Risultati per: La nevralgia post-erpetica

Stroke, Volume 56, Issue Suppl_1, Page AWP145-AWP145, February 1, 2025. Objective:A thorough exploration of neighborhood environmental impacts on post-discharge stroke outcomes is lacking and crucial to identifying populations at high risk. We assess neighborhood economic and demographic characteristics associated with 90-day death or readmission post-stroke hospitalization.Methods:The study population included 1329 stroke survivors in the prospective Florida Stroke Registry’s Transition of Care Stroke Disparities Study (91% ischemic stroke, 56% males, 51.5% Non-Hispanic White, 22.6% non-Hispanic Black, 21.8% Hispanic, median age 64). Publicly available data on the neighborhood (Zip+4) characteristics included socioeconomic status (NSES), race/ethnic composition, and business densities (food, tobacco/alcohol, gyms, medical services), which were used in factor analysis to create four main factors. Structured telephone interviews at 90 days post-discharge assessed stroke outcomes (death or readmission). Logistic regression models examined associations between the neighborhood characteristics and death/readmission, adjusting for individual demographics (race/ethnicity, sex, age), vascular risk factors and stroke severity obtained from Get with the Guidelines-Stroke®, and individual social/economic conditions (insurance, social support, living arrangement) from patient interviews.Results:Within 90 days post-discharge, 208 patients experienced death or readmission. Four main factors explained 56% of the variance in 24 neighborhood characteristics, of which factor 1 was associated with a 20% increased risk of death/readmission. Factor 1 was characterized by Hispanic dominance (above median %Hispanic), lower NSES (higher %below the poverty line, densely populated), and highly urbanized (primary Rural-Urban Commuting Area (RUCA) code of 1, higher densities of tobacco outlets, alcohol outlets, restaurants, grocery stores, gyms, and pharmacies).Conclusions:Living in predominantly Hispanic, highly urbanized, crowded neighborhoods with lower SES, predicted poor stroke outcomes independent of individual health or SES conditions. These findings can help inform the target population for community interventions aimed at improving stroke mortality and readmission rates.

Stroke, Volume 56, Issue Suppl_1, Page AWP373-AWP373, February 1, 2025. Cardiac arrest (CA) often leads to severe memory impairment, largely due to extensive neuronal loss in brain areas critical for cognitive function, including the hippocampus and amygdala. We demonstrated that physical exercise (PE) following asphyxia CA (ACA) mitigates contextual memory deficits in male rats. Intriguingly, this effect occurs without direct protection of the hippocampus and amygdala, as evidenced by significant cell death in both regions. Instead, PE post-ACA reduces neuronal loss in the medial septum (MS), a forebrain structure essential for regulating limbic system oscillations, and thus memory. This study aims to investigate whether PE post-ACA preserves oscillatory activity within the limbic circuitry and whether it ameliorates other forms of cognitive deficits in both sexes.Methods:Male and female rats are subjected to 8’ ACA. After 5 days of recovery, the animals undergo 5 consecutive days of treadmill running, followed by a battery of cognitive tests. Approximately one-month post-ACA, the animals are anesthetized with urethane for in vivo oscillatory recordings.Results:Having acquired fear conditioning (Figs. 1a and 1d), the animals were tested for cued fear memory and extinction two days later. Post-ACA exercised animals displayed a significant increase in freezing levels compared to non-exercised animals in response to a single re-exposure to the tone, indicating preserved cued fear memory (Fig. 1c). After continuous tone presentations, only the exercised animals displayed a significant decrease in freezing, suggesting they were able to extinguish their fear response (Fig. 1f). The Y-maze test revealed a significant increase in spontaneous alternation in exercised animals (Fig. 1g), indicating improved working memory. These outcomes were not influenced by locomotion (Fig. 1h) or anxiety (Fig. 1i), as confirmed by the open field test. We are currently performing the oscillatory recordings in different limbic system regions.Conclusion:PE post-ACA mitigates different forms of long- and short-term memory deficits in both sexes. This improvement is likely mediated by the preservation of oscillatory power in the MS and hippocampus (to be confirmed), highlighting a potential mechanism by which PE exerts its neuroprotective effects.

