypic) Classification of Stroke

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