A novel score for early prediction of urinary tract infection risk in patients with acute ischemic stroke: a nomogram-based retrospective cohort study.

This study aimed to construct and externally validate a user-friendly nomogram-based scoring model for predicting the risk of urinary tract infections (UTIs) in patients with acute ischemic stroke (AIS). A retrospective real-world cohort study was conducted on 1748 consecutive hospitalized patients with AIS. Out of these patients, a total of 1132 participants were ultimately included in the final analysis, with 817 used for model construction and 315 utilized for external validation. Multivariate regression analysis was applied to develop the model. The discriminative capacity, calibration ability, and clinical effectiveness of the model were evaluated. The overall incidence of UTIs was 8.13% (92/1132), with Escherichia coli being the most prevalent causative pathogen in patients with AIS. After multivariable analysis, advanced age, female gender, National Institute of Health Stroke Scale (NIHSS) score ≥ 5, and use of urinary catheters were identified as independent risk factors for UTIs. A nomogram-based SUNA model was constructed using these four factors (Area under the receiver operating characteristic curve (AUC) = 0.810), which showed good discrimination (AUC = 0.788), calibration, and clinical utility in the external validation cohort. Based on four simple and readily available factors, we derived and externally validated a novel and user-friendly nomogram-based scoring model (SUNA score) to predict the risk of UTIs in patients with AIS. The model has a good predictive value and provides valuable information for timely intervention in patients with AIS to reduce the occurrence of UTIs.

Ischemic insular damage and stress ulcer in patients of acute ischemic stroke.

BACKGROUND AND AIMS: Stress ulcer (SU) is a common complication in patients with acute ischemic stroke. The relationship of infarction location and the incidence of SU was unclear. Herein, we aim to investigate the association between ischemic insular damage and the development of SU. METHODS: Data were retrieved from the SPARK study (Effect of Cardiac Function on Short-Term Functional Prognosis in Patients with Acute Ischemic Stroke). We included the patients who had experienced an ischemic stroke within 7 days. The diagnosis of SU was based on clinical manifestations, including hematemesis, bloody nasogastric tube aspirate, or hematochezia. Evaluation of ischemic insular damage was conducted through magnetic resonance imaging. Cyclo-oxygenase regression analysis and Kaplan-Meier survival curves were used to assess the relationship between ischemic insular damage and the occurrence of SU. RESULTS: Among the 1357 patients analyzed, 110 (8.1%) developed SUs during hospitalization, with 69 (6.7%) experiencing infarctions in the anterior circulation. After adjusting for potential confounders, patients with ischemic insular damage exhibited a 2.16-fold higher risk of developing SUs compared to those without insular damage (p = .0206). Notably, among patients with infarctions in the anterior circulation, those with insular damage had a 2.21-fold increased risk of SUs (p = .0387). Moreover, right insular damage was associated with a higher risk of SUs compared to left insular damage or no insular damage (p for trend = .0117). Kaplan-Meier curves demonstrated early separation among groups, persisting throughout the follow-up period (all p < .0001). CONCLUSIONS: This study identified a significant independent correlation between ischemic insular damage, particularly on the right side, and the development of SU during hospitalization, indicating the need to consider prophylactic acid-suppressive treatment for patients with ischemic insular damage.

Circulating HMGB1 in acute ischemic stroke and its association with post-stroke cognitive impairment.

