Vascular Risk Research Articles (Page 6)

Systemic disease burden is well reflected in the retinal microvasculature, but it is not established whether optical coherence tomography angiography (OCTA) parameters can reliably reflect coronