Stroke最新文献

{"title":"Effect of Argatroban Plus Dual Antiplatelet in Branch Atherosclerosis Disease: A Randomized Clinical Trial.","authors":"Jinghan Xu, Yinglin Liu, Huazedan Wang, Rong Sun, Hongjian Zhao, Xindong Liu, Yuanyuan Li, Juan Yang, Bei Zhang, Lanying He, Liang Gong, Xin Ding, Xuejun Xu, Ronghua Xu, Jian Wang","doi":"10.1161/STROKEAHA.124.048872","DOIUrl":"10.1161/STROKEAHA.124.048872","url":null,"abstract":"<p><strong>Background: </strong>Branch atherosclerosis disease (BAD) is prone to early neurological deterioration (END). The purpose of this study was to assess the efficacy and safety of argatroban plus dual antiplatelet therapy (DAPT) for preventing END in high-risk branch atherosclerosis disease patients.</p><p><strong>Methods: </strong>This multicenter, open-label, blinded end point, randomized controlled trial including branch atherosclerosis disease patients with mild stroke (National Institutes of Health Stroke Scale score ≤5) was conducted at 4 centers in China from May 18, 2021 to February 8, 2023. Within 48 hours after symptom onset, patients were randomly assigned to receive argatroban plus DAPT or DAPT alone in a 1:1 ratio. The primary end points were the incidence of END (National Institutes of Health Stroke Scale score increase ≥2) within 7 days and excellent functional outcome (modified Rankin Scale score of 0 to 1) at 90 days.</p><p><strong>Results: </strong>A total of 111 patients were randomized, with 11 excluded for specific reasons, resulting in 100 patients included in the modified intention-to-treat population. Among the 100 patients, 49 received argatroban plus DAPT and 51 received DAPT alone, 63 (63.0%) were men, and the median age was 64 (range, 55-74) years. END occurred in 20.4% (10/49) of the argatroban plus DAPT group and 47.1% (24/51) of the DAPT group (risk difference, 26.7% [95% CI, 14.1-39.2]; risk ratio, 2.31 [95% CI, 1.49-3.58]; <i>P</i>=0.006). At the 90-day follow-up, 87.8% (43/49) in the argatroban plus DAPT group and 68.6% (35/51) in the DAPT group achieved an excellent functional outcome (risk difference, -19.1% [95% CI, -30.3 to -8.0]; risk ratio, 0.78 [95% CI, 0.67-0.91]; <i>P</i>=0.025). There was 1 minor hemorrhage in each group.</p><p><strong>Conclusions: </strong>Argatroban plus DAPT is a safe and effective strategy to reduce END occurrence and improve 90-day functional outcome in high-risk branch atherosclerosis disease patients.</p><p><strong>Registration: </strong>URL: https://www.chictr.org.cn; Unique Identifier: ChiCTR21000 46487.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1662-1670"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12180705/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143982738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cost-Effectiveness Analysis of Early Minimally Invasive Removal of Intracerebral Hemorrhage.","authors":"Janel Hanmer, Jonathan Arnold, Alex Hall, Jonathan J Ratcliff, Jason W Allen, Michael Frankel, David W Wright, Daniel L Barrow, Gustavo Pradilla, Kenneth J Smith","doi":"10.1161/STROKEAHA.124.048493","DOIUrl":"10.1161/STROKEAHA.124.048493","url":null,"abstract":"<p><strong>Background: </strong>Supratentorial intracerebral hemorrhage (ICH) is common and often devastating. In a randomized controlled trial, ICH evacuation with minimally invasive trans-sulcal parafascicular surgery (MIPS) improved functional outcomes at 180 days compared with medical management (MM), primarily in patients with lobar hemorrhages. The cost-effectiveness of MIPS compared with MM is explored.</p><p><strong>Methods: </strong>A Markov model compared costs and outcomes using ENRICH trial (Early Minimally Invasive Removal of Intracerebral Hemorrhage) data for MIPS versus MM over the 6-month trial duration. Costs were 2020 US$ and effectiveness was quality-adjusted life years. Monthly model transitions between modified Rankin Scale score health states were estimated from trial data. Costs were obtained from US databases and literature. MIPS device costs were $5705/patient. Primary outcomes were total hospital costs from the hospital perspective and the incremental cost-effectiveness ratio between MIPS and MM (ie, the 6-month cost difference between strategies divided by quality-adjusted life year difference) from the healthcare perspective for patients with lobar ICH. Sensitivity analyses were performed.