Stroke最新文献

{"title":"Carbenoxolone Modulates Dopamine D2 Receptor-Associated Inflammatory Responses After Ischemic Stress.","authors":"Yusuke Ikeuchi, Shunsuke Yamashita, Masaaki Kohta, Hiroyasu Shose, Rikuo Nishii, Shunsuke Yamanishi, Hiroaki Nagashima, Kazuhiro Tanaka, Kohkichi Hosoda, Yuko Ogawa, Akihiko Taguchi, Yoshihiro Muragaki, Takashi Sasayama","doi":"10.1161/STROKEAHA.126.056562","DOIUrl":"https://doi.org/10.1161/STROKEAHA.126.056562","url":null,"abstract":"<p><strong>Background: </strong>Despite advances in reperfusion therapy, ischemic brain injury remains a major cause of disability. Astrocytes play a central role in postischemic inflammation and tissue remodeling, but the molecular drivers of their reactive state transitions remain unclear. Here, we investigated whether carbenoxolone modulates reactive astrocyte phenotypes through astrocytic <i>Drd2</i> signaling after cerebral ischemia.</p><p><strong>Methods: </strong>In vivo rat cerebral ischemia-reperfusion model and in vitro oxygen-glucose deprivation/reperfusion paradigms were used. Infarct volume and neurological outcomes were assessed in vivo. Transcriptomic profiling was performed by RNA sequencing, followed by validation of representative genes using quantitative real-time polymerase chain reaction. Functional effects were evaluated in astrocytes and neuron-astrocyte coculture systems, and the involvement of <i>Drd2</i> was examined using genetic knockdown approaches.</p><p><strong>Results: </strong>Carbenoxolone reduced infarct volume and improved neurological outcomes both in the acute phase and 14 days after cerebral ischemia-reperfusion in rats. RNA sequencing revealed that carbenoxolone attenuated inflammatory signaling and reduced the expression of reactive astrocyte markers, including interleukin-1 beta and <i>Cd44</i>. RNA sequencing identified <i>Drd2</i> as a prominently upregulated gene in carbenoxolone-treated rats compared with saline controls. These transcriptional changes were validated at both the mRNA level by quantitative real-time polymerase chain reaction and the protein level by Western blotting. Functionally, under oxygen-glucose deprivation/reperfusion conditions, carbenoxolone enhanced cell survival in astrocytes and neuron-astrocyte cocultures, but not in neurons alone, indicating an astrocyte-mediated protective effect. Genetic silencing of <i>Drd2</i> increased the reactive astrocyte marker Cd44 (cluster of differentiation 44) under basal conditions and partially attenuated carbenoxolone-induced cytoprotection after oxygen-glucose deprivation/reperfusion.</p><p><strong>Conclusions: </strong>Carbenoxolone modulates postischemic inflammatory responses and reactive astrocyte-associated programs, with evidence supporting a role for <i>Drd2</i> signaling in these effects. These findings provide mechanistic insight into carbenoxolone-mediated neuroprotection and suggest <i>Drd2</i> signaling as a potential therapeutic target in ischemic brain injury.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128357","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":"Subjective Social Status and Outcomes After Stroke: A Prospective Cohort Study.","authors":"Doo Young Kim, E Alison Holman, Steven C Cramer","doi":"10.1161/STROKEAHA.126.056914","DOIUrl":"10.1161/STROKEAHA.126.056914","url":null,"abstract":"<p><strong>Background: </strong>Subjective social status (SSS) represents self-perceived social position and may affect poststroke recovery. Despite impacting various medical outcomes, SSS remains understudied in stroke. We hypothesized that higher SSS is associated with better stroke recovery at 3- and 12 months poststroke.