Publications by authors named "Xunming Ji"

372 Publications

Outcomes in Endovascular Therapy for Basilar Artery Occlusion: Intracranial Atherosclerotic Disease . Embolism.

Aging Dis 2021 Apr 1;12(2):404-414. Epub 2021 Apr 1.

8Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.

Acute ischemic stroke due to basilar artery occlusion (BAO) carries a very poor prognosis. Functional outcomes in BAO patients undergoing endovascular therapy (EVT) may differ according to the specific pathological mechanisms. We aimed to explore the impact of the underlying pathological mechanisms on prognosis at 90-days and long-term follow-up in BAO patients treated with EVT. We analyzed consecutive BAO patients undergoing EVT from December 2012 to December 2018 at a single center (Xuanwu Hospital). Patients were classified into either an intracranial atherosclerotic disease (ICAD) group or an embolic group according to the corresponding angiographic findings. The baseline characteristics and functional outcomes were compared between the two groups. Multivariable logistic regression analysis was performed. Among the 167 patients enrolled, 78 patients (46.7%) were in the ICAD group and 89 patients (53.3%) were assigned to the embolic group. Overall, 149 patients (89.2%) achieved successful reperfusion post-EVT. There were no significant differences in functional outcomes at 90-days and long-term follow-up between the two groups. Similarly, a Kaplan-Meier survival analysis showed similar long-term survival probabilities (P = 0.438). The pathological mechanism was not associated with functional independence (OR, 1.818; 95% CI, 0.694-4.761; P = 0.224), favorable outcome (OR, 1.476; 95% CI, 0.592-3.681; P = 0.403), or mortality (OR, 1.249; 95% CI, 0.483-3.226; P = 0.646). However, based on subgroup analysis, embolic BAO versus ICAD was significantly associated with better functional independence in those aged 60 years and younger (OR, 4.513; 95% CI, 1.138-17.902). In this study, no differences in either 90-days or long-term functional outcomes between ICAD-related BAO and embolic BAO patients undergoing EVT were observed. However, in BAO patients aged ≤ 60 years, the pathological mechanism of embolism was associated with better functional independence.
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http://dx.doi.org/10.14336/AD.2020.0704DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7990363PMC
April 2021

Safety and efficacy of remote ischemic conditioning for the treatment of intracerebral hemorrhage: A proof-of-concept randomized controlled trial.

Int J Stroke 2021 Apr 7:17474930211006580. Epub 2021 Apr 7.

Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China.

Background: Remote ischemic conditioning can promote hematoma resolution, attenuate brain edema, and improve neurological recovery in animal models of intracerebral hemorrhage.

Aims: This study aimed to evaluate the safety and preliminary efficacy of remote ischemic conditioning in patients with intracerebral hemorrhage.

Methods: In this multicenter, randomized, controlled trial, 40 subjects with supratentorial intracerebral hemorrhage presenting within 24-48 h of onset were randomly assigned to receive medical therapy plus remote ischemic conditioning for consecutive seven days or medical therapy alone. The primary safety outcome was neurological deterioration within seven days of enrollment, and the primary efficacy outcome was the changes of hematoma volume on CT images. Other outcomes included hematoma resolution rate at 7 days ([hematoma volume at 7 days - hematoma volume at baseline]/hematoma volume at baseline), perihematomal edema (PHE), and functional outcome at 90 days.

Results: The mean age was 59.3 ± 11.7 years and hematoma volume was 13.9 ± 4.5 mL. No subjects experienced neurological deterioration within seven days of enrollment, and no subject died or experienced remote ischemic conditioning-associated adverse events during the study period. At baseline, the hematoma volumes were 14.19 ± 5.07 mL in the control group and 13.55 ± 3.99 mL in the remote ischemic conditioning group, and they were 8.54 ± 3.99 mL and 6.95 ± 2.71 mL at seven days after enrollment, respectively, which is not a significant difference ( > 0.05 each). The hematoma resolution rate in the remote ischemic conditioning group (49.25 ± 9.17%) was significantly higher than in the control group (41.92 ± 9.14%; MD, 7.3%; 95% CI, 1.51-13.16%;  = 0.015). The absolute PHE volume was 17.27 ± 8.34 mL in the control group and 12.92 ± 7.30 mL in the remote ischemic conditioning group at seven days after enrollment, which is not a significant between-group difference ( = 0.087), but the relative PHE in the remote ischemic conditioning group (1.77 ± 0.39) was significantly lower than in the control group (2.02 ± 0.27; MD, 0.25; 95% CI, 0.39-0.47;  = 0.023). At 90-day follow-up, 13 subjects (65%) in the remote ischemic conditioning group and 12 subjects (60%) in the control group achieved favorable functional outcomes (modified Rankin Scale score ≤ 3), which is not a significant between-group difference ( = 0.744).

Conclusions: Repeated daily remote ischemic conditioning for consecutive seven days was safe and well tolerated in patients with intracerebral hemorrhage, and it may be able to improve hematoma resolution rate and reduce relative PHE. However, the effects of remote ischemic conditioning on the absolute hematoma and PHE volume and functional outcomes in this patient population need further investigations. http://www.clinicaltrials.gov. Unique identifier: NCT03930940.
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http://dx.doi.org/10.1177/17474930211006580DOI Listing
April 2021

SDL Index Predicts Stroke-Associated Pneumonia in Patients After Endovascular Therapy.

Front Neurol 2021 16;12:622272. Epub 2021 Feb 16.

Department of Neurosurgery, Xuanwu Hospital of Capital Medical University, Beijing, China.

This study aimed to develop and validate a novel index to predict SAP for AIS patients who underwent endovascular treatment. A study was conducted in an advanced comprehensive stroke center from January 2013 to December 2019 aiming to develop and validate a novel index to predict SAP for AIS patients who underwent endovascular treatment. This cohort consisted of a total of 407 consecutively registered AIS patients who underwent endovascular therapy, which was divided into derivation and validation cohorts. Multiple blood parameters as well as demographic features, vascular risk factors, and clinical features were carefully evaluated in the derivation cohort. The independent predictors were obtained using multivariable logistic regression. The scoring system was generated based on the β-coefficients of each independent risk factor. Ultimately, a novel predictive model: the SDL index (stroke history, dysphagia, lymphocyte count < 1.00 × 10/μL) was developed. The SDL index showed good discrimination both in the derivation cohort (AUROC: 0.739, 95% confidence interval, 0.678-0.801) and the validation cohort (AUROC: 0.783, 95% confidence interval, 0.707-0.859). The SDL index was well-calibrated (Hosmer-Lemeshow test) in the derivation cohort ( = 0.389) and the validation cohort ( = 0.692). We therefore divided our population into low (SDL index = 0), medium (SDL index = 1), and high (SDL index ≥ 2) risk groups for SAP. The SDL index showed good discrimination when compared with two existing SAP prediction models. The SDL index is a novel feasible tool to predict SAP risk in acute ischemic stroke patients post endovascular treatment.
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http://dx.doi.org/10.3389/fneur.2021.622272DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7921145PMC
February 2021

Remote Ischemic Postconditioning vs. Physical Exercise After Stroke: an Alternative Rehabilitation Strategy?

Mol Neurobiol 2021 Feb 24. Epub 2021 Feb 24.

Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA.

There remain debates on neuroprotection and rehabilitation techniques for acute ischemic stroke patients. Therapeutic physical exercise following stroke has shown promise but is challenging to apply clinically. Ischemic conditioning, which has several clinical advantages, is a potential neuroprotective method for stroke rehabilitation that is less understood. In the present study, the rehabilitative properties and mechanisms of physical exercise and remote ischemic postconditioning (RIPostC) after stroke were compared and determined. A total of 248 adult male Sprague-Dawley rats were divided into five groups: (1) sham, (2) stroke, (3) stroke with intense treadmill exercise, (4) stroke with mild treadmill exercise, and (5) stroke with RIPostC. Focal ischemia was evaluated by infarct volume and neurological deficit. Long-term functional outcomes were represented through neurobehavioral function tests: adhesive removal, beam balance, forelimb placing, grid walk, rota-rod, and Morris water maze. To further understand the mechanisms underlying neurorehabilitation and verify the presence thereof, we measured mRNA and protein levels of neuroplasticity factors, synaptic proteins, angiogenesis factors, and regulation molecules, including HIF-1α, BDNF, TrkB, and CREB. The key role of HIF-1α was elucidated by using the inhibitor, YC-1. Both exercise intensities and RIPostC significantly decreased infarct volumes and neurological deficits and outperformed the stroke group in the neurobehavioral function tests. All treatment groups showed significant increases in mRNA and protein expression levels of the target molecules for neurogenesis, synaptogenesis, and angiogenesis, with intermittent further increases in the RIPostC group. HIF-1α inhibition nullified most beneficial effects and indicative molecule expressions, including HIF-1α, BDNF, TrkB, and CREB, in both procedures. RIPostC is equally, or superiorly, effective in inducing neuroprotection and rehabilitation compared to exercise in ischemic rats. HIF-1α likely plays an important role in the efficacy of neuroplasticity conditioning, possibly through HIF-1α/BDNF/TrkB/CREB regulation.
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http://dx.doi.org/10.1007/s12035-021-02329-6DOI Listing
February 2021

Self-Assembly of Size-Controlled m-Pyridine-Urea Oligomers and Their Biomimetic Chloride Ion Channels.

Angew Chem Int Ed Engl 2021 Feb 23. Epub 2021 Feb 23.

Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Beijing Advanced Innovation Center for Big Data-based Precision Medicine, Capital Medical University, Beijing, 100069, China.

The m-pyridine urea (mPU) oligomer was constructed by using the intramolecular hydrogen bond formed by the pyridine nitrogen atom and the NH of urea and the intermolecular hydrogen bond of the terminal carbonyl group and the NH of urea. Due to the synergistic effect of hydrogen bonds, mPU oligomer folds and exhibits strong self-assembly behaviour. Affected by folding, mPU oligomer generates a twisted plane, and one of its important features is that the carbonyl group of the urea group orientates outwards from the twisted plane, while the NHs tend to direct inward. This feature is beneficial to NH attraction for electron-rich species. Among them, the trimer self-assembles into helical nanotubes, and can efficiently transport chloride ions. This study provides a novel and efficient strategy for constructing self-assembled biomimetic materials for electron-rich species transmission.
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http://dx.doi.org/10.1002/anie.202102174DOI Listing
February 2021

Analysis of microRNA expression in cerebral ischemia/reperfusion after mild therapeutic hypothermia treatment in rats.

Ann Transl Med 2021 Jan;9(2):168

Department of Neurosurgery, Xuanwu Hospital of Capital Medical University, Beijing, China.

Background: This study aimed to explore the molecular mechanism of mild hypothermia in in the treatment of cerebral ischemia, microRNA (miRNA) microarrays and bioinformatics analysis were employed to examine the miRNA expression profiles of rats with mild therapeutic hypothermia after middle cerebral artery occlusion (MCAO).

Methods: MCAO was induced in Male Sprague-Dawley rats. Mild hypothermia treatment began from the onset of ischemia and maintained for 3 hours. miRNA expressions following focal cerebral ischemia and mild hypothermia treatment were profiled using microarray technology. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to analyze the functions of the target genes in mild therapeutic hypothermia after MCAO. 60 min before MCAO, mimics and inhibitor of miR-291b were injected into the right lateral ventricle respectively, then the infarct volume and neuronal apoptosis were analyzed.

Results: Six upregulated miRNAs and 6 downregulated miRNAs were detected 4 hours after mild therapeutic hypothermia, and after 24 hours, 41 and 10 miRNAs were upregulated and downregulated, respectively. The target genes of the differentially expressed genes were mainly related with multicellular organism development and the mucin type O-glycan biosynthesis pathway was the most enriched KEGG pathway. Among the differentially expressed miRNAs, miR-291b was selected to assess the effects of mild therapeutic hypothermia in MCAO rats. At 24 hours after mild therapeutic hypothermia, miR-291b overexpression was proved to exhibit neuroprotective effects.