</p><p><strong>Results: </strong>From the hospital perspective, MIPS costs were $2782 less per patient than MM ($74 252 versus $77 034), with MIPS having decreased the intensive care unit hospital length of stay, non-MIPS neurosurgery, mortality, and rehospitalization. From the healthcare perspective, including hospital and nonhospital costs, MIPS in lobar ICH cost $8850 less and gained 0.068 quality-adjusted life year per patient compared with MM; thus MIPS was dominant (less costly and more effective). Results were robust to individual parameter variation over plausible ranges and, with all parameters varied simultaneously in a probabilistic sensitivity analysis, MIPS was dominant in >93% of 10 000 model iterations and favored in >99% at $100 000/quality-adjusted life year gained (a common US benchmark).</p><p><strong>Conclusions: </strong>In the ENRICH randomized controlled trial, MIPS cost less and was more effective compared with MM from both hospital and healthcare perspectives for patients with lobar ICH.</p><p><strong>Registration: </strong>URL: https://clinicaltrials.gov/; Unique identifier: NCT02880878.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1799-1806"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144039293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Topographic Localization of Chronic Cerebellar Ischemic Lesions: Implications for Underlying Cause.","authors":"Markus Kneihsl, Arsany Hakim, Martina B Goeldlin, Mattia Branca, Sabine Fenzl, Stefanie Abend, Thomas Gattringer, Christian Enzinger, Jesse Dawson, Benno Gesierich, Anna Kopczak, Remco J Hack, Minne N Cerfontaine, Julie W Rutten, Saskia A J Lesnik Oberstein, Marco Pasi, Urs Fischer, Marco Duering, Thomas R Meinel","doi":"10.1161/STROKEAHA.124.049337","DOIUrl":"10.1161/STROKEAHA.124.049337","url":null,"abstract":"<p><strong>Background: </strong>Chronic cerebellar lesions of presumed ischemic origin are frequently found in patients with ischemic stroke and as incidental findings. However, the differentiation of embolic lesions from lesions caused by cerebral small vessel disease (SVD) is unclear. We aimed to investigate whether the location of chronic cerebellar ischemic lesions (deep versus cortical) indicates the underlying cause (embolic versus SVD).</p><p><strong>Methods: </strong>This study was a post hoc data analysis from the multinational ELAN trial (Early Versus Late Initiation of Direct Oral Anticoagulants in Patients With Postischemic Stroke With Atrial Fibrillation), which included patients with acute ischemic stroke and atrial fibrillation cohort between 2017 and 2022. For comparison, data from 2 cohorts (DiViNAS [Disease Variability in NOTCH3-Associated SVD] and VASCAMY [Vascular and Amyloid Predictors of Neurodegeneration and Cognitive Decline in Nondemented Subjects]) consisting of participants with hereditary cerebral SVD (ie, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) were analyzed (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy cohort). Brain magnetic resonance imaging scans were evaluated for presence and location of chronic cerebellar ischemic lesions. The association between these lesions and the severity of supratentorial SVD was analyzed using univariable and multivariable models, adjusting for key covariables.</p><p><strong>Results: </strong>In the atrial fibrillation cohort (N=790), 278 (35%) patients had chronic cerebellar ischemic lesions (cortical: n=242; deep: n=36). In multivariable analyses, features of cerebral SVD were associated with deep cerebellar ischemic lesions (summary SVD score; odds ratio per point, 2.5 [95% CI, 1.5-3.5]; <i>P</i><0.001), while there was no association of SVD markers and cortical cerebellar ischemic lesions (summary SVD score; odds ratio per point, 1.1 [95% CI, 0.9-1.3]; <i>P</i>=0.107). In the cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy cohort (N=257), chronic cerebellar ischemic lesions (n=108 [42%]) were almost exclusively identified in deep cerebellar regions (n=101, 94%).