Stroke, Volume 56, Issue Suppl_1, Page AWP146-AWP146, February 1, 2025. Background:Prior literature has reported patterns of racial differences in percutaneous endoscopic gastrostomy (PEG) placement for patients with post-stroke dysphagia. Reasons for this disproportion are not well understood, but critical for clinical decision making. Long-term implications for PEG placement are considerable, given complication rates and that reducing oral intake can significantly impact recovery of swallow function. In this population-based study, we evaluated the influence of patient-related factors and stroke characteristics on PEG placement.Methods:All patients, 18 years or older, hospitalized with either ischemic or hemorrhagic stroke in Greater Cincinnati in 2010, 2015, and 2020 were considered for this study. Patients who died within 3 days or transferred to hospice care were not included. Demographics and clinical characteristics of Black and White individuals were compared. Multivariable logistic regression was then used to examine the association between Black race and PEG placement after adjustment for potential confounders. Univariable and multivariable logistic regression analysis (dependent = PEG) was used to determine influential factors for PEG placement. Patient and stroke characteristics between Black and Non-Black patients were compared using Chi-square tests, two-sample t-tests, or Wilcoxon rank-sum tests.Results:The final sample included 2315 cases, of whom 28.2% were Black (653/2315) and 54.1% were women (1254/2315). Black individuals with stroke were younger (p

Stroke, Volume 56, Issue Suppl_1, Page AWMP91-AWMP91, February 1, 2025. Background and Objective:Carotid artery stenting (CAS) is a procedure that has been established as a safe and effective alternative to carotid endarterectomy in high surgical risk patients. There are procedural questions that remain unanswered, specifically, the safety of pre-stent balloon angioplasty versus post-stent versus both. The objective of our study is to understand the risk and safety of these procedural techniques.Methods:Multicenter retrospective data related to angioplasty balloons, stents, complications due to pre and post-stent angioplasty along with the modified Rankin score (mRS) before and after the procedure were collected from January of 2015 until December of 2022. Statistical analysis was performed to correlate this data with risks of complications and clinical outcomes.Results:A total of 1355 patients were enrolled. We found that patients who underwent pre-stent angioplasty, or both (pre and post-stent angioplasty) had a higher risk of complications compared to those who only had post-stent angioplasty. There were more complications in patients who did not undergo post-stent angioplasty as compared to those who did undergo angioplasty (p=0.018, OR=0.513). Follow-up MRS at 30-90 days was higher if the balloons in both pre-stent angioplasty (p=0.016) and post-stent angioplasty (p=0.020) stent angioplasty were not inflated to nominal pressure. Follow up MRS was statistically higher (p=0.01) in patients with open-cell stents than closed-cell stents. Open-cell stents were more likely to undergo post-stent angioplasty (p

Stroke, Volume 56, Issue Suppl_1, Page AWP140-AWP140, February 1, 2025. Background:Maximizing long-term home time (HT) for acute ischemic stroke (AIS) patients has patient-centered and health-system benefits. We evaluated the influence of early (30-day) post-acute care (PAC) pathways on 1-year HT.Methods:We analyzed a cohort of Medicare AIS patients at a 7-hospital stroke certified health system (2016 to 2020). Clinical data extracted from an EMR-driven registry were linked to PAC utilization information retrieved from a CMS Qualified Entity with ≥80% data for the Texas state population (including 100% of Medicare Fee-for-Service). All claims within 1 year of hospitalization were collated and grouped into corresponding care pathways. One-year HT (i.e., number of days at home across 1-year period) was calculated utilizing discharge dates from various healthcare settings. Low HT was defined as

