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Ann Clin Transl Neurol. 2019 Aug;6(8):1546-1551. doi: 10.1002/acn3.50834. Epub 2019 Jul 10.

Microbleed prevalence and burden in anticoagulant-associated intracerebral bleed.

Author information

1
Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
2
Department of Neurology, University of Tennessee Health Science Center, Memphis, Tennessee.
3
Second Department of Neurology, "Attikon" University Hospital, School of Medicine, National & Kapodistrian University of Athens, Athens, Greece.
4
Department of Neurology, St. Josef-Hospital, Ruhr University of Bochum, Bochum, Germany.
5
Department of Neurology, Geisinger Medical Center, Danville, Pennsylvania.
6
Division of Neurology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
7
Department of Neurology, Henry Ford Hospital, Detroit, Michigan.
8
Department of Neurology, West Virginia University Charleston Division, Charleston, West Virginia.
9
Stroke Unit and Division of Cardiovascular Medicine, University of Perugia, Perugia, Italy.
10
Department of Neurology, Essentia Health-Duluth Clinic, Duluth, Minnesota.
11
Department of Critical Care Medicine, MedStar Washington Hospital Center, Washington, DC.
12
Acute Stroke Unit, Metropolitan Hospital, Piraeus, Greece.
13
Laboratory of Haematology and Blood Bank Unit (A.T.), "Attikon" Hospital, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
14
Second Department of Neurosurgery, "Attikon University Hospital", School of Medicine, National & Kapodistrian University of Athens, Athens, Greece.
15
Department of Neurology, School of Medicine, University of Crete, Crete, Greece.

Abstract

Prior studies suggest an association between Vitamin K antagonists (VKA) and cerebral microbleeds (CMBs); less is known about nonvitamin K oral anticoagulants (NOACs). In this observational study we describe CMB profiles in a multicenter cohort of 89 anticoagulation-related intracerebral hemorrhage (ICH) patients. CMB prevalence was 51% (52% in VKA-ICH, 48% in NOAC-ICH). NOAC-ICH patients had lower median CMB count [2(IQR:1-3) vs. 7(4-11); P < 0.001]; ≥5 CMBs were less prevalent in NOAC-ICH (4% vs. 31%, P = 0.006). This inverse association between NOAC exposure and high CMB count persisted in multivariable logistic regression models adjusting for potential confounders (OR 0.10, 95%CI: 0.01-0.83; P = 0.034).

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