Search Results for: Nuovo test rapido per distinguere le infezioni virali

Stroke, Volume 56, Issue Suppl_1, Page AWP181-AWP181, February 1, 2025. Background:Timely intervention is crucial for patients with acute ischemic stroke. The RapidAI imaging system (RAPID) was implemented to enhance the speed and efficiency of care delivery. We evaluated the impact of RAPID on various metrics in the patient care pathway.Methods:In this retrospective observational study, we analyzed consecutive patients who presented to our hospital ER with acute ischemic stroke and who were treated with Intravenous Thrombolysis (IVT) or mechanical thrombectomy between December 20, 2014, and April 20, 2024. Patients were divided into pre-RAPID (n =186) and post-RAPID (n =264) groups based on the implementation date of the RAPID system (September 1, 2019). We compared Door to Non-contrast CT (NCCT), Door to CT Angiography (CTA) / Perfusion Imaging, Door to IVT, and Door to Puncture / first pass for thrombectomy, between the two groups using Fisher’s exact test.Results:For Door to CT, no significant difference was observed between pre-RAPID and post-RAPID groups; 74% of patients in the post-RAPID group and 71% in the pre-RAPID group received NCCT within 45 minutes (p= 0.44). Significant improvements were observed in Door to CTA/Perfusion times; 90% of patients received vessel or perfusion imaging within 150 minutes post-RAPID compared to 70% pre-RAPID (p= 0.01), and 87% received imaging within 120 minutes post-RAPID compared to 70% pre-RAPID (p= 0.031). For Door to IVT, 96% of patients received treatment within 120 minutes post-RAPID compared to 82% pre-RAPID (p= 0.015). For thrombectomy, there was a trend toward faster door to puncture post-RAPID; 70% of patients were treated within 150 minutes post-RAPID compared to 62% pre-RAPID (p= 0.36), and 90% were treated within 210 minutes post-RAPID compared to 81% pre-RAPID (p= 0.12). Similarly, a trend toward faster Door to First Pass times was observed post-RAPID, with 88% treated within 240 minutes compared to 80% pre-RAPID (p= 0.20).Conclusions:RapidAI Implementation was associated with significant improvements in key workflow metrics, notably in Door to Vessel/Perfusion Imaging and Door to IVT. These findings suggest that RAPID enhances the efficiency of patient care delivery in acute ischemic stroke. Further studies with larger sample sizes are warranted.

Stroke, Volume 56, Issue Suppl_1, Page ATMP32-ATMP32, February 1, 2025. Introduction:Facilitating evidence-based uptake of new medication regimens for disease prevention is a well-recognized public health challenge. Using data from GWTG-Stroke, researchers previously reported that, after minor ischemic stroke (NIHSS 0-3), the use of aspirin-clopidogrel for stroke prevention is highly variable despite guideline recommendations. We sought to explore potential changes in dual antiplatelet therapy (DAPT) use in patients with moderate ischemic stroke (NIHSS 4-5) after the publication of the THALES (The Acute Stroke or Transient Ischemic Attack Treated With Ticagrelor and ASA for Prevention of Stroke and Death) trial in 2020.Methods:We used the GWTG-Stroke registry to describe patterns of DAPT use in the U.S. from 2019 to 2023. All patients with a final diagnosis of ischemic stroke, NIHSS 4-5, hospital arrival within 24 hours, who lacked an indication for anticoagulation (e.g., atrial fibrillation) and were not treated with thrombolysis/thrombectomy were included in our study. Patients with NIHSS 4-5 (moderate stroke) were not included in prior randomized controlled trials of aspirin-clopidogrel for short-term stroke prevention but were included in THALES. We reported basic demographic features of our cohort and used the Cochran-Armitage trend test to report changes in aspirin-ticagrelor use by year.Results:We identified a total of 40,624 acute ischemic stroke patients with NIHSS 4-5 during the study period. The mean age was 68 years and 47% of patients were women. We found that a total of 20,293 (50%) patients were discharged on aspirin-clopidogrel whereas 1,335 (3.5%) were discharged on aspirin-ticagrelor. The use of both DAPT regimens significantly increased over time (Figure 1, p

