Search Results for: Tumore prostata, test della saliva piu’ attendibile del PSA

Stroke, Volume 56, Issue Suppl_1, Page ATP268-ATP268, February 1, 2025. Introduction:Xylitol, a sugar alcohol with a global market estimated at 161,500 metric tons, has been linked to increased thrombosis and risk of stroke and heart attack. Older adults with obesity and metabolic syndrome may have decreased elimination of the xylitol metabolite xylose, which may explain the higher observed risk of thrombosis and stroke in older adults who consume foods with sugar alcohols. MicroRNAs (miRs) have been associated with thrombosis and the blood clotting cascade and can provide additional insight about pathogenesis or biomarkers to help establish safe dietary intake guidelines. However, multiomics studies of both xylitol metabolites and these miRs in humans have not been done. This study aims to measure these associations in a sample of adults with obesity and metabolic syndrome.Methods:We analyzed data from a subset ofN=70 obese adults with metabolic syndrome who had both baseline metabolome and miR data from the PRYSMS randomized controlled trial. Pearson’s correlations were used to test associations between xylitol, xylose, and 20 miRs associated with thrombosis and the clotting cascade, using the false discovery rate method to adjust for multiple comparisons.Results:Participants were 55 ± 6 years (range 32-65) and 24% male. The mean BMI was 35.2 ± 7.4 kg/m2, HbA1c was 5.9% ± 0.4, fasting blood glucose was 103 ± 13 mg/dL, HDL cholesterol was 49 ± 10 mg/dL, and triglycerides were 173 ± 63 mg/dL. Xylose concentrations were inversely correlated with six miRs (miR-15b, miR-151a-3p, miR-151a-5p, miR-151b, miR-24-3p, and miR-27a-3p). Relevant target proteins of these miRs may include Factor XI (F11), Fibrinogen Alpha (F1 or FGG_A), Coagulation Factor VIII (F8), Von Wilebrand Factor (VWF), and Toxoplasma gondii (TFP1).Conclusion:Our findings demonstrate an inverse association between xylose levels and six miRs associated with thrombosis and the clotting cascade in adults with obesity and metabolic syndrome. Xylitol metabolite concentration was not associated with any miRs in our sample, suggesting that circulating xylose may be a better indicator of clotting risk. Dietary intake of xylitol-containing foods may provide additional detail about these associations. Future research should explore multiomics relationships to refine and validate these results, to provide a more complex understanding of the biological processes involved for people at risk of T2D and stroke, and to help establish safe guidelines for dietary xylitol intake.

Stroke, Volume 56, Issue Suppl_1, Page ATP293-ATP293, February 1, 2025. Background and Objectives:Left subclavian artery (LSA) is more prone to atherosclerosis than the right one. The study was designed to investigate whether aortic arch types (AAT) was associated with the lateralization of subclavian artery stenosis (SAS).Methods:In this observational prospective registry study, we reviewed the digital subtraction angiography (DSA) database from our comprehensive stroke center between 2015-2023. Patients (age ≥ 18 years) with clinically manifest atherosclerotic vessel disease or risk factors for atherosclerosis and a normal branching pattern of the aortic arch were included. AAT and degree of SAS were determined by DSA. Breslow-Day test and multinomial logistic regression models were performed to identify the association between AAT and SAS.Results:A total of 7,470 patients (mean [SD] age, 57.4 [14.9] years; 5,098 [68.3%] male and 2,372 [31.8%] female; 2,430 [32.5%] aged < 60 years) were included. Among the 7,470 patients, 771 (10.3%) were detected with SAS, including 518 (6.9%) on the left side, 173 (2.3%) on the right side and 80 (1.1%) on the bilateral side. Frequency of AAT Ι, ΙΙ and ΙΙΙ were 1,741 (23.3%), 5,047 (67.6%), and 682 (9.1%) respectively. LSA is more susceptible to atherosclerotic stenosis than right subclavian artery (RSA) with AAT Ι (any degree stenosis: 6.0% vs 2.4%, p < 0.001) and ΙΙ (any degree stenosis: 8.4% vs 2.9%, p < 0.001). We found no significant difference in occurrence of stenosis between LSA and RSA among patient with AAT ΙΙΙ (any degree of stenosis: 10.4% vs 9.2%, p = 0.521) (Figure1). The Breslow-Day test showed that there existed significant differences in the odd ratio (ORs) for the side of subclavian artery across each stratum of AAT (p

