40 research outputs found

    Proximal Arterial Occlusion in Acute Ischemic Stroke with Low NIHSS Scores Should Not Be Considered as Mild Stroke

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    <div><p>Background</p><p>Untreated acute mild stroke patients have substantial 90-day disability rates and worse outcomes than those who are treated with thrombolysis. There is little information regarding which patients with acute mild stroke will benefit from thrombolysis. We sought to investigate factors that are associated with early neurological deterioration (END) and poor prognosis in patients with acute mild stroke.</p><p>Methods</p><p>This was a retrospective study of consecutively registered patients with acute mild stroke (NIHSS ≤3) at our tertiary stroke center between October 2008 and December 2011. END was defined as an increase in NIHSS ≥2 points between hospital days 0 and 5. Modified Rankin Scale (mRS) scores of 0–1 at 90 days post-stroke were defined as favorable outcomes.</p><p>Results</p><p>A total of 378 (mean age, 65.9±13.0 years) patients were included in this study. END occurred in 55 patients (14.6%). IV-thrombolysis was performed in only 9 patients. Symptomatic arterial occlusion on the initial MRA was independently associated with END (OR, 2.206; 95% CI, 1.219–3.994; <i>p</i> = 0.009) by multivariate logistic regression. Of the 119 patients with symptomatic arterial occlusion, ICA occlusion was independently associated with END (OR, 8.606; 95% CI, 2.312–32.043; <i>p</i> = 0.001).</p><p>Conclusions</p><p>This study demonstrates that symptomatic arterial occlusion may be an important predictor of END in patients with acute mild stroke. It may therefore be important to consider that acute ischemic stroke with symptomatic arterial occlusion and low NIHSS scores may not represent mild stroke in acute periods.</p></div

    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

    General characteristics of subjects.

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    <p>Baseline NIHSS scores, onset to visit time, and initial blood glucose levels were analyzed using the Mann-Whitney <i>U</i> test after tests of normality.</p><p>END, early neurological deterioration; TOAST, Trial of Org 10172 in Acute Stroke Treatment; LAA, large artery atherosclerosis; CE, cardioembolism; SVO, small vessel occlusion; UD, undetermined; NIHSS, National Institutes of Health Stroke Scale; PAI, perforating artery infarcts; PI, pial infarcts; BI, border zone infarcts; TI, territorial infarcts; LI, lacunar infarcts; IVT, intra-venous thrombolysis; IAR, intra-arterial revascularization.</p>*<p>Lesion patterns were analyzed only in patients with lesions in anterior circulation.</p

    The distribution of occlusion sites according to END type.

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    <p><b>MCA and ICA occlusions contributed most frequently to severe END.</b> (Abbreviation: MCAO, middle cerebral artery occlusion; ICAO, internal carotid artery occlusion; VBAO, vertebrobasilar artery occlusion; otherAO, other arterial occlusion; no RAO, no relevant arterial occlusion).</p

    The distribution of various types of END and mRS scores of 0–1 and 0–2 at 90 days in terms of baseline NIHSS scores (<sup>*</sup><i>p</i> for trends <0.05).

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    <p>The distribution of various types of END and mRS scores of 0–1 and 0–2 at 90 days in terms of baseline NIHSS scores (<sup>*</sup><i>p</i> for trends <0.05).</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
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