Stroke, Volume 56, Issue Suppl_1, Page ATP325-ATP325, February 1, 2025. Introduction:The Cameron County Hispanic Cohort (CCHC) represents a random sample of the Hispanic community residing in Cameron County, Texas. Participants were invited, regardless of their medical history, to participate every five years and went through extensive interviews and laboratory workout. This is the first report on the incidence of stroke in this cohort and provides a comprehensive examination for the associations between strokes and several cardiometabolic indicators.Methods:We conducted a case-cohort analysis to measure the associations between incident stroke and several cardiometabolic risk factors in the CCHC. Strokes were self-reported and we exclude subjects who reported strokes at their first visit as well as those who did not report on their stroke status. Chi square and Student t-test were used to test for univariate associations of several cardiometabolic indicators with incident strokes. We ran logistic regression models to estimate the associations of several cardiometabolic indicators with incident strokes after adjusting for age, diabetes, and hypertension. We used multiple imputation to estimate missing values for variables with more than 25% missingness. All analyses were conducted in R software (version 4.4.2)Results:The cumulative incidence for strokes was 0.02 (87 out of 4692 subjects). Those who presented with incident strokes were older (mean(sd): 61.4 (13.9) vs. 45.3 (15.9)), more likely to be diabetic (44 (50.6%) vs. 759 (16.5%)), and hypertensive (58 (66.7%) vs. 1194 (25.9%)), have higher inflammatory profile (e.g., C-Reactive Protein) (11.0 (26.3)vs. 7.92 (14.8)), thicker carotid intima (0.796 (0.250) vs. 0.681 (0.179)), lower left ventricular ejection fraction (60.8 (8.69) vs. 63.9 (4.89)), and higher left ventricular mass (159 (45.7) vs. 141 (36.9)) when compared to those without strokes at baseline. Adjusted logistic regression models comparing those with strokes to those without strokes at baseline showed that Low Density Lipoprotein (OR: 0.99, 95%CI: 0.98 – 0.99) and metabolic syndrome (OR: 0.53, 95%CI: 0.33-0.84) to be significantly associated (p

Stroke, Volume 56, Issue Suppl_1, Page ATP311-ATP311, February 1, 2025. Introduction:Immune Checkpoint Inhibitors (ICIs) used for treatment of malignancies might promote atherosclerosis and increase the risk of ischemic stroke (IS). We aimed to compare IS characteristics of patients with non-small cell lung cancer (NSCLC) who received ICIs compared to those who did not. We hypothesized that IS associated with atherosclerosis will be more common among those treated with ICIs than other treatments.Methods:A retrospective single center study of patients,18 or older, with NSCLC presenting between 2013 and 2023, treated with either ICIs, chemotherapy, or a combination and had an IS any time following treatment. Patients without vessel imaging were excluded. We collected demographics and stroke characteristics. Two sample Mann-Whitney U and chi-square test were used to compare demographics and stroke etiologies among patients who received chemotherapy and those who received ICIs with or without chemotherapy.Results:A total of 58 patients were identified, 22 received chemotherapy only and 36 received ICIs. The mean age was 68.8, with 50% male (29/58). ICI treated groups had significantly more stage IV diagnoses (chemotherapy only 3.6%, ICI 67%, p=0.04). There was no difference in median time from treatment to stroke onset in days between groups; chemotherapy 90.5 (range 27-386) vs. ICI 337.5 (range 95-665), p= 0.39. The stroke etiology in those treated with chemotherapy alone were as follows: Large artery atherosclerosis (3), cardioembolic (8), small vessel disease (5), ESUS (5), other (1). For those treated with either ICI alone or ICI and chemotherapy: Large artery atherosclerosis (5), cardioembolic (6), small vessel disease (2), ESUS (23), other (0). Stroke etiology consistent with embolic stroke with unknown source (ESUS) was more common in the ICI group (chemotherapy only 2.3%, ICI 64%, p=0.02).Conclusions:Contrary to prior research suggesting atherogenesis with ICI, the most common stroke etiology in the ICI group was ESUS.