Background: Ischemic stroke frequently leads to a condition known as post-stroke cognitive impairment (PSCI). Timely recognition of individuals susceptible to developing PSCI could facilitate the implementation of personalized strategies to mitigate cognitive deterioration. High mobility group box 1 (HMGB1) is a protein released by ischemic neurons and implicated in inflammation after stroke. Circulating levels of HMGB1 could potentially serve as a prognostic indicator for the onset of cognitive impairment following ischemic stroke. Objective: To investigate the predictive value of circulating HMGB1 concentrations in the acute phase of ischemic stroke for the development of cognitive dysfunction at the 3-month follow-up. Methods: A total of 192 individuals experiencing their initial episode of acute cerebral infarction were prospectively recruited for this longitudinal investigation. Concentrations of circulating HMGB1 were quantified using an enzyme-linked immunosorbent assay (ELISA) technique within the first 24 hours following hospital admission. Patients underwent neurological evaluation including NIHSS scoring. Neuropsychological evaluation was conducted at the 3-month follow-up after the cerebrovascular event, employing the Montreal Cognitive Assessment (MoCA) as the primary tool for assessing cognitive performance. Multivariable logistic regression models were employed to investigate the relationship between circulating HMGB1 concentrations and cognitive dysfunction following stroke, which was operationalized as a MoCA score below 26, while controlling for potential confounders including demographic characteristics, stroke severity, vascular risk factors, and laboratory parameters. Results: Of 192 patients, 84 (44%) developed PSCI. Circulating HMGB1 concentrations were significantly elevated in individuals who developed cognitive dysfunction following stroke compared to those who maintained cognitive integrity (8.4 ± 1.2 ng/mL vs 4.6 ± 0.5 ng/mL, respectively; p < 0.001). The prevalence of PSCI showed a dose-dependent increase with higher HMGB1 quartiles. After controlling for potential confounders such as demographic factors (age, gender, and education), stroke severity, vascular risk factors, and laboratory parameters in a multivariable logistic regression model, circulating HMGB1 concentrations emerged as a significant independent predictor of cognitive dysfunction following stroke (regression coefficient = 0.236, p < 0.001). Conclusion: Circulating HMGB1 concentrations quantified within the first 24 hours following acute cerebral infarction are significantly and independently correlated with the likelihood of developing cognitive dysfunction at the 3-month follow-up, even after accounting for potential confounding factors. HMGB1 may be a novel biomarker to identify patients likely to develop post-stroke cognitive impairment for targeted preventive interventions.

Acute ischemic stroke in tuberculous meningitis.

Background: The underlying mechanism for stroke in patients with tuberculous meningitis (TBM) remains unclear. This study aimed to investigate the predictors of acute ischemic stroke (AIS) in TBM and whether AIS mediates the relationship between inflammation markers and functional disability. Methods: TBM patients admitted to five hospitals between January 2011 and December 2021 were consecutively observed. Generalized linear mixed model and subgroup analyses were performed to investigate predictors of AIS in patients with and without vascular risk factors (VAFs). Mediation analyses were performed to explore the potential causal chain in which AIS may mediate the relationship between neuroimaging markers of inflammation and 90-day functional outcomes. Results: A total of 1,353 patients with TBM were included. The percentage rate of AIS within 30 days after admission was 20.4 (95% CI, 18.2-22.6). A multivariate analysis suggested that age ≥35 years (OR = 1.49; 95% CI, 1.06-2.09; P = 0.019), hypertension (OR = 3.56; 95% CI, 2.42-5.24; P < 0.001), diabetes (OR = 1.78; 95% CI, 1.11-2.86; P = 0.016), smoking (OR = 2.88; 95% CI, 1.68-4.95; P < 0.001), definite TBM (OR = 0.19; 95% CI, 0.06-0.42; P < 0.001), disease severity (OR = 2.11; 95% CI, 1.50-2.90; P = 0.056), meningeal enhancement (OR = 1.66; 95% CI, 1.19-2.31; P = 0.002), and hydrocephalus (OR = 2.98; 95% CI, 1.98-4.49; P < 0.001) were associated with AIS. Subgroup analyses indicated that disease severity (P for interaction = 0.003), tuberculoma (P for interaction = 0.008), and meningeal enhancement (P for interaction < 0.001) were significantly different in patients with and without VAFs. Mediation analyses revealed that the proportion of the association between neuroimaging markers of inflammation and functional disability mediated by AIS was 16.98% (95% CI, 7.82-35.12) for meningeal enhancement and 3.39% (95% CI, 1.22-6.91) for hydrocephalus. Conclusion: Neuroimaging markers of inflammation were predictors of AIS in TBM patients. AIS mediates < 20% of the association between inflammation and the functional outcome at 90 days. More attention should be paid to clinical therapies targeting inflammation and hydrocephalus to directly improve functional outcomes.

Can the Glasgow prognostic score predict ischemic stroke in patients with infective endocarditis?

OBJECTIVE: The Glasgow prognosis score is a simple parameter calculated using serum levels of albumin and C-reactive protein. The aim of this study was to examine whether this parameter may predict ischemic stroke in patients with infective endocarditis. METHODS: A total of 80 patients who were diagnosed with definitive infective endocarditis according to Duke criteria between 2016 and 2023 were included in the study. Glasgow prognosis score was based on serum levels of albumin and C-reactive protein. In imaging methods, patients were divided into two groups according to whether they had a stroke or not. These two groups were compared in terms of biochemical parameters, and infective endocarditis findings on echocardiography and Glasgow prognosis score. RESULTS: We found that the results were statistically similar except for serum C-reactive protein (Group 1: 54.9±71.1 and Group 2: 39±70.7; p=0.03), neutrophil (Group 1: 19.8±10.8*109/L and Group 2: 13.3±7.3*109/L; p=0.014), albumin (Group 1: 2.3±0.6 and Group 2: 2.8±0.5; p=0.03), and Glasgow prognosis score (Group 1: median 2, min.-max. (1-2) and Group 2: median 1, min.-max. (0-1); p=0.004). In the receiver operating characteristics analysis, Glasgow prognosis score had 82.4% sensitivity and 58.3% specificity in predicting ischemic stroke if the Glasgow prognosis score cutoff was ≥1. In multivariate logistic regression analysis, chronic renal failure [odds ratio (OR): 1.098; 95% confidence interval: 1.054-1.964; p=0.044], age (OR: 1.050; 95%CI 1.006-1.096; p=0.024), and Glasgow prognosis score (OR: 0.695; 95%CI 0.411-0.949; p=0.035) were independent variables in predicting ischemic stroke. CONCLUSION: High Glasgow prognosis score is an independent predictor of ischemic stroke in patients with infective endocarditis. Glasgow prognosis score, determined using albumin and C-reactive protein levels, is a simple and practical index for predicting the prognosis of patients hospitalized with infective endocarditis.

Leukocyte counts and ratios as potential predictors of large vessel occlusion in acute ischemic stroke: A retrospective cohort study.

Leukocyte counts and ratios are independent biomarkers to determine the severity and prognosis of acute ischemic stroke (AIS). In AIS, the connection between leukocytes and large vessel occlusion (LVO) is uncertain. This study aims to determine the relationship between the existence of LVO and leukocyte counts and ratios on admission to AIS. Patients were retrospectively evaluated within six hours of AIS starting between January 2019 and April 2023. On admission, blood specimens were collected, and leukocyte subtype counts were promptly analyzed. Computed tomography or digital subtraction angiography were utilized to verify the existence of LVO. Regression analysis and receiver operating characteristic (ROC) curves were employed to investigate the connections between the counts and ratios of leukocytes and the existence of LVO, as well as the discriminatory ability of these variables in predicting LVO. Total white blood cell (WBC) count, neutrophil count, and neutrophil-to-lymphocyte ratio (NLR) were substantially higher in the LVO existence group compared to the LVO absence group, whereas the ratio of eosinophils to neutrophils (ENR × 102) was lower (P < .001, respectively). Significant associations were observed between total WBC counts, neutrophil counts, NLR, and ENR × 102 and the existence of LVO (P < .001, respectively). Total WBC counts, neutrophil counts, NLR, and ENR × 102 had respective areas under the curves (AUC) of 0.730, 0.748, 0.704, and 0.680 for identifying LVO. Our results show that in AIS patients, the existence of LVO is independently associated with elevated total WBC and neutrophil counts, high NLR, and low ENR × 102 levels. Neutrophil and total WBC counts, as well as NLR and levels of ENR × 102, may serve as potential biomarkers for predicting LVO. Neuroinflammation, based on the existence of LVO, should be given particular attention in future investigations.

Role of the gut microbiota in complications after ischemic stroke.

Ischemic stroke (IS) is a serious central nervous system disease. Post-IS complications, such as post-stroke cognitive impairment (PSCI), post-stroke depression (PSD), hemorrhagic transformation (HT), gastrointestinal dysfunction, cardiovascular events, and post-stroke infection (PSI), result in neurological deficits. The microbiota-gut-brain axis (MGBA) facilitates bidirectional signal transduction and communication between the intestines and the brain. Recent studies have reported alterations in gut microbiota diversity post-IS, suggesting the involvement of gut microbiota in post-IS complications through various mechanisms such as bacterial translocation, immune regulation, and production of gut bacterial metabolites, thereby affecting disease prognosis. In this review, to provide insights into the prevention and treatment of post-IS complications and improvement of the long-term prognosis of IS, we summarize the interaction between the gut microbiota and IS, along with the effects of the gut microbiota on post-IS complications.

Rare instances of concomitant acute myocardial infarction and stroke.

Cardio-cerebral infarction (CCI) is a term coined to describe concomitant myocardial infarction and acute ischemic stroke. Acute myocardial infarction and stroke, as separate events, constitute some of the most important causes for disability and mortality in aging societies. Stroke can either occur simultaneously with myocardial infarction or become a serious complication of myocardial infarction and/or its treatment. The frequency of CCI has been reported at a 0.009% incidence rate in stroke patients and is associated with an extremely high mortality. Because of the rare occurrence of CCI, there are currently no guidelines for assessing its diagnosis and optimal treatment. Therefore, currently, the management of CCI cases needs to be individualized. Hopefully, in the future, the results of large clinical trials or prospective registries are expected to enhance our understanding of managing concomitant acute MI and stroke. In this review we have focused on the current literacy in the diagnosis and treatment of CCIs. The paper illustrates potential distinct scenarios of CCI through the analysis of three patient cases (Fig. 5, Ref. 65). Text in PDF www.elis.sk Keywords: myocardial infarction, stroke, cardio-cerebral infarction, carotid artery stenting, cardiac surgery.

ADAMTS13 deficiency exacerbates neuroinflammation by targeting matrix metalloproteinase-9 in ischemic brain injury.

Our design aimed to explore the potential involvement of matrix metalloproteinase-9 (MMP-9) in the inflammatory response associated with acute ischemic stroke (AIS). We also aimed to preliminarily examine the potential impact of a disintegrin-like and metalloprotease with thrombospondin type I repeats-13 (ADAMTS13) on MMP-9 in AIS. We conducted oxygen-glucose deprivation models of microglia cells and mice models of AIS with middle cerebral artery occlusion (MCAO). We assessed the expression pattern of MMP-9 with western blotting (WB) and real-time quantitative PCR both in vivo and in vitro. MMP-9 downregulation was achieved by using ACE inhibitors such as trandolapril. For the MCAO model, we used ADAMTS13-deficient mice. We then evaluated the related neurological function scores, cerebral edema and infarct volume. The levels of inflammation-related proteins, such as COX2 and iNOS, were assessed using WB, and the expression of inflammatory cytokines was measured via enzyme-linked immuno sorbent assay in vivo. Our findings indicated that MMP-9 was up-regulated while ADAMTS13 was down-regulated in the MCAO model. Knockdown of MMP-9 reduced both inflammation and ischemic brain injury. ADAMTS13 prevented brain damage, improved neurological function and decreased the inflammation response in mice AIS models. Additionally, ADAMTS13 alleviated MMP-9-induced neuroinflammation in vivo. It showed that ADAMTS13 deficiency exacerbated ischemic brain injury through an MMP-9-dependent inflammatory mechanism. Therefore, the ADAMTS13-MMP-9 axis could have therapeutic potential for the treatment of AIS.

Study of Serum Electrolytes (Sodium and Potassium) Abnormalities in Acute Stroke.

Stroke is the common cause of death and disability worldwide, as well as in Bangladesh. Serum electrolytes abnormalities or dyselectrolytaemia is one of the major acute complications of stroke. Dyselectrolytaemia or serum electrolytes (sodium and potassium) abnormalities are more common in patients with acute stroke that can be easily measured. The study was planned to find out the serum electrolytes (sodium and potassium) abnormalities in acute stroke patients. This cross-sectional study was conducted in the Department of Neurology and Medicine, Mymensingh Medical College and Hospital from January 2019 to June 2020. Total 84 purposively selected patients with acute strokes were evaluated following informed written consent. Diagnosis was confirmed by neuroimaging of brain. Moreover, serum electrolytes level was measured for each patient. Data were collected by interviews, clinical examinations & laboratory investigations of the patients using a case record form and analysis was carried out by the help of SPSS 25.0. Mean age of the patients with acute strokes were 57.65±15.79 years. About two thirds (60.7%) of the patients were male and the remaining (39.3%) were female. Sodium imbalances were observed in 32.2% and potassium imbalances in 25.0% cases. About 66.7% haemorrhagic strokes patients and 42.2% ischaemic strokes patients had dyselectrolytaemia (p<0.05). More than twenty eight percent (28.6%) of all stroke patients had hyponatraemia, which was more common (35.9%) among haemorrhagic strokes patients (p<0.05). Of all stroke patients 21.4% had hypokalaemia, which was more common (28.2%) in haemorrhagic strokes patients (p<0.05). This study reveals that, serum electrolytes (sodium and potassium) abnormalities are more common in haemorrhagic than ischaemic strokes, which is mainly hyponatraemia and hypokalaemia.

Investigation of the Association between Bilateral Selective Anterograde Cerebral Perfusion and Postoperative Ischemic Stroke in Obese Patients with Emergency Surgery for Acute Type A Aortic Dissection.

Background and objectives: The relationship between cerebral perfusion and new postoperative ischemic stroke in obese patients is not well defined. The aim of this study was to investigate the association between selective bilateral anterograde cerebral perfusion and new postoperative ischemic stroke in obese patients with emergency surgery for acute type A aortic dissection. Materials and methods: A total of 292 patients with emergency surgery for acute type A aortic dissection were included in this study. Patients with hemorrhagic stroke or ischemic stroke with severe neurological dysfunction at admission that were not candidates for surgery; patients who died in the first 48 h after intensive care admission and patients with incomplete medical records were excluded. Results: The mean age was 59.42 ± 10.68 years and the mean Euroscore was 9.12 ± 1.63. Obesity was present in 76.4%, the incidence of new postoperative ischemic stroke was 27.5%, and the postoperative mortality rate was 26.7%. The mean cardiopulmonary bypass time was 206.81 ± 75.48 min, the aortic cross-clamp time was 118.2 ± 46.42 min, and 90% of cases required cerebral perfusion. The mean cerebral perfusion time was 30.8 ± 24.41 min. Obese patients had a higher frequency of in-hospital death (p = 0.009), smoking (p = 0.036), hypertension (p = 0.023), left common carotid artery dissection (p < 0.001), right common carotid artery dissection (p = 0.029), femoral artery cannulation (p = 0.026), aortic root replacement (p = 0.009), aortic valve replacement (p = 0.005) and early reintervention for bleeding (p = 0.004). Using logistic regression, selective bilateral anterograde cerebral perfusion over 40 min in obese patients was independently associated with new postoperative ischemic stroke (OR = 2.35; 95%CI = 1.36-4.86; p = 0.021). Conclusions: A patient-tailored strategy for cerebral perfusion should be considered in obese patients, considering the high atheromatous burden of the supra-aortic vessels in these patients and the potential risk of atheromatous embolization associated with this technique.

Dysphagia in Ischaemic Stroke Patients: One Centre Retrospective Study.

The aim of this study was to examine the frequency of dysphagia in patients with ischaemic stroke. It was crucial to evaluate the relationship between swallowing disorders and selected demographic and clinical indicators. Additionally, the association between various patient feeding methods and selected demographic and clinical factors was assessed. Based on the analysis of medical documentation, we identified the most important clinical parameters, including demographic data, the frequency of stroke risk factors, the location of the ischaemic lesion, cortical involvement, stroke severity as measured by the NIHSS (Nationale Institutes of Health Stroke Scale), and the methods of feeding post-stroke patients. Dysphagia was observed in 65.9% of the patients in the study group. Hypertension was the most common chronic illness in the studied population of ischemic stroke patients (91.8% of patients). Diet modification (35.7%) and PEG (25%) were the frequent methods of feeding in patients with confirmed dysphagia. Age played a significant role in determining the feeding methods in patients with dysphagia. Patients with a PEG (Percutaneous Endoscopic Gastrostomy) tube were the oldest (79.37 ± 10.80) and 75% of them had pneumonia. Early identification of swallowing difficulties in stroke patients is critical in determining an appropriate and safe feeding plan, as well as initiating logopedics therapy to improve swallowing efficacy and minimize pulmonary complications.

Development of insomnia in patients with stroke: A systematic review and meta-analysis.

BACKGROUND AND AIM: Stroke is a serious threat to human life and health, and post-stroke insomnia is one of the common complications severely impairing patients' quality of life and delaying recovery. Early understanding of the relationship between stroke and post-stroke insomnia can provide clinical evidence for preventing and treating post-stroke insomnia. This study was to investigate the prevalence of insomnia in patients with stroke. METHODS: The Web of Science, PubMed, Embase, and Cochrane Library databases were used to obtain the eligible studies until June 2023. The quality assessment was performed to extract valid data for meta-analysis. The prevalence rates were used a random-efect. I2 statistics were used to assess the heterogeneity of the studies. RESULTS: Twenty-six studies met the inclusion criteria for meta-analysis, with 1,193,659 participants, of which 497,124 were patients with stroke.The meta-analysis indicated that 150,181 patients with stroke developed insomnia during follow-up [46.98%, 95% confidence interval (CI): 36.91-57.18] and 1806 patients with ischemic stroke (IS) or transient ischemic attack (TIA) developed insomnia (47.21%, 95% CI: 34.26-60.36). Notably, 41.51% of patients with the prevalence of nonclassified stroke developed insomnia (95% CI: 28.86-54.75). The incidence of insomnia was significantly higher in patients with acute strokes than in patients with nonacute strokes (59.16% vs 44.07%, P < 0.0001).Similarly, the incidence of insomnia was significantly higher in the patients with stroke at a mean age of ≥65 than patients with stroke at a mean age of <65 years (47.18% vs 40.50%, P < 0.05). Fifteen studies reported the follow-up time. The incidence of insomnia was significantly higher in the follow-up for ≥3 years than follow-up for <3 years (58.06% vs 43.83%, P < 0.05). Twenty-one studies used the Insomnia Assessment Diagnostic Tool, and the rate of insomnia in patients with stroke was 49.31% (95% CI: 38.59-60.06). Five studies used self-reporting, that the rate of insomnia in patients with stroke was 37.58% (95% CI: 13.44-65.63). CONCLUSIONS: Stroke may be a predisposing factor for insomnia. Insomnia is more likely to occur in acute-phase stroke, and the prevalence of insomnia increases with patient age and follow-up time. Further, the rate of insomnia is higher in patients with stroke who use the Insomnia Assessment Diagnostic Tool.

Personalised stroke evaluation and management: tailoring individualised patient care for hereditary haemorrhagic telangiectasia.

SummaryHereditary haemorrhagic telangiectasia (HHT) has an estimated prevalence of 1 in 5000-8000 individuals globally with pulmonary arteriovenous malformations (PAVMs) affecting approximately 15%-50% of HHT patients. Ischaemic stroke is a known complication of PAVMs that affects ≤30% of patients with PAVMs. Studies have shown that patients with PAVMs have ischaemic stroke a decade earlier than routine stroke. The predominant mechanism of ischaemic stroke in HHT patients is paradoxical embolism due to PAVMs, but most HHT-related PAVMs are asymptomatic. Additionally, HHT is often underdiagnosed in patients and poses a challenge to physicians due to its rarity. We present a case of a patient with ischaemic stroke who was subsequently diagnosed with HHT and found to have a PAVM on further evaluation. This case highlights the importance of using an individualised patient-centred stroke evaluation and screening for PAVMs in patients who had a stroke with possible or suspected HHT and definite HHT.

Time­dependent changes in blood cells, NIHSS and mRS according to reperfusion treatment type in stroke patients who developed hemorrhagic complication.

Hemorrhagic complications may be seen following reperfusion therapy with rtPA and/or thrombectomy after acute ischemic stroke (AIS). Neutrophils, lymphocytes, and platelets have important roles in the inflammatory and immune responses that develop in these patients. We investigated time­dependent changes in blood cells, NIHSS and mRS values according to type of reperfusion therapy in AIS patients who developed cerebral hemorrhage. In AIS patients who underwent rtPA and/or thrombectomy and developed cerebral hemorrhage within the first 24 hours after treatment, leukocyte, neutrophil, lymphocyte, platelet counts and their ratios were recorded on admission, 1st, 3rd, and 7th days. NIHSS values on admission, 3rd days and mRS values on admission, discharge, and the 3rd month were recorded. These values were compared according to the type of reperfusion therapy. Out of 436 AIS patients, rtPA was applied in 50.5%, thrombectomy in 28.2%, and rtPA+thrombectomy in 21.3%. Hemorrhage developed in 25.5% of the patients. Patients treated with thrombectomy had a greater rate of cerebral hemorrhage. Pre­stroke mRS values were lower in all therapy types than mRS scores at discharge and the 3rd month. The NIHSS scores did not differ significantly in 3 days. Depending on the type of reperfusion treatment, there are a few time­dependent significant changes observed in the blood cell counts and ratios. In conclusion, there is a relation between the type of reperfusion therapy and the time­dependent changes in blood cells and ratios as well as mRS scores among AIS patients who have undergone rtPA and/or thrombectomy and developed cerebral hemorrhage.