</p><p><strong>Methods: </strong>In this prospective cohort study, patients were enrolled between October 2016 and February 2020. We examined associations between 3-month SSS score and clinician-reported, performance, and patient-reported outcomes at 3- and 12-month assessments. Ordinal multivariable regression analysis evaluated 3-month SSS score as a predictor of 12-month modified Rankin Scale score.</p><p><strong>Results: </strong>The 494 participants had a median age of 63.5 years; 200 (41%) were female, and median (interquartile range) acute National Institutes of Health Stroke Scale score was 4 (2-8). Scores on SSS showed no meaningful associations with performance outcomes and some associations with clinician-reported outcomes (eg, 3-month modified Rankin Scale: ρ, -0.12 [95% CI, -0.21 to -0.03], false discovery rate-adjusted <i>P</i>=0.017; 12-month modified Rankin Scale: ρ_12mo, -0.18 [95% CI, -0.27 to -0.09], false discovery rate-adjusted <i>P</i>=0.001). Conversely, higher SSS showed strong, consistent correlations with patient-reported outcomes, including less psychological distress and higher Stroke Impact Scale-Activities of Daily Living (ρ_3mo, 0.18 [95% CI, 0.09-0.26]; ρ_12mo, 0.17 [95% CI, 0.07-0.26]; all false discovery rate-adjusted <i>P</i><0.05). Item-level analyses of Stroke Impact Scale-Activities of Daily Living revealed that SSS remained most strongly and consistently linked to complex Stroke Impact Scale-Activities of Daily Living motor tasks over time. In ordinal multivariable regression adjusted for age, sex, stroke subtype, initial severity, and the selected objective socioeconomic status proxies (eg, educational attainment, employment, and marital status), 3-month SSS score significantly predicted 12-month modified Rankin Scale score (β, 0.14 [95% CI, 0.02-0.26]; <i>P</i>=0.014).</p><p><strong>Conclusions: </strong>In patients with predominantly mild stroke, 3-month SSS score may serve as a significant social determinant of health that is associated with long-term functional recovery, a relationship closely linked with psychological distress. SSS scores at 3 months poststroke may identify vulnerable patients, enabling development, validation, and targeted application of interventions that optimize stroke recovery.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128500","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":"Persistence of Association of Blood Biomarkers With Risk of Recurrent Stroke on Long-Term Follow-Up: Population-Based Study.","authors":"Linxin Li, Annette I Burgess, Julia Duerden, Katherine Onions, Helen C Segal, Peter M Rothwell","doi":"10.1161/STROKEAHA.126.056325","DOIUrl":"10.1161/STROKEAHA.126.056325","url":null,"abstract":"<p><strong>Background: </strong>Raised inflammatory biomarkers predict an increased short-term risk of recurrent vascular events after stroke or transient ischemic attack, but it is uncertain whether the hazard is maintained thereafter. In the absence of previous population-based studies, we aimed to determine the predictive value of biomarkers for the long-term risk of recurrent stroke in intensively treated patients following transient ischemic attack or stroke.</p><p><strong>Methods: </strong>We studied 12 blood biomarkers related to inflammation, neuronal cell damage, and thrombosis soon after transient ischemic attack or stroke in a population-based study (OXVASC [Oxford Vascular Study]; 2002-2011) with follow-up to 2025. We used Cox and negative binomial regressions to assess associations between each log-transformed biomarker (per SD increase) and recurrent stroke (first event and total number), adjusted for age, sex, and baseline vascular risk factors.