Conclusions: The results showed that miRNAs might play a pivotal role in mild therapeutic hypothermia in cerebral ischemia/reperfusion injury. Further understanding of the mechanism and function of miRNAs would help to illuminate the mechanism of mild therapeutic hypothermia in cerebral ischemia/reperfusion injury.
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http://dx.doi.org/10.21037/atm-21-143DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7867934PMC
January 2021

Pathogenesis and Management in Cerebrovenous Outflow Disorders.

Aging Dis 2021 Feb 1;12(1):203-222. Epub 2021 Feb 1.

1Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China.

In keeping with its status as one of the major causes of disability and mortality worldwide, brain damage induced by cerebral arterial disease has been the subject of several decades of scientific investigation, which has resulted in a vastly improved understanding of its pathogenesis. Brain injury mediated by venous etiologies, however, such as cerebral, jugular, and vertebral venous outflow disturbance, have been largely ignored by clinicians. Unfortunately, this inattention is not proportional to the severity of cerebral venous diseases, as the impact they exact on the quality of life of affected patients may be no less than that of arterial diseases. This is evident in disease sequelae such as cerebral venous thrombosis (CVT)-mediated visual impairment, epilepsy, and intracranial hypertension; and the long-term unbearable head noise, tinnitus, headache, dizziness, sleeping disorder, and even severe intracranial hypertension induced by non-thrombotic cerebral venous sinus (CVS) stenosis and/or internal jugular venous (IJV) stenosis. In addition, the vertebral venous system (VVS), a large volume, valveless vascular network that stretches from the brain to the pelvis, provides a conduit for diffuse transmission of tumors, infections, or emboli, with potentially devastating clinical consequences. Moreover, the lack of specific features and focal neurologic signs seen with arterial etiologies render cerebral venous disease prone to both to misdiagnoses and missed diagnoses. It is therefore imperative that awareness be raised, and that as comprehensive an understanding as possible of these issues be cultivated. In this review, we attempt to facilitate these goals by systematically summarizing recent advances in the diagnosis and treatment of these entities, including CVT, CVS stenosis, and IJV stenosis, with the aim of providing a valid, practical reference for clinicians.
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http://dx.doi.org/10.14336/AD.2020.0404DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7801276PMC
February 2021

Ischemic Conditioning Ameliorated Hypertension and Vascular Remodeling of Spontaneously Hypertensive Rat via Inflammatory Regulation.

Aging Dis 2021 Feb 1;12(1):116-131. Epub 2021 Feb 1.

1Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, 10053, China.

Vascular remodeling is an initial step in the development of hypertension. Limb remote ischemic conditioning (LRIC) is a physiological treatment that induces endogenous protective effect during acute ischemic injury. However, the impact of long-term LRIC on hypertension, a chronic disease, is unknown. In this study, we aimed to investigate the LRIC effect on blood pressure and vascular remodeling in spontaneously hypertensive rat (SHR) model and patients with prehypertension and early-stage hypertension. LRIC of rats was performed once a day for 6-weeks. Blood pressure, vascular remodeling (cross-sectional area, extracellular deposition, and smooth muscle cell area), inflammation (inflammatory factors, and inflammatory cells) were compared among normotensive Wistar-Kyoto rats (WKY), WKY RIC group, SHR control group, and SHR RIC. Long-term LRCI treatment (twice a day for 4-weeks) was performed on patients with prehypertension or early-stage hypertension. Blood pressure and pulse wave velocity (PWV) were analyzed before and after LRIC treatment. LRIC treatment decreased blood pressure in SHR (n = 9-10). LRIC ameliorated vascular remodeling by decreasing cross-sectional area, suppressing deposition of the extracellular matrix, and hypertrophy of smooth muscle cell in conduit artery and small resistance artery (n = 7). LRIC decreased proinflammatory factors while increasing the anti-inflammatory factors in the circulation (n = 5). LRIC decreased circulating monocyte and natural killer T-cell levels (n = 5). Furthermore, LRIC treatment decreased blood pressure and improved vascular stiffness in patients (n = 20). In conclusion, long term LRIC could decrease blood pressure and ameliorate vascular remodeling via inflammation regulation. LRIC could be a preventive treatment for people with blood pressure elevation or prehypertension.
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http://dx.doi.org/10.14336/AD.2020.0320DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7801289PMC
February 2021

Identifying Biomarkers Associated with Venous Infarction in Acute/Subacute Cerebral Venous Thrombosis.

Aging Dis 2021 Feb 1;12(1):93-101. Epub 2021 Feb 1.

7Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China.

Among cerebral venous thrombosis (CVT) patients, those with venous infarction have more severe clinical presentations and worse outcomes. Identifying biomarkers associated with venous infarction in CVT may help understand the pathogenesis and provide potentially useful therapeutic markers. Fifty-two CVT patients were prospectively recruited and divided into three groups: acute/subacute CVT with venous infarction (ASVI, n=30), without venous infarction (ASOVI, n=13), and chronic CVT (n=9). Blood brain barrier (BBB) permeability-related proteins, including claudin-5, occludin, matrix metalloproteinase-9, glial fibrillary acidic protein, and S100B, and inflammation-related factor high-sensitivity C-reactive protein (hs-CRP), were tested in serum and/or cerebrospinal fluid upon admission. We compared these biomarkers between the three groups and investigated their associations with venous infarction and clinical symptom severity in acute/subacute CVT patients on admission using the NIH Stroke Scale (NIHSS). Serum hs-CRP was significantly higher in acute/subacute CVT patients than chronic CVT patients. For acute/subacute CVT patients, levels were significantly higher in the ASVI group than the ASOVI group for serum claudin-5 (medians 2.80 vs. 2.50 mg/I, respectively, P = 0.039) and hs-CRP (medians 17.25 vs. 2.27 mg/l, respectively, P = 0.003). Both these biomarkers, analyzed as categorical or continuous variables, were also significantly associated with venous infarction in acute/subacute CVT patients after logistic regression analysis. Additionally, hs-CRP was positively correlated with the NIHSS ( = 0.710, P < 0.001) on admission in acute/subacute CVT patients. In CVT patients, venous infarction was associated with BBB disruption and potentially inflammation. Hs-CRP might serve as a biomarker reflecting the clinical severity of CVT in the acute/subacute stages.
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http://dx.doi.org/10.14336/AD.2020.0405DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7801269PMC
February 2021

Loss of Wip1 aggravates brain injury after ischaemia/reperfusion by overactivating microglia.