</p><p><strong>Conclusions: </strong>Chronic cerebellar ischemic lesions in deep but not cortical regions were associated with supratentorial cerebral SVD. Therefore, cerebral SVD is likely the primary cause of chronic ischemic lesions in deep cerebellar regions, while cortical cerebellar lesions are more likely attributable to embolic etiologies.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT03148457.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1823-1831"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanical Thrombectomy for Large Ischemic Stroke: A Critical Appraisal of Evidence From 6 Randomized Controlled Trials.","authors":"Amrou Sarraj, Shinichi Yoshimura, Götz Thomalla, Xiaochuan Huo, Caroline Arquizan, Albert J Yoo, Takeshi Morimoto, Martin Bendszus, Bertrand Lapergue, Thanh N Nguyen, Bruce C V Campbell, Vincent Costalat, Jens Fiehler, Tudor G Jovin, Osama O Zaidat, Zhongrong Miao","doi":"10.1161/STROKEAHA.125.050402","DOIUrl":"10.1161/STROKEAHA.125.050402","url":null,"abstract":"<p><p>Recently, 6 randomized trials evaluated the efficacy and safety of endovascular thrombectomy in patients with large core stroke. This review examines the differences in clinical and imaging eligibility and their impact on the interpretation of evidence and potential neuroimaging workflow. Pending results of a planned patient-level meta-analysis, it also evaluates clinical outcomes and thrombectomy treatment effect across those trials, overall and within selected clinical and imaging subgroups most relevant to clinical practice. Additionally, the implications of extending thrombectomy eligibility to patients with large core stroke on stroke systems of care and societal benefits are discussed.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1917-1927"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144102735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurostimulant Use for Rehabilitation and Recovery After Stroke: A Narrative Literature Review.","authors":"Helene Chesnais, Kelly L Sloane, Jens Witsch, Christopher Favilla, Scott E Kasner, Aaron Rothstein","doi":"10.1161/STROKEAHA.124.048677","DOIUrl":"10.1161/STROKEAHA.124.048677","url":null,"abstract":"<p><strong>Background: </strong>Stroke often results in significant impairments across various domains, including movement, language, cognition, and mood. Neurostimulants have been proposed as potential therapeutic interventions to enhance recovery in these areas.</p><p><strong>Methods: </strong>This narrative literature review examines clinical trials investigating the efficacy of neurostimulants in poststroke recovery. It evaluates outcomes related to aphasia, motor deficits, cognition, fatigue, and depression.</p><p><strong>Results: </strong>The qualitative analysis included 34 trials testing the following neurostimulants: methylphenidate (n=6), amphetamines (n=8), memantine (n=2), modafinil (n=2), levodopa (n=14), amantadine (n=1), bromocriptine (n=3), and ropinirole (n=1). Of the 34 studies, 31 were randomized, placebo-controlled (double-blind, n=27; single-blind, n=2; unblinded n=2), 2 were randomized and not placebo-controlled, and 1 was not randomized. Study design was either multiarm (n=23), crossover (n=10), or used subjects as their own control (n=1). Mean sample size was 49.4 (5-593).</p><p><strong>Conclusions: </strong>Current evidence suggests that memantine may be effective for aphasia, although few phase III trials exist, whereas bromocriptine and amphetamines lack sufficient evidence for long-term recovery of aphasia. Levodopa may improve motor aphasias but has not shown long-term benefits for motor recovery. Similarly, ropinirole has not been shown to improve poststroke motor outcomes. Methylphenidate has limited efficacy for cognitive improvement but may enhance poststroke functionality and mood. Modafinil may help with poststroke fatigue. In conclusion, there are promising results of positive effects of neurostimulants with few side effects, though studies are limited by heterogeneous designs and small sample sizes. Neurostimulant efficacy must be assessed in conjunction with specific rehabilitation modalities as part of larger, well-designed studies to best understand their effects on impairment.