</p><p><strong>Results: </strong>Of 1292 consecutive patients (mean/SD age, 73.1/13.2 years; 47.8% male), 365 recurrent strokes occurred in 280 patients during 11 336 patient-years. All inflammatory biomarkers were associated with 10-year risk of recurrence, with little impact of adjustment for other risk factors (adjusted incidence rate ratio: IL-6 [interleukin-6], 1.21 [95% CI, 1.04-1.42]; CRP [C-reactive protein], 1.29 [95% CI, 1.11-1.49]; TNFR-1 [tumor necrosis factor receptor-1], 1.24 [95% CI, 1.05-1.46]; and NGAL [neutrophil gelatinase-associated lipocalin], 1.15 [95% CI, 0.99-1.33]). Moreover, number of elevated (top quartile) inflammatory markers was associated with higher burden of recurrence (incidence rate ratio, 1.31 [95% CI, 1.15-1.50]; <i>P</i><0.001), with no diminution over time (90 days: hazard ratio, 1.24 [95% CI, 0.98-1.57]; 90 days-1 year: 1.24 [95% CI, 0.95-1.62]; 1-5 years: 1.22 [95% CI, 1.01-1.47]; and 5-10 years: 1.34 [95% CI, 1.06-1.68]), and similar associations for transient ischemic attack and minor stroke. Biomarkers related to neuronal cell damage or thrombosis were generally less predictive of recurrent stroke.</p><p><strong>Conclusions: </strong>Inflammatory biomarkers were more predictive of long-term recurrent stroke than neuronal or thrombotic biomarkers, particularly when several inflammatory markers were raised. Predictive value was independent of other vascular risk factors and did not diminish with duration of follow-up, supporting trials of anti-inflammatory strategies for long-term secondary prevention.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"3035-3045"},"PeriodicalIF":11.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13619134/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148664518","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":"Colchicine for the Prevention of Vascular Events After an Acute Intracerebral Hemorrhage: A Placebo-Controlled Trial.","authors":"Aristeidis H Katsanos, Kelvin K H Ng, Thalia S Field, Aravind Ganesh, Joanna D Schaafsma, Shirin Jalini, Ashfaq Shuaib, Lauren M Mai, Amy Y X Yu, Laura C Gioia, Regan Cooley, Dar Dowlatshahi, Abhilekh Srivastava, Georgios Tsivgoulis, Angela Wang, Kumar Balasubramanian, Kevin W Reeh, Amanda Taylor, Robert G Hart, Ashkan Shoamanesh","doi":"10.1161/STROKEAHA.126.055934","DOIUrl":"10.1161/STROKEAHA.126.055934","url":null,"abstract":"<p><strong>Background: </strong>There is a need for novel treatments that lower the risk of major adverse cardiovascular events and secondary inflammatory brain injury after an intracerebral hemorrhage (ICH).</p><p><strong>Methods: </strong>We performed a double-blind, placebo-controlled, pilot randomized clinical trial at 11 centers across Canada to determine the feasibility of testing colchicine after an acute ICH. We recruited adults presenting within 48 hours of ICH onset with vascular neuroimaging evidence or risk factors for atherosclerosis. Participants were randomized to oral colchicine 0.5 mg daily or placebo and followed to a common study termination date. The primary feasibility outcome was the recruitment rate (participants/center per year). Secondary feasibility outcomes included retention of participants at 6 months and medication adherence at 12 months. This trial is registered (URL: https://www.clinicaltrials.gov; Unique identifier: NCT05159219).</p><p><strong>Results: </strong>Between August 2022 and March 2024, 52 participants were allocated to colchicine 0.5 mg daily and 48 participants to placebo daily. Participants were, on average, 68 years old, and 60% were male. The mean time from ICH onset to randomization was 35 hours. The average recruitment rate was 8.9 participants/site per year. Retention at 6 months was 92% (colchicine 91% versus placebo 93%). Following randomization, 14 participants (27%) in the colchicine group and 13 participants (27%) in the placebo group permanently discontinued the study drug. Excluding participants who died or permanently discontinued the study intervention, 12-month medication adherence was 97%, with similar rates between the colchicine and placebo groups (100% versus 93%). We detected no difference in predefined exploratory efficacy or safety end points between the 2 groups over the median follow-up time of 364 days.