ARTICLE
Predictors of new remote cerebral microbleeds
after IV thrombolysis for ischemic stroke
Tim Bastian Braemswig, MD, Kersten Villringer, MD, Guillaume Turc, MD, PhD, Hebun Erdur, MD,
Jochen B. Fiebach, MD, Heinrich J. Audebert, MD, Matthias Endres, MD, Christian H. Nolte, MD,*
and Jan F. Scheitz, MD*
Neurology
®
2019;92:e1-e9. doi:10.1212/WNL.0000000000006915
Correspondence
Dr. Braemswig
tim-bastian.braemswig@
charite.de
Abstract
Objective
To assess the frequency, associated factors, and underlying vasculopathy of new remote cerebral
microbleeds (CMB), as well as the risk of concomitant hemorrhagic complications related to
new CMBs, after IV thrombolysis (IVT) in acute stroke patients.
Methods
We conducted an observational study using data from our local thrombolysis registry. We
included consecutive stroke patients with MRI (3T)-based IVT and a follow-up MRI the next
day between 2008 and 2017 (n = 396). Only CMBs located outside of the ischemic lesions were
considered. We also performed a meta-analysis on new CMBs after IVT that included 2
additional studies.
Results
In our cohort, new remote CMBs occurred in 16/396 patients (4.0%) after IVT and the
distribution was strictly lobar in 13/16 patients (81%). Patients with preexisting CMBs with
a strictly lobar distribution were significantly more likely to have new CMBs after IVT (p =
0.014). In the random-effects meta-analysis (n = 741), the pooled cumulative frequency of new
CMBs after IVT was 4.4%. A higher preexisting CMB burden (>2) was associated with a higher
likelihood of new CMBs (odds ratio [OR] 3.6, 95% confidence interval [CI] 1.3–10.3) and new
CMBs were associated with the occurrence of remote parenchymal hemorrhage (OR 28.8, 95%
CI 8.6–96.4).
Conclusions
New remote CMBs after IVT occurred in 4% of stroke patients, mainly had a strictly lobar
distribution, and were associated with IVT-related hemorrhagic complications. Preexisting
CMBs with a strictly lobar distribution and a higher CMB burden were associated with new
CMBs after IVT, which may indicate an underlying cerebral amyloid angiopathy.
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*These authors contributed equally to this work.
From the Klinik und Hochschulambulanz f¨ ur Neurologie (T.B.B., H.E., H.J.A., M.E., C.H.N., J.F.S.), Charit´ e–Universit¨ atsmedizin Berlin, Corporate Member of Freie Universit¨ at Berlin,
Humboldt-Universit¨ at zu Berlin, and Berlin Institute of Health; Berlin Institute of Health (BIH) (T.B.B., H.E., M.E., C.H.N., J.F.S.), Berlin, Germany; Center for Stroke Research Berlin (CSB)
(T.B.B., K.V., G.T., J.B.F., H.J.A., M.E., C.H.N., J.F.S.), Charit´ e – Universit¨ atsmedizin Berlin, Berlin, Germany; Department of Neurology (G.T.), Hˆ opital Sainte-Anne, Universit´ e Paris
Descartes; INSERM U894 (G.T.), France; DZHK (German Centre for Cardiovascular Research) (M.E., C.H.N., J.F.S.), partner site Berlin, Berlin, Germany; German Center for Neurode-
generative Diseases (DZNE) (M.E.), partner site Berlin, Berlin, Germany.
Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.
Copyright © 2019 American Academy of Neurology e1
Copyright ª 2019 American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
Published Ahead of Print on January 23, 2019 as 10.1212/WNL.0000000000006915