Stroke, Volume 56, Issue Suppl_1, Page AWP185-AWP185, February 1, 2025. Introduction:Branch atheromatous disease involving the lenticulostriate artery (LSA) is strongly associated with early neurological deterioration. We aimed to investigate whether an apparent thalamostriate vein (TSV) or brush sign on susceptibility-weighted imaging (SWI) can predict infarct growth.Methods:Consecutive patients with the small subcortical infarction of the LSA presenting within 24 h of onset were retrospectively evaluated. MRI, including SWI, was performed on admission and within 1 week of admission. An apparent TSV was defined as a difference in the diameter of the TSV between the right and left sides on SWI upon admission. Infarct growth was defined as an increase in infarct size on axial or coronal diffusion-weighted imaging from 1 point.Results:Of the 76 patients (median age, 76 [67.25–82] years, 48 male) with the small subcortical infarction of the LSA, 22 (median age, 75.5 [64.75–82.5] years, 13 male) presented with an apparent TSV and/or brush sign. On univariable logistic analysis, only the presence of apparent TSV and/or brush sign (OR, 3.12; 95% CI, 1.11–8.73;p=0.03) was associated with infarct growth. In multivariable logistic regression analysis, age (OR, 1.07; 95% CI, 1.01–1.14;p=0.02) and infarct growth (OR, 4.46; 95% CI, 1.37–14.54;p=0.01) were independently associated with progressive paralysis.Conclusion:An apparent TSV or brush sign could indicate infarct growth in cases of the small subcortical infarction of the LSA.

Stroke, Volume 56, Issue Suppl_1, Page ATP312-ATP312, February 1, 2025. Background/Objectives:Perioperative stroke is a significant cause of morbidity and mortality in patients undergoing cardiac, vascular, and neurosurgical procedures. We assessed the rate, characteristics, risk factors and survival outcomes of perioperative stroke following surgical resection of glioma.Design:This is a retrospective chart review of a single quaternary care center of patients with glioma between 2005-2021 who underwent resection. Stroke within 30 days of surgical resection was identified based on the radiology read of MRI brain for ischemic stroke and CT brain for hemorrhagic stroke that was obtained as part of clinical care. This was then confirmed retrospectively by a neurologist who reviewed imaging and medical records, excluding expected post-operative changes. Descriptive analysis and logistic regression were conducted. Overall survival was estimated with Kaplan-Meier methods from the date of surgery to death and compared with the log rank test.Results:Out of 738 patients who underwent surgical resection of their glioma and underwent brain MRI or CT head, 20 (2.71%) had radiographic evidence of strokes, with the mean (SD) time from surgery to stroke 5.4 (16.2) days. Of these, 13 (65%) had ischemic strokes, 7 (35%) had hemorrhagic strokes. Out of all perioperative strokes, 9 (45%) were symptomatic (total incidence of 1.2%), and 11 (55%) were asymptomatic. Patients who had a stroke were older [mean (SD); 60.4 (13.7) vs. 52.8 (15.0) years; p=0.026], had a higher rate of atrial fibrillation (p= 0.002), and had comorbid hyperlipidemia (p=0.039) and hypertension (p=0.047). Descriptive analysis of this cohort is summarized in Table 1. Older age, carrying a diagnosis of atrial fibrillation, and having hyperlipidemia were associated with higher odds of having a perioperative stroke (Table 2). In an attempt to generate a multivariate logistic model, stepwise selection yielded no significant results likely due to the low number of strokes in this cohort. The median survival for patients with stroke was 24.6 months (95% CI:21.8-32.1), which was lower than for patients who did not suffer a stroke (29.3 months, 95% CI: 25.6-32.9) (p=0.052).Conclusion:Older age, atrial fibrillation, hyperlipidemia, and hypertension were associated with perioperative stroke risk after glioma resection. Future studies should evaluate underlying mechanisms and stroke etiologies to better identify high risk patients.