</p><p><strong>Conclusions: </strong>It is feasible to test low-dose colchicine after an acute ICH. Future randomized clinical trials should account for the high rates of early permanent study drug discontinuation in this patient population.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT05159219.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"2971-2980"},"PeriodicalIF":11.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13619137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148679982","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":"Independent Association of RNF213 p.R4810K With Extracranial Carotid Artery Disease Beyond Intracranial Atherosclerosis.","authors":"Masamitsu Takashima, Takuya Kiyohara, Kuniyuki Nakamura, Yuichi Ozaki, Fumitaka Yoshino, Go Hashimoto, Masaoki Hidaka, Noriyuki Sahara, Fumi Irie, Yoshinobu Wakisaka, Ryu Matsuo, Masahiro Kamouchi, Tetsuro Ago","doi":"10.1161/STROKEAHA.126.055878","DOIUrl":"10.1161/STROKEAHA.126.055878","url":null,"abstract":"<p><strong>Background: </strong>The <i>RNF213</i> p.R4810K variant, a susceptibility variant for moyamoya disease, has also been linked to intracranial atherosclerotic disease (ICAD). However, its association with extracranial carotid artery disease (ECAD), particularly whether this association is independent of concomitant ICAD and whether it differs by stenosis severity, remains unclear.</p><p><strong>Methods: </strong>We conducted a multicenter registry-based observational study of patients with acute ischemic stroke (AIS) or transient ischemic attack enrolled in the Fukuoka Stroke Registry. Patients were genotyped for <i>RNF213</i> p.R4810K and classified as noncarriers (G/G) or variant carriers (G/A or A/A). ECAD was defined as ≥50% stenosis or occlusion of the extracranial carotid arteries. Multivariable logistic regression was used to assess the association between <i>RNF213</i> p.R4810K and ECAD after adjusting for vascular risk factors and ICAD, and stratified analyses were performed by ICAD status. ECAD severity was modeled ordinally (none, moderate, severe, and occlusion) using a partial proportional-odds model.</p><p><strong>Results: </strong>Of 15 569 registry patients with AIS or transient ischemic attack, 13 994 were included in the present analysis after exclusions (mean age, 73±12 years; 59.5% men). The <i>RNF213</i> p.R4810K variant was identified in 359 patients (2.6%). ECAD was present in 2181 patients (15.6%), including 78 variant carriers. Variant carriers had significantly higher odds of ECAD after adjustment for vascular risk factors and ICAD (odds ratio, 1.69 [95% CI, 1.29-2.22]). This association was consistent irrespective of ICAD status (<i>P</i>_{heterogeneity}=0.32). In severity analyses, the association strengthened stepwise with increasing ECAD severity; the largest effect estimate was for occlusion (odds ratio, 4.55 [95% CI, 2.81-7.38]).</p><p><strong>Conclusions: </strong>The <i>RNF213</i> p.R4810K variant was associated with ECAD independent of concomitant ICAD and showed a graded association with ECAD severity. Extracranial disease expression may involve modifiers distinct from those driving ICAD.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"3046-3054"},"PeriodicalIF":11.