Stroke Vasc Neurol 2021 Jan 15. Epub 2021 Jan 15.

Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing, China.

Background And Purpose: The inflammatory response mediated by microglia/macrophages is closely related to cerebral ischaemia/reperfusion injury. Wild-type p53-induced protein phosphatase 1 (Wip1), a serine/threonine phosphatase, is expressed in various tissues. A growing number of reports have suggested that Wip1 is a negative regulator of inflammation in peripheral tissue; however, its role in the central nervous system (CNS) remains unclear. This study aimed to clarify whether Wip1 can inhibit CNS inflammation by regulating microglia/macrophage functions after ischaemic injury.

Methods: A model of middle cerebral artery occlusion and reperfusion was established in mice. CNS inflammation was simulated by lipopolysaccharide treatment of primary microglia. Laser speckle imaging was used to monitor regional cerebral blood flow. Behavioural outcomes were assessed with a TreadScan gait analysis system. TTC staining was used to evaluate the infarct volume, and western blotting and immunofluorescence staining were applied to detect the phenotypical transformation of microglia. ELISA was performed to detect the levels of inflammatory factors.

Results: Wip1 expression was increased after ischaemia/reperfusion. Wip1-knockout (KO) mice displayed more severe brain injury than wild-type mice, as indicated by aggravated motor dysfunction, greater brain infarct volumes and higher expression of inflammatory cytokines (interleukin-6 and tumour necrosis factor alpha) in the brain. We also found that Wip1 depletion increased microglial/macrophage activation in both in vitro and in vivo models, which all showed activation of microglia/macrophages. Lentivirus- reversed the injury induced by Wip1-KO.

Conclusions: Our results suggest that Wip1 may inhibit neuroinflammation by inhibiting microglial/macrophage activation after brain ischaemia/reperfusion injury.
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http://dx.doi.org/10.1136/svn-2020-000490DOI Listing
January 2021

Risk Factors for Severe Residual Headache in Cerebral Venous Thrombosis.

Stroke 2021 Jan 7;52(2):531-536. Epub 2021 Jan 7.

China-America Institute of Neuroscience (K.J., C.Z., L.W., W.L., M.J., M.C., D.W., X.J.), Xuanwu Hospital, Capital Medical University, Beijing, China.

Background And Purpose: Which factors will influence the presence of severe residual headache after cerebral venous thrombosis (CVT) is unclear. The purpose of this study was to identify risk factors for severe residual headache in a large single-center cohort of patients with CVT.

Methods: We consecutively included eligible patients with CVT from a prospective stroke registry. Severe residual headache was defined as a residual headache attack requiring bed rest or hospital admission within 1 month before the last follow-up visit. We identified the risk factors of severe residual headache in all survivors and in those with favorable functional outcome (a modified Rankin Scale score, 0-2).

Results: A total of 325 patients' data were analyzed. At the last follow-up (median 13 months), 43 patients (13.2%) reported severe headache. In the multivariable analysis, isolated intracranial hypertension (odds ratio [OR], 3.309 [95% CI, 1.434-7.634]; =0.005), CVT recurrence (OR, 4.722 [95% CI, 1.639-13.602]; =0.004), and no recanalization (OR, 10.158 [95% CI, 4.194-24.600]; <0.001) were independently associated with severe headache. Severe headache was more frequent in patients with unfavorable outcome (11/25 [44.0%] versus 32/300 [10.7%]; <0.001). In patients with favorable outcome, the risk factors for severe headache were isolated intracranial hypertension (OR, 3.236 [95% CI, 1.268-8.256]; =0.014) and no recanalization (OR, 7.863 [95% CI, 3.120-19.812]; <0.001).

Conclusions: Isolated intracranial hypertension, CVT recurrence, and no recanalization increased the risk for severe residual headache after CVT.
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http://dx.doi.org/10.1161/STROKEAHA.120.029820DOI Listing
January 2021

SERPINC1 novel mutation (c.637C > T p. Gln213Ter) in a cerebral venous sinus thrombosis case and treatment with agatroban.

Thromb Res 2021 Mar 17;199:35-37. Epub 2020 Dec 17.

Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.

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http://dx.doi.org/10.1016/j.thromres.2020.12.011DOI Listing
March 2021

Response by Hui et al to Letter Regarding, "Efficacy and Safety of Recanalization Therapy for Acute Ischemic Stroke With Large Vessel Occlusion".

Stroke 2021 01 28;52(1):e47. Epub 2020 Dec 28.

Department of Neurosurgery (X.J.), Xuanwu Hospital, Capital Medical University, Beijing, China.

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http://dx.doi.org/10.1161/STROKEAHA.120.032522DOI Listing
January 2021

EphrinB2-EphB2 signaling for dendrite protection after neuronal ischemia and oxygen-glucose deprivation .

J Cereb Blood Flow Metab 2020 Dec 16:271678X20973119. Epub 2020 Dec 16.

Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA.

