Risultati per: Gestione del dolore post-operatorio

Stroke, Volume 56, Issue Suppl_1, Page ATP398-ATP398, February 1, 2025. Introduction:RNS60 is a proprietary 0.9% saline solution with an elevated oxygen concentration. Previously, we showed that 13 days of daily RNS60 treatment after transient middle cerebral artery occlusion (tMCAo) stroke reduced brain pathology (e.g., infarction, amyloid pathology, neuronal death, microglial activation, and white matter damage) while increasing microvascular perfusion and memory (Baena Caldas et al. 2024). Here, we examine earlier brain-protective effects of daily RNS60 treatment 4 days after stroke.Methods:Male C57BL/6J mice, 3-4 months old, were randomly divided into sham surgery or unilateral 60-minute tMCAo. Each group was subdivided into three treatment arms: an experimental arm receiving daily intraperitoneal injections of 0.2 mL of stabilized RNS60, and control arms of pressurized normal saline with the same oxygen content as RNS60 (PNS60) or normal saline (NS). Injections began 2 hours after stroke, once daily for 3 days. An additional group without treatment was used as a control. Treatment group assignments were blinded throughout the study. On day 4, mice from each group were euthanized to assess infarct volume using TTC staining, or were perfused with 4% PFA to perform immunohistochemistry.Results:Four days after ischemic stroke, daily injections of RNS60 treatment significantly reduced early post-stroke vasogenic edema by 41% and infarct size by 39% compared to controls. These RNS60 brain-protective effects were related to decreased expression of hypoxia-inducible factor 1α (HIF1α), suggesting that RNS60 treatment may reduce hypoxia.Conclusion:RNS60-treated mice exhibit early and long-term significant brain protection after ischemic stroke associated with decreased expression of HIF1α, suggesting reduced hypoxia in the ischemic brain. Ongoing studies aim to identify the effect of RNS60 on blood brain barrier integrity to further elucidate the underlying molecular mechanism.

Stroke, Volume 56, Issue Suppl_1, Page ATP370-ATP370, February 1, 2025. Introduction:Despite efforts to improve stroke outcomes in patients, a translational gap exists between preclinical and clinical studies. Due to this gap, the Stroke Preclinical Assessment Network has incorporated the corner test (CoT) for behavioral outcome as a primary measure for evaluating whether a treatment is successful or not. Standard behavioral analysis for CoT uses the laterality index to detect if there is mouse turning preference on a scale from -1 to 1. We sought to determine if a deep learning approach using “DeepLabCut” could be applied towards enriching our CoT data to better evaluate aspects of mouse locomotion.Methods:Six C57/Bl6 mice were subjected to an 1 hr transient middle cerebral artery occlusion in the right hemisphere of the brain. CoT were recorded with an isometric view and performed at both baseline (BL) prior to the stroke and one day post stroke (D1). The same set of six mice performed 10 turns per CoT, totalling to 60 turns for BL and 60 turns for D1. The pose estimation model was made using a ResNet-101 neural network trained on 1064 manually-labeled frames, with the assistance of “DeepLabCut” software packages. Videos were analyzed by the pose estimation model and sequentially processed through a newly developed R script and DLC Analyzer R script. Turns were defined as in SPAN with a 90 degree head turn upon vibrissae contact on both sides of the corner boards. Turn latency was defined as the time lapsed during a turn, and head turn speed as the average speed during a turning event.Results:The average laterality index showed clear preference towards ipsilateral turning in all D1 mice (-1.0 ± 0.04, N = 6). Furthermore, a comparison between BL data and respective D1 data showed significantly longer turn latencies and slower head turn speeds (p < 0.05) for D1 mice. The average turn latency for BL mice was 3.58 ± 0.57 s, which was 4.6 times shorter than that of D1 mice (16.45 ± 3.11 s). The average speed for BL mice was 2.01 cm/s ±0.21, which was 2.3 times faster than that of D1 mice (0.86 ± 0.14 cm/s).Conclusion:This deep learning approach enriches current stroke behavioral analysis methods by offering additional quantitative information upon which behavior can be assessed. Future studies can use these behavioral metrics for stratification or correlation with variables of interest (e.g. infarct size) to provide a more refined assessment of preclinical stroke behavior.