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148819476","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":"Prevalence and Clinical Relevance of Antiphospholipid Antibodies in Ischemic Stroke: A Systematic Review and Meta-Analysis.","authors":"Nathan W Watson, Syed Bukhari, Sina Rashedi, Mariana Pfeferman, Francisco Ujueta, Bassil Bacare, Brittany N Weber, Mehrdad Zarghami, Yogendra Kanthi, Eric A Secemsky, Jean M Connors, Geoffrey D Barnes, Sacha Uljon, Samuel Z Goldhaber, Jeffrey I Weitz, Karen H Costenbader, Harlan M Krumholz, Gregory Piazza, Mary Cushman, Christopher D Anderson, Mitchell S V Elkind, Behnood Bikdeli","doi":"10.1161/STROKEAHA.126.055247","DOIUrl":"10.1161/STROKEAHA.126.055247","url":null,"abstract":"<p><strong>Background: </strong>Antiphospholipid antibodies (aPL) are associated with an increased risk of thrombosis. However, individual studies have reported conflicting findings regarding the prevalence of aPL in patients with ischemic stroke and their association with first or recurrent events.</p><p><strong>Methods: </strong>Systematic searches of PubMed and Embase through May 13, 2025 were conducted to identify case-control, cohort, or cross-sectional studies investigating 3 questions related to aPL seropositivity (defined as positivity for either immunoglobulin G/immunoglobulin M anticardiolipin antibody, immunoglobulin G/immunoglobulin M anti-β2 glycoprotein I antibody, or a lupus anticoagulant): (1) the prevalence of aPL seropositivity among individuals with ischemic stroke; (2) the association between aPL seropositivity and the risk of first ischemic stroke; and (3) the association between aPL seropositivity and the risk of recurrent ischemic stroke. Random-effects models with inverse weighting were used to calculate pooled prevalences and odds ratios (OR) with 95% CIs. Risk of bias was assessed using the ROBINS-I tool.</p><p><strong>Results: </strong>A total of 52 studies were included (40 case-control, 12 cohort). The pooled prevalence of seropositivity for any aPL among patients with ischemic stroke (51 studies, 9438 patients) was 19.1% (95% CI, 15.4%-23.0%; <i>I</i>²=95.8%). aPL seropositivity was associated with higher odds of first ischemic stroke (43 studies, 19 097 patients; OR, 2.93 [95% CI, 2.31-3.73]; <i>I</i>²=68.7%). The strongest associations were for lupus anticoagulant (OR, 6.69 [95% CI, 2.94-15.2]; <i>I</i>²=92.6%) and immunoglobulin G anticardiolipin antibody (OR, 2.56 [95% CI, 1.96-3.35]; <i>I</i>²=92.5%). The odds of recurrent ischemic stroke among patients with versus without any aPL seropositivity were not significantly different (OR, 1.20 [95% CI, 0.87-1.67]; 9 studies, 2873 patients, <i>I</i>²=11.4%).</p><p><strong>Conclusions: </strong>Seropositivity for any aPL was present in nearly 1-in-5 patients with ischemic stroke and was associated with increased odds of ischemic stroke at presentation.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"3024-3034"},"PeriodicalIF":11.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13528693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148841265","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":"Antithrombotic Therapy in Secondary Stroke Prevention: 10 Clinical Pearls Every Clinician Should Know.","authors":"Matteo Foschi, Lucio D'Anna, Federico De Santis, Raffaele Ornello, Simona Sacco","doi":"10.1161/STROKEAHA.126.056567","DOIUrl":"https://doi.org/10.1161/STROKEAHA.126.056567","url":null,"abstract":"","PeriodicalId":21989,"journal":{"name":"Stroke","volume":"57 10","pages":"e491-e494"},"PeriodicalIF":11.