TY - RPRT A1 - McCarron, R. M. A1 - Doron, D. A. A1 - Sirén, Anna-Leena A1 - Feuerstein, G. Z. A1 - Heldman, E. A1 - Pollard, H. B. A1 - Spatz, M. A1 - Hallenbeck, J. M. T1 - Agonist-stimulated release of von Willebrand factor and procoagulant factor VIII in rats with and without risk factors for stroke [Research Report] N2 - Lipopolysaccharidc (LPS)-induced (i.v. or i.c.v., 1.8 mg/kg) release of von Willebrand factor (vWF) ·was examined in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. SHR rats releascd significantly (P < 0.05) more vWF than WKY rats in response to LPS. LPS also inhibited factor VIII procoagulant activity (FVIII: c) which may indicate an increase in thrombin activity. Cultured cerebrovascular endothelial cells (EC) derived from both SHR and WKY rats, as weil as human umbilical vein EC (HUVEC) cultures constitutively released vWF. Treatment with agonists including LPS, thrombin and tumor necrosis factor-a (TNFa) did not affect the in vitro secretion of vWF by cerebrovascular EC cultures but significantly upregulated vWF release by HUVEC cultur~s. Preincubation of cerebrovascular EC cultures with interleukin-1 OL-l) ± TNFa or co-culturing in the presence of LPS-activated syngeneic monocytes had no effect on vWF secretion. The findings demoostrate that conditions of hypertension may affect endothelial cells and make them more responsive to agonist Stimulation and thereby increase secretion of vWF, an important factqr in hemostasis as weil as thrombosis. The capacity of LPS to significantly affect the in vivo secretion of vWF in SHR and WKY rats but not cultured cerebrovascular EC indicates that observed elevations in plasma vWF were not derived from cerebrovascular EC. lt is suggested that hypertension may function as a risk factor for thrombotic stroke by influencing factors involved in coagulation processes, such as vWF and factor VIII : c. KW - Neurobiologie KW - von Willebrand factor KW - Hypertension KW - Lipopolysaccharide KW - Endothelial cell KW - Stroke KW - Monocyte Y1 - 1994 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-62945 ER - TY - JOUR A1 - Kleinschnitz, Christoph A1 - Göbel, Kerstin A1 - Meuth, Sven G. A1 - Kraft, Peter T1 - Glatiramer acetate does not protect from acute ischemic stroke in mice N2 - Background The role of the immune system in the pathophysiology of acute ischemic stroke is increasingly recognized. However, targeted treatment strategies to modulate immunological pathways in stroke are still lacking. Glatiramer acetate is a multifaceted immunomodulator approved for the treatment of relapsing-remitting multiple sclerosis. Experimental studies suggest that glatiramer acetate might also work in other neuroinflammatory or neurodegenerative diseases apart from multiple sclerosis. Findings We evaluated the efficacy of glatiramer acetate in a mouse model of brain ischemia/reperfusion injury. 60 min of transient middle cerebral artery occlusion was induced in male C57Bl/6 mice. Pretreatment with glatiramer acetate (3.5 mg/kg bodyweight) 30 min before the induction of stroke did not reduce lesion volumes or improve functional outcome on day 1. Conclusions Glatiramer acetate failed to protect from acute ischemic stroke in our hands. Further studies are needed to assess the true therapeutic potential of glatiramer acetate and related immunomodulators in brain ischemia. KW - Glatiramer acetate KW - Stroke KW - Inflammation KW - Neurodegeneration Y1 - 2014 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-110528 ER - TY - JOUR A1 - Heuschmann, Peter U. A1 - Montellano, Felipe A. A1 - Ungethüm, Kathrin A1 - Rücker, Viktoria A1 - Wiedmann, Silke A1 - Mackenrodt, Daniel A1 - Quilitzsch, Anika A1 - Ludwig, Timo A1 - Kraft, Peter A1 - Albert, Judith A1 - Morbach, Caroline A1 - Frantz, Stefan A1 - Störk, Stefan A1 - Haeusler, Karl Georg A1 - Kleinschnitz, Christoph T1 - Prevalence and determinants of systolic and diastolic cardiac dysfunction and heart failure in acute ischemic stroke patients: The SICFAIL study JF - ESC Heart Failure N2 - Aims Ischaemic stroke (IS) might induce alterations of cardiac function. Prospective data on frequency of cardiac dysfunction and heart failure (HF) after IS are lacking. We assessed prevalence and determinants of diastolic dysfunction (DD), systolic dysfunction (SD), and HF in patients with acute IS. Methods and results The Stroke‐Induced Cardiac FAILure in mice and men (SICFAIL) study is a prospective, hospital‐based cohort study. Patients with IS underwent a comprehensive assessment of cardiac function in the acute phase (median 4 days after IS) including clinical examination, standardized transthoracic echocardiography by expert sonographers, and determination of blood‐based biomarkers. Information on demographics, lifestyle, risk factors, symptoms suggestive of HF, and medical history was collected by a standardized personal