Stroke, Volume 56, Issue Suppl_1, Page A24-A24, February 1, 2025. Objectives:To investigate the correlation between iron deposition changes in the lesioned thalamic nuclei and the presence and severity of central post-stroke pain (CPSP) after thalamic infarction using quantitative susceptibility mapping (QSM) technique.Methods:We consecutively enrolled patients with unilateral chronic thalamic infarction with radiological examination conformed . Detailed and multidimensional pain characteristics measured as follows: Douleur Neuropathique 4 (DN4) questionnaire for validation of neuropathic pain diagnosis, Short-Form McGill Pain Questionnaire (SF-MPQ) for comprehensive representation of pain experience, Present Pain Intensity index (PPI) for current pain severity upon examination, and Visual Analogue Scale (VAS) for overall pain feeling since symptom onset. Age- and sex-matched stoke-free healthy controls were recruited simultaneously. High resolution structural image 3D-T1 BRAVO and QSM sequences were obtained with 3.0T MRI. The voxel-lesion-symptom-mapping (VLSM) was used to determine lesioned thalamic nuclei at the high risk for CPSP. Then ipsilateral QSM values of the whole thalamus and subregions were compared with contralateral side and healthy controls. Partial correlation analysis were performed to explore the relationship between QSM value and pain severity.Results:Finally, 28 CPSP patients, 33 non-CPSP patients and 55 healthy controls were included in the study. Our results indicated no significant difference in overall QSM values of the whole thalamus among the groups. The VLSM results showed lesion involving ventral posterolateral nuclei (VPL) was highly orrelaed with occurance of CPSP (pFWE=0.0092.). The QSM values of each subnuclei in the thalamus ipsilateral to infarction were lower compared with the contralateral side and healthy controls (p

Stroke, Volume 56, Issue Suppl_1, Page ATP392-ATP392, February 1, 2025. Diabetes is a widespread disease, and stroke is one of the serious complications of diabetes. Antidiabetic therapy increases the risk of recurrent hypoglycemia (RH). We have previously shown that RH exposure leads to severe post-ischemic hypoperfusion at least up to 80 minutes after ischemia and increases the extent of ischemic brain injury in insulin-treated diabetic (ITD) rats. However, the total duration for which these perfusion deficits last is unknown. Thus, we evaluated cerebral blood flow up to 7 days post-ischemia in RH-exposed ITD rats using laser speckle imaging. Diabetic male rats were treated for hyperglycemia using insulin pellets, were assigned randomly to either hyperinsulinemic euglycemia (ITD+RH+Glucose control; n=7) or hyperinsulinemic hypoglycemia (ITD+RH; n=7) groups (3 h duration) (Figure B-C) and were subjected to transient global cerebral ischemia overnight after the last episode of hyperinsulinemic euglycemia or hyperinsulinemic hypoglycemia. We evaluated cerebral perfusion at baseline (pre-ischemia), 1 h, 24 h, 3 d, 5 d, and 7 d post-ischemia. The cerebral ischemia in RH-exposed ITD rats resulted in a significant decrease in percentage change in cerebral blood flow as compared to the control rats when quantified 1 hour (23%, p

Stroke, Volume 56, Issue Suppl_1, Page ATP150-ATP150, February 1, 2025. Introduction:Stroke is a significant global health challenge, impacting physical and mental well-being, with many neuropsychiatric symptoms contributing to worse functional outcomes. Post-stroke depression (PSD) is a common neuropsychiatric consequence of stroke, affecting approximately one third of stroke survivors. PSD is associated with worse functional outcomes, higher mortality rates, and reduced quality of life.Hypothesis:We hypothesize that patients with higher stroke severity scores on admission will have higher levels of immediate depressive symptoms and have a smaller household population.Methods:This study examines the predictive power of immediate post-stroke depressive symptoms and functional outcomes at 3- and 12- months post hospitalization. 130 patients with Ischemic stroke were enrolled and completed a standard battery of questionnaires during their hospitalization. Post-stroke depression was measured via PHQ-9 scores, with scores above 5 denoting moderate to severe depressive symptoms. Acute stroke severity was measured using the National Institute of Health Stroke Scale (NIHSS), with increasing scores indicating more severe strokes.Results:Analyzing stroke severity and PSD development among patients with ischemic stroke, our statistical analyses revealed that larger household size significantly protects against PSD. For acute stroke injury, we found that patients living with fewer people at baseline are more likely to have a higher NIHSS score (p

Stroke, Volume 56, Issue Suppl_1, Page ATMP102-ATMP102, February 1, 2025. Background:Atrial Fibrillation (AF) occurs in about one-fourth of patients with Embolic Stroke of Undetermined Source (ESUS). Accurate prediction of post-stroke AF upon discharge from an index stroke admission informs a personalized post-stroke monitoring strategy of AF and interventions. While clinical risk scores predict AF, machine learning (ML) models have shown superior performance.However, traditional ML approaches only use expert-derived predictors available in an electronic health record (EHR) and thus may miss variables that would potentially increase the accuracy of prediction.Aims:This study aims to enhance AF prediction by augmenting expert-derived predictors with an unbiased selection of full diagnostic codes and medication histories up to index strokes. Through embedding learning with hypergraph neural networks, we generate compact representations of high-dimensional data to improve prediction accuracy by capturing complex feature interactions.Methods:We analyzed data from 510 ESUS patients (55.3% female, mean age 61.4 years) from 2015 to 2023 at Emory Healthcare. We focus on experiments using a logistic regression (LR) model to predict AF from different sets of features. At baseline, we use 58 clinically motivated predictors, including comorbidities characterized by 17 ICD codes manually extracted based on literature, and 41 other features extracted from lab results, echocardiographic and ECG. To directly model the full history of comorbidities and medications, another baseline uses the full 1530 ICD codes plus the 41 other features (1571 in total). In contrast, the embedding method uses the full 1530 ICD codes to generate condensed, informative embedding vectors (32-dimensional), eventually getting 32+41=73 features. To generate the embedding, a hypergraph neural network was trained on a larger stroke cohort (n=7956) to model the interactions between the 1530 ICD codes. A nested cross-validation approach was employed within 5-fold splits, and ROC-AUC scores were recorded.Result:Among 510 ESUS patients, 107 (21.0%) developed AF (mean age 67.9 years, 57% female). We compared the performance of LR model with different features from ICD codes (Table 1). The results show that the learned 32-dim embedding vectors improves the prediction of post-ESUS AF.Conclusion:The embedding technique can significantly enhance predictive performance by integrating comprehensive medical information, maximizing the use of available data for improved outcomes.

Stroke, Volume 56, Issue Suppl_1, Page AWP62-AWP62, February 1, 2025. Introduction:Cerebrovascular diseases are the third leading cause of disability worldwide, which can occur due to the effects of Post-stroke Cognitive Impairment (PSCI) and Post-Stroke Depression (PSD). Higher morbidity and mortality are associated with both conditions following a stroke, but there is a lack of research on this topic in developing countries. We studied the prevalence of stroke and PSCI and PSD in a representative sample of the Brazilian population aged over 50 years, as well as the factors associated with both conditions.Methods:We performed a retrospective analysis of the ELSI-Brazil study, a nationally representative sample of adults aged 50 and over, including 9412 individuals. Individuals self-reported their sociodemographic characteristics, previous medical history, including prior stroke (transient ischemic attack, ischemic and hemorrhagic stroke), other chronic health conditions and disability in basic (b-ADL) and instrumental activities of daily living (i-ADL). Depression was defined as a score above 4 in the CESD-8 scale. Cognitive impairment was defined through a composite z-score including episodic memory, semantic memory, prospective memory, verbal fluency and orientation. After adjustments by age, sex and education, it was defined as a score below -1.0. Statistical analysis was performed using STATA/SE 17.0 software. Logistic regression was used to study the associated variables with PSD and PSCI.Results:From the total sample, 536 (5.3%) reported previous stroke. Of these, 58.6% had PSD and 31.8% had PSCI. Individuals who had a stroke were more likely to be older, male, of black race, have lower education, and more chronic health conditions. They also had higher disability in b-ADL and i-ADL, with higher depression and higher cognitive impairment. In the logistic regression, being a woman, having more chronic health conditions and higher disability in i-ADL were associated with PSD, while only being of black race was associated with PSCI.Conclusion:More than half of individuals with a previous stroke had depression and approximately a third had cognitive impairment. PSD was associated with being a woman, more chronic health conditions and higher disability in i-ADL. PSCI was associated with black race. Understanding the factors associated with PSD and PSCI is important to reduce stroke-related disability and promote better quality of life in individuals with previous stroke.

Stroke, Volume 56, Issue Suppl_1, Page ATP136-ATP136, February 1, 2025. Background:The STRACK project aims to improve post-stroke patient management and the transition from acute to primary care thanks to improvements in patient pathways and monitoring cardiovascular risk factors: heart failure, diabetes, atrial fibrillation, dyslipidemia and hypertension. Collaboration between primary care centers and hospital staff was essential for the project’s success by delivering personalized care and home monitoring devices to patients through access to a digital platform. STRACK was launched with a european value-based contracting process and Roche Diag. as partner.Methods:The three-year project was launched in May 2021, during first year all specialties and professionals participated in the development and planning of the project and were trained in the use of the devices and own digital platform.First STRACK patient was enrolled in May 2022. Once these post-stroke patients have been identified, they are given a personalized monitoring plan depending on the individuals’ risk factors, the personalized care and rehabilitation plans are tracked and followed. For a year post-discharge, a nursing and administrative team follows the data that the patient enters remotely or is automatically available on their mobile application.Results:STRACK has evolved the continuum of care by 421patient in July 2024 and ongoing, by integrating comprehensive monitoring of cardiometabolic risk factors (heart failure, diabetes, atrial fibrillation, dyslipidemia, hypertension) into a patient discharge plan, identified as key to avoiding stroke recurrence and improving control of vascular risk factors are monitored.Preliminary results of 231 patients (May 2022-2023) with full one year follow-up comparing with historical cohort (May 2018-2019) showed: Reduction in unnecessary visits (weighted): -26,3%. Reduction in admissions for stroke recurrence or related to stroke, (heart attack, angina, peripheral embolism, etc.): Stroke, 30days: -100%; Related to stroke, (365d: -47,7%; 30d: -57,0%). Reduction in cardiovascular admissions ( 30d: -100%; 365d: -31,4%). Best treatment adherence: 81,2% (72% previously)Conclusion:The great value of STRACK is knowing the evolution of stroke patients post-discharge through strict self-monitoring of clinical parameters, following prior health education. STRACK has managed to achieve reduction in stroke recurrence and adverse events and readmissions for cardiovascular risk factors, reducing emergency visits for vascular events.

Stroke, Volume 56, Issue Suppl_1, Page AWP54-AWP54, February 1, 2025. Introduction:Post-stroke fatigue is prevalent and significantly impacts quality of life chronically after stroke. Its underlying biological mechanisms remain largely unknown. Here we set out to understand the persistence of post-stroke fatigue and to use plasma proteomics to identify candidate mechanisms.Methods:We acquired neurocognitive assessments and blood draws from 250 stroke survivors from two sites at baseline (median 8 mo after stroke, range 5-120 mo), and 131 participants one year later. The Functional Assessment of Chronic Illness-Fatigue (FACIT) scale was used to assess fatigue, with no fatigue defined as FACIT >41, any fatigue as FACIT≤41, and severe fatigue as FACIT

Stroke, Volume 56, Issue Suppl_1, Page ATP380-ATP380, February 1, 2025. Recent research on neurodegenerative diseases has highlighted a pathophysiological cascade characterized by abnormal lipid accumulation within the brain. Although progress has been made, the role of lipid metabolism following stroke remains unclear. This study aims to further explore changes in lipid metabolism after stroke, with a specific focus on the endoplasmic reticulum transmembrane protein 97 (TMEM97), which has emerged as a promising therapeutic target due to its critical role in cholesterol metabolism.Spatial transcriptomic analyses following experimental stroke induction in mice revealed neuronal upregulation of crucial genes involved in lipid metabolism pathways, including LDLR, acetyl-CoA acetyltransferase 1, and elongation of very long-chain fatty acids protein 6, indicating dynamic adaptations post-stroke or under cellular stressors.Initial findings demonstrate TMEM97 expression predominantly within neurons in vivo (mouse model). In an in vitro model of lipid starvation using mouse neural progenitor cells (MNPCs), pharmacological inhibition of lysosomal lipid release leads to increased expression of TMEM97. Interestingly, when TMEM97 was knocked down in MNPCs using lentiviral shRNA transfection, these cells exhibited no significant difference in neutral lipid accumulation compared to control cells. However, upon treatment with the lysosomal lipid release inhibitor, a significant increase in neutral lipid accumulation was observed exclusively in the TMEM97 knockdown cells.Furthermore, Thapsigargin-induced endoplasmic reticulum (ER) stress in the MNPCs reduced TMEM97 expression, while also increasing low-density lipoprotein (LDL) uptake and the mRNA levels of the LDL receptor (LDLR). The observed elevation of neuronal LDLR expression in vitro closely aligns with the heightened expression of LDLR in vivo, suggesting a coordinated modulation of lipid metabolism pathways triggered by ER stress in response to stroke or metabolic stress induction. This synchronous upregulation of LDLR underscores the crucial role of ER stress as a potential trigger for this regulatory response. Additionally, considering the known involvement of TMEM97 in lipid homeostasis within the ER, it further highlights the intricate interplay between these proteins in post-stroke lipid metabolism regulation.Our findings provide a compelling starting point for further exploring TMEM97’s significance in post-ischemic lipid homeostasis.

