Database : MEDLINE
Search on : cerebral and infarction [Words]
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[PMID]: 29479056
[Au] Autor:Zhong Z; Wu H; Ye M; Yang Y; Luo W; Wu Y; Wu H; Zhong M; Zhao P
[Ad] Address:Center for Cardiovascular Diseases, Meizhou People's Hospital (Huangtang Hospital), Meizhou Hospital Affiliated to Sun Yat-sen University, Meizhou, Guangdong, China (mainland).
[Ti] Title:Association of APOE Gene Polymorphisms with Cerebral Infarction in the Chinese Population.
[So] Source:Med Sci Monit;24:1171-1177, 2018 Feb 26.
[Is] ISSN:1643-3750
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND Apolipoprotein E (ApoE) is a multifunctional protein that plays an important role in lipoprotein metabolism. However, the relationship between APOE gene polymorphisms and cerebral infarction in the Chinese population remains unclear. Therefore, we studied the role of APOE gene polymorphisms in patients with cerebral infarction in a Chinese population. MATERIAL AND METHODS This study involved 906 patients with cerebral infarction and 1,141 individuals without cerebral infarction who served as controls. APOE genotypes were identified in all participants who participated in the study. Factors influencing cerebral infarction were also analyzed. RESULTS Statistically significant variances in the distribution and frequencies of the APOE genotypes in the patients were observed (ε2/ε3 versus ε2/ε4 versus ε3/ε3=22.85% versus 7.62% versus 56.95%) and controls (ε2/ε3 versus ε2/ε4 versus ε3/ε3=17.27% versus 2.72% versus 66.87%; p<0.001). Univariate analysis showed that the APOE ε3/ε3 genotype [OR, 0.393 (95% CI, 0.237-0.653); p<0.001] and ε3/ε4 genotype [OR, 0.376 (95% CI 0.221-0.637); p<0.001] played a protective role against cerebral infarction in Chinese men. CONCLUSIONS Statistically significant variances in the distribution and frequencies of the APOE genotypes of the patients and controls were observed. The study demonstrated that the APOE ε3/ε3 and ε3/ε4 genotypes played a protective role against cerebral infarction in Chinese men, but not women. Additionally, the ε2/ε4 genotype may be a potential risk factor in men, whereas ε3/ε4 genotype may play a potential protective role against this disease in women.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

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[PMID]: 29458087
[Au] Autor:Zhao H; Zhang Y; Zhang Y; Shen Y; Zhang Y; Bi F; Xiao B; Zhang H; Ye W; Zhang H; Liao Y
[Ad] Address:Department of Neurology, Xiangya Hospital, Central South University, Changsha, China; Department of Neurology, The First Affiliated Hospital of Xiamen University, Xiamen, China.
[Ti] Title:NGF/FAK signal pathway is implicated in angiogenesis after acute cerebral ischemia in rats.
[So] Source:Neurosci Lett;672:96-102, 2018 Feb 16.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Neurogenesis in the cerebral infarction after an ischemic event is important to the rehabilitation of patients. However, the mechanism of angiogenesis around cerebral ischemia is not clear. Our study designed to test whether the nerve growth factor (NGF)-P-focal adhesion kinase (FAK) signaling pathway for associations with angiogenesis plays a key role in post-acute cerebral ischemia of rats. Firstly, we implanted the Matrigel, a carrier of basement membrane matrix, into the abdominal skin of rats to identify the relevant components of the NGF-P-FAK signaling pathway related to angiogenesis. Secondly, we used a model established by ligation of the middle cerebral artery (MCA) to observe the effect of the same signal pathway on angiogenesis in the subventricular and subgranular zones of the dentate gyrus(SVG and SGZ). The results showed that the tissue scores was significantly increased by NGF. However, the tissue scores was signifcaintly decreased by FAK inhibitor TAE226. Furthermore, CD31 and α-SMA were significantly increased by NGF and were decreased by anti-NGF and TAE226 in Matrigel. The P-FAK protein expression in Matrigel was markedly increased by NGF and decreased by TAE226. In the SVZ and SVG of cerebral ischemia, the numbers of BrdU-positive cells were significantly increased by NGF and decreased by TAE226, respectively. Our findings suggest that the therapy targeting the NGF-P-FAK signaling pathway may be an option for patients suffering from cerebral ischemia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29294343
[Au] Autor:Singh S; Houng AK; Reed GL
[Ad] Address:Department of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA. Electronic address: satishsingh@email.arizona.edu.
[Ti] Title:Matrix Metalloproteinase-9 Mediates the Deleterious Effects of α2-Antiplasmin on Blood-Brain Barrier Breakdown and Ischemic Brain Injury in Experimental Stroke.