interview. Applying current guidelines, cardiac dysfunction was classified based on echocardiographic criteria into SD (left ventricular ejection fraction < 52% in men or <54% in women) and DD (≥3 signs of DD in patients without SD). Clinically overt HF was classified into HF with reduced, mid‐range, or preserved ejection fraction. Between January 2014 and February 2017, 696 IS patients were enrolled. Of them, patients with sufficient echocardiographic data on SD were included in the analyses {n = 644 patients [median age 71 years (interquartile range 60–78), 61.5% male]}. In these patients, full assessment of DD was feasible in 549 patients without SD (94%). Prevalence of cardiac dysfunction and HF was as follows: SD 9.6% [95% confidence interval (CI) 7.6–12.2%]; DD in patients without SD 23.3% (95% CI 20.0–27.0%); and clinically overt HF 5.4% (95% CI 3.9–7.5%) with subcategories of HF with preserved ejection fraction 4.35%, HF with mid‐range ejection fraction 0.31%, and HF with reduced ejection fraction 0.78%. In multivariable analysis, SD and fulfilment of HF criteria were associated with history of coronary heart disease [SD: odds ratio (OR) 3.87, 95% CI 1.93–7.75, P = 0.0001; HF: OR 2.29, 95% CI 1.04–5.05, P = 0.0406] and high‐sensitive troponin T at baseline (SD: OR 1.78, 95% CI 1.31–2.42, P = 0.0003; HF: OR 1.66, 95% CI 1.17–2.33, P = 0.004); DD was associated with older age (OR 1.08, 95% CI 1.05–1.11, P < 0.0001) and treated hypertension vs. no hypertension (OR 2.84, 95% CI 1.23–6.54, P = 0.0405). Conclusions A substantial proportion of the study population exhibited subclinical and clinical cardiac dysfunction. SICFAIL provides reliable data on prevalence and determinants of SD, DD, and clinically overt HF in patients with acute IS according to current guidelines, enabling further clarification of its aetiological and prognostic role. KW - Stroke KW - Heart failure KW - Cardiac dysfunction| Brain natriuretic peptide KW - Troponin Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-225656 VL - 8 IS - 2 ER - TY - THES A1 - Beaucamp, Marcel T1 - Prädiktion des Verschlusses großer intrakranieller Arterien anhand präklinischer Schlaganfallscores T1 - Prediction of large vessel oclusions by using preclinical stroke scores N2 - 2015 konnte in mehreren Studien ESCAPE, EXTENDED IA, MR CLEAN, REVASCAT, SWIFT-PRIME eine signifikante Überlegenheit der mechanischen Thrombektomie verglichen mit der alleinigen i. v. Lysetherapie mit rtPA bezogen auf Revaskularisierung bei Patienten mit einer LVO (large vessel occlusion) nachgewiesen werden. Diese neue Therapiemöglichkeit erforderte eine Aufteilung der Patienten die von einer Thrombektomie profitieren (LVO) und der Patienten, die keiner Thrombektomie zugeführt werden können (nLVO). Die zentrale Fragestellung der Studie ist: Kann ein symptomorientierter Schlaganfallscore die Wahrscheinlichkeit eines großen intrakraniellen Gefäßverschlusses mit hinreichender Präzision vorhersagen und kann auf Basis dieser Vorhersage ein Patient direkt in ein übergeordnetes Schlagfanfallzentrum gebracht werden, obwohl sich dadurch eine Bridging Lysetherapie verzögern würde? Um diesen Fragen auf den Grund zu gehen führten wir eine monozentrische Querschnittstudie durch, in deren Rahmen 215 Patienten rekrutiert wurden. Die Rekrutierung erfolgte mittels eines aus Subitems bereits etablierter Schlafanfallscores (FAST, CPSS, LAPSS, 3ISS, RACE), zusammengesetzten Fragebogens. Die ausgefüllten Fragebögen wurde in Excel digitalisiert und mittels SPSS, Signifikanz und Odds Ratio berechnet. Anschließend wurde aus den signifikanten Subitems mit der höchsten Odds Ratio ein neuer einfach anzuwendender Schlaganfallscore, bestehend aus den präklinisch erhobenen Daten gebildet (Würzburg Score of Large Vessel Occlusions, WOLVE- Score). Weiter wurden Signifikanz, Odds Ratio, Sensitivität und Spezifität des WOLVE-Score mit denen der oben genannten etablieren Scores verglichen. N2 - 2015 several publications ESCAPE, EXTENDED IA, MR CLEAN, REVASCAT, SWIFT-PRIME proofed a significant superiority of the mechanical thrombectomy in Patients suffering from a LVO (large vessel occlusion) concerning revascularization rates compared to i. v. thrombolysis with rtPA, alone. This newly discovered therapy required a new distribution of patients who could profit from a thrombectomy (LVO) and those who would not profit from a thrombectomy (nLVO). The key question is: Can a symptom related stroke score predict the probability of a large vessel occlusion with a sufficient precision and is it possible to admit a patient to a comprehensive stroke center based on this prediction, even though an early bridging thrombolysis is delayed. To answer this question we performed a cross-sectional study in which 215 patients were recruited by using a composite questionnaire consisting of subitems from established stroke scores (FAST, CPSS, LAPSS, 