Stroke, Volume 56, Issue Suppl_1, Page A60-A60, February 1, 2025. Introduction:Over 70% of patients experience post-stroke cognitive impairment (PSCI), which can lead to functional decline. Outpatient stroke clinics often lack a consistent and validated cognitive assessment protocol for follow-ups. This increases the risk of missed diagnosis of PSCI, which is often determined based on the subjective assessment of cognitive functioning by patients or caregivers. Our goal was to assess the practice of unstructured PSCI screening at our stroke clinic and test if a cognitive screening protocol would improve PSCI detection in follow-up patients.Methods:We led a quality improvement project to identify root causes of the problem and plan interventions for introducing a feasible cognitive screening protocol. We performed a baseline chart review on 79 stroke patients seen at the clinic to assess documentation of discussion of cognitive symptoms during visits. We developed a pre-screening survey to assess educational level, post-stroke rehabilitation participation, and vascular risk factors. We enrolled 30 follow-up patients with either an ischemic or hemorrhagic stroke. An examiner conducted a short-form MoCA (MoCA-sf) test and a CLCE-24 questionnaire for subjective cognitive complaints (SCC) on each patient. We collected data from the electronic record on discharge mRS and NIHSS scores and measured time spent on screening to assess feasibility.Results:In baseline chart review, 65% of 79 patients did not have any discussion of cognitive symptoms documented during their visit before our intervention. In our initial screening results, 53% of patients screened positive for cognitive impairment (

Stroke, Volume 56, Issue Suppl_1, Page AWP78-AWP78, February 1, 2025. Introduction:Dysphagia affects approximately 30-80% of ischemic stroke patients. While most patients recover swallowing functions within a week, 10-50% may experience persistent issues for up to six months post-stroke. Early enteral access is critical for providing hydration, nutrition, and medication to these patients. Stroke patients often require specialized nutritional support through feeding tubes. At a large urban academic comprehensive stroke center, we identified an opportunity to develop a model that supports and streamlines feeding tube placement for this population to enhance care quality and improve patient outcomes.Methods:This retrospective study evaluated enteral feeding support in 43 post-acute stroke patients from October 2023 through July 31st. We compared tube placements and outcomes between nursing staff and a dietitian-led enteral access team. Nursing staff used standard NG tube procedures, while the dietitian-led team employed advanced techniques, including an electromagnetic device and bridle retention system to enhance tube stability and reduce need for replacements. We also assessed discharges to acute rehabilitation with bridled small-bore tubes who would have otherwise required PEG placement.Results:Out of 43 patients, 7 patients had NG tubes placed by nursing staff and 36 by the dietitian-led team. All 7 patients required replacement and were ultimately escalated to the dietitian-led team. The dietitian-led team achieved greater tube stability using advanced techniques and required only 1 replacement. A total of 13 patients were discharged to rehabilitation with bridled tubes.Conclusion:In conclusion, we found that a dietitian-led enteral access team can maintain high-quality care and satisfaction through advanced enteral tube placement techniques. Additionally, a subset of patients were able to defer PEG placement allowing for additional time for recovery from dysphagia. Future considerations include evaluating nurse workload reduction, decreased hospital stays, and accelerated rehabilitation placement with early, secure enteral access.

