• Duncan Wilson, David J Seiffge, Christopher Traenka, Ghazala Basir, Jan C Purrucker, Timolaos Rizos, Oluwaseun A Sobowale, Hanne Sallinen, Shin-Joe Yeh, Teddy Y Wu, Marc Ferrigno, Rik Houben, SchreuderFloris H B MFHBMFrom the Stroke Research Center (D.W., C.S., D.J.W.) and Neuroradiological Academic Unit (H.R.J.), Department of Brain Repair and Rehabilitation, Institute of Neurology, and Department of Statistical Science (G.A.), UCL, London, U, Luke A Perry, Jun Tanaka, Marion Boulanger, Rustam Al-Shahi Salman, Hans R Jäger, Gareth Ambler, Clare Shakeshaft, Yusuke Yakushiji, ChoiPhilip M CPMCFrom the Stroke Research Center (D.W., C.S., D.J.W.) and Neuroradiological Academic Unit (H.R.J.), Department of Brain Repair and Rehabilitation, Institute of Neurology, and Department of Statistical Science (G.A.), UCL, London, UK; Strok, Julie Staals, Charlotte Cordonnier, Jiann-Shing Jeng, Roland Veltkamp, Dar Dowlatshahi, Stefan T Engelter, Adrian R Parry-Jones, Atte Meretoja, David J Werring, and And the CROMIS-2 collaborators.
• From the Stroke Research Center (D.W., C.S., D.J.W.) and Neuroradiological Academic Unit (H.R.J.), Department of Brain Repair and Rehabilitation, Institute of Neurology, and Department of Statistical Science (G.A.), UCL, London, UK; Stroke Center and Neurology (D.J.S., C.T., S.T.E.), University Hospital Basel, University of Basel, Switzerland; Ottawa Hospital Research Institute and University of Ottawa (G.B., D.D.), Canada; Department of Neurology (J.C.P., T.R.), Heidelberg University Hospital, Germany; Manchester Academic Health Sciences Center (O.A.S., A.R.P.-J.), Salford Royal NHS Foundation Trust, UK; Department of Neurology (H.S., A.M.), Helsinki University Hospital, Finland; Stroke Center & Department of Neurology (S.-J.Y., J.-S.J.), Department of Neurology, National Taiwan University Hospital, Taipei; Department of Medicine and neurology at the Royal Melbourne Hospital (T.Y.W., A.M.), University of Melbourne, Parkville, Australia; U1171-Degenerative & Vascular Cognitive Disorders (M.F., C.C.), Univ Lille, Inserm, CHU Lille, France; Department of Neurology (R.H., F.H.B.M.S., J.S.), Maastricht University Medical Center, the Netherlands; Department of Neurosciences (J.A.P., P.M.C.C.), Eastern Health, Melbourne, Australia; Division of Neurology, Department of Internal Medicine (J.T., Y.Y.), Saga University Faculty of Medicine, Japan; Division of Clinical Neurosciences (M.B., R.A.-S.S.), Center for Clinical Brain Sciences, School of Clinical Sciences, University of Edinburgh; Department of Stroke Medicine, Division of Brain Sciences (R.V.), Imperial College London, UK; and Neurorehabilitation Unit (S.T.E.), University of Basel and University Center for Medicine of Aging, Felix Platter Hospital, Switzerland.
• Neurology. 2017 May 2; 88 (18): 1693-1700.

ObjectiveIn an international collaborative multicenter pooled analysis, we compared mortality, functional outcome, intracerebral hemorrhage (ICH) volume, and hematoma expansion (HE) between non-vitamin K antagonist oral anticoagulation-related ICH (NOAC-ICH) and vitamin K antagonist-associated ICH (VKA-ICH).MethodsWe compared all-cause mortality within 90 days for NOAC-ICH and VKA-ICH using a Cox proportional hazards model adjusted for age; sex; baseline Glasgow Coma Scale score, ICH location, and log volume; intraventricular hemorrhage volume; and intracranial surgery. We addressed heterogeneity using a shared frailty term. Good functional outcome was defined as discharge modified Rankin Scale score ≤2 and investigated in multivariable logistic regression. ICH volume was measured by ABC/2 or a semiautomated planimetric method. HE was defined as an ICH volume increase >33% or >6 mL from baseline within 72 hours.ResultsWe included 500 patients (97 NOAC-ICH and 403 VKA-ICH). Median baseline ICH volume was 14.4 mL (interquartile range [IQR] 3.6-38.4) for NOAC-ICH vs 10.6 mL (IQR 4.0-27.9) for VKA-ICH (p = 0.78). We did not find any difference between NOAC-ICH and VKA-ICH for all-cause mortality within 90 days (33% for NOAC-ICH vs 31% for VKA-ICH [p = 0.64]; adjusted Cox hazard ratio (for NOAC-ICH vs VKA-ICH) 0.93 [95% confidence interval (CI) 0.52-1.64] [p = 0.79]), the rate of HE (NOAC-ICH n = 29/48 [40%] vs VKA-ICH n = 93/140 [34%] [p = 0.45]), or functional outcome at hospital discharge (NOAC-ICH vs VKA-ICH odds ratio 0.47; 95% CI 0.18-1.19 [p = 0.11]).ConclusionsIn our international collaborative multicenter pooled analysis, baseline ICH volume, hematoma expansion, 90-day mortality, and functional outcome were similar following NOAC-ICH and VKA-ICH.Copyright © 2017 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.

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