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1853-1871"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12187543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144015020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"14,15-EET Maintains Mitochondrial Homeostasis to Inhibit Neuronal Pyroptosis After Ischemic Stroke.","authors":"Huixia Geng, Jing Tang, Zhen Li, Yanshuo Zhang, Congwei Ye, Yibo Zhang, Xiaohui Li, Yunxia Li, Yanming Wang, Yi Wang, Xinrui Lv, Lai Wang","doi":"10.1161/STROKEAHA.124.049143","DOIUrl":"10.1161/STROKEAHA.124.049143","url":null,"abstract":"<p><strong>Background: </strong>Neuronal pyroptosis is involved in neuronal cell death and neurological damage after cerebral ischemia-reperfusion. 14,15-Epoxyeicosatrienoic acid (14,15-EET) can reduce neuronal loss induced by cerebral ischemia-reperfusion by regulating mitochondrial biological processes. However, it remains unclear how 14,15-EET regulates mitochondrial homeostasis, inhibits neuronal pyroptosis, and promotes neurological functional recovery after cerebral ischemia-reperfusion.</p><p><strong>Methods: </strong>Mice with middle cerebral artery occlusion and reperfusion were used as an animal model to study the cerebral ischemia-reperfusion disease. The neurological function of mice was performed at 1, 3, and 5 days to test the therapeutic effects of 14,15-EET. Transmission electron microscope imaging and Nissl staining were used to analyze neuronal morphological structure, mitophagy, and neuronal pyroptosis. Western blot and transcriptome were used to detect the levels of mitophagy and neuronal pyroptosis signaling pathway-related molecules. HT22 cells were used in in vitro studies to detect the mechanism by which 14,15-EET reduces neuronal pyroptosis after oxygen-glucose deprivation/reoxygenation treatment.</p><p><strong>Results: </strong>14,15-EET treatment reduced cerebral infarct volumes and improved neurological functional recovery in mice after cerebral ischemia-reperfusion. 14,15-EET treatment maintained the morphological structure of neurons in the ischemic penumbra area as well as the dendritic spine density in mice after cerebral ischemia-reperfusion. The upregulation of NLRP1 (NOD-like receptor thermal protein domain associated protein 1), IL (interleukin)-1β, caspase-1, and GSDMD (gasdermin D) induced by cerebral ischemia-reperfusion was inhibited, and the expression of mitophagy proteins Parkin and LC3B (microtubule-associated protein 1 light chain 3 B) was increased by 14,15-EET treatment. Transcriptome profiling found that 14,15-EET exerts a neuroprotection role in promoting neural function recovery by activating the WNT (wingless-type mouse mammary tumor virus integration site family) signaling pathway. We found that 14,15-EET upregulated the WNT pathway proteins such as WNT1, WNT3A, β-catenin, and p-GSK-3β (phosphorylation of glycogen synthase kinase 3β) in vivo and in vitro. The WNT signaling pathway inhibitor XAV-939 reduced the expression of mitophagy protein Parkin and upregulated the expression of caspase-1 and GSDMD in HT22 cells with oxygen-glucose deprivation/reoxygenation and 14,15-EET treatment.</p><p><strong>Conclusions: </strong>14,15-EET regulates mitochondrial homeostasis to inhibit neuronal pyroptosis, thereby promoting the recovery of neurological function in mice after cerebral ischemia-reperfusion. These results provide new ideas for maintaining mitochondrial homeostasis and inhibiting neuronal pyroptosis after cerebral ischemia-reperfusion.