Stroke, Volume 56, Issue Suppl_1, Page A156-A156, February 1, 2025. Background:Brain inflammation following ischemic stroke exacerbates neuronal injury. Early immune cell infiltration into the brain after ischemia is correlated with increased risk of subsequent stroke and higher three-month mortality. However, direct mechanisms that underly this immune cell recruitment remain unclear, preventing the development of successful therapeutics. Recent work has identified mast cells as early responders in stroke that incite inflammation, yet how these cells are activated remains unknown. We hypothesized that Mrgprb2, a mast cell receptor known to trigger neurogenic inflammation, initiates mast cell activity in stroke, and that inhibition of this receptor can attenuate stroke injury.Methods:We performed MCA occlusion (MCAO) on wild-type and Mrgprb2-null (Mrgprb2-/-) mice and assessed stroke volume, and behavior. We used flow cytometry and ELISA for immune cell and cytokine profiling to evaluate inflammation. Human stroke patient dura and blood was sampled to assess mast cell activity and to identify potential ligands for Mrgprb2 activation. Lastly, we used osthole, a Mrgprb2 inhibitor, as a post-MCAO treatment to determine if pharmacologic inhibition can attenuate post-stroke deficits in mice.Results:We found that Mrgprb2 is activated in meningeal mast cells after stroke, causing mast cell degranulation and release of chemokines that attract immune cells. Mrgprb2-/-mice exhibited reduced brain inflammation after stroke, leading to attenuated infarct size, and reduced mortality. Further, we show evidence that Mrgprb2-/-mice recruited fewer skull bone marrow neutrophils into the brain, suggesting a novel mechanism whereby mast cells regulate skull bone marrow recruitment. We demonstrated that the human ortholog of this receptor, MRGPRX2, is expressed in human meningeal mast cells, and that these cells are activated in stroke patients. Further, substance P, a known ligand of Mrgprb2/X2, is increased in stroke patient serum. Lastly, osthole-treated mice have reduced post-stroke brain inflammation and improved functional outcomes, confirming that pharmacologic inhibition of Mrgprb2 is a promising therapeutic strategy.Conclusions:Our study identifies Mrgprb2 as a key receptor which triggers mast cell activity in stroke and initiates brain inflammation. Mrgprb2/X2 provides a specific and druggable target to attenuate post-stroke inflammation and holds potential to meaningfully alter the clinical course for stroke patients.

Stroke, Volume 56, Issue Suppl_1, Page AWP16-AWP16, February 1, 2025. Introduction:Currently, no level A evidence exists for the optimal rescue strategy for cases at high risk for re-occlusion following endovascular thrombectomy (EVT) in acute ischemic stroke. Glycoprotein IIb/IIIa inhibitors, which inhibit platelet aggregation and adhesion, show promise as adjunctive therapy, potentially yielding favorable outcomes, especially in residual stenosis cases.Methods:In this retrospective review study, we included patients aged ≥18 who underwent EVT at a comprehensive stroke center with TICI 2b or 2c outcome (admitted between 2019 – 2024), who were noted to have high-risk residual stenosis on angiography after EVT. We defined high-risk post-EVT stenosis as any stenosis with ≥50% lumen stenosis, associated dissection, re-occlusion during thrombectomy, and severe residual luminal irregularity. We excluded patients who had a clear contraindication to Eptifibatide, received a stent, or if the luminal stenosis was related to reactive vasospasm and any cases with TICI 0, 1, or TICI 3 scores.Results:Our sample size was 60 (51.7% male, 48.3% female, mean age 63.9). Mean National Institute of Health Stroke Scale (NIHSS) on admission was 16.6; 36.7% (n=22) received eptifibatide. The rate of re-occlusion was significantly lower in patients who received eptifibatide compared to those who did not (9.1% vs. 36.8%, p=0.032). There was no difference in pre-stroke modified Rankin scale (mRS), NIHSS on admission, mortality, discharge mRS, or 90-day mRS between these two groups, nor between patients who received intravenous thrombolysis (IVT) vs. those who did not. However, among the 16 patients who received IVT, those who also received eptifibatide had significantly lower mean discharge NIHSS (5.0 vs. 13.6, p=0.028), discharge mRS (1.3 vs. 4.5, p=0.009), and 90-day mRS (1.0 vs. 4.1, p=0.038) than those who did not. Ordinal logistic regression of discharge mRS and 90-day mRS in IVT recipients with vs. without eptifibatide usage also revealed significant odds of lower mRS at both timepoints with eptifibatide (OR 7.23, p=0.011 and OR 5.2, p=0.030 respectively).Conclusions:Eptifibatide use is associated with lower re-occlusion rates in patients with residual high-risk stenosis after EVT. Among IVT recipients with post-EVT residual stenosis, eptifibatide use is associated with improved discharge mRS, discharge NIHSS, and 90-day mRS. Given our limited sample size, these findings need to be evaluated further with larger Randomized Control Trials.