Stroke, Volume 56, Issue Suppl_1, Page A142-A142, February 1, 2025. Introduction:Mechanical thrombectomy (MT) dramatically improves the outcome for patients with acute ischemic stroke due to large vessel occlusion (LVO). There are racial and socioeconomic disparities in access to MT. In addition, while thrombectomy-specific data are limited, there are clear urban-rural disparities in access to acute stroke care.Hypothesis:We hypothesized that in a rural state in which the Emergency Medical System (EMS) routes all suspected stroke patients to the nearest available stroke center of any level, there would be a significant association between rural LVO patient location and lower rates of MT.Methods:As part of an ongoing statewide stroke system implementation initiative, Stroke STAT, we prospectively collected data on patients presenting to EMS with suspected stroke due to LVO from 4/30/22 to 10/9/23. As of March, 2023, the Alabama acute stroke system included 10 centers performing thrombectomy (including Comprehensive Stroke Centers (Level 1) and Thrombectomy capable Stroke Centers (Level 2a) out of 81 hospitals in the stroke system. All thrombectomy performing hospitals are located in urban areas, as shown in theFigure. We collected zip and rural-urban commuting area (RUCA) codes of initial EMS contact, age, sex, ethnicity, race, initial NIHSS score, reperfusion treatment rates with thrombolysis or MT, and whether the patient was transferred from one hospital to another in the acute period (transferred). Differences were assessed using Chi-squared, t-test and the appropriate non-parametric methods at 0.05 significance.Results:There were 2,692 patients with suspected stroke due to LVO in the study period, including 1,921 with urban and 771 with rural point of initial EMS contact. There were 497 patients with LVO, including 293 (59%) who underwent MT. As shown inTable 1, there were no differences in rates of MT by age, sex, ethnicity, or race. As shown inTable 2, rural and urban patients had equal access to tPA, but rural patients were less likely to receive MT 80/179 (45%) vs. 213/318 (67%) (p

Stroke, Volume 56, Issue Suppl_1, Page ATP264-ATP264, February 1, 2025. Introduction:Children with cardiac diseases are at an increased risk to develop ischemic stroke that can lead to lifelong neurological deficits. Blood pressure is an important modifiable factor associated with poor neurological outcomes. However, there lacks sufficient evidence to provide patient specific blood pressure guidelines post pediatric ischemic stroke.Objective:We evaluated blood pressure mean and changes in pediatric patients with cardiac diseases within the first 48hours cardiac critical care unit (CCCU) after an arterial ischemic stroke.Method:We conducted a retrospective study of children diagnosed with acute arterial ischemic stroke admitted to the CCCU. We reviewed data on demographics, clinical outcome, radiologic, hemodynamic parameters, and medication. Ischemic lesion volume size was obtained from Diffusion-Weighted Imaging by a full-trained neuroradiologist. Blood pressure percentile was obtained based on age, sex, and the 50thheight range. We contrasted the blood pressure with age and admission year matched CCCU controls without a history of stroke. We used linear regression to model blood pressure trends, t-test to compare continuous data, and chi square analyses to compare discrete data points.Results:Twenty-nine stroke patients (34% female, median age 2.1 years and range 17 years) were included. The majority of patients aged up to 3 years-old, presented with congenital heart defects (69%). Older patients presented more often with acquired heart disease (40%). Blood pressure means and trends differed by age, cardiac disease, and neurological outcomes. Younger patients and those with congenital heart defects had higher blood pressure compared to controls. Older patients or those with acquired heart diseases tended to have lower systolic blood pressure and higher diastolic blood pressure than their control. A third of patients with neurological deficits presented with an average blood pressure greater than the 95thpercentile, while patients with normal neurological status at discharge all had an average blood pressure inferior to the 50thpercentile. Higher blood pressure was associated with worst neurological outcomes, and larger ischemic brain volume size.Conclusion:Patients with cardiac disease have age and cardiac anomaly specific blood pressure after an acute ischemic stroke. Further research into these differences and blood pressure management in this group is crucial to lessening the burden of stroke on this at risk population.