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1883-1896"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143995399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Dietary Fiber Intake and Stroke Among US Adults: From NHANES and Mendelian Randomization Analysis.","authors":"Siran Lai, Guiting Zhou, Yue Li, Yuling Zhang, Yue An, Fuyuan Deng, Kunsheng Wu, Peijian Liu, Qingmin Chu, Rui Peng","doi":"10.1161/STROKEAHA.124.049093","DOIUrl":"10.1161/STROKEAHA.124.049093","url":null,"abstract":"<p><strong>Background: </strong>There is debate on the link between dietary fiber intake and stroke risk. The purpose of this study was to look at how it impacts dietary fiber intake and stroke risk, as well as mortality among stroke survivors. Two-sample Mendelian randomization was also used to investigate the causal relationship.</p><p><strong>Methods: </strong>This research examined information from 1453 patients with stroke participating in the National Health and Nutrition Examination Survey from 1999 to 2018. To assess the incidence of stroke, we conducted a survey-weighted multivariate logistic regression analysis and subgroup analysis. To evaluate the mortality associated with stroke, we used Kaplan-Meier survival analysis combined with survey-weighted Cox regression models. Using 2-sample Mendelian randomization and inverse-variance weighted method, we established a causal relationship between dietary fiber intake and stroke. The article was organized according to Strengthening the Reporting of Observational Studies in Epidemiology and Strengthening the Reporting of Observational Studies in Epidemiology Using Mendelian Randomization guidelines.</p><p><strong>Results: </strong>In the fully adjusted model, dietary fiber intake was negatively associated with stroke (odds ratio, 0.98 [95% CI, 0.97-0.99]; <i>P</i><0.0001; T3 versus T1; odds ratio, 0.71 [95% CI, 0.57-0.88]; <i>P</i>=0.002). A stable linear negative relevance was confirmed between dietary fiber intake and stroke risk (nonlinear <i>P</i>=0.566) by the multivariate adjusted spline regression model. According to the survey-weighted multivariate Cox regression model, dietary fiber intake significantly reduced all-cause mortality (T3 versus T1; odds ratio, 0.68 [95% CI, 0.47-0.97]; <i>P</i>=0.04). Further Kaplan-Meier survival analysis indicated that higher intake of dietary fiber improved the survival of patients with stroke (<i>P</i>=0.02325). The 2-sample Mendelian randomization analysis showed that genetic prediction supported a causal relationship between increased dietary fiber intake and reduced risk of small vessel stroke (odds ratio, 0.8326 [95% CI, 0.7051-0.9833]; <i>P</i>=0.0309).</p><p><strong>Conclusions: </strong>There is a stable negative correlation between dietary fiber intake and stroke risk. High fiber intake is associated with reduced all-cause mortality among stroke survivors. Additionally, genetic prediction further demonstrates a causal relationship between dietary fiber and reduced risk of small vessel stroke.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1786-1798"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12180701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex Differences in Prescription, Initiation, and Discontinuation of Secondary Prevention Medications After Stroke.","authors":"Lachlan L Dalli, Nadine E Andrew, Muideen T Olaiya, Dominique A Cadilhac, Joosup Kim, David Ung, Amanda G Thrift, Hoang T Phan, Seana Gall, Mark R Nelson, Monique F Kilkenny","doi":"10.1161/STROKEAHA.124.050207","DOIUrl":"10.1161/STROKEAHA.124.050207","url":null,"abstract":"<p><strong>Background: </strong>Women less frequently receive secondary prevention medications at discharge poststroke than men. It is unclear whether similar sex differences exist in the long term poststroke, after accounting for age and clinical characteristics. We aimed to evaluate sex differences in medication prescription, initiation, and discontinuation poststroke or transient ischemic attack.