In order to rescue neuronal function, neuroprotection should be required not only for the neuron soma but also the dendrites. Here, we propose the hypothesis that ephrin-B2-EphB2 signaling may be involved in dendritic degeneration after ischemic injury. A mouse model of focal cerebral ischemia with middle cerebral artery occlusion (MCAO) method was used for EphB2 signaling test in vivo. Primary cortical neuron culture and oxygen-glucose deprivation were used to assess EphB2 signaling in vitro. siRNA and soluble ephrin-B2 ectodomain were used to block ephrin-B2-Ephb2 signaling. In the mouse model of focal cerebral ischemia and in neurons subjected to oxygen-glucose deprivation, clustering of ephrin-B2 with its receptor EphB2 was detected. Phosphorylation of EphB2 suggested activation of this signaling pathway. RNA silencing of EphB2 prevented neuronal death and preserved dendritic length. To assess therapeutic potential, we compared the soluble EphB2 ectodomain with the NMDA antagonist MK801 in neurons after oxygen-glucose deprivation. Both agents equally reduced lactate dehydrogenase release as a general marker of neurotoxicity. However, only soluble EphB2 ectodomain protected the dendrites. These findings provide a proof of concept that ephrin-B2-EphB2 signaling may represent a novel therapeutic target to protect both the neuron soma as well as dendrites against ischemic injury.
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http://dx.doi.org/10.1177/0271678X20973119DOI Listing
December 2020

Association between high-sensitivity C-reactive protein levels and clinical outcomes in acute ischemic stroke patients treated with endovascular therapy.

Ann Transl Med 2020 Nov;8(21):1379

Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.

Background: Increasing evidence demonstrates that high-sensitivity C-reactive protein (hs-CRP) is an independent prognostic predictor in acute ischemic stroke (AIS) patients. The purpose of this study is to investigate the association between hs-CRP levels and clinical outcomes in AIS patients receiving endovascular therapy (EVT).

Methods: This observational study was based on a prospective registry study. AIS patients receiving EVT from December 2012 to January 2019 were included. The modified Rankin Scale (mRS) scores at the 90-day and long-term follow-up were evaluated as clinical outcomes. Multivariable logistic regression analysis was conducted to adjust for confounders. Receiver operating characteristic (ROC) curve analysis was performed based on significant predictors of favorable outcomes in the logistic regression analysis. Patients were divided into two groups according to the cutoff value. Clinical outcomes were compared between groups. Survival probability was assessed using Kaplan-Meier survival analysis.

Results: Multivariable logistic regression analysis of the 362 enrolled AIS patients demonstrated that age (P=0.030), National Institutes of Health Stroke Scale (NIHSS) score (P=0.023), hs-CRP levels (P<0.001), and symptomatic intracranial hemorrhage (sICH) (P=0.006) were independently predictive of favorable outcomes. ROC curve analysis indicated that the hs-CRP level was predictive of favorable outcomes at the 90-day follow-up with a cutoff value of 8.255 mg/L. The mRS scores between patients with hs-CRP <8.255 mg/L and patients with hs-CRP ≥8.255 mg/L at the 90-day [2 (IQR, 1-2) 4 (IQR, 3-6), P<0.001] and long-term follow-up [1 (IQR, 0-2) 4 (IQR, 2-6), P<0.001] were significantly different. Patients with hs-CRP ≥8.255 mg/L had significantly increased risk of poor clinical outcomes at the 90-day and long-term follow-up compared with those with hs-CRP <8.255 mg/L (P<0.001 each).

Conclusions: Elevated hs-CRP levels were associated with poor clinical outcomes in AIS patients receiving EVT.
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http://dx.doi.org/10.21037/atm-20-3820DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723633PMC
November 2020

Normobaric Oxygen May Ameliorate Cerebral Venous Outflow Disturbance-Related Neurological Symptoms.

Front Neurol 2020 13;11:599985. Epub 2020 Nov 13.

Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China.

Cerebral venous outflow disturbance (CVOD) has begun to garner the attention of researches owing to a series of clinical symptoms that impose a significant impact on people's quality of life. Herein, we aimed to investigate whether normobaric oxygen (NBO) can ameliorate CVOD-induced neurological symptoms. This was one part of the prospective trial registered in ClinicalTrials.gov (NCT03373292). A total of 37 CVOD patients were divided into the NBO group (5-8 L/min of oxygen inhalation, 1 h per time, 3 times daily, = 19) and the control group (without oxygen inhalation, = 18) randomly. The assessments were performed at admission, 1-week hospitalization, and 6-month follow-up. Quantitative electroencephalogram (qEEG) data were recorded prior to and post 1 h of NBO in some patients. R software was used for data analysis. No NBO-related adverse events were observed during the whole NBO intervention process. The 1-week Patient Global Impression of Change (PGIC) scale showed that the symptom improvement occurred in nine patients in the NBO group (47.4%) while none in the control group ( = 0.001). NBO could improve headache evaluated with visual analog scale (pre-NBO vs. post-NBO: 4.70 ± 2.16 vs. 2.90 ± 2.03, = 0.024) and Headache Impact Test-6 (53.40 ± 12.15 vs. 50.30 ± 13.04, = 0.041). As for 6-month PGIC follow-up, eight out of 14 cases (57.1%) in the NBO group reported improvement, while only one out of 12 patients in the control group replied mild improvement ( = 0.014). The qEEG revealed that NBO reduced the ratio of theta to alpha power (0.65 ± 0.38 vs. 0.56 ± 0.35, = 0.030) over the fronto-central electrodes. To sum up, NBO may be a safe and effective approach to attenuate CVOD-related symptoms (especially for headache) by brain functional improvement resulting from increasing oxygen supply to the brain tissues.
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http://dx.doi.org/10.3389/fneur.2020.599985DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7691288PMC
November 2020

Premorbid Use of Statin and Outcome of Acute Ischemic Stroke After Intravenous Thrombolysis: A Meta-Analysis.

Front Neurol 2020 12;11:585592. Epub 2020 Nov 12.

China-America Institute of Neuroscience, Xuanwu Hospital, Capital Medical University, Beijing, China.