Stroke, Volume 56, Issue Suppl_1, Page AWP186-AWP186, February 1, 2025. Background and Purpose:Primary aldosteronism (PA) is characterized by the autonomous overproduction of aldosterone leading to the risk of occurrence of acute ischemic stroke (AIS), but the exact prevalence of PA is unknown in patients with AIS. PA induces oxidative stress and inflammation through vascular endothelial cells, which may damage small vessel disease (SVD). We conducted a prospective study to investigate the prevalence of screening and definite diagnosis of PA in patients with AIS. Next, we aimed to reveal whether SVD markers could be associated with PA.Methods:We screened consecutive patients with AIS who participated in our prospective study to investigate the prevalence of PA and followed up for PA evaluation from October 2020 to December 2022. Inclusion criteria were patients with AIS hospitalized and diagnosed with hypertension. Exclusion criteria were patients taking medications affecting renin, aldosterone, and catecholamines. The screening criteria for PA was defined as the aldosterone-to-renin ratio > 200. Final diagnosis of PA was judged by endocrinologist if one of the captopril challenge test, saline infusion test, and furosemide-upright test was positive following discharge. We evaluated total SVD score based on white matter hyperintensities (separately scored by periventricular hyperintensity [PVH] and deep and subcortical white matter hyperintensity), cerebral microbleeds (CMBs; categorized into deep, lobar, and infratentorial lesions), enlarged perivascular spaces (separately scored in basal ganglia and centrum semiovale), and old lacunes on MRI.Results:We included 120 patients with AIS (93 [78%] male, median age 62 years, Figure 1). The screening for PA was positive in 33 (28%) patients and 8 (7%) patients were finally diagnosed with definite PA. In Poisson regression analysis with a robust variance estimator, total SVD score was related to positive PA screening (prevalence ratio [PR] 1.261, 95% CI 1.021-1.556,p= 0.031) and definite PA diagnosis (PR 1.946, 95% CI 1.229-3.082,p= 0.005, Figure 2). In terms of each SVD marker, severe PVH, and deep and lobar CMBs were associated with positive PA screening and definite PA diagnosis (Figure 3).Conclusions:Twenty-eight percent of patients with AIS were positive for PA screening, and then about a quarter of them were confirmed as definite PA. SVD burden, especially PVH, and deep and lobar CMBs, might be associated with positive screening and definite diagnosis of PA.

Stroke, Volume 56, Issue Suppl_1, Page ATP314-ATP314, February 1, 2025. Introduction:Blood pressure (BP) control after a stroke is crucial in lowering the risk of stroke recurrence. Our prior work found that over 60% of patients recently discharged from a regional health system with stroke did not achieve BP control according to current guidelines. Less is known about the impact of insurance type and co-morbidities on post-stroke BP control.Objective:To analyze the relationship between insurance type, comorbidities and post-stroke BP control among patients within a regional health system.Methods:This report is an observational cohort study. Patients were admitted between 2013-2021 for ischemic and hemorrhagic stroke and had seen a PCP/PCAPP (primary care physician/primary care advance practice provider) in a regional health system or affiliated outpatient clinics using the EPIC electronic health record. We excluded patients who died during hospitalization, were lost to follow-up, or were on dialysis.Results:The analysis included 2,750 patients. Six months after hospital discharge, the insurance coverage among stroke survivors with uncontrolled BP ( >130/80 mm Hg) was 61.1% for public, 35.8% for private, 1.9% for other/unknown, and 1.3% for self-pay. In comparison, among those with controlled BP (

Stroke, Volume 56, Issue Suppl_1, Page A82-A82, February 1, 2025. Background:Spontaneous intracerebral hemorrhage (sICH) is a neurological condition characterized by the rupture of blood vessels within the brain, resulting in the formation of a hematoma and subsequent brain injury. Tobacco use is a major modifiable risk factor for sICH and is associated with worsened outcomes following the occurrence of sICH. Tobacco use is also correlated with worsened outcomes following sICH. Previously, we observed that prior chronic exposure to nicotine results in increased hematoma volume following collagenase-induced sICH when compared to saline-exposed animals. This study aims to evaluate the effect of prior chronic nicotine exposure on long-term outcomes post-sICH.Hypothesis:Prior chronic nicotine exposure will result in more significant brain damage following an autologous blood injection-induced sICH.Methods:Young male and female (estrous matched) rats were randomly assigned to a saline (control) or nicotine-exposed group. Rats received nicotine or saline via. osmotic pumps for 2-3 weeks. The pump was removed before the induction of sICH by the stereotaxic injection of autologous blood into the striatum. The autologous blood injection-induced sICH model was used to obtain equal hematoma volume in all experimental groups. Rats then underwent perfusion fixation, and brains were harvested for histopathological analysis. Paraffin-embedded brain blocks were cut into 10 µm coronal sections between bregma -2.0 to +2.0, stained with hematoxylin and eosin, scanned with a high-resolution scanner, and analyzed using ImageJ to measure lesion area. Student’s t-test was used to determine significant differences in mean lesion volume between treatment groups. Two-way ANOVA was used to assess the interaction effect between sex and lesion volume.Results:For the male group, the brain lesion volume in nicotine-exposed rats was significantly (p