Stroke, Volume 56, Issue Suppl_1, Page A107-A107, February 1, 2025. Introduction:Atrial fibrillation diagnosed after stroke (AFDAS) is common and differs from known atrial fibrillation (KAF), the most common cause of cardioembolic stroke. Because identification of AFDAS warrants administration of oral anticoagulants for secondary prevention, extended cardiac monitoring is often used, yet it is unclear who is most at risk for developing AFDAS. We aimed to determine whether prediction of AFDAS improves when adding genetic risk to clinical risk predictors in a real world clinical population of stroke survivors.Methods:We retrospectively included patients with stroke between June 2003 and April 2017. Characteristics and outcomes were obtained from a data repository at Mass General Brigham (MGB), with chart review of AF diagnosis. Genome-wide polygenic risk scores (PRS) for AF were calculated using recent GWAS summary statistics. Clinical risk was determined using ReCHARGE-AF, a clinical post-stroke AF prediction score recalibrated from the CHARGE-AF score. For a subgroup, we obtained information on rare cardiomyopathy loss-of function genetic variants associated with AF risk. We determined whether patients had KAF, AFDAS or no AF, and used descriptive statistics to compare groups. We used Cox proportional hazards models to predict AFDAS, and calculated c-statistics to determine predictive validity at 1 month, 1 year and 5 years after stroke. We compared performance of clinical and genetic risk models through the DeLong test. We used 1,000-iteration bootstrapping to determine whether the addition of PRS improves model prediction.Results:Of 1004 stroke patients, 900 (90%) were non-Hispanic white, with a mean age of 67. KAF was present in 239 (23.8%) patients, and 87 (8.7%) developed AFDAS. Patients with KAF and AFDAS had higher ReCHARGE-AF scores, higher rates of surface monitors and ILRs, and were more likely to have a high PRS, but did not differ in the presence of rare variants. Addition of PRS to clinical risk was associated with an increased performance at 30 days (AUC 0.784 vs 0.665, p < 0.01), 1 year (AUC 0.738 vs 0.659, p = 0.02) and 5 years (AUC 0.757 vs 0.708, p = 0.01). Addition of PRS was associated with improved discrimination, better reclassification, and a median improvement in risk score.Conclusion:Prediction of AFDAS can be improved by adding polygenic risk scores to clinical risk prediction tools. Future studies are necessary to determine the feasibility of incorporating polygenic risk prediction for AFDAS.

Stroke, Volume 56, Issue Suppl_1, Page ADP44-ADP44, February 1, 2025. Introduction:Patient reported outcomes post-stroke may be more sensitive to meaningful differences than the modified Rankin Scale (mRS). We aimed to compare patient reported outcomes (PROMs) in Mexican Americans (MAs) and non-Hispanic Whites (NHWs) in a community-based study. We also explored the correlation of PROMs with the mRS at 3 months post-stroke.Methods:All patients with ischemic and hemorrhagic stroke (ICH) from mid 2019-2023 in the Brain Attack Surveillance in Corpus Christi (BASIC) project were enrolled. PROMs and mRS were assessed at 3 months post-stroke. PROMs were assessed by the Patient-Reported Outcomes Measurement Information System, (PROMIS), Work and Social Adjustment Scale (WSAS), Economic Quality of Life Survey (EQOL) and ability to return to work and driving.For unadjusted analyses, medians and IQRs were reported for continuous and ordinal variables, with t-test p-values. Chi-squared tests were used for binary variables. For adjusted models, logistic, multinomial, or proportional-odds cumulative logit models were used as appropriate. Multitier inverse probability weighting (IPW) addressed sample attrition, and covariates included age, sex, initial NIHSS, comorbidity count, ischemic vs ICH, and previous stroke.Results:A total of 913 patients were included. Table 1 provides the main results. In the adjusted analysis, MA had significantly lower (worse) PROMIS Global Mental Health score (mean ethnic difference: -2.24, 99% CI: -3.93 to -0.54, p