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075946","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":"Beyond the Threshold: Continuous Creatinine Change and Outcomes After Endovascular Thrombectomy for Acute Ischemic Stroke.","authors":"Ghil Schwarz, Angelo Cascio Rizzo, Gareth Ambler, Pawel Wrona, Agnieszka Slowik, Aleksandra Bodzioch, Mohamed F Doheim, Alhamza R Al-Bayati, Raul G Nogueira, Ana Paiva Nunes, Patricia Ferreira, Matteo Paolucci, Andrea Zini, Luigi Simonetti, Norbert Leško, Jakub Fedorko, Zuzana Gdovinová, Luca Scarcia, Erwah Kalsoum, Firas Farhat, Morin Beyeler, Adnan Mujanovic, Marcel Arnold, Torcato Meira, Marta Morais, Leonor Francisco, Marcin Wiącek, Paulina Pudło, Halina Bartosik-Psujek, Patricia Calleja, Fernando Ostos, David Seoane, Negrila Anca, Razvan Alexandru Radu, Cristina Tiu, Sami Al Kasab, Ahmad Abu Qdais, Imad Samman Tahhan, Oscar Ayo-Martin, Francisco Hernández-Fernández, Maria Paya, Juan David Molina-Nevo, Beata Maria Labuz-Roszak, Danilo Toni, Karolina Moszko, Mateusz Łukasz Roszak, Manuela De Michele, Elena Barrile, Prasanna Eswaradass, Margaret L Houghton, Tiffany Barkley, Amir Ali, Jelle Demeestere, Wayne Martin Bauknight, Sunil Anil Sheth, Louise Maes, Anke Wouters, João Pedro Marto, José Blazer Costa, Nicola Davide Loizzo, Andrea Romi, Carmelo Tiberio Currò, Piotr Luchowski, Maksymilian Seweryn, Konrad Rejdak, Piers Klein, Mohamad Abdalkader, Valentina Saia, Antioco Sanna, Tiziana Tassinari, Maurizio Acampa, Francesca Rosini, Rossana Tassi, Marta Ewa Bilik, Anna Maria Bandzarewicz-Samcik, Jiangyong Min, Naser HajAissa, Marilena Mangiardi, Sabrina Anticoli, Enrico Pampana, Carlos Hervás-Testal, Ricardo Rigual, Blanca Fuentes, Davide Strambo, Carl Manuata Tetaria, Guillaume Saliou, Andrea Salvatore Caramma, Davide Maimone, Pier Andrea Rizzo, Marco Moci, Irene Scala, Antonio Cruz-Culebras, Rocío Vera Lechuga, Sebastian Garcia Madrona, Giovanni Merlino, Mariarosaria Valente, Arianna Todesco, Manuel Bolognese, Lehel-Barna Lakatos, Grzegorz Marek Karwacki, Paolo Candelaresi, Vincenzo Andreone, Carlo Maurea, Roberto Tarletti, Angelica Mele, Antonio Ciacciarelli, Michele Alessiani, Gabriella Monteforte, David Pakizer, Martin Roubec, David Školoudík, Fenne Vandervorst, Sylvie De Raedt, Martijn Verdam, Josef Bartoš, Martin Šrámek, Valentina Mazzoleni, Luca Quilici, Dario Alimonti, Jessica Moller, Ilaria Maestrini, Marina Diomedi, Giordano Lacidogna, Osama O Zaidat, Eugene Lin, Mohammad AlMajali, Claudio Baracchini, Matteo Zaccagnino, Federica Viaro, Alessandro Pezzini, Giulia Avola, Chiara Ferraro, Milena Świtońska, Paulina Sobieszak-Skura, Grzegorz Meder, Lukas Mayer-Suess, Michael Knoflach, Elke Ruth Gizewski, Matthew R Common, Patrick Nicholson, Sarah Power, Marta Małgorzata Nowakowska-Kotas, Michał Pula, Maciej Guzinski, Soledad Pérez Sánchez, Joan Montaner, Alexandra Sevilla Bravo, Simona Marcheselli, Francesca Vodret, Costanza Rapillo, Liliana Pereira, Miguel Rodrigues, Adam Jaros, Martin Kovar, Jan Vojik, Gloria Valcamonica, Serena Gallo Cassarino, Alessandra Cardillo, Marco Petruzzellis, Silvia Grimaldi, Nicola Marrone, Ameer E Hassan, Samantha Miller, Mohammad W Khasawneh, Valentina Poretto, Simone Tonello, Saverio Tollot, Aleksander Dębiec, Jacek Staszewski, Adam Stepien, Francisco Bernardo, Jorge Ferrao, Marialuisa Zedde, Rosario Pascarella, Alessandra Sanna, Rossella Meloni, Kati Delibas, Simona Sacco, Maria Grazia Vittorini, Raffaele Ornello, Marina Mannino, Valeria Terruso, Marco Filizzolo, Emily Hall, Christine Roffe, Małgorzata Dorobek, Justyna Zielinska-Turek, Giuseppe Scopelliti, Leonardo Pantoni, Guglielmo Carlo Pero, Antonio Macera, Amedeo Cervo, Simone Bellavia, Marco Longoni, Mine Sezgin, Yavuz Dilmen, Esme Ekizoglu, Georgios Tsivgoulis, Aikaterini Theodorou, Vlad Eugen Tiu, Cristina Aura Panea, Simona Petrescu, Mariangela Piano, Thanh N Nguyen, Maria Sessa","doi":"10.1161/STROKEAHA.126.056847","DOIUrl":"https://doi.org/10.1161/STROKEAHA.126.056847","url":null,"abstract":"<p><strong>Background: </strong>Contrast-associated acute kidney injury (CA-AKI) after endovascular thrombectomy (EVT) worsens outcomes in acute ischemic stroke, but threshold-based definitions do not capture prognostic information from subthreshold changes. We tested whether early creatinine change within 48 hours of EVT conveys graded prognostic information beyond dichotomous CA-AKI.