[So] Source:Neuroscience;376:40-47, 2017 Dec 30.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:During acute brain ischemia, α2-antiplasmin markedly enhances brain injury, blood-brain barrier breakdown and matrix metalloproteinase-9 (MMP-9) expression. Although α2-antiplasmin inhibits fibrin thrombus-degradation, and MMP-9 is a collagen-degrading enzyme altering blood-brain barrier, both have similar deleterious effects on the ischemic brain. We examined the hypothesis that MMP-9 is an essential downstream mediator of α2-antiplasmin's deleterious effects during brain ischemia. Middle cerebral artery thromboembolic stroke was induced in a randomized, blinded fashion in mice with increased blood levels of α2-antiplasmin. There was a robust increase in MMP-9 expression (immunofluorescence) in the ischemic vs. the non-ischemic hemisphere of MMP-9 but not MMP-9 mice, 24 h after stroke. Brain swelling and hemorrhage were significantly increased in the ischemic vs. the non-ischemic hemisphere of MMP-9 mice. By comparison to MMP-9 mice, the ischemic hemispheres of MMP-9 mice showed a ∼6-fold reduction in brain swelling (p < 0.001) and a ∼9-fold reduction in brain hemorrhage. Brain infarction (p < 0.0001) and TUNEL-positive cell death (p < 0.001) were significantly diminished in the ischemic hemisphere of MMP-9 mice vs. MMP-9 mice. Ischemic breakdown of the blood-brain barrier and fibrin deposition were also significantly reduced in MMP-9 mice vs. MMP-9 mice (p < 0.05), as measured by quantitative immunofluorescence. We conclude that MMP-9 deficiency ablates many of the deleterious effects of high α2-antiplasmin levels, significantly reducing blood-brain barrier breakdown, TUNEL-positive cell death, brain hemorrhage, swelling and infarction. This suggests that the two molecules may be in a shared pathway in which MMP-9 is essential downstream for the deleterious effects of α2-antiplasmin in ischemic stroke.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 28456933
[Au] Autor:Tang X; Liu K; Hamblin MH; Xu Y; Yin KJ
[Ad] Address:Pittsburgh Institute of Brain Disorders & Recovery, Department of Neurology, University of Pittsburgh School of Medicine, S514 BST, 200 Lothrop Street, Pittsburgh, PA, 15213, USA.
[Ti] Title:Genetic Deletion of Krppel-Like Factor 11 Aggravates Ischemic Brain Injury.
[So] Source:Mol Neurobiol;55(4):2911-2921, 2018 Apr.
[Is] ISSN:1559-1182
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Krppel-like factors (KLFs) belong to the zinc finger family of transcription factors, and their function in the CNS is largely unexplored. KLF11 is a member of the KLF family, and we have previously demonstrated that peroxisome proliferator-activated receptor gamma-mediated cerebral protection during ischemic insults needs recruitment of KLF11 as its critical coactivator. Here, we sought to determine the role of KLF11 itself in cerebrovascular function and the pathogenesis of ischemic stroke. Transient middle cerebral artery occlusion (MCAO) was performed in KLF11 knockout and wild-type control mice, and brain infarction was analyzed by TTC staining. BBB integrity was assessed by using Evans Blue and TMR-Dextran extravasation assays. KLF11 KO mice exhibited significantly larger brain infarction and poorer neurological outcomes in response to ischemic insults. Genetic deficiency of KLF11 in mice also significantly aggravated ischemia-induced BBB disruption by increasing cerebrovascular permeability and edema. Mechanistically, KLF11 was found to directly regulate IL-6 in the brains of ischemic mice. These findings suggest that KLF11 acts as a novel protective factor in ischemic stroke. Elucidating the functional importance of KLF11 in ischemia may lead us to discover novel pharmacological targets for the development of effective therapies against ischemic stroke.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1705
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1007/s12035-017-0556-9

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[PMID]: 29523650
[Au] Autor:Reidler P; Thierfelder KM; Fabritius MP; Sommer WH; Meinel FG; Dorn F; Wollenweber FA; Duering M; Kunz WG
[Ad] Address:From the Department of Radiology (P.R., K.M.T., M.P.F., W.H.S., W.G.K.) and Department of Neuroradiology (F.D.), University Hospital, LMU Munich, Germany; Institute of Diagnostic and Interventional Radiology, University Medical Center Rostock, Germany (K.M.T., F.G.M.); and Institute for Stroke and D
[Ti] Title:Thalamic Diaschisis in Acute Ischemic Stroke: Occurrence, Perfusion Characteristics, and Impact on Outcome.
