17 research outputs found

    The presence and severity of cerebral small vessel disease increases the frequency of stroke in a cohort of patients with large artery occlusive disease

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    <div><p>Background</p><p>Cerebral small vessel disease (SVD) commonly coexists with large artery atherosclerosis (LAA).</p><p>Aim</p><p>We evaluate the effect of SVD on stroke recurrence in patients for ischemic stroke with LAA.</p><p>Methods</p><p>We consecutively collected first-ever ischemic stroke patients who were classified as LAA mechanism between Jan 2010 and Dec 2013. Univariate and multivariate Cox analyses were performed to evaluate the association between the 2-year recurrence and demographic, clinical, and radiological factors. To evaluate the impact of SVD and its components on recurrent stroke, we used the Kaplan-Meier analysis. SVD was defined as the presence of severe white matter hyperintensity (WMH) or old lacunar infarction (OLI) or cerebral microbleeds (CMB). We also compared frequency and burden of SVD among recurrent stroke groups with different mechanisms.</p><p>Results</p><p>Among a total of 956 participants, 92 patients had recurrent events. Recurrence group showed a higher frequency of severe WMH, OLI, asymptomatic territorial infarction, and severe stenosis on the relevant vessel in multivariate analysis. The impact of SVD and its components on recurrent stroke was significant in any ischemic recurrent stroke, and the presence of SVD was continuously important in stroke recurrence regardless of its mechanism, including recurrent LAA stroke, recurrent small vessel occlusion stroke, and even recurrent cardioembolic stroke. Additionally, the recurrence rate increased in dose-response manner with the increased number of SVD components.</p><p>Conclusions</p><p>Cerebral SVD is associated with recurrent stroke in patients with LAA. Additionally, it may affect any mechanisms of recurrent stroke and even with a dose response manner.</p></div

    Recurrent stroke with the number of components of small vessel disease.

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    <p>Number of components of small vessel disease showed a dose-response manner with 2-year recurrent stroke both in the Kaplan-Meier analysis (<i>P</i> < 0.001) (A) and univariate Cox regression analysis adjusted by survival time (<i>P</i> < 0.001) (B).</p

    Recurrent stroke between with and without SVD, severe WMH, OLI, or CMB.

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    <p>Recurrent stroke rate was significantly higher in the group with small vessel disease (A) (<i>P</i> < 0.001), severe white matter hyperintensity (B) (<i>P</i> < 0.001), old lacunar infarction (C) (<i>P</i> < 0.001), or cerebral microbleeds (D) (<i>P</i> < 0.001).</p

    Temporal changes in the neutrophil to lymphocyte ratio and the neurological progression in cryptogenic stroke with active cancer

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    <div><p>Background</p><p>Ischemic stroke patients with active cancer frequently experience early neurological deterioration (END); however, the predictors of END are not well studied. The neutrophil to lymphocyte ratio (NLR) has recently been described as a predictor of poor outcomes in cancer and stroke. However, its role in cancer-related stroke has not been addressed.</p><p>Aim</p><p>We aimed to evaluate the association between the NLR and END in cancer-related stroke patients.</p><p>Methods</p><p>We included 85 cryptogenic stroke patients with active cancer. END was defined as an increase ≥ 4 on the total National Institutes of Health Stroke Scale (NIHSS) score within 72 hours of admission. The NLR was calculated as the ratio of the absolute neutrophil count to the absolute lymphocyte count. We obtained the NLR during the following three periods: at admission, 1–3 days after admission (D 1–3 NLR) and 4–7 days after admission (D 4–7 NLR).</p><p>Results</p><p>END occurred in 15 (18%) of the 85 patients. END was significantly associated with the initial NIHSS score, infarction volume, and the D 1–3 NLR. In multivariate analysis, a higher D 1–3 NLR, measured before END events, remained an independent predictor of END [adjusted odds ratio = 2.78, 95% confidence interval = 1.09–7.08, <i>P</i> = 0.032]. In terms of temporal changes in the NLR, the END group showed a tendency toward temporal increase in the NLR at D 1–3 (<i>P</i> = 0.061) with subsequent decrements in the D 4–7 NLR (<i>P</i> = 0.088), while the non-END group showed no significant changes in the NLR between periods.</p><p>Conclusions</p><p>This study demonstrated that a higher NLR could predict END events in cryptogenic stroke patients with active cancer. However, the results should be confirmed in further large prospective studies.</p></div

    Dynamic changes in the NLR between the with and without END groups.

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    <p>The END group showed consistently higher NLRs than the non-END group, especially in the D 1–3 NLR (Mann-Whitney test, <i>P</i> = 0.002), with a tendency toward a transient increase at D 1–3 (A). Differences in the NLR values between admission and the D 1–3 NLR and between the D 1–3 NLR and the D 4–7 NLR were also significant between the with and without END groups (<i>P</i> = 0.036 and <i>P</i> = 0.025, respectively) (B).</p
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