</p><p><strong>Methods: </strong>We performed a secondary analysis of the CAN-REST (Contrast-Associated Nephropathy After Endovascular Stroke Treatment; REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT06596603) registry, a retrospective multicenter observational cohort study of 6638 EVT-treated adults with acute ischemic stroke enrolled at 73 centers in 16 countries between January 1 and December 31, 2023. Early creatinine change was quantified as the natural logarithm ratio of 48-hour creatinine to baseline creatinine (ln[48-hour/baseline creatinine]), with CA-AKI defined per Kidney Disease: Improving Global Outcomes criteria (≥0.3 mg/dL or ≥1.5× baseline rise within 48 hours). Multivariable logistic regression adjusted for prespecified baseline and periprocedural covariates examined associations with 90-day modified Rankin Scale shift and in-hospital mortality; linear versus restricted cubic spline specification was selected by likelihood ratio testing, and contrasts were estimated at ±10%, ±25%, and ±50%.</p><p><strong>Results: </strong>Greater creatinine worsening within 48 hours of EVT was independently associated with an unfavorable 90-day modified Rankin Scale shift (adjusted common odds ratio per 1-unit log-ratio increase, 1.48 [95% CI, 1.07-2.04]; linear) and in-hospital mortality (nonlinear dose-response, of larger magnitude). A 10% increase in creatinine at 48 hours-well below Kidney Disease: Improving Global Outcomes threshold-was associated with worse functional outcome (adjusted common odds ratio, 1.04 [95% CI, 1.01-1.07]) and death (adjusted odds ratio, 1.22 [95% CI, 1.13-1.32]); a 10% decrease in creatinine at 48 hours was associated with lower odds of both outcomes (adjusted common odds ratio, 0.96 [95% CI, 0.93-0.99] and 0.74 [95% CI, 0.65-0.86]). The functional-outcome association concentrated at upper modified Rankin Scale cut-points (severe disability, death); effect modification by baseline renal function was not significant.</p><p><strong>Conclusions: </strong>Early creatinine change after EVT conveys graded, outcome-specific prognostic information extending below formal CA-AKI thresholds, with a dose-response detectable at changes as modest as ±10%, complementing binary CA-AKI as a framework for post-EVT renal risk assessment.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT06596603.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":""},"PeriodicalIF":11.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149114935","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 Recent Mechanical Risk Factors for Venous Thrombosis and Young-Onset Cryptogenic Ischemic Stroke.","authors":"Julija Valančienė, Pauli Ylikotila, Riikka Lautamäki, Marialuisa Zedde, Teresa Grimaldi, Tomi Sarkanen, Essi Ryödi, Dalius Jatužis, Kristina Ryliškienė, Diana Zakarkaitė, Bettina von Sarnowski, Raila Busch, Lauri Tulkki, Jani Pirinen, Nicolas Martinez-Majander, Radim Licenik, Phillip Ferdinand, Cheryl Oxley, Janika Kõrv, Piibe Muda, Tuukka A Helin, Lotta Joutsi-Korhonen, Tímea Szántó, Alessandro Pezzini, Carlo Mario Lombardi, Georgios Tsivgoulis, Satu Suihko, Heli Tolppanen, Ana Catarina Fonseca, Patricia Martínez-Sánchez, Laura Amaya-Pascasio, Sofie Abels, Frank-Erik de Leeuw, Nilufer Yesilot, Mine Sezgin, Ulrike Waje-Andreassen, Sahrai Saeed, Petra Redfors, Odd Bech-Hanssen, Juha Huhtakangas, Marja Hedman, Pekka Jäkälä, Hugo Ten Cate, Eva Gerdts, Mika Lehto, Juha Sinisalo, Jukka Putaala","doi":"10.1161/STROKEAHA.125.054299","DOIUrl":"10.1161/STROKEAHA.125.054299","url":null,"abstract":"<p><strong>Background: </strong>In young adults, the risk factors (RFs) for cryptogenic ischemic stroke (CIS) remain unclear. We aimed to investigate the association between recent mechanical venous thrombosis RFs (VTRFs) and young-onset CIS in this multicenter sex- and age-matched case-control study.