Complement Proteins in Serum Astrocyte-Derived Exosomes Are Associated with Poststroke Cognitive Impairment in Type 2 Diabetes Mellitus Patients.

Background: The complement system plays crucial roles in cognitive impairment and acute ischemic stroke (AIS). High levels of complement proteins in plasma astrocyte-derived exosomes (ADEs) were proven to be associated with Alzheimer's disease. We aimed to investigate the relationship of complement proteins in serum ADEs with poststroke cognitive impairment in type 2 diabetes mellitus (T2DM) patients. Methods: This study analyzed 197 T2DM patients who suffered AIS. The Beijing version of the Montreal Cognitive Assessment (MoCA) was used to assess cognitive function. Complement proteins in serum ADEs were quantified using ELISA kits. Results: Mediation analyses showed that C5b-9 and C3b in serum ADEs partially mediate the impact of obstructive sleep apnea (OSA), depression, small vessel disease (SVD), and infarct volume on cognitive function at the acute phase of AIS in T2DM patients. After adjusting for age, sex, time, and interaction between time and complement proteins in serum ADEs, the mixed linear regression showed that C3b and complement protein Factor B in serum ADEs were associated with MoCA scores at three-, six-, and twelve-months after AIS in T2DM patients. Conclusions: Our study suggested that the impact of OSA, depression, SVD, and infarct volume on cognitive impairment in the acute stage of AIS may partially mediate through the complement proteins in serum ADEs. Additionally, the complement proteins in serum ADEs at the acute phase of AIS associated with MoCA scores at three-, six-, twelve months after AIS in T2DM patients.REGISTRATION: URL: http://www.chictr.org.cn/,ChiCTR1900021544.

Clinical and neuroanatomical predictors of post-stroke fatigue.

INTRODUCTION: Post-stroke fatigue (PSF) has been described as early exhaustion with tiredness that develops during physical or mental activity and generally does not improve with rest. There are inconsistent findings on the relationship between the characteristics of the ischemic brain lesion and PSF. However, some studies suggest that specific neuroanatomical and neuroplastic changes could explain post-stroke fatigue. The aim was to evaluate the severity of PSF in relation to the location and the size of the ischemic lesion in acute stroke patients to establish possible predictors of PSF. PATIENTS AND METHODS: We performed a prospective observational study to establish potential early predictors of long-term PSF, which was assessed using the Fatigue Assessment Scale six months after ischemic stroke. After segmenting brain infarcts on Diffusion-Weighted Imaging (DWI) images, we studied the association with PSF using Voxel-Based Lesion-Symptom Mapping (VLSM). RESULTS: Out of 104 patients, 61 (59 %) reported PSF. Female sex and history of diabetes mellitus were associated with a greater risk of developing PSF. The association of PSF with female sex was confirmed in a replication cohort of 50 patients. The ischemic lesion volume was not associated with PSF, and VBLSM analysis did not identify any specific brain area significantly associated with PSF. CONCLUSIONS: PSF is frequent in stroke patients, especially women, even after six months. The absence of neuroanatomical correlates of PSF suggests that it is a multifactorial process with biological, psychological, and social risk factors that require further study.

Early neurological changes following endovascular therapy for acute stroke due to intracranial atherosclerotic disease.