The association between the premorbid use of statin and the early outcomes of acute ischemic stroke (AIS) after intravenous thrombolysis (IVT) remains uncertain. We performed a meta-analysis of observational studies to evaluate the influence of the premorbid use of statin on functional outcome and symptomatic intracranial hemorrhage (SIH) in AIS after IVT. Relevant studies were identified by search of PubMed, Embase, and Cochrane's Library databases. Only studies with multivariate analyses were included. A random-effect model, incorporating inter-study heterogeneity, was used to pool the results. Twenty observational studies with 20,752 AIS patients who were treated with IVT were included. The pooled results showed that the premorbid use of statin was not associated with improved 3-month favorable functional outcome [odds ratio (OR): 1.05, 95% confidence interval (CI): 0.87-1.26, = 0.60, = 52%), 3-month functional independence (OR: 1.13, 95% CI: 0.96-1.33, = 0.15, = 52%), or 3-month mortality (OR: 1.12, 95% CI: 0.94-1.34, = 0.20, = 20%). Moreover, the premorbid use of statin was associated with an increased risk of SIH in AIS after IVT (OR: 1.48, 95% CI: 1.12-1.95, = 0.006, = 60%). Subgroup analyses according to study design, adjustment of baseline low-density lipoprotein cholesterol, and definitions of SIH showed consistent results (-values for subgroup difference all >0.05). The premorbid use of statin is not associated with improved functional outcomes or mortality but is associated with a higher risk of SIH in AIS patients after IVT.
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http://dx.doi.org/10.3389/fneur.2020.585592DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7688895PMC
November 2020

Intra-arterial Cold Saline Infusion in Stroke: Historical Evolution and Future Prospects.

Aging Dis 2020 Dec 1;11(6):1527-1536. Epub 2020 Dec 1.

3Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.

Acute ischemic stroke (AIS) is a perpetual threat to life and functionality due to its high morbidity and mortality. In the past several decades, therapeutic hypothermia has garnered interest as an effective neuroprotective method in the setting of AIS. However, traditional hypothermic methods have been criticized for their low cooling efficiency and side effects. Intra-arterial cold saline infusion (IA-CSI), as a novel hypothermic method, not only minimizes these side effects, but is also perfectly integrated with widely accepted recanalization modalities in AIS, thereby serving as a promising prospect for clinical translation. In this article, we review the historical development of IA-CSI, summarize major studies of IA-CSI in rodents, large animals, and humans to date, and suggest insight into future development prospects in the field of AIS. We hope that this article will provide inspiration for the future application of hypothermia in AIS patients.
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http://dx.doi.org/10.14336/AD.2020.0325DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673854PMC
December 2020

Serum Occludin as a Biomarker to Predict the Severity of Acute Ischemic Stroke, Hemorrhagic Transformation, and Patient Prognosis.

Aging Dis 2020 Dec 1;11(6):1395-1406. Epub 2020 Dec 1.

6Department of Pharmaceutical Sciences, College of Pharmacy, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.

Blood-brain barrier (BBB) damage plays an important role in overall brain injury following acute ischemic stroke (AIS). We investigated the potential utility of serum occludin, a BBB damage biomarker, in predicting the severity of AIS, hemorrhagic transformation (HT) and patient prognosis. A total of 243 patients, suspected of suffering an AIS and admitted to the emergency room at Xuanwu Hospital between November 2018 to March 2019, were enrolled in this study. Serum occludin levels were measured by enzyme linked immunosorbent assay and clinical data were collected from each patient. Receiver operating characteristic curves (ROC) were used to analyze the relationship between serum occludin and AIS. Multiple logistic regression analysis was used to analyze the relationship between serum occludin and stroke prognosis. Serum occludin levels were significantly elevated in acute stroke cases compared with those with stroke-like symptoms (P<0.001). In the moderate and severe cerebral infarction (CI) groups, serum occludin levels were significantly higher than those in the mild CI group (P<0.001). Patients with HT had higher occludin levels than non-HT patients (P<0.05). In addition, serum occludin level of patients with poor prognosis was significantly higher than that of the patients with good prognosis for non-reperfusion therapy. The ROC curve showed that serum occludin could reasonably predict HT and poor prognosis. Moreover, serum occludin were independently associated with 90-day poor prognosis. These findings suggest that the serum occludin levels could be used to identify early acute stroke cases and may predict the severity of AIS and HT as well as the prognosis at 90 days.
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http://dx.doi.org/10.14336/AD.2020.0119DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673856PMC
December 2020

A systemic review into carotid plaque features as predictors of restenosis after carotid endarterectomy.

J Vasc Surg 2020 Nov 27. Epub 2020 Nov 27.

Department of Vascular Ultrasonography, Xuanwu Hospital, Capital Medical University, Beijing, China; Center of Vascular Ultrasonography, Beijing Institute of Brain Disorders, Beijing, China.

Objective: Restenosis after carotid endarterectomy (CEA) limits its long-term efficacy for stroke prevention. Thus, it is of utmost importance to identify the factors that predispose a patient to restenosis after CEA. This systemic review aims to survey the current literature regarding restenosis after CEA and discuss the predictive value of carotid plaque features.

Methods: A systemic review of studies on the predictive value of carotid plaque features for restenosis after CEA was conducted according to the PRISMA guidelines. PubMed/MEDLINE and Embase databases were searched up to March 20, 2020. Two authors independently extracted the data and assessed the risk of bias with the Quality in Prognosis Studies tool. Given the heterogeneity in the measurement of prognostic factors, types of CEA, and clinical outcomes, a qualitative synthesis was performed.