</p><p><strong>Methods: </strong>Five hundred forty-six patients aged 18 to 49 years (median age, 41 [34-46] years; 47.3% women) with a recent CIS and 546 stroke-free community-based controls were included in the study across 19 European centers between October 2013 and November 2022. Mechanical VTRFs, including surgical treatment, nonsurgical intervention, injury, and immobilization occurring within 90 days prestroke, were assessed using standardized, structured interviews. Conditional logistic regression was used to assess the association of mechanical VTRFs with CIS. Age, sex, level of education, and traditional and nontraditional stroke RFs were included as confounders.</p><p><strong>Results: </strong>Mechanical VTRFs within 14 days prestroke were more prevalent in cases than controls (15.4% versus 9.6%) and independently associated with CIS after adjustment for demographics and traditional stroke RFs (odds ratio [OR], 1.67 [95% CI, 1.05-2.67]). In age-stratified analysis, this association remained significant after additional adjustment for nontraditional RFs in 18- to 39-year-olds (OR, 2.36 [95% CI, 1.02-5.46]) but was not significant in the 40- to 49-year age group (OR, 1.50 [95% CI, 0.73-3.08]). In addition, mechanical VTRFs were associated with CIS in cases with clinically relevant patent foramen ovale in a fully adjusted model (OR, 2.06 [95% CI, 1.21-3.51]) but not in those without (OR, 1.29 [95% CI, 0.76-2.18]). No significant associations were observed for mechanical VTRFs occurring >14 days before stroke. Baseline blood thrombophilia markers did not differ between cases with and without mechanical VTRFs 0 to 14 or 15 to 90 days before stroke.</p><p><strong>Conclusions: </strong>Recent mechanical VTRFs occurring within 14 days preceding stroke contribute to the risk of young-onset CIS, particularly in younger individuals and those with a clinically relevant patent foramen ovale. This risk does not appear to be conveyed by thrombophilic factors assessed.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT01934725.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"3010-3023"},"PeriodicalIF":11.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13619135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148819449","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":"Evidence Update for Minimally Invasive Surgical Evacuation of Supratentorial Spontaneous Intracerebral Hemorrhage: A Science Advisory From the American Heart Association.","authors":"Stacey Q Wolfe, Sepideh Amin-Hanjani, Christine Tschoe, Scott D Simon, Christopher P Kellner, Kevin N Sheth","doi":"10.1161/STR.0000000000000529","DOIUrl":"10.1161/STR.0000000000000529","url":null,"abstract":"<p><p>Recent evidence has reignited interest in the role of surgical intervention for improving outcomes after spontaneous intracerebral hemorrhage. Historically, the surgical management of intracerebral hemorrhage has been limited due to concerns regarding procedural risks and lack of functional improvement. However, recent advances in minimally invasive surgical techniques suggest improvements in functional recovery, broadening consideration for surgical treatment of certain patients, such as those with lobar hemorrhage after spontaneous intracerebral hemorrhage. This science advisory summarizes randomized evidence for minimally invasive surgical evacuation of intracerebral hemorrhage compared with medical management, including considerations related to patient selection, care pathways, and surgical technique.</p>","PeriodicalId":21989,"journal":{"name":"Stroke","volume":" ","pages":"e659-e669"},"PeriodicalIF":11.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809070","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}