</p><p><strong>Methods: </strong>A retrospective cohort study using person-level linked data from the Australian Stroke Clinical Registry (42 hospitals; Victoria and Queensland; 2012-2016). We included all adults with first-ever ischemic stroke, intracerebral hemorrhage, or transient ischemic attack who survived >60 days post-discharge. For each major class of secondary prevention medication (antihypertensive, antithrombotic, or lipid lowering), we evaluated sex differences in prescription at hospital discharge, initiation within 60 days, and discontinuation within 2 years post-discharge. Sex differences were assessed using multivariable models, adjusted for sociodemographics and comorbidities. Where effect modification by age was found (<i>P</i>_interaction≤0.05), age-specific odds ratios were reported.</p><p><strong>Results: </strong>Among 8108 women (median age, 74.3 years) and 10 344 men (median age, 70.5 years) with first-ever stroke (≈8% intracerebral hemorrhage) or transient ischemic attack, women were less likely to be prescribed antihypertensive medications on discharge (odds ratio, 0.82 [95% CI, 0.74-0.91]). Women were less likely to initiate antihypertensive (odds ratio, 0.76 [95% CI, 0.69-0.84]) and antithrombotic (odds ratio, 0.89 [95% CI, 0.82-0.96]) medications within 60 days than men. While there was no overall difference in discontinuation between men and women, interactions were observed with age (<i>P</i>_interaction, all <0.002). Younger women (aged <45 years) and older women (aged >90 years) were more likely to discontinue secondary prevention medications than men of equivalent age.</p><p><strong>Conclusions: </strong>Sex differences exist for prescription, initiation, and discontinuation of secondary prevention medications poststroke. With many sex differences being age specific, there is a critical need for targeted interventions to improve prevention medication use in these patient subgroups.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1769-1778"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144048227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sitting Time, Leisure-Time Physical Activity, and Risk of Mortality Among US Stroke Survivors: A Prospective Cohort Study From the NHANES 2007 to 2018.","authors":"Chuanchuan Yu, Yalin Cao, Qifang Liu, Hongwen Tan, Guiling Xia, Baolin Chen, Fawang Du, Kui Lu, Gustavo Saposnik","doi":"10.1161/STROKEAHA.124.049672","DOIUrl":"10.1161/STROKEAHA.124.049672","url":null,"abstract":"<p><strong>Background: </strong>Stroke survivors are highly sedentary and engage in minimal physical activity. This study aimed to investigate the independent and joint effects of daily sitting time and leisure-time physical activity on survival among stroke survivors.</p><p><strong>Methods: </strong>The nationally representative cohort included 1446 stroke survivors (weighted population, 6 968 723) from the National Health and Nutrition Examination Survey from 2007 to 2018. Mortality data were obtained through December 31, 2019. Leisure-time physical activity was categorized as inactive (0 min/wk), insufficiently active (1 to <150 min/wk), and sufficiently active (≥150 min/wk). Daily sitting time was categorized as <6, 6 to <8, and ≥8 h/d. Survival analyses of all-cause and specific mortality were performed by weighted Cox proportional hazards regression models.</p><p><strong>Results: </strong>This cohort study comprised 55.0% females, 68.7% non-Hispanic White, and had a weighted mean (SE) age of 64.6 (0.5) years. Overall, 70.3% were inactive, 42.3% sat at least 8 h/d, and 34.9% were both inactive and sat at least 8 h/d. During a median of 5.2 years of follow-up, 494 deaths occurred, including 171 associated with cardiovascular disease (CVD) and 323 associated with non-CVD. Active stroke survivors had a lower risk of all-cause (hazard ratio [HR], 0.26 [95% CI, 0.17-0.40]), CVD (HR, 0.26 [95% CI, 0.13-0.53]), and non-CVD (HR, 0.26 [95% CI, 0.15-0.46]) mortality compared with inactive stroke survivors. Sitting at least 8 h/d was associated with higher risks of all-cause (HR, 1.50 [95% CI, 1.13-1.99]) and non-CVD (HR, 1.61 [95% CI, 1.18-2.20]) mortality compared with sitting <6 h/d. In the joint analyses, stroke survivors who were inactive or insufficiently active and sat for at least 8 h/d had the highest risks of all-cause (HR, 3.73 [95% CI, 2.07-6.73]), CVD (HR, 3.32 [95% CI, 1.33-8.29]), and non-CVD (HR, 3.91 [95% CI, 1.70-8.95]) mortality when compared with those who were active and sat for <6 h/d. When stratifying by leisure-time physical activity, daily sitting time was not associated with mortality among active stroke survivors. These observations were confirmed in sensitivity analyses.