Results: Twenty-one articles with a sample size that ranged from 11 to 1203 were included in this systematic review. Based on the presence of calcification in original carotid plaques, two progression patterns of restenosis were hypothesized: patients with calcified plaques may experience a temporary increase in the intima-media thickness (IMT) followed by a decrease in IMT after CEA, whereas patients with noncalcified plaques may experience a gradual increase in IMT after CEA. Accordingly, patients with a high calcium score may have a high restenosis rate within 6 months after CEA and a low restenosis rate thereafter. Thus, the late restenosis rate in patients with uniformly echogenic plaques was lower than that in patients with uniformly echolucent plaques. Pathologically, a lipid-rich, inflammatory carotid plaque is associated with a decreased risk of restenosis within 1 year after CEA, mainly owing to the relatively mild reactive intimal hyperplasia at the surgical site and active inflammation in the remaining media and adventitia. Molecular predictors for restenosis included a Mannose-binding lectin 2 genotype, preoperative C-reactive protein, serum homocysteine, apolipoprotein J, vitamin C, and telomere length of carotid plaques.

Conclusions: This review demonstrated that carotid plaque features, including imaging features, cellular composition, and molecular features, are correlated with the risk of restenosis after CEA. A comprehensive evaluation of plaque characteristics may help to stratify the risk of restenosis after CEA.
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http://dx.doi.org/10.1016/j.jvs.2020.10.084DOI Listing
November 2020

Hamartin: An Endogenous Neuroprotective Molecule Induced by Hypoxic Preconditioning.

Front Genet 2020 30;11:582368. Epub 2020 Sep 30.

Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China.

Hypoxic/ischemic preconditioning (HPC/IPC) is an innate neuroprotective mechanism in which a number of endogenous molecules are known to be involved. Tuberous sclerosis complex 1 (TSC1), also known as hamartin, is thought to be one such molecule. It is also known that hamartin is involved as a target in the rapamycin (mTOR) signaling pathway, which functions to integrate a variety of environmental triggers in order to exert control over cellular metabolism and homeostasis. Understanding the role of hamartin in ischemic/hypoxic neuroprotection will provide a novel target for the treatment of hypoxic-ischemic disease. Therefore, the proposed molecular mechanisms of this neuroprotective role and its preconditions are reviewed in this paper, with emphases on the mTOR pathway and the relationship between the expression of hamartin and DNA methylation.
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http://dx.doi.org/10.3389/fgene.2020.582368DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7556298PMC
September 2020

Ultrasound-Based Carotid Plaque Characteristics Help Predict New Cerebral Ischemic Lesions after Endarterectomy.

Ultrasound Med Biol 2021 Feb 3;47(2):244-251. Epub 2020 Nov 3.

Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China.

The aim of this study was to identify the ultrasound-based carotid plaque characteristics associated with new cerebral ischemic lesions after carotid endarterectomy (CEA). Between January 2013 and December 2018, carotid duplex ultrasound was performed in 1061 patients who underwent CEA. Brain magnetic resonance diffusion-weighted imaging (DWI) was performed pre-operatively and within 30 d after CEA. New cerebral ischemic lesions on DWI were observed in 169 patients. The cutoff value gray-scale median (GSM) used to distinguish DWI-positive from DWI-negative patients was 30.5, with an area under the receiver operating characteristic curve of 0.837. A larger proportion of multiple DWI lesions were observed in the GSM ≤30.5 group (59.5% vs. 41.5%, p = 0.030). Univariate and multivariate analyses identified GSM ≤30.5, ulcerated carotid plaques and pre-operative ischemic symptoms as predictors of post-operative cerebral DWI lesions. Our results indicate that ultrasound-based carotid plaque characteristics help predict new cerebral ischemic lesions after CEA.
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http://dx.doi.org/10.1016/j.ultrasmedbio.2020.09.025DOI Listing
February 2021

rs1769793 variant reduces expression in skeletal muscle and hippocampus and contributes to high aerobic capacity in hypoxia.

Proc Natl Acad Sci U S A 2020 11 27;117(47):29283-29285. Epub 2020 Oct 27.

Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, China;

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http://dx.doi.org/10.1073/pnas.2010073117DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7703601PMC
November 2020

Clinical Classification and Collateral Circulation in Chronic Cerebrospinal Venous Insufficiency.

Front Neurol 2020 23;11:913. Epub 2020 Sep 23.

Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China.

As an indispensable part of the cerebral venous system, the extracranial cerebrospinal venous system is not fully recognized. This study aimed to analyze the clinical classification and imaging characteristics of chronic cerebrospinal venous insufficiency (CCSVI) quantitatively. A total of 128 patients, who were diagnosed as CCSVI by jugular ultrasound and contrast-enhanced magnetic resonance venography (CE-MRV), were enrolled from May 2018 through May 2019. For the patients with possible extraluminal compression, computed tomography venography (CTV) was applied to estimate the degree of internal jugular venous stenosis (IJVS) and rank the vertebral venous collateral circulation. The causes of extraluminal compression induced IJVS included osseous compression (78.95%), carotid artery (24.21%), sternocleidomastoid muscle (5.79%), swollen lymph node (1.05%), and unknown reasons (5.26%). The subtypes of non-compression CCSVI included the high jugular bulb (77.27%), fenestration of the internal jugular vein (IJV) (7.27%), internal jugular phlebectasia (2.73%), tortuous IJV (0.91%), IJV thrombosis (14.55%), and elongated venous valves with/without erythrocyte aggregation (13.64%). For extraluminal compression induced IJVS, the ratio of severe vertebral venous expansion was higher in the severe IJVS group than that in the mild IJVS group ( < 0.001). The IJVS degree was higher in the severe vertebral venous expansion group than in the mild vertebral venous expansion group ( < 0.001). A multimodal diagnostic system is necessary to improve the diagnostic accuracy of CCSVI. The vertebral venous system is an important collateral circulation for CCSVI, which may be a promising indicator for evaluating IJVS degree.
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http://dx.doi.org/10.3389/fneur.2020.00913DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7538781PMC
September 2020

Remote Ischemic Perconditioning for the Treatment of Acute Ischemic Stroke.

JAMA Neurol 2020 Sep 28. Epub 2020 Sep 28.

Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China.

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http://dx.doi.org/10.1001/jamaneurol.2020.3555DOI Listing
September 2020

Long-term outcome of endovascular therapy for acute basilar artery occlusion.