Stroke, Volume 56, Issue Suppl_1, Page AWP294-AWP294, February 1, 2025. Background:Racial disparities have been well described in cardiovascular disease. However, the impact of race on the risk of stroke among infective endocarditis (IE) patients is not well understood.Objective:This study aims to investigate the racial disparities in the risk of stroke and clinical outcomes among IE patients.Method:The TriNeTX Global Collaborative Network database was used to identify patients aged ≥18 years of age from January 2000 to May 2023 which included IE patients. Patients were categorized into two groups, one with Black or African American and another with White race patients. Both groups were followed for 12 months. Propensity score-matched analysis (PSM) (1:1) was performed on age, gender, BMI, hypertension, diabetes mellitus, chronic kidney disease, hemoglobin level, LDL level, left ventricular ejection fraction and various drugs including beta blockers, ACEi and ARBi. Primary outcome was ischemic stroke, while secondary outcomes were all-cause mortality, heart failure, cardiogenic shock, MACE (composite of all-cause mortality, heart failure, and ischemic stroke), and acute kidney injury (AKI).Result:After 1:1 propensity score matching, the study cohort comprised 9, 814 Black patients and 9, 814 White patients. The mean age of patients was comparable between both groups (59.8 and 63.1 years). IE patients were having a comparable risk of ischemic stroke among both the races after 1 month (RR, 1.17 (95% CI: 0.96-1.42), P = 0.11), however, the risk of ischemic stroke was significantly higher among Black patients after 1 year (RR, 1.18 (95% CI:1.02-1.36), P = 0.024) when compared with White patients. Black patients were having a significantly higher risk of all-cause mortality after one month (RR, 0.818 (95% CI: 0.74-0.89), P

Stroke, Volume 56, Issue Suppl_1, Page ATP284-ATP284, February 1, 2025. Enrichment is the prospective use of any patient characteristic to select a study population at higher risk in which detection of a drug effect is more likely than it would be in an unselected population. Patients with post-stroke cognitive impairment (PSCI) found to have higher risk of stroke recurrence in a recently completed meta-analysis. The goal of this study is to test whether PSCI based patient selection may represent enrichment strategy for secondary stroke prevention clinical trial. This is a subgroup analysis of Insulin Resistance Intervention after Stroke (IRIS) trial. In IRIS trial, patients were randomized to receive pioglitazone vs. placebo and had a baseline Modified Mini-Mental State Examination (3MS, where 3MS ≤ 88 was indicative of global PSCI. The primary endpoint of the study was recurrent stroke or MI. We estimated the hazard ratio (HR) for the effect of pioglitazone among those with global PSCI. To determine the sample size for a subsequent trial enriched by including only subjects with global PSCI, we make the following assumptions: (1) time to event follows an exponential distribution in both the pioglizone and placebo groups where the hazard rate for the placebo group is assumed to be the same as in the IRIS trial among those with global PSCI; (2) hazards for the pioglitizon and placebo groups are proportional over the course of the study; and (3) subjects are randomized to pioglitazone or placebo in equal proportions.Data on n = 3,338 patients of original cohort of n = 3,876 were analyzed, and n = 473 among them had PSCI at baseline. During 5-years of follow-up, n=246 patients experienced recurrent stroke, and n = 118 had MI. In patients with PSCI HR was 0.56 (95% CI 0.34 – 0.92) suggesting a 44% reduction in the hazard rate for secondary stroke or MI after 5 years of follow-up in the pioglitizone group compared to the placebo. If we conservatively assume that the true HR = 0.56 (closer to the null of HR = 1 than what was observed in the IRIS trial), then a total sample size of n= 967 willl proivde 90% power using a two-sided log-rank test at the 5% significance level. This conservative sample size corresponds to a 75% reduction in the sample size that was required for the IRIS Trial. PSCI screening may represent enrichment strategy for secondary stroke prevention clinical trial potentially reducing sample size by 75%. PSCI screening-based enrichment can be tested in phase 2 secondary stroke prevention trial.