3ISS, RACE). The questionnaire was digitalized in Ecxel. Statistical calculations of the significancy and the odds ratio were conducted in SPSS. The significant subitems with the highest odds ratio were used to construct a new simple stroke score for LVO recognition in the field (Würzburg Score of Large Vessel Occlusions, WOLVE- Score). Eventually the significancy, odds ratio sensitivity and specificity of the WOLVE-Score were calculated and compared to the ones of the established scores. KW - Schlaganfall KW - Gefäßverschluss KW - Score KW - Thrombektomie KW - Revaskularisierung KW - Stroke KW - Score KW - LVO Y1 - 2021 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-215117 ER - TY - JOUR A1 - Padberg, Inken A1 - Knispel, Petra A1 - Zöllner, Susanne A1 - Sieveking, Meike A1 - Schneider, Alice A1 - Steinbrink, Jens A1 - Heuschmann, Peter U. A1 - Wellwood, Ian A1 - Meisel, Andreas T1 - Social work after stroke: identifying demand for support by recording stroke patients' and carers' needs in different phases after stroke JF - BMC Neurology N2 - Background Previous studies examining social work interventions in stroke often lack information on content, methods and timing over different phases of care including acute hospital, rehabilitation and out-patient care. This limits our ability to evaluate the impact of social work in multidisciplinary stroke care. We aimed to quantify social-work-related support in stroke patients and their carers in terms of timing and content, depending on the different phases of stroke care. Methods We prospectively collected and evaluated data derived from a specialized “Stroke-Service-Point” (SSP); a “drop in” center and non-medical stroke assistance service, staffed by social workers and available to all stroke patients, their carers and members of the public in the metropolitan region of Berlin, Germany. Results Enquiries from 257 consenting participants consulting the SSP between March 2010 and April 2012 related to out-patient and in-patient services, therapeutic services, medical questions, medical rehabilitation, self-help groups and questions around obtaining benefits. Frequency of enquiries for different topics depended on whether patients were located in an in-patient or out-patient setting. The majority of contacts involved information provision. While the proportion of male and female patients with stroke was similar, about two thirds of the carers contacting the SSP were female. Conclusion The social-work-related services provided by a specialized center in a German metropolitan area were diverse in terms of topic and timing depending on the phase of stroke care. Targeting the timing of interventions might be important to increase the impact of social work on patient’s outcome. KW - Social support KW - Stroke KW - Rehabilitation KW - Social work KW - Patient-centered care Y1 - 2016 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-164691 VL - 16 IS - 111 ER - TY - RPRT A1 - Wang, X. A1 - Sirén, Anna-Leena A1 - Liu, Y. A1 - Yue, T-L. A1 - Barone, F. C. A1 - Feuerstein, G. Z. T1 - Upregulation of intercellular adhesion molecule-1 (ICAM-1) on brain microvascular endothelial cells in rat ischemic cortex [Research Report] N2 - The expression of intercellular adhesion molecule 1 (ICAM-1) was studied in rat focal ischemic cortex. A significant increase in ICAM-1 mRNA expression in the ischemic cortex over Ievels in contralateral (nonischemic) site was observed by means of Northern blot analysis following either permanent or temporary occlusion with reperfusion of the middle cerebral artery (PMCAO or MCAO with reperfusion) in spontaneously hypertensive rats. In the ischemic cortex, Ievels of ICAM-1 mRNA increased significantly at 3 h (2.6-fold, n = 3, P < 0.05), peaked at 6 to 12 h (6.0-fold, P < 0.01) and remained elevated up to 5 days (2.5-fold, P < 0.05) after PMCAO. The profile of ICAM-1 mRNA expression in the ischemic cortex following MCAO with reperfusion was similar to that following PMCAO, except that ICAM-1 mRNA was significantly increased as early as 1 h (6.3-fold, n = 3, P < 0.05) and then gradually reached a peak at 12 h (12-fold, P < 0.01) after reperfusion. ICAM-1 mRNA expression in ischemic cortex following PMCAO was significantly greater in hypertensive rats than in two normotensive rat strains. Immunostaining using anti-ICAM-1 antiborlies indicated that upregulated ICAM-1 expressionwas localized to endotheIial cells of intraparenchymal blood vessels in the ischemic but not contralateral cortex. The data suggest that an upregulation of ICAM-1 mRNA and protein on brain capillary endothelium may play an important rote in leukocyte migration into ischemic brain tissue. KW - Neurobiologie KW - Intercellular adhesion molecule 1 KW - Focal brain ischemia KW - Stroke KW - Reperfusion KW - lnflammation Y1 - 1994 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-62952 ER -