Evidence map›Paper›PMID 27491738›Full record

SynthesisStroke2016

Leukoaraiosis, Cerebral Hemorrhage, and Outcome After Intravenous Thrombolysis for Acute Ischemic Stroke: A Meta-Analysis (v1).

Andreas Charidimou, Marco Pasi, Marco Fiorelli, Sara Shams, Rüdiger von Kummer, Leonardo Pantoni, Natalia Rost

Erratum issuedOpen access · bronzeAbstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Stroke, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 3 pooled it
7.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 3 syntheses or guidelines pooled it, 92 citations in OpenAlex.

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  20. sTWEAK is a leukoaraiosis biomarker associated with neurovascular angiopathy.Annals of clinical and translational neurology · 2022
    Observational
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 4 countries.

Andreas CharidimouFrom J. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston (A.C., M.P., N.R.); Harvard Medical School, Boston, MA (A.C., M.P., N.R.); Department of Neurology and Psychiatry, Sapienza University of Rome, Viale dell'Università 30, Italy (M.F.); Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden (S.S.); Institute of Diagnostic and Interventional Neuroradiology, Dresden University Stroke Centre, Germany (R.v.K.); and NEUROFARBA Department, Neuroscience Section, University of Florence, Italy (M.P., L.P.). andreas.charidimou.09@ucl.ac.uk.
Marco PasiFrom J. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston (A.C., M.P., N.R.); Harvard Medical School, Boston, MA (A.C., M.P., N.R.); Department of Neurology and Psychiatry, Sapienza University of Rome, Viale dell'Università 30, Italy (M.F.); Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden (S.S.); Institute of Diagnostic and Interventional Neuroradiology, Dresden University Stroke Centre, Germany (R.v.K.); and NEUROFARBA Department, Neuroscience Section, University of Florence, Italy (M.P., L.P.).
Marco FiorelliFrom J. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston (A.C., M.P., N.R.); Harvard Medical School, Boston, MA (A.C., M.P., N.R.); Department of Neurology and Psychiatry, Sapienza University of Rome, Viale dell'Università 30, Italy (M.F.); Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden (S.S.); Institute of Diagnostic and Interventional Neuroradiology, Dresden University Stroke Centre, Germany (R.v.K.); and NEUROFARBA Department, Neuroscience Section, University of Florence, Italy (M.P., L.P.).
Sara ShamsFrom J. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston (A.C., M.P., N.R.); Harvard Medical School, Boston, MA (A.C., M.P., N.R.); Department of Neurology and Psychiatry, Sapienza University of Rome, Viale dell'Università 30, Italy (M.F.); Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden (S.S.); Institute of Diagnostic and Interventional Neuroradiology, Dresden University Stroke Centre, Germany (R.v.K.); and NEUROFARBA Department, Neuroscience Section, University of Florence, Italy (M.P., L.P.).
Rüdiger von KummerFrom J. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston (A.C., M.P., N.R.); Harvard Medical School, Boston, MA (A.C., M.P., N.R.); Department of Neurology and Psychiatry, Sapienza University of Rome, Viale dell'Università 30, Italy (M.F.); Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden (S.S.); Institute of Diagnostic and Interventional Neuroradiology, Dresden University Stroke Centre, Germany (R.v.K.); and NEUROFARBA Department, Neuroscience Section, University of Florence, Italy (M.P., L.P.).
Leonardo PantoniFrom J. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston (A.C., M.P., N.R.); Harvard Medical School, Boston, MA (A.C., M.P., N.R.); Department of Neurology and Psychiatry, Sapienza University of Rome, Viale dell'Università 30, Italy (M.F.); Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden (S.S.); Institute of Diagnostic and Interventional Neuroradiology, Dresden University Stroke Centre, Germany (R.v.K.); and NEUROFARBA Department, Neuroscience Section, University of Florence, Italy (M.P., L.P.).
Natalia RostFrom J. Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston (A.C., M.P., N.R.); Harvard Medical School, Boston, MA (A.C., M.P., N.R.); Department of Neurology and Psychiatry, Sapienza University of Rome, Viale dell'Università 30, Italy (M.F.); Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden (S.S.); Institute of Diagnostic and Interventional Neuroradiology, Dresden University Stroke Centre, Germany (R.v.K.); and NEUROFARBA Department, Neuroscience Section, University of Florence, Italy (M.P., L.P.).
Harvard University · USKarolinska University Hospital · SETechnische Universität Dresden · DEUniversity of Florence · IT

Funding

MRI-GENetics Interface Exploration_MRI-GENIE_StudyR01NS086905 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROST, NATALIA S · 2015 to 2019
$3.3M
Statins augment small vessel function and improve stroke outcomesR01NS082285 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROST, NATALIA S · 2013 to 2017
$2.6M
NINDS NIH HHS R01 NS082285NINDS NIH HHS R01 NS086905
6 · The paper itself

Abstract

background and purposeWe performed a meta-analysis to assess whether leukoaraiosis on brain computed tomographic scans of acute ischemic stroke patients treated with intravenous thrombolysis is associated with an increased risk of symptomatic intracerebral hemorrhage (sICH) or poor functional outcome at 3 to 6 months after stroke, or both.

methodsWe searched PubMed and pooled relevant data in meta-analyses using random effects models. Using odds ratios (OR), we quantified the strength of association between the presence and severity of leukoaraiosis and post-thrombolysis sICH or 3- to 6-month modified Rankin Score >2.

resultsEleven eligible studies (n=7194) were pooled in meta-analysis. The risk of sICH was higher in patients with leukoaraiosis (OR, 1.55; 95% confidence interval [CI], 1.17-2.06; P=0.002) and severe leukoaraiosis (OR, 2.53; 95% CI, 1.92-3.34; P<0.0001) compared with patients without leukoaraiosis. Leukoaraiosis was an independent predictor of sICH in 6 included studies (n=4976; adjusted OR, 1.75; 95% CI, 1.35-2.27; P<0.0001). OR for leukoaraiosis and poor 3- to 6-month outcome was 2.02 (95% CI, 1.54-2.65; P<0.0001), with significant statistical heterogeneity (I(2), 75.7%; P=0.002). In adjusted analyses, leukoaraiosis was an independent predictor of poor outcome (n=3688; adjusted OR, 1.61; 95% CI, 1.44-1.79; P<0.0001). In post hoc analyses, including only leukoaraiosis patients in randomized controlled trials (IST-3 [third International Stroke Trial], NINDS [National Institute of Neurological Disorders and Stroke], ECASS-1-2 [European Cooperative Acute Stroke Study]; n=2234), tissue-type plasminogen activator versus control was associated with higher sICH risk (OR, 5.50; 95% CI, 2.49-12.13), but lower poor outcome risk (OR, 0.75; 95% CI, 0.60-0.95).

conclusionsLeukoaraiosis might increase post-intravenous thrombolysis sICH risk and poor outcome poststroke. Despite increased sICH risk, intravenous tissue-type plasminogen activator treatment has net clinical benefit in patients with leukoaraiosis. Given the risk of bias/confounding, these results should be considered hypothesis-generating and do not justify withholding intravenous thrombolysis.

Indexed as

Brain IschemiaCerebral HemorrhageFibrinolytic AgentsHumansLeukoaraiosisStrokeThrombolytic TherapyTissue Plasminogen ActivatorTreatment OutcomeFibrinolytic AgentsTissue Plasminogen Activatorcerebral small vessel diseaseintracerebral hemorrhageleukoaraiosisthrombolysiswhite matter hyperintensities

Identifiers

PMID27491738
PMCPMC4995119
OpenAlexW2493756592

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.