Stroke, Volume 56, Issue Suppl_1, Page ADP41-ADP41, February 1, 2025. Introduction&Objective:Stroke care is fragmented with reported 30-day readmission rates as high as 10-15%. Novel, cost effective strategies to improve care coordination and address social determinants of care are needed. We sought to evaluate the clinical and financial impact of a home-based stroke care delivery model colloquially called Stroke Mobile (SM).Methods:Patients discharged to home, home health, rehab or skilled nursing facility followed by home from an Ochsner Health hospital in the New Orleans region between July 2021 through December 2022 with stroke (ischemic stroke, TIA, ICH) and on a value-based contract were eligible for the study. Patients were seen at home by an RN and health educator within 30 days of discharge followed by monthly for 3 consecutive months. Thereafter, patients were seen periodically as determined by the care team up to a year. Patients seen by the SM team were compared to a propensity matched control group comprising of patients eligible for care service by the SM team but not enrolled in the program during the study period. Propensity score matching was performed using age, gender, race and chronic conditions as covariates and “nearest neighbor” algorithm with 1:3 match ratio. Parametric (independent sample t-test) and non-parametric (Wilcoxon rank sum, Chi-square) tests were used to test the difference in overall cost (per member per month (pmpm)), 30-day readmissions, and cost of readmission between groups with an error rate set to

Stroke, Volume 56, Issue Suppl_1, Page ADP10-ADP10, February 1, 2025. Introduction:Stroke center designation generally specifies required education for nurses. Our system provides stroke education to hundreds of nurses annually. Traditionally this education has been provided via live or remote lectures or online modules, where content is static, and students play a passive role. In that model, testing is performed at the conclusion of instructional units, known in education as summative assessment. We sought to create a learning environment that is more engaging and interactive, utilizing newer educational technologies.Methods:We investigated educational technologies developed for the K-12 educational space. We sought a platform that would provide the ability to monitor and assess students’ performance during live lectures and provide real-time feedback. Our choice of educational tool, the Nearpod© App, enables presentation of multiple question types (single and multiple choice, matching, polls) and allows the monitoring of students’ performance in real time. We used Nearpod© to track attendance, compliance, and test responses of individual nurses.Ninety-eight nurses took part in our educational sessions during the period of September 2020 through November 2020. Sets of multiple-choice questions were presented on a smartphone, tablet, or computer during live presentations. The responses were monitored in real-time by a member of the educational team. Based on individual and group responses, the educators were able to provide immediate feedback, adjust instruction, and emphasize material learned.Results:The technology was easily and enthusiastically adopted by all nurses. No difficulties with technical implementation were encountered. Nurses received immediate feedback. We were able to track attendance, graph results, and provide live feedback and immediate test results to all nurses. Educators were able to assess which material required more focus and emphasize those specific topics. We achieved high compliance and competencies with our stroke specific education.Conclusions:Educational technology tools from non-medical settings can be easily adapted to nursing education. This technology can assist nurse educators with providing hospital wide topic specific nursing education, tracking attendance and compliance, and providing live feedback. It can be easily adapted to nursing education in institutions seeking to meet the educational requirement for disease specific certification.

Stroke, Volume 56, Issue Suppl_1, Page ATP287-ATP287, February 1, 2025. Background:Chronic kidney disease (CKD) is a known risk factor for stroke that leads to significant long-term disability. Efferocytosis, the process by which microglia engulf and clear apoptotic cells, is essential for stroke recovery. However, its impairment can hinder recovery and worsen the outcomes. Desidustat, an oral hypoxia-inducible factor-prolyl hydroxylase inhibitor, has emerged as a promising treatment for anemia associated with CKD. Despite its clinical potential, its effects on microglial efferocytosis and subsequent effects on stroke recovery have not yet been studied.Objective:To evaluate the mechanistic role of desidustat in mitigating CKD-induced defective microglial efferocytosis and enhancing sensorimotor recovery following embolic stroke.Methods:CKD was induced in adult C57BL/6 mice by oral administration of adenine (50 mg/kg) for 28 days. Acute Ischemic stroke was induced in mice with CKD using an embolic model. Sensorimotor function tests (modified neurological severity score and corner test) were performed for up to 4-weeks post-stroke. Inflammation, apoptosis, and the effect of CKD on microglial efferocytosis following stroke were assessed 72 h post-stroke using in vitro and in vivo functional assays. Desidustat 15 mg/kg was administered orally starting on day 14 of adenine treatment and continued for 28 days post-stroke in mice with CKD. Human-induced microglial cells were used to evaluate the mechanistic role of desidustat in promoting efferocytosis of apoptotic neurons.Results:Mice with CKD exhibited elevated blood urea nitrogen and creatinine levels, accompanied by tubulointerstitial abnormalities and vascular fibrosis in the kidneys. Stroke induction in mice with CKD resulted in increased cerebral inflammation and reduced microglial efferocytosis 72 h post-stroke which was concomitant with worse neurological outcomes and sensorimotor function tests for up to 4 weeks as compared to controls. Desidustat treatment significantly reduced cerebral inflammation and enhanced microglial efferocytosis (72 h post-stroke) and improved neurological recovery and sensorimotor function for up to 4 weeks. In vitro mechanistic studies revealed that desidustat directly enhanced efferocytosis in a human microglial-neuronal co-culture assay.Conclusion:Our results demonstrated that desidustat treatment enhances microglial efferocytosis and improves neurological outcomes and sensorimotor deficits following ischemic stroke in mice.