Stroke, Volume 56, Issue Suppl_1, Page A90-A90, February 1, 2025. Introduction:Post-Stroke Cognitive Impairment (PSCI) is increasingly recognized as a major factor in long-term disability. Therefore, new therapies that enhance post-stroke brain function (plasticity) are appealing in translational research. Activation of the cation channel TRPM2 after middle cerebral artery occlusion (MCAO) induces PSCI-like symptoms, such as memory impairment and deficits in Long-Term Potentiation (LTP). Determining the mediator of chronic TRPM2 channel activation may implicate a novel contributor to LTP deficit. The enzyme CD38 may be this mediator, as it produces the TRPM2 activator ADPr. Here, we investigate astrocytic CD38’s role in MCAO and TRPM2-induced deficits.Methods:LTP was assessed through Extracellular Field Recordings from CA3-CA1 synapses of Acute Hippocampal Slices. Immunofluorescence stained for GFAP and CD38 in hippocampal sections. Wt or CD38-/-mice were subjected to 60-minute MCAO, or Sham, and assessed for LTP 7 days later. Wt or TRPM2-/-mice received Intracranial Administration (200nL, 1012gc/mL) of AAV-CD38-eGFP (astrocyte CD38 overexpression) or AAV-eGFP (control) to the right ventral CA1 and assessed for LTP after 21 days. All mice were 8-12-week-old males. Differences between groups were determined with either Welch’s T-Test or One-Way ANOVA followed by post-hoc test.Results:We observed increased expression of CD38, colocalized with GFAP (astrocyte marker), in the hippocampus 7 days post-MCAO. Sham Wt mice exhibited robust LTP, not observed in Wt MCAO (Wt-Sham: 176% +/- 33.9 vs Wt-MCAO: 135% +/- 23, p < 0.05). Conversely, CD38-/-mice displayed robust LTP after either Sham or MCAO, depicting protection of synaptic plasticity (CD38-/--Sham: 175.2% +/- 24.1, CD38-/--MCAO: 184.8% +/- 27.3). AAV-CD38-eGFP astrocytic overexpression vector produced impairment in LTP in the Wt mice compared to the empty vector control (Wt-eGFP: 195.6% +/- 46 vs Wt-CD38:141.5% +/- 38.7, p < 0.05). No differences were observed in TRPM2-/-mice injected with either virus. (TRPM2-/--eGFP: 180.3% +/- 39.4, TRPM2-/--CD38 174% +/- 54.1)Conclusions:Our study implicates astrocytic CD38 as a novel inducer of hippocampal synaptic plasticity impairment. CD38 is increased following injury and required for MCAO-induced LTP deficit. Additionally, overexpression is sufficient to impair LTP in uninjured mice, in a TRPM2-dependent manner. Astrocytic CD38 is a novel target for PSCI and the likely upstream mediator of chronic TRPM2 activation.

Stroke, Volume 56, Issue Suppl_1, Page ATMP10-ATMP10, February 1, 2025. Introduction:An optimal strategy for the treatment of intracranial atherosclerotic disease (ICAD) has remained unclear, despite medical therapy (antiplatelet therapy and LDL control management) or endovascular therapy (angioplasty or stenting). Recently, cilostazol plus other antiplatelet agents combined therapy (CT) has been reported to reduce recurrent stroke, and eicosapentaenoic acid (EPA) has been reported to reduce the risk of cardiovascular events and plaque progression. Therefore, our hypothesis is that the addition of CT and EPA therapy may reduce stroke recurrence and further regression of stenosis.Methods:Patients with symptomatic and asymptomatic intracranial artery stenosis treated and followed at our institution from January 2009 to December 2023 were included in this study: 198 ICAD lesions in 155 patients (mean follow-up 11 months) were retrospectively evaluated. Each patient was divided into antiplatelet therapy alone (AA) (monotherapy (MT) or CT), antiplatelet therapy plus statin (AS), and antiplatelet therapy plus statin and EPA (AE). Antiplatelet drug monotherapy was aspirin, clopidogrel, or prasugrel and combination therapy was any of them plus cilostazol. ICAD was assessed by MRA and the stenosis rate was calculated by the warfarin-aspirin symptomatic intracranial disease (WASID) method.Results:The improvement in stenosis was significantly better with CT than with MT (Median% interquartile range(IQR)= CT: 21.71% (11.33-41.40) vs. MT: 9.15% (2.69-25.78), P

Stroke, Volume 56, Issue Suppl_1, Page AWMP114-AWMP114, February 1, 2025. Introduction:Clonal Hematopoiesis of Indeterminate Potential (CHIP) is characterized by the expansion of a blood-cell clone due to somatic mutation in hematopoietic stem cells, in the absence of other hematologic abnormalities. Initially, CHIP was identified as a risk factor for hematologic cancer, but recently, many studies have implicated it as a risk factor for cardiovascular disease. CHIP is also considered a risk factor for subarachnoid hemorrhage. However, the causality between CHIP and aneurysm rupture, as well as the mechanism by which CHIP promotes aneurysm rupture, remains unclear. Our study aimed to assess whether CHIP promotes the development of intracranial aneurysm rupture and investigate its mechanisms in mice. We induced intracranial aneurysms on chimeric mice with partial bone marrow transplantation of TET2-knockout hematopoietic stem cells, widely used to recapitulate human CHIP to test our hypothesis.Methods:We used competitive bone marrow transplantation as a model of CHIP. We used the C57BL/6 congenic mice that express the CD45.1 allele as a recipient and TET2-knockout mice that carry CD45.2 alleles as a donor. C57BL/6 CD45.1+/CD45.2- congenic mice were transplanted with suspensions of bone marrow cells containing 10% CD45.1-/CD45.2+ TET2-/- cells and 90% CD45.1+/CD45.2- TET2+/+ cells as a TET2-derived CHIP model. We induced intracranial aneurysms by a combination of elastase injection and DOCA-salt hypertension at 8 weeks later. We evaluated the formation and rupture rates of intracranial aneurysms and the survival curve. The qPCR was used to reveal molecular change in the intracranial artery. From the result of qPCR, we utilized IL-6 monoclonal antibody and NLRP3 inhibitor as a treatment for CHIP-related intracranial aneurysm rupture.Results:First, CHIP mice show clonal expansion of TET2-knockout cells in flow cytometry (Fig.1). Our studies demonstrated increased aneurysmal rupture rates in CHIP mice of both sexes (Fig.2). Second, Inflammatory cytokines including IL-6, IL-1β, and NLRP3 were elevated in qPCR (Fig.3). Lastly, both IL-6 monoclonal antibody and NLRP3 inflammasome inhibitor significantly decreased aneurysm rupture rate in CHIP mice.Conclusions:Our study showed that CHIP promotes the development of intracranial aneurysm rupture. Its mechanism is through the upregulation of inflammatory cytokines. Our findings suggest that IL-6 and NLRP3 are promising therapeutic targets for CHIP-related intracranial aneurysm rupture.

Stroke, Volume 56, Issue Suppl_1, Page ATMP44-ATMP44, February 1, 2025. Introduction:Understanding factors that contribute to missed diagnoses of acute ischemic stroke (AIS) may improve diagnostic accuracy. Prior studies have focused on the failure of non-neurologists to recognize AIS. The aim of this study was to understand the characteristics of stroke-alerted patients whose symptoms were misattributed to a stroke mimic by the responding vascular neurology team.Methods:A retrospective chart review was conducted on patients seen by the vascular neurology team as a stroke alert at a single Joint-Commission-certified Comprehensive Stroke Center between 1/2021-2/2022. Patients whose symptoms were erroneously attributed to a stroke mimic at the time of assessment but later confirmed by MRI as AIS (“missed stroke”) were compared to 200 consecutive cases of stroke patients who were correctly diagnosed (“accurate stroke”) and 200 who were correctly diagnosed with a stroke mimic (“accurate mimic”). Patient characteristics were compared with univariate analysis, using chi square or Kruskal-Wallis H test as appropriate.Results:1823 stroke alerts were reviewed to identify 40 patients with missed stroke (incidence 2.2%) of which the median age was 66 years (IQR 58-81), median NIHSS was 5 (IQR 1-18), and 40% presented within the 4.5h-treatment window for thrombolysis. Patients with missed strokes were more likely female than those with accurate strokes (57% vs 39%, p