Stroke, Volume 56, Issue Suppl_1, Page ADP28-ADP28, February 1, 2025. Background:Microglia-mediated inflammatory response directly affects ischemic stroke outcome. Autophagy is crucial in inflammatory response after cerebral ischemia. NLRC5 can be a positive or negative regulator of inflammatory signaling cascades, but its role after ischemic stroke is unstudied.Methods:Single-cell RNA sequencing and immunofluorescence staining were used to explore the expression and localization of NLRC5 in mice brain. Conditional (microglia-specific) NLRC5-knockout mice (TMEM119CreERTNLRC5f/f) and their littermate control mice (NLRC5f/f) were subjected to MCAO. Histopathological and behavioral methods were performed to assess ischemic injury in mice. In vitro, oxygen-glucose deprivation (OGD) and OGD neuronal supernatant were used to stimulate microglia to simulate post-stroke inflammatory microenvironment. Primary microglia were extracted from litters of wide type and NLRC5-global-KO mice for proteomic detection after OGD. Mass spectrometry was used to investigate the interaction of NLRC5 with other proteins. A series of cellular and molecular biological techniques were used to evaluate the proinflammatory response, autophagy activity and protein–protein interactions etc.Results:mRNA and protein expression of NLRC5 were increased after MCAO from 1 to 7 days. NLRC5 was mainly expressed in microglia rather than neurons and astrocytes. After MCAO, the cerebral infarction volume of TMEM119CreERTNLRC5f/fmice was smaller than that ofNLRC5f/fmice, and neurological impairment was slighter. In the ischemic penumbra tissue of TMEM119CreERTNLRC5f/fmice, autophagy level increased, microglia activation decreased, and inflammation decreased. In vitro experiments, NLRC5 knockdown promoted autophagy level of primary microglia and BV2 in the inflammatory environment, and the inflammatory response was reduced. Proteomic results showed that after OGD, the autophagy levels of NLRC5-global-KO primary microglia were increased compared to that of wide type mice. Additionally, the protein levels of EIF5A, EIF5A hypusination and ATG3 increased in NLRC5-KO primary microglia after OGD. Mass spectrometry revealed that NLRC5 could bind to EIF5A. Specific binding sites and mechanisms need further study.Conclusions:Down-regulation of microglia NLRC5 can increase hypusination level of EIF5A, increase ATG3 transcription, thus promote autophagy, inhibit neuroinflammation, and protect brain injury after ischemic stroke.

Stroke, Volume 56, Issue Suppl_1, Page ADP26-ADP26, February 1, 2025. Introduction:Short interspersed nuclear elements (SINEs) are an abundant class of noncoding retrotransposons that can be transcribed by RNA polymerase III. Some SINEs have also been shown to act as genomic enhancers, thus giving rise to what are known as enhancer SINE-RNAs (eSINE-RNAs). The function of these novel RNAs within the post-stroke brain remains virtually unexplored. In this study, we map the genome-wide cortical expression of eSINE-RNAs in response to stroke, characterize their cell-type&subcellular localization, and determine their role in affecting post-stroke infarct volumes.Methods:Ischemic stroke was induced in male C57BL/6N mice using 1h middle cerebral artery occlusion (MCAO) followed by 6h of reperfusion (or sham surgery). Genome-wide RNA-seq and H3K27ac ChIP-seq (n=3/group/experiment) were performed on ipsilateral cortices to identify stroke-responsive enhancer RNA transcripts, which were then overlaid with genomic SINEs to identify eSINE-RNAs. Immunohistochemistry and RNA-FISH were used in tandem to determine the cell-type and subcellular localization of several highly expressed eSINE-RNAs. Select eSINE-RNAs were ablated via intracerebroventricular injection of antisense oligonucleotides followed by 1h MCAO and 24h reperfusion. Infarct volumes following knockdown were evaluated using cresyl violet staining (n=5-7/group).Results:We discovered 46 eSINE-RNAs upregulated in the cortex following MCAO, 33 of which were unique to stroke and not detected in the sham group. These RNAs were derived from several families of SINEs, including 24 from the B1 family, 20 from the B2 family, and one each from the less ubiquitous ID and MIR families. The expression of several abundant eSINE-RNAs was specific to the nuclei of neurons within the prospective infarct and peri-infarct territories, including the sensorimotor cortex and hippocampus. Ablation of select eSINE-RNAs resulted in significantly higher infarct volumes versus controls, suggesting that these eSINE-RNAs serve a neuroprotective role in the brain following ischemic stroke.Conclusion:Our study is the first report to characterize the expression of eSINE-RNAs in the post-stroke brain and begin to elucidate their function as regulators of post-stroke pathophysiology. Our results suggest that the transcription of eSINE-RNAs represents a robust neuroprotective response to transient focal ischemia, thus positioning them as potential molecular targets for modulating post-stroke outcomes.