[So] Source:Stroke;, 2018 Mar 09.
[Is] ISSN:1524-4628
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND PURPOSE: Ipsilateral thalamic diaschisis (ITD) describes the reduction of thalamic function, metabolism, and perfusion resulting from a distant lesion of the ipsilateral hemisphere. Our aim was to evaluate the perfusion characteristics and clinical impact of ITD in acute middle cerebral artery stroke, which does not directly affect the thalamus. METHODS: One hundred twenty-four patients with middle cerebral artery infarction were selected from a prospectively acquired cohort of 1644 patients who underwent multiparametric computed tomography (CT), including CT perfusion for suspected stroke. Two blinded readers evaluated the occurrence of ITD, defined as ipsilateral thalamic hypoperfusion present on ≥2 CT perfusion maps. Perfusion alterations were defined according to the Alberta Stroke Program Early CT Score regions. Final infarction volume and subacute complications were assessed on follow-up imaging. Clinical outcome was quantified using the modified Rankin Scale. Multivariable linear and ordinal logistic regression analysis were applied to identify independent associations. RESULTS: ITD was present in 25/124 subjects (20.2%, ITD+). In ITD+ subjects, perfusion of the caudate nucleus, internal capsule, and lentiform nucleus was more frequently affected than in ITD- patients (each with <0.001). In the ITD+ group, larger cerebral blood flow ( =0.002) and cerebral blood volume ( <0.001) deficit volumes, as well as smaller cerebral blood flow-cerebral blood volume mismatch ( =0.021) were observed. There was no independent association of ITD with final infarction volume or clinical outcome at discharge in treatment subgroups (each with >0.05). ITD had no influence on the development of subacute stroke complications. CONCLUSIONS: ITD in the form of thalamic hypoperfusion is a frequent CT perfusion finding in the acute phase in middle cerebral artery stroke patients with marked involvement of subcortical areas. ITD does not result in thalamic infarction and had no independent impact on patient outcome. Notably, ITD was misclassified as part of the ischemic core by automated software, which might affect patient selection in CT perfusion-based trials.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 56466 MEDLINE  
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[PMID]: 29523557
[Au] Autor:Jansen IGH; Mulder MJHL; Goldhoorn RB; MR CLEAN Registry investigators
[Ti] Title:Endovascular treatment for acute ischaemic stroke in routine clinical practice: prospective, observational cohort study (MR CLEAN Registry).
[So] Source:BMJ;360:k949, 2018 Mar 09.
[Is] ISSN:1756-1833
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To determine outcomes and safety of endovascular treatment for acute ischaemic stroke, due to proximal intracranial vessel occlusion in the anterior circulation, in routine clinical practice. DESIGN: Ongoing, prospective, observational cohort study. SETTING: 16 centres that perform endovascular treatment in the Netherlands. PARTICIPANTS: 1488 patients included in the Multicentre Randomised Controlled Trial of Endovascular Treatment for Acute Ischaemic Stroke in the Netherlands (MR CLEAN) Registry who had received endovascular treatment, including stent retriever thrombectomy, aspiration, and all alternative methods for acute ischaemic stroke within 6.5 hours from onset of symptoms between March 2014 and June 2016. MAIN OUTCOME MEASURES: The primary outcome was the modified Rankin Scale (mRS) score, ranging from 0 (no symptoms) to 6 (death) at 90 days after the onset of symptoms. Secondary outcomes were excellent functional outcome (mRS score 0-1), good functional outcome (mRS score 0-2), and favourable functional outcome (mRS score 0-3) at 90 days; score on the extended thrombolysis in cerebral infarction scale at the end of the intervention procedure; National Institutes of Health Stroke Scale score 24-48 hours after intervention; and complications that occurred during intervention, hospital admission, or three months' follow up period. Outcomes and safety variables in the MR CLEAN Registry were compared with the MR CLEAN trial intervention and control arms. RESULTS: A statistically significant shift was observed towards better functional outcome in patients in the MR CLEAN Registry compared with the MR CLEAN trial intervention arm (adjusted common odds ratio 1.30, 95% confidence interval 1.02 to 1.67) and the MR CLEAN trial control arm (1.85, 1.46 to 2.34). The reperfusion rate, with successful reperfusion defined as a score of 2B-3 on the extended thrombolysis in cerebral infarction score, was 58.7%, the same as for patients in the MR CLEAN trial. Duration from onset of stroke to start of endovascular treatment and from onset of stroke to successful reperfusion or last contrast bolus was one hour shorter for patients in the MR CLEAN Registry. Symptomatic intracranial haemorrhage occurred in 5.8% of patients in the MR CLEAN Registry compared with 7.7% in the MR CLEAN trial intervention arm and 6.4% in the MR CLEAN trial control arm. CONCLUSION: In routine clinical practice, endovascular treatment for patients with acute ischaemic stroke is at least as effective and safe as in the setting of a randomised controlled trial.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review
[do] DOI:10.1136/bmj.k949

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[PMID]: 29438705
[Au] Autor:Deng L; Wan H; Zhou H; Yu L; He Y
[Ad] Address:Zhejiang Chinese Medical University, Binwen Road, Hangzhou, Zhejiang, China.