Stroke, Volume 56, Issue Suppl_1, Page ATMP12-ATMP12, February 1, 2025. Background:Atherosclerotic carotid artery disease is associated with a high risk of major adverse cardiac events (MACE) even with optimal risk factor management and surgical interventions such as carotid endarterectomy (CEA). Aortic stenosis (AS) is an age-related valve disease that is associated with a high rate of MACE. An artificial intelligence-based AS estimation algorithm (AI-AS) can identify AS with high accuracy using electrocardiogram. This study evaluates the prognostic value of AI-AS in patients with carotid artery disease undergoing CEA.Methods:We included patients with carotid artery disease undergoing CEA at Mayo Clinic from 2002-2023 if they had >30 days of follow-up and an electrocardiogram within one year before CEA. The electrocardiogram closest to the CEA date was used to calculate AI-AS (AS probability ranging from 0-1). MACE was defined as the composite of cardiac events, ischemic cerebrovascular accidents, and all-cause mortality during follow-up after CEA. A receiver operating characteristic curve and the Youden index were used to identify the optimal AI-AS cut-off value for predicting MACE. Kaplan Meier plot was used to depict MACE-free survival. Regression models were used to evaluate the predictive value of AI-AS for future MACE adjusting for clinical covariates.Results:A total of 665 patients with a median age of 72 [IQR:66, 78] years and 438 (65.9%) males were included. Over a median follow-up time of 7.1 [IQR:2.7, 11.5] years, MACE occurred in 419 (63%) of the patients, including 187 (44.6%) mortality, 161 (38.4%) cardiac events, and 71 (16.9%) cerebrovascular accidents. Median AI-AS was 0.32 [IQR:0.09, 0.55] in the total cohort, 0.34 [IQR:0.12, 0.56] in patients with MACE, and 0.30 [IQR:0.07, 0.53] in patients without MACE (P=0.038). AI-AS was a significant predictor of MACE (HR:2.38, 95%CI:1.64-3.46, P

Stroke, Volume 56, Issue Suppl_1, Page A98-A98, February 1, 2025. Background:Middle cerebral artery steno-occlusive disease (MCAD) has been recognized as a different clinical entity from moyamoya disease (MMD). Although MCAD can progress to MMD, the extent to which patients actually progress and the risk factors for this progression have not been fully elucidated.Methods:We retrospectively reviewed patients with MCAD who underwentRNF213genotyping. Demographic features,RNF213p.R4810K mutation, medical history, and longitudinal changes in angiography were analyzed.Results:Sixty patients with 81 affected hemispheres were enrolled. During the follow-up period 17 patients developed MMD, and theRNF213p.R4810K mutation was the only factor significantly associated with progression to MMD (odds ratio, 16.1; 95% CI, 2.13–731;P= 0.001). The log-rank test demonstrated that patients with the mutation had a higher risk of progression to MMD (P =0.007), stenosis progression (P =0.010), and symptomatic cerebral infarction or hemorrhage (P =0.026). In Cox regression analysis the p.R4810K mutation remained a significant factor after adjusting for age group (childhood or adult onset) at diagnosis (hazard ratio, 8.42; 95%CI, 1.10–64.4). Hemisphere-based analysis also showed that the mutation was associated with a higher risk of progression to the MMD hemisphere (P =0.002), stenosis progression (P =0.005), and cerebral infarction or hemorrhage (P =0.012).Conclusions:TheRNF213p.R4810K mutation was identified as a risk factor for progression from MCAD to MMD.Genotyping for this mutation may contribute to risk stratification in MCAD.

Stroke, Volume 56, Issue Suppl_1, Page AWMP105-AWMP105, February 1, 2025. Introduction:Accurate prediction of the risk of ischemic stroke (IS) is vital for prevention and would be aided by multimodal biomarkers integrating genetic, clinical, and functional data. The role of imaging and EKG based atrial measurements, other than atrial fibrillation (AF), in IS prediction is uncertain and many strokes remain cryptogenic despite extensive work-up. As an exploratory step to improve stroke evaluation by including atrial traits, we developed a novel multimodal deep learning model integrating demographic and clinical variables with atrial phenotypic and genotypic data.Methods:We collected individuals from UK Biobank (UKBB) and defined ischemic stroke (IS) by the UKBB Algorithmically Defined Outcome (ADO). We developed a multimodal multi-layer perceptron with late fusion (MMLP-LF) model to predict whether a subject has IS by integrating five data modalities from UKBB: 1) MRI and EKG derived atrial traits, 2) lead genetic variants (P