Stroke, Volume 56, Issue Suppl_1, Page A133-A133, February 1, 2025. Introduction:Moyamoya is a progressive steno-occlusive cerebrovascular arteriopathy of bilateral anterior circulation. The pathophysiology is elusive, and once established, moyamoya is typically inexorably progressive.Hypothesis:We hypothesized that the left-sided circulation is more vulnerable to steno-occlusive arteriopathy compared to the right, which may reflect differences in mechanical stress from blood flow.Methods:All children with moyamoya cared for between 1/1/2009 and 7/1/2024 at a single institution were identified through an IRB-approved, retrospective study. The charts and neuroimaging at the time of diagnosis were reviewed to assess symmetry of steno-occlusion. Chi-square test was used for statistical analysis, with p-value

Stroke, Volume 56, Issue Suppl_1, Page A111-A111, February 1, 2025. Background:Neutrophil infiltration plays a pivotal role in exacerbating brain injury following subarachnoid hemorrhage (SAH). Integrin α9, highly expressed on activated neutrophils, facilitates their adhesion and transendothelial migration. Once infiltrated, neutrophils aggravate inflammatory response and can impair microglial efferocytosis. Defective efferocytosis may results in accumulation of apoptotic cells, persistent inflammation, and resultant poor recovery following SAH. Despite the known role of integrin α9 in promoting cerebral inflammation, the impact neutrophil integrin α9 on microglial efferocytosis and subsequent SAH outcomes remains unknown.Hypothesis:Integrin α9 dependent neutrophil transendothelial migration impedes microglial efferocytosis, promotes cerebral inflammation, and mediates poor SAH recovery.Methods:Neutrophil specific integrin α9 knockout mice (α9fl/flMrp8Cre+/-) and littermate controls (α9fl/flMrp8Cre-/-) were subjected to the endovascular perforation model to induce SAH. Sensorimotor tests (modified neurological severity score, corner, and cylinder test) and cognitive function tests (Y-maze and novel object recognition test) were performed up to 4-weeks. Neutrophil infiltration, inflammation, apoptosis, and blood brain barrier (BBB) disruption were quantified 24-hr post-SAH. In vitro and in vivo functional assays were carried out to assess the neutrophil integrin α9-dependent effects on microglial efferocytosis.Results:Mice with SAH exhibited increased integrin α9 levels on infiltrated neutrophils as compared to mice with sham-surgery.α9fl/flMrp8Cre+/-mice showed improved sensorimotor and cognitive recovery (up to 4-weeks) (Fig 1), reduced neutrophil infiltration, BBB damage, neuronal apoptosis as compared to controls.α9fl/flMrp8Cre+/-mice exhibited reduced brain neutrophil elastase levels along with enhanced microglial efferocytosis of apoptotic neurons. In vitro mechanistic studies revealed that reduced transendothelial migration ofα9-/-neutrophils directly contributed to the enhanced microglial efferocytosis of apoptotic neurons (Fig 2). Pharmacological targeting of integrin α9 with macitentan significantly improved SAH outcomes, reduced neutrophil infiltration, BBB damage, neuronal apoptosis, and showed enhanced microglial efferocytosis (Fig 3).Conclusions:Our study uncovered a previously unrecognized role of neutrophil integrin α9 in microglial efferocytosis and post-SAH sensorimotor and cognitive recovery.