</p><p><strong>Conclusions: </strong>This study highlights the potential benefits of enhancing leisure-time physical activity and reducing sitting time to lower mortality rates among stroke survivors.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1738-1747"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-Term Exposure to Ambient Particulate Matter and Structural Brain Changes in Older Adults.","authors":"Giulia Grande, Bolin Wu, Jing Wu, Grégoria Kalpouzos, Erika J Laukka, Tom Bellander, Debora Rizzuto","doi":"10.1161/STROKEAHA.124.048096","DOIUrl":"10.1161/STROKEAHA.124.048096","url":null,"abstract":"<p><strong>Background: </strong>Accumulating evidence links air pollution exposure to late-life cognitive deterioration. Whether air pollution alters brain structure remains poorly understood. Thus, we aimed to quantify the association between long-term exposure to particulate matter ≤2.5 µm and ≤10 µm (PM_2.5 and PM₁₀, respectively) and late-life brain structural changes.</p><p><strong>Methods: </strong>In the Swedish National Study on Aging and Care in Kungsholmen, Stockholm, 555 participants free from dementia underwent brain magnetic resonance imaging (MRI) scans at baseline and after 6 years (cohorts <78 years) or after 3 and 6 years (cohorts aged ≥78 years). After the exclusion of participants with neurological conditions (including previous stroke) and suboptimal MRI quality, we had 457 participants with available repeated MRI examinations, where total brain tissue volume, ventricles, hippocampus, and white matter hyperintensities volumes were assessed. PM_2.5 and PM₁₀ have been assessed since 1990 using dispersion models at residential addresses. Brain volumes have been standardized using baseline mean and SD. Long-term exposure to PM_2.5 and PM₁₀ in relation to the baseline and longitudinal brain MRI volumes were tested through multiadjusted (age, sex, educational level, smoking, socioeconomic status, and neighborhood household mean income) linear regression models.</p><p><strong>Results: </strong>At study entry, the mean (SD) age of the participants was 70 (SD, 8.9) years and 41% were males. Individuals who before baseline had been exposed to levels of PM_2.5 or PM₁₀ above the median (8.5 and 14.9 μg/m³, respectively) had smaller total brain tissue volume (β, -0.20 [95% CI, -0.33 to -0.06] and β, -0.14 [95% CI, -0.28 to -0.01], respectively) at baseline than those with lower PM_2.5 and PM₁₀ levels. Participants exposed during the follow-up to PM_2.5>8.7 μg/m³ had on average an annual shrinkage of total brain tissue volume of 0.22 (95% CI, -0.43 to -0.01) and an annual increase of 0.25 (95% CI, 0.07-0.43) of the white matter hyperintensities as compared with participants exposed to PM_2.5<8.7 μg/m³. No association was detected between PM₁₀ and an annual rate of change in brain MRI volumes.</p><p><strong>Conclusions: </strong>Long-term exposure to comparatively low levels of PM_2.5 was associated with a greater load of structural brain changes, encompassing brain atrophy and vascular pathology. These findings, in a dementia- and cerebrovascular disease-free sample, underscore the importance of addressing air pollution as a modifiable risk factor for late-life cognitive decline, and highlight the need for targeted interventions to prevent its detrimental effects on brain integrity.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"1816-1822"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12180693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144015019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}