17 research outputs found

    Use of Antithrombotics after Hemorrhagic Transformation in Acute Ischemic Stroke

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    <div><p>Backgrounds</p><p>There have been neither appropriate guidelines nor clinical studies about the use of antithrombotics after hemorrhagic transformation (HT). We sought to find whether the use of antithrombotics after hemorrhagic infarction might be associated with aggravation of HT and neurological deterioration.</p><p>Methods</p><p>This retrospective study included prospectively registered consecutive patients with acute ischemic stroke and HT in our tertiary stroke center. We focused on the hemorrhagic infarction. Aggravation of HT was defined as either enlargement of the original HT or newly developed HT within the infarcted area by visual analysis. We analyzed relationships between antithrombotics and HT, and neurological deterioration after HT in patients with hemorrhagic infarction. In addition, we assessed composite outcomes including neurological deterioration, vascular events, and death at 1month after HT. We analyzed relationships between antithrombotics after discharge and composite outcomes within 1month after HT.</p><p>Results</p><p>222 patients were finally analyzed. Of the 150 patients with hemorrhagic infarction, 75 (50.0%) were type 1. The use of warfarin after detection of hemorrhagic infarction more frequently increased aggravation of HT than did the use of antiplatelets (4 of 24 vs 3 of 69; <i>p</i> = 0.094), but neither warfarin nor antiplatelets caused more HT than no medication. In addition, the use of antithrombotics after hemorrhagic infarction was not significantly associated with neurological deterioration after HT. The frequency of composite events at 1months was significantly lower in patients treated with antithrombotics than those treated without (<i>p</i> = 0.041).</p><p>Conclusion</p><p>In conclusion, the results of this study suggest that antithrombotics can safely be used after hemorrhagic infarction and may not be associated with neurological deterioration and aggravation of HT. Further studies are needed to confirm our results.</p></div

    The associations between use of antithrombotics with aggravation of hemorrhagic transformation by multivariate logistic regression analysis in patients with hemorrhagic infarction (N = 150).

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    <p>Aggravation of HT; Model 1: Adjusted by age and initial NIHSS. Model 2: Adjusted by age, initial NIHSS, and thrombolysis.</p><p>END; adjusted by age, initial NIHSS and thrombolysis.</p

    General characteristics of subjects with hemorrhagic transformation at initial MRI and all imaging.

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    <p>HTN, hypertension; DM, diabetes mellitus; NIHSS, National Institutes of Health Stroke Scale; IV, intravenous; IA, intra-arterial; HT, hemorrhagic transformation; END, early neurological deterioration; FU, follow-up.</p><p>*N = 65 (due to loss of follow-up).</p

    Aspirin Resistance in the Acute Stages of Acute Ischemic Stroke Is Associated with the Development of New Ischemic Lesions

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    <div><p>Background</p><p>Aspirin is a primary antiplatelet agent for the secondary prevention of ischemic stroke. However, if aspirin fails to inhibit platelet function, as is expected in acute ischemic stroke (AIS), it may increase the rate of early clinical events. Therefore, we sought to determine whether aspirin resistance in the acute stage was associated with early radiological events, including new ischemic lesions (NILs).</p><p>Methods</p><p>This study was a single-center, prospective, observational study conducted between April 2012 and May 2013. Aspirin 300 mg was initially administered followed by maintenance doses of 100 mg daily. The acute aspirin reaction unit (aARU) was consistently measured after 3 hours of aspirin loading. An aARU value ≥550 IU was defined as biological aspirin resistance (BAR). NILs on follow-up diffusion-weighted imaging (DWI) were defined as lesions separate from index lesions, which were not detected on the initial DWI.</p><p>Results</p><p>A total of 367 patients were analyzed in this study. BAR in aARU was detected in 60 patients (16.3%). On follow-up DWI, 81 patients (22.1%) had NILs, which were frequently in the same territory as the index lesions (79%), pial infarcts (61.7%), and located within the cortex (59.3%). BAR was independently associated with NILs on follow-up DWI (adjusted OR 2.00, 95% CIs 1.01–3.96; p = 0.047).</p><p>Conclusion</p><p>In conclusion, BAR in aARU could be associated with NILs on follow-up DWI in AIS. Therefore, a further prospective study with a longer follow-up period is necessary to evaluate the clinical implications of aARU in AIS.</p></div

    General characteristics of the patients.

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    <p>National Institutes of Health Stroke Scale, NIHSS; TOAST, the Trial of Org 10172 in Acute Stroke Treatment; LAA, Large artery atherosclerosis; SVO, small vessel occlusion.</p><p>General characteristics of the patients.</p
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