Stroke, Volume 56, Issue Suppl_1, Page A113-A113, February 1, 2025. Background:Early detection and intervention of cerebral ischemia is critical to improving patient outcomes. Optical brain pulse monitoring (OBPM) is a unique technique that offers non-invasive, continuous monitoring of brain hemodynamics via brain pulse waveform visualization. This method has the potential to identify ischemic changes and facilitate expeditious intervention. Here, we assessed OBPM signal changes during middle cerebral artery occlusion (MCAo) and following reperfusion in a clinically relevant sheep model to enable pre-clinical waveform characterization.Methods:Eleven Merino wethers underwent MCAo for 4 hours followed by reperfusion for 6 hours. Brain tissue oxygen monitoring (PbtO2; n=11) and OBPM (n=11) were performed in the MCAo hemisphere overlying the MCA territory, while intracranial pressure (ICP; n=11) and OBPM (n=6) were performed in the contralateral MCA territory. OBPM measurements were taken at baseline, MCAo, and following reperfusion. Magnetic resonance imaging (MRI) was used to measure infarct volume at 1 hour post reperfusion. Brain pulse waveforms were grouped into 5 classes by 3 blinded observers. Interrater agreement and frequency distributions were analyzed using Fleiss k and Fischer’s exact test, respectively. Generalized estimating equations (GEE) identified neuromonitoring changes (OBPM, StO2%, PbtO2, ICP) at each time point, adjusted with the Benjamini-Hochberg method.Results:Observers were in moderate agreement (k=0.433;p0.99). One waveform class was observed only during MCAo. Reductions in brain pulse amplitude were found during MCAo when infarct volume was controlled for (p

Stroke, Volume 56, Issue Suppl_1, Page ADP33-ADP33, February 1, 2025. Background:Absence of a perfusion Mismatch (MM) profile suggests that the volume of salvageable penumbral tissue is small or absent. There is uncertainty regarding the benefit of endovascular therapy (EVT) in large ischemic core patients without MM. Although these patients were eligible for recent prospective randomized trials, few ultimately were enrolled. We sought to compare the expected percentage of MM versus No MM encountered in clinical practice compared to enrollment in large core clinical trials stratified by time since last known well.Methods:We used a retrospective multicenter international study of patients with anterior circulation large vessel occlusion strokes, baseline MR or CT perfusion (MRP, CTP), and definitive last known well (LKW) within 24 hours. We compared this to the SELECT2 and ANGEL-ASPECT randomized clinical trials of EVT in large core ischemic stroke. A MM profile was defined as mismatch ratio ≥1.2 and penumbral volume ≥10ml. Large core was defined as ≥50ml on CTP (volume of relative cerebral blood flow

Stroke, Volume 56, Issue Suppl_1, Page ADP47-ADP47, February 1, 2025. Introduction:Chronic kidney disease (CKD) is a risk factor for intracerebral hemorrhage (ICH) and for worse outcomes following ICH. In this study, we examined the relationship between kidney function, ICH, and brain iron deposition, using quantitative susceptibility mapping (QSM) and cerebral microbleeds (CMB) as intermediate biomarkers. We hypothesized that kidney function is an independent risk factor for QSM/CMB, and that high QSM/CMB burden is an independent risk factor for ICH.Methods:A retrospective cohort of spontaneous ICH and non-ICH patients with CT/MR imaging was identified. For each patient, eGFR along with age, sex, race, ethnicity, hypertension, diabetes (DM), heart disease, and hyperlipidemia were abstracted. CMB volume as well as intracranial arterial calcification (IAC) volume were extracted using custom convolutional neural networks. QSM was derived using the Graz total generalized variation method. All results were visually verified for accuracy by an expert neuroradiologist. Univariate analysis for QSM/CMB risk factors was assessed using Pearson correlation and t-test, while multivariate analysis was assessed using linear regression. Univariate analysis of ICH risk factors was assessed using t-test and Chi-square, while multivariate analysis was assessed using logistic regression.Results:Among 155 patients in this study, 39 were ICH patients. In all patients, eGFR was significantly inversely correlated with QSM (r=-0.30, p=0.02) and CMB (r=-0.24, p=0.04); significant differences were also observed across CKD stages for both QSM/CMB (ANOVA; p

Stroke, Volume 56, Issue Suppl_1, Page A116-A116, February 1, 2025. Background:Ischemic stroke triggers a chronic B-lymphocyte response in the stroke core that is required for delayed post-stroke cognitive decline in mice. Because immune cells primarily infiltrate into connected subcortical axonal tracts after stroke, we hypothesized that degenerating axons promulgate a persistent neuroinflammation that is critical for late cognitive decline. To test this, we utilized mice deficient in Sarm1 (Sarm1-/-),a molecular trigger of axon degeneration and the loss of which leads to axonal protection after injury.Methods:Wildtype andSarm1-/-male mice (N=9 per condition) underwent distal MCA stroke followed by transient hypoxia, which reliably leads to infarct-induced neurodegeneration 7 weeks after injury. Innate (monocytes) and adaptive (T, B lymphocytes) immune cell infiltration were evaluated via immunohistochemistry 1&7 weeks after stroke. Cognition was assessed using the Barnes maze at both time points after stroke.Results:Absence ofSarm1resulted in robust axonal protection after ischemic stroke. In connected thalamic region, mean immunostained intensity of axons was 166 in wildtype vs. 267 inSarm1-/-(p < 0.005) 1 week, and 106 vs. 201 (p < 0.005) 7 weeks after stroke. Compared to wildtype mice,Sarm1-/-mice had an attenuated innate immune response in connected subcortical white matter 1 week after stroke (% area of CD68+ reactivity was 35 ± 5% in WT vs. 19 ± 4% inSarm1-/-(p < 0.01), while peri-infarct CD68 was not different. Moreover, loss ofSarm1reduced B220+ B-cell infiltration into the infarct 7 weeks after stroke. Percent area of B220+ reactivity was 30 ± 8% in WT vs 15 ± 7% inSarm1-/-(p

Stroke, Volume 56, Issue Suppl_1, Page ATP265-ATP265, February 1, 2025. Objective:Stroke–heart syndrome (SHS) leads to poorer prognosis in patients with acute ischemic stroke (AIS), which makes early identification and prevention of SHS crucial. Therefore, the primary objective of this study was to establish a nomogram-based risk prediction model for SHS following endovascular therapy (EVT) in anterior circulation stroke.Methods:This retrospective observational study recruited consecutive AIS patients undergoing EVT between January 2014 and June 2021. Utilizing the least absolute shrinkage and selection operator (LASSO) regression and multivariate logistic regression analysis, we screened for variables that demonstrated strong associations with SHS. Significant variables were included to construct risk prediction model and visualized with nomogram. Multiple methods were employed to comprehensively assess the accuracy and calibration of the prediction model. The modified Rankin Scale (mRS) score was utilized to assess the prognosis of patients at 3 months.Results:A sample of 218 patients was incorporated into the study. The incidence of SHS within two weeks after EVT is 13.8%. After multiple analyses, age (OR 1.060, 95% CI 1.021–1.100, P = 0.002), hyperlipidemia (OR 3.400, 95% CI 1.289–8.968, P = 0.013), creatinine (OR 1.023, 95% CI 1.000–1.046, P = 0.049), and total anterior circulation infarct (TACI, OR 4.875, 95% CI 1.984–11.980, P = 0.001) were included in the risk prediction model. The model has good discriminatory capacity (AUC = 0.812), calibration (Hosmer-Lemeshow test P = 0.855, Brier score = 0.098), and robustness (internal cross-validation AUC = 0.811). SHS independently increased the risk of 3-month unfavorable prognosis (OR 3.267, 95% CI 1.159–9.212, P = 0.025) and mortality (OR 3.484, 95% CI 1.154–10.516, P = 0.027).Conclusions:SHS significantly increases unfavorable prognosis risk and mortality in AIS patients with EVT. The prediction model based on age, hyperlipidemia, TACI, and creatinine exert good predictive efficacy for early SHS.