Stroke, Volume 56, Issue Suppl_1, Page ADP56-ADP56, February 1, 2025. Introduction:We discovered a marked upregulation of MMP-12 levels in the brain following an ischemic stroke and demonstrated that reducing MMP-12 levels in otherwise healthy rodents decreases brain damage and facilitates functional recovery. This study aimed to assess the effectiveness of MMP-12 gene silencing in improving sensorimotor function recovery in aged mice and hypertensive rats.Methods:Both male and female C57BL/6 mice (≥16 months old) and male spontaneously hypertensive rats (SHRs) (2-3 months old) were subjected to 35-min and 1-h transient right middle cerebral artery occlusion (MCAO), respectively. Appropriate cohorts of animals (25 mice/group; 18 rats/group) received either control shRNA or MMP-12 shRNA plasmids (1 mg/kg) formulated as nanoparticles that were administered intravenously via tail vein 2 h after reperfusion. In mice, stroke symptoms were evaluated using the neurological deficit score at 2-4 hours and 1 day after reperfusion, while the modified neurological severity score was used in rats. Sensorimotor functions were assessed using the sticky tape test, pole test, and rotarod test at baseline (before MCAO) and at regular intervals post-MCAO (days 3, 5, and 7 in mice, and days 1, 3, 5, 7, and 14 in rats).Results:MMP-12 expression in the ischemic brain was significantly increased by 35-min MCAO in aged mice and 1-h MCAO in SHRs, as was previously observed in healthy young mice and rats that were subjected to 1-h and 2-h MCAO, respectively. In comparison to the control shRNA treatment, MMP-12 shRNA treatment facilitated a greater mean recovery of somatosensory function in aged mice (sticky tape latency was significant on day 3 and day 5; sticky tape interaction was significant on day 5) and in SHRs (sticky tape ratio was significant on day 14). Furthermore, MMP-12 shRNA treatment resulted in a greater mean recovery of motor function across all tested time points in aged mice (pole descent score was significant on day 7; rotarod latency was significant on day 7) and in SHRs (rotarod latency was significant on day 5 and day 14).Conclusions:Reducing MMP-12 expression in the ischemic brain facilitates the recovery of both somatosensory and motor function in aged mice and hypertensive rats after transient focal cerebral ischemia. Our findings further reinforce the potential benefits of MMP-12 gene silencing as a therapeutic approach for improving recovery outcomes in stroke patients.

Stroke, Volume 56, Issue Suppl_1, Page ATP1-ATP1, February 1, 2025. Background and Objective:The effect of time from onset to treatment on reperfusion in an extended time window remains unexplored. This study aimed to investigate the relationship between the time to treatment and the probability of reperfusion in acute ischemic stroke patients with large vessel occlusion treated with tenecteplase in an extended time window, using data from the Chinese Acute tissue-Based imaging selection for Lysis In Stroke Tenecteplase (CHABLIS-T) trials.Methods:This study included patients treated with intravenous tenecteplase from the CHABLIS-T1 and CHABLIS-T2 clinical trials, both of which screened patients in the extended window using CT perfusion (CTP) imaging. Major reperfusion was assessed through follow-up CTP or digital subtraction angiography (DSA) imaging. Time variables, including the time from last known normal (LKN) /symptom onset to hospital arrival/ administration of tenecteplase were entered as continuous, categorical, and cubic spline variables in multivariable logistic regression models to explore their association with the probability of post-thrombolytic reperfusion.Results:A total of 199 patients arrived within 4.5-24 hours from LKN were included in this study, of whom 67 achieved post-thrombolytic major reperfusion. Cubic spline analysis indicated a linear correlation between time variables and the probability of reperfusion. Therefore, time variables were entered as continuous or categorical variables in the regression models. Multivariable logistic regression analysis revealed that a longer time from LKN to hospital arrival was associated with a lower probability of major reperfusion (continuous variable: OR=0.998, P=0.018,Figure 1). Similarly, a longer time from LKN to thrombolysis was associated with a lower probability of reperfusion (continuous variable: OR=0.996, P=0.020,Figure 2; categorical variable: OR=0.043, P=0.005,Figure 3). The analysis of time from symptom onset to hospital arrival/thrombolysis and reperfusion drew similar resultsConclusion:In acute ischemic stroke patients with large vessel occlusion treated with tenecteplase in an extended time window, a longer time to treatment was associated with a lower probability of post-thrombolytic reperfusion. Therefore, rapid reperfusion treatment should still be required even in patients with large vessel occlusion in an extended time window with a good collateral flow, in order to optimize treatment effect.

