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J Stroke. 2017 Jan;19(1):67-76. English. Original Article.
Purrucker JC , Haas K , Wolf M , Rizos T , Khan S , Kraft P , Poli S , Dziewas R , Meyne J , Palm F , Jander S , Möhlenbruch M , Heuschmann PU , Veltkamp R , , .
Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany.
Institute of Clinical Epidemiology and Biometry, University Würzburg, Germany.
Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.
Department of Neurology, University Hospital Würzburg, Würzburg, Germany.
Department of Neurology, Tübingen University, Tübingen, Germany.
Department of Neurology, University Hospital Münster, Germany.
Department of Neurology, University Hospital Schleswig-Holstein, Kiel, Germany.
Department of Neurology, Klinikum Ludwigshafen, Ludwigshafen, Germany.
Department of Neurology, Heinrich-Heine-University, Medical Faculty, Düsseldorf, Germany.
Comprehensive Heart Failure Center, and Clinical Trial Center, University Hospital Würzburg, Würzburg, Germany.
Department of Stroke Medicine, Imperial College London, London, United Germany.

BACKGROUND AND PURPOSE: To evaluate the frequency and outcome of haemorrhagic transformation (HT) after ischaemic stroke in patients treated with non-vitamin K antagonist oral anticoagulants (NOACs). METHODS: Patients with stroke on treatment with a NOAC were prospectively enrolled in this multicentre observational study between February 2012 and 2015. Brain imaging at admission and follow-up imaging until day 7 were reviewed for HT. Functional outcome was assessed by the modified Rankin scale (mRS) before the index event, at discharge, and at 3-months. RESULTS: 231 patients without recanalisation therapy (no-RT), and 32 patients with RT were eligible for analysis. Any HT was present at admission in 9/231 no-RT patients (3.9%, 95% CI 2.0 to 7.3) and in none of the patients with RT. In patients with follow-up imaging (no-RT, n=129, and RT, n=32), HT was present in 14.0% (no-RT; 95% CI, 8.9 to 21.1), and 40.6% (RT, 95% CI, 25.5 to 57.8), respectively. After adjustment for stroke severity, this difference between the no-RT and RT groups became non-significant. Symptomatic ICH was observed in 1 patient per group. HT was not associated with unfavourable outcome (mRS 3-6) at 3-months in multivariable analysis. Resumption of OAC after stroke was delayed in patients with HT compared to those without (15 d [IQR, 5–26] vs. 1 d [0–4], P<0.001). CONCLUSIONS: The frequency and severity of HT after stroke on NOAC appears similar to previous reports for vitamin K antagonists and no anticoagulation. Whether asymptomatic HT should delay resumption of preventive anticoagulation requires further investigation.

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