[Ti] Title:Protective effect of hydroxysafflor yellow A alone or in combination with acetylglutamine on cerebral ischemia reperfusion injury in rat: A PET study using F-fuorodeoxyglucose.
[So] Source:Eur J Pharmacol;825:119-132, 2018 Feb 10.
[Is] ISSN:1879-0712
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Hydroxysafflor yellow A (HSYA) and acetylglutamine (NAG) are extensively applied in the treatment of brain injury. In this study, we investigated the neuroprotective effect and underlying mechanism of HSYA alone or together with NAG using a rat model of cerebral ischemia reperfusion injury. Male Sprague-Dawley (SD) rats (n = 5) were intraperitoneally injected with 5, 10, 20 mg/kg HSYA, 300 mg/kg NAG and 10 mg/kg HSYA+300 mg/kg NAG after the onset of reperfusion and once each day for the following 7 days. After assessing the neurological deficit and infarct volume, we used F-FDG-PET to evaluate the regional cerebral metabolic rate of glucose consumption, immunohistochemical analysis to detect the expression of GFAP, NGF, Bcl-2, Bax, caspase-3 and ICAM-1 in brain tissue at day 7 after cerebral I/R injury. Meanwhile, the mRNA levels of ICAM-1, IL-1, TNF-α and NF-κB were determined by qRT-PCR, the protein levels of Bcl-2, Bax and caspase-3 were detected by western blot. The results indicated that HSYA significantly up-regulated glucose metabolism, improved neurological function, decreased cerebral infarction volume. HSYA alone or together with NAG attenuated apoptosis and inflammation by up-regulating GFAP, NGF and Bcl-2 expression, suppressing the expression of Bax, caspase-3 and ICAM-1, IL-1, TNF-α and NF-κB. These finding suggested that HSYA exerted neuroprotection against cerebral I/R injury by modulating inflammation and apoptosis process, and HSYA in combination with NAG possessed a synergetic effect on protecting cerebral I/R brain injury.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

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[PMID]: 29353043
[Au] Autor:Tanaka M; Ishihara Y; Mizuno S; Ishida A; Vogel CF; Tsuji M; Yamazaki T; Itoh K
[Ad] Address:Laboratory of Molecular Brain Science, Graduate School of Integrated Arts and Sciences, Hiroshima University, Hiroshima, 739-8521, Japan; Laboratory for Pharmacotherapy and Experimental Neurology, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Kagawa, 769-2193, Japan.
[Ti] Title:Progression of vasogenic edema induced by activated microglia under permanent middle cerebral artery occlusion.
[So] Source:Biochem Biophys Res Commun;496(2):582-587, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Brain edema is a severe complication that accompanies ischemic stroke. Increasing evidence shows that inflammatory cytokines impair tight junctions of the blood-brain barrier, suggesting the involvement of microglia in brain edema. In this study, we examined the role of microglia in the progression of ischemic brain edema using mice with permanent middle cerebral artery occlusion. The intensity of T2-weighted imaging (T2WI) in the cerebral cortex and the striatum was elevated 3 h after occlusion and spread to peripheral regions of the ischemic hemisphere. Merged images of 2,3,5-triphenyl tetrazolium chloride staining and T2WI revealed the exact vasogenic edema region, which spread from the ischemic core to outside the ischemic region. Microglia were strongly activated in the ischemic region 3 h after occlusion and, notably, activated microglia were observed in the non-ischemic region 24 h after occlusion. Pretreatment with minocycline, an inhibitor of microglial activation clearly suppressed not only vasogenic edema but also infarct formation. We demonstrated in this study that vasogenic edema spreads from the ischemic core to the peripheral region, which can be elicited, at least in part, by microglial activation induced by ischemia.