J Cereb Blood Flow Metab 2020 Sep 21:271678X20958587. Epub 2020 Sep 21.

Department of Neurosurgery, Capital Medical University, Beijing, China.

The long-term functional outcome of acute basilar artery occlusion (BAO) patients who received modern endovascular therapy (EVT) is unclear. We sought to assess the long-term functional outcome of BAO patients treated with EVT and determine the prognostic factors associated with favorable outcome. We enrolled consecutive BAO patients who received EVT between December 2012 and December 2018 in this observational study. Baseline characteristics and outcomes were presented. Multivariable logistic regression analysis was performed to identify the prognostic factors associated with long-term outcome. Among the 177 BAO patients included in this study, 80 patients (45.2%) obtained favorable outcome and 97 patients (54.8%) had unfavorable outcome at long-term follow-up with a median observation time of 12 months (interquartile range, 3-19). A total of 67 patients (37.9%) died. National Institutes of Health Stroke Scale (NIHSS), posterior circulation Alberta Stroke Program Early Computed Tomography Score (pc-ASPECTS), time from stroke onset to recanalization, and recanalization condition were identified as independent predictors for long-term outcome. Over 40% of BAO patients who were treated with modern EVT achieved favorable outcome at long-term follow-up. NIHSS, pc-ASPECTS, time from stroke onset to recanalization, and recanalization condition were identified as independent prognostic factors of long-term outcome.
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http://dx.doi.org/10.1177/0271678X20958587DOI Listing
September 2020

Remote ischemic conditioning enhances oxygen supply to ischemic brain tissue in a mouse model of stroke: Role of elevated 2,3-biphosphoglycerate in erythrocytes.

J Cereb Blood Flow Metab 2020 Sep 15:271678X20952264. Epub 2020 Sep 15.

Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China.

Oxygen supply for ischemic brain tissue during stroke is critical to neuroprotection. Remote ischemic conditioning (RIC) treatment is effective for stroke. However, it is not known whether RIC can improve brain tissue oxygen supply. In current study, we employed a mouse model of stroke created by middle cerebral artery occlusion (MCAO) to investigate the effect of RIC on oxygen supply to the ischemic brain tissue using a hypoxyprobe system. Erythrocyte oxygen-carrying capacity and tissue oxygen exchange were assessed by measuring oxygenated hemoglobin and oxygen dissociation curve. We found that RIC significantly mitigated hypoxic signals and decreased neural cell death, thereby preserving neurological functions. The tissue oxygen exchange was markedly enhanced, along with the elevated hemoglobin P50 and right-shifted oxygen dissociation curve. Intriguingly, RIC markedly elevated 2,3-biphosphoglycerate (2,3-BPG) levels in erythrocyte, and the erythrocyte 2,3-BPG levels were highly negatively correlated with the hypoxia in the ischemic brain tissue. Further, adoptive transfusion of 2,3-BPG-rich erythrocytes prepared from RIC-treated mice significantly enhanced the oxygen supply to the ischemic tissue in MCAO mouse model. Collectively, RIC protects against ischemic stroke through improving oxygen supply to the ischemic brain tissue where the enhanced tissue oxygen delivery and exchange by RIC-induced 2,3-BPG-rich erythrocytes may play a role.
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http://dx.doi.org/10.1177/0271678X20952264DOI Listing
September 2020

Publisher Correction: Rapid endothelial cytoskeletal reorganization enables early blood-brain barrier disruption and long-term ischaemic reperfusion brain injury.

Nat Commun 2020 08 25;11(1):4335. Epub 2020 Aug 25.

Center of Cerebrovascular Disease Research, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15213, USA.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.
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http://dx.doi.org/10.1038/s41467-020-18263-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7447756PMC
August 2020

Glycosylated Hemoglobin A1c Predicts Intracerebral Hemorrhage with Acute Ischemic Stroke Post-Mechanical Thrombectomy.

J Stroke Cerebrovasc Dis 2020 Sep 15;29(9):105008. Epub 2020 Jun 15.

Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China. Electronic address:

Background: Intracerebral hemorrhage, including symptomatic intracerebral hemorrhage, is a serious post-mechanical thrombectomy complication in patients with acute ischemic stroke. We aimed to determine whether glycosylated hemoglobin A1c parameters could predict intracerebral hemorrhage in this patient population.

Methods: We enrolled patients with acute occlusion of the internal carotid artery or proximal middle cerebral artery and who had undergone mechanical thrombectomy. According to the glycosylated hemoglobin A1c level (%) assessed during the hospital stay, the patients were divided into two groups: > 6.5% and ≤ 6.5%. Intracerebral hemorrhage was evaluated and classified based on cranial computed tomography scans obtained within 24-48 h or when neurological conditions worsened. We assessed the outcome at the end of 90 days using the modified Rankin Scale scores.

Results: Among 202 patients, 86 (42.6%) suffered intracerebral hemorrhage, while 25 (12.4%) had symptomatic intracerebral hemorrhage; 35.6% of the patients had a favorable outcome (modified Rankin Scale scores 0-2). Multivariable analysis demonstrated an association of glycosylated hemoglobin A1c > 6.5% with intracerebral hemorrhage. Furthermore, glycosylated hemoglobin A1c > 6.5% was independently associated with symptomatic intracerebral hemorrhage (OR, 2.136; 95% CI, 1.279-3.567; P = 0.004). In addition, glycosylated hemoglobin A1c > 6.5% was significantly associated with increased mortality (OR, 1.511; 95% CI, 1.042-2.191; P = 0.029) and negatively associated with favorable outcome (OR, 0.480; 95% CI, 0.296-0.781; P = 0.003) at 90 days.

Conclusions: Glycosylated hemoglobin A1c is an independent predictor of intracerebral hemorrhage (specifically, symptomatic intracerebral hemorrhage) in patients with acute ischemic stroke treated with mechanical thrombectomy. Further studies are needed to validate these findings.
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http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2020.105008DOI Listing
September 2020