Stroke, Volume 56, Issue Suppl_1, Page ADP13-ADP13, February 1, 2025. Background:People with stroke are at high risk of dementia. There have been reductions in stroke case fatality and disability but temporal trends in the incidence and absolute burden of post-stroke dementia have not been described.Methods:We did a population-wide analysis of over 15 million people in Ontario, Canada between 2002-2022. Using linked administrative databases, we identified all 90-day dementia-free survivors of first acute ischemic stroke or intracerebral hemorrhage (ICH). We evaluated dementia incidence from 90-days after stroke onwards using a validated definition which included hospitalization, physician claims, and dementia medications. We calculated 1-year and 5-year incidence of dementia as percentages and per 100 person-years for each fiscal year, age-/sex-standardized by the 2002 population and with follow-up until March 2022. We stratified incidence trends by sex, stroke type, and severity (90-day home time of

Stroke, Volume 56, Issue Suppl_1, Page ATP263-ATP263, February 1, 2025. Introduction:Children with arteriopathy 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 is a lack of sufficient evidence to provide patient specific blood pressure guidelines post pediatric ischemic stroke.Objective:We aimed to evaluate blood pressure averages and changes in pediatric patients with arteriopathy within the first 48 hours in intensive care after an arterial ischemic stroke.Method:We conducted a retrospective study of children diagnosed with acute arterial ischemic stroke admitted to the pediatric intensive care unit (PICU). We reviewed data on demographics, clinical outcome, radiologic, hemodynamic signs, and medication within PICU. 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 rang. We also contrasted blood pressures of stroke patients with age and admission year matched 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:Forty-five patients (49% female, median age 7.8 years, range age 17 years) were included. Arteriopathy disease included Dissection, Moyamoya, Focal Cerebral Arteriopathy and Vasculitis. Despite only a minority of patients being on vasoactive medications, patients with arteriopathy had higher blood pressures compared to age-matched control PICU patients in the first 48 hours. In addition, 31% of arteriopathy patients had an average systolic blood pressure greater than the 95thpercentile for the first two days after an acute arterial ischemic stroke, versus only 14% of their control (p-value < 0.05). Neurological deficits and increased brain ischemic lesion volume were associated with higher blood pressures.Conclusion:Understanding blood pressure trends and outcomes after an ischemic stroke in children at risk is crucial to guide the management of this modifiable factor. Blood pressure in children with arteriopathy is increased after an ischemic stroke compared to controls admitted to PICU. Further research into the etiology of differences observed here and blood pressure management is crucial to reducing the burden of pediatric ischemic stroke on this at risk population.

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 A114-A114, February 1, 2025. Introduction:Post-stroke neuroinflammation is a hallmark of ischemic stroke. This study investigates the role of IGSF6 in microglia during ischemic stroke and its contribution to neuroinflammatory responses and brain injury following stroke.Methods:IGSF6 expression was examined in murine microglia under various inflammatory stimuli. Using a middle cerebral artery occlusion (MCAO) model, we evaluated the impact of microglialIgsf6knockdown (Igsf6-KD) on neuroinflammation and ischemic outcomes. Pro-inflammatory cytokine levels were measured using qPCR and ELISA in bothIgsf6-KD and wild-type (WT) mice, and functional outcomes were assessed through neurological tests. Subcellular localization and cytokine trafficking studies were conducted using immunofluorescence, electron microscopy, and protein interaction assays.Results:IGSF6 expression was significantly upregulated in microglia following MCAO. Knockdown of Igsf6 in microglia resulted in reduced secretion of pro-inflammatory cytokines (TNF, IL-6, CCL2, CCL5) at day 1 post-stroke, despite unchanged mRNA levels. Morphological analysis of microglia fromIgsf6-KD mice revealed a less reactive phenotype. Additionally,Igsf6-KD mice exhibited a reduction in infarct volume and improved functional outcomes, including enhanced performance on rotarod, grip strength, and foot-fault tests.Mechanistically, IGSF6 was shown to localize to the trans-Golgi network (TGN) and mediate cytokine trafficking. Knockdown ofIgsf6disrupted this process, reducing the secretion of key cytokines without affecting their transcription or translation.Conclusions:Microglial IGSF6 exacerbates post-stroke neuroinflammation by promoting the secretion of pro-inflammatory cytokines. Its knockdown attenuates neuroinflammatory responses, reduces ischemic brain injury, and improves functional recovery. These findings highlight the detrimental role of IGSF6 in stroke pathology and suggest that targeting IGSF6 may offer therapeutic benefits for mitigating neuroinflammation and improving outcomes after ischemic stroke.

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