[Mh] MeSH terms primary: Brain Edema/etiology
Brain/pathology
Infarction, Middle Cerebral Artery/complications
Microglia/pathology
[Mh] MeSH terms secundary: Animals
Brain Edema/pathology
Disease Progression
Infarction, Middle Cerebral Artery/pathology
Male
Mice, Inbred ICR
Water/analysis
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:059QF0KO0R (Water)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180122
[St] Status:MEDLINE

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[PMID]: 29306591
[Au] Autor:Yoshida K; Aburakawa Y; Suzuki Y; Kuroda K; Kimura T
[Ad] Address:Department of Neurology, Asahikawa Medical Center, National Hospital Organization, Asahikawa, Hokkaido, Japan. Electronic address: yoshidak@asahikawa.hosp.go.jp.
[Ti] Title:The Frequency and Risk Factors for Ischemic Stroke in Myotonic Dystrophy Type 1 Patients.
[So] Source:J Stroke Cerebrovasc Dis;27(4):914-918, 2018 Apr.
[Is] ISSN:1532-8511
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Patients with myotonic dystrophy type 1 have several cardiac abnormalities, especially myocardial conduction disorders. Few studies have investigated cerebral infarction. We investigated the frequency of both symptomatic and asymptomatic ischemic strokes in patients with myotonic dystrophy type 1. METHODS: Patients who were diagnosed with myotonic dystrophy type 1 using genetic testing or clinical examinations at Asahikawa Medical Center were included. We retrospectively reviewed their medical history, neuroradiological imaging, electrocardiograms, and treatment. Their CHADS2 and CHA2DS2-VASc scores were calculated. RESULT: A total of 108 patients were diagnosed with myotonic dystrophy type 1. Magnetic resonance imaging was performed in 72 and 1 patient whose results were not available was excluded. Among these, 2 patients had atrial flutter and 3 had atrial fibrillation. Regarding the CHADS2 score, 11 patients scored more than 2. Regarding the CHA2DS2-VASc score, 22 patients scored more than 2. Ischemic strokes were found in 9 patients with 1 having an atrial flutter and 4 having atrial fibrillation. All patients with stroke had CHADS2 and CHA2DS2-VASc scores higher than 2. There were significant differences between the 2 groups in atrial fibrillation (P < .001), CHADS2 score (P < .001), and CHA2DS2-VASc score (P < .001). CONCLUSIONS: Ischemic stroke in patients with myotonic dystrophy type 1 is associated with atrial fibrillation. The CHADS2 score seems to be useful for the management of patients with myotonic dystrophy type 1. Repeated electrocardiograms are necessary for managing these patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  10 / 56466 MEDLINE  
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[PMID]: 29246672
[Au] Autor:Yasaka M; Koretsune Y; Yamashita T; Oda E; Matsubayashi D; Ota K; Kobayashi M; Matsushita Y; Kaburagi J; Ibusuki K; Takita A; Iwashita M; Yamaguchi T
[Ad] Address:Department of Cerebrovascular Medicine and Neurology, National Hospital Organization, Kyushu Medical Center, Fukuoka, Japan. Electronic address: yasaka@kyumed.jp.
[Ti] Title:Recurrent Stroke and Bleeding Events after Acute Cardioembolic Stroke-Analysis Using Japanese Healthcare Database from Acute-Care Institutions.
[So] Source:J Stroke Cerebrovasc Dis;27(4):1012-1024, 2018 Apr.
[Is] ISSN:1532-8511
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: To understand the reality of patients who experienced a cardioembolic stroke (CES) is important because of the high incidence of recurrent stroke and the need to account for bleeding risk in relation to the need for anticoagulation treatment. We elucidated the current real-world medical care in patients who had a CES and identified the risk factors for recurrent stroke. METHODS AND RESULTS: The study comprised 9804 patients who were diagnosed with CES between April 2008 and September 2013 as identified in a healthcare database used by acute-care institutions in Japan. We analyzed the incidence and risk factors of stroke and bleeding events in CES patients. The incidence of stroke was 10.3% during the median observation period of 68 days, mainly consisting of recurrent CES (8.5%). The incidence of bleeding events and intracranial bleeding was 10.3% and 7.0%, respectively. The recurrence of ischemic stroke was significantly lower, and brain hemorrhage was significantly higher in the anticoagulation treatment group. The factors related to an increased risk of stroke were a history of cerebral infarction or transient ischemic attack, diabetes, and increase of CHA DS -VASc and CHADS scores. The risk factors for bleeding events were hypertension, renal dysfunction, and use of proton pump inhibitors (PPIs). CONCLUSIONS: The patients who experienced CES had a high rate of recurrent stroke or CES, mainly consisting of recurrent CES. Although anticoagulation may be beneficial for reducing recurrence of ischemic stroke, careful management is required given consideration of increased risk of brain hemorrhage during anticoagulation treatment, especially for patients with hypertension, renal dysfunction, and use of PPIs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process


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