Stroke, Volume 56, Issue Suppl_1, Page A158-A158, February 1, 2025. Introduction:Clearing necrotic tissue from lesions by microglia/macrophage is crucial for recovery after acute ischemic stroke (AIS). Lysosomal activity is key for efferocytosis. In the chronic phase, reduced lysosomal activity impairs clearance, causing residual debris and worsening cognitive impairment. Migrasomes, formed during cellular migration, help maintain other organelles like mitochondria.Hypothesis:This study explored how migrasomes in microglia/macrophage help load damaged lysosomes for expulsion, preserving lysosomal quality and efferocytosis post-stroke.Methods:Male C57BL/6 mice including wild-type (WT) andTspan14conditional knockout (Tspan14fl/flLyz2Cre, TSPAN14 CKO) underwent transient middle cerebral artery occlusion (tMCAO). Migrasome production and TSPAN14 expression were evaluated through staining and nano flow cytometry. Neurobehavioral performance was measured by rotarod, foot fault, novel object recognition, and water maze tests up to 14 days post-stroke. In vitro, bone marrow-derived macrophages (BMDM) were cultured with blebbistatin to inhibit migrasome production. BMDM efferocytosis of dead neurons was assessed by staining and flow cytometry.Results:In cultures, 76.9% of migrasomes from BMDM engulfing dead neurons contained damaged lysosomes. Inhibiting migrasome production in BMDM impaired efferocytosis and increased damaged lysosome accumulation. TSPAN14 on the lysosomal membrane mediated lysosome sorting into migrasomes. Migrasomes from TSPAN14 CKO BMDM engulfing dead neurons had 62.3% less lysosomal content than those from WT BMDM, though their numbers were similar (P

Stroke, Volume 56, Issue Suppl_1, Page A150-A150, February 1, 2025. Background and Purpose:Stroke is a leading cause of long-term disability, often resulting in functional and cognitive impairments that significantly reduce quality of life. While racial and ethnic differences in clinical outcomes after stroke are well-documented, the impact of post-stroke disability on patient-centered outcome measures, which account for physical, emotional, and sociocultural factors, remains insufficiently understood. This study aimed to investigate racial and ethnic differences in post-stroke quality of life among participants in the SHINE trial.Methods:This is a post-hoc analysis of the Stroke Hyperglycemia Insulin Network Effort (SHINE) trial. Self-reported race, ethnicity, and the 12-item Stroke Specific Quality of Life (SSQOL) Scale at 90-day follow-up were used for correlation analyses, adjusted for age, sex, hypertension, diabetes, stroke size, recurrent stroke, and 90-day modified Rankin Scale. The SSQOL is a patient-centered outcome measure that assesses health-related quality of life specific to stroke survivors across 12 domains (Table 1).Results:A total of 907 ischemic stroke patients with hyperglycemia (mean age 65±12.8, 44.7% female, 80.9% with diabetes) were included in this study. At 90-day follow-up, no significant differences were found in overall SSQOL summary scores by race/ethnicity. However, Hispanic patients reported significantly lower scores in self-care (p < .0001) (Figure 1), vision (p = .015), and upper extremity function (p = .007), while Black patients reported lower energy (p = 0.012).Discussion:These findings indicate that Hispanic and Black stroke survivors experience lower quality of life in specific domains after adjusting for stroke severity and other potential confounders. In addition to clinical outcomes, it is crucial to understand stroke survivors’ perceptions of their quality of life which can inform more culturally competent care. Future research should validate these associations and examine the role of socio-economic factors in shaping post-stroke quality of life to promote effective and equitable care in line with the WHO 2030 Rehabilitation agenda.