BACKGROUND: Endovascular therapy (EVT) reduces functional disability in patients with acute large vessel occlusion (LVO). However, the early neurological change after EVT may be limited in patients with intracranial atherosclerotic disease (ICAD). METHODS: We analyzed the Japanese Registry of NeuroEndovascular Therapy (JR-NET) 4 which was a retrospective, nationwide, multicenter registry of patients with LVO between 2015 and 2019. We compared the early neurological change, efficacy and safety of EVT for acute LVO in ICAD and other etiologies. The primary outcome was NIHSS improvement ≥10 points, and secondary outcome were NIHSS worsening ≥4 points 7 days after EVT, effective reperfusion rate, 30-day functional outcomes, and safety outcomes. RESULTS: Among the 6710 enrolled patients, 610 (9.1%) had ICAD. The ICAD group was younger (mean 72.0 vs. 75.8 years) and predominantly male (63.4% vs. 56.0%), had lower NIHSS scores before EVT (median 16 vs. 18), and underwent percutaneous transluminal angioplasty and stenting more frequently (43.0% vs. 4.4%, 12.3% vs. 4.4%). In the ICAD group, NIHSS improvement was significantly lower (adjusted odds ratio (aOR) [95% confidence interval (95%CI)] 0.52 [0.41-0.65]), NIHSS worsening was significantly higher (aOR [95%CI] 1.76 [1.31-2.34]), and effective reperfusion was significantly lower (aOR [95%CI] 0.47 [0.36-0.60]). Fewer patients with ICAD had modified Rankin scale 0-2 at 30 days (aOR [95%CI] 0.60 [0.47-0.77]). The risk of acute reocclusion was more prominent in the ICAD group (aOR [95%CI] 4.03 [1.98-8.21]). CONCLUSIONS: Improvement in neurological severity after EVT was lower in patients with LVO and ICAD.

Prognosis of patients with coexisting obesity and malnutrition after ischemic stroke: A cohort study.

BACKGROUND: The double burden of malnutrition, defined as the coexistence of obesity and malnutrition, is an increasing global health concern and is unclear in patients after ischemic stroke. The current study explored the combined impacts of obesity and malnutrition on patients with ischemic stroke. METHODS: We conducted a single-center prospective cohort study with patients with ischemic stroke enrolled in Minhang Hospital in China between January 2018 and December 2022. Patients were stratified into four categories based on their obesity (defined by body mass index) and nutritional status (classified according to the Controlling Nutritional Status score): (1) nourished nonobese, (2) malnourished nonobese, (3) nourished obese, and (4) malnourished obese. The primary end points were poor outcomes and all-cause mortality at 3 months. RESULTS: A total of 3160 participants with ischemic stroke were included in our study, of which 64.7% were male and the mean age was 69 years. Over 50% of patients were malnourished. At 3-month follow-up, the malnourished nonobese had the worst outcomes (34.4%), followed by the malnourished obese (33.2%), nourished nonobese (25.1%), and nourished obese (21.8%; P < 0.001). In multivariable analyses, with nourished nonobese group as the reference, the malnourished nonobese group displayed poorer outcomes (odds ratio [OR], 1.395 [95% CI, 1.169-1.664], P < 0.001) and higher all-cause mortality (OR, 1.541 [95% CI, 1.054-2.253], P = 0.026), but only a nonsignificant increase in poor prognosis rate (33.2% vs. 25.1%, P = 0.102) and mortality (4.2% vs. 3.6%, P = 0.902) were observed in the malnourished obese group. CONCLUSION: A high prevalence of malnutrition is observed in the large population suffering from ischemic attack, even in the obese. Malnourished patients have the worst prognosis particularly in those with severe nutritional status regardless of obesity, while the best functional outcomes and the lowest mortality are demonstrated in nourished obese participants.

Secondary stroke prevention in people with atrial fibrillation: treatments and trials.

Atrial fibrillation is one of the most common cardiac arrhythmias and is a major cause of ischaemic stroke. Recent findings indicate the importance of atrial fibrillation burden (device-detected, subclinical, or paroxysmal and persistent or permanent) and whether atrial fibrillation was known before stroke onset or diagnosed after stroke for the risk of recurrence. Secondary prevention in patients with atrial fibrillation and stroke aims to reduce the risk of recurrent ischaemic stroke. Findings from randomised controlled trials assessing the optimal timing to introduce direct oral anticoagulant therapy after a stroke show that early start (ie, within 48 h for minor to moderate strokes and within 4-5 days for large strokes) seems safe and could reduce the risk of early recurrence. Other promising developments regarding early rhythm control, left atrial appendage occlusion, and novel factor XI inhibitor oral anticoagulants suggest that these therapies have the potential to further reduce the risk of stroke. Secondary prevention strategies in patients with atrial fibrillation who have a stroke despite oral anticoagulation therapy is an unmet medical need. Research advances suggest a heterogeneous spectrum of causes, and ongoing trials are investigating new approaches for secondary prevention in this vulnerable patient group. In patients with atrial fibrillation and a history of intracerebral haemorrhage, the latest data from randomised controlled trials on stroke prevention shows that oral anticoagulation reduces the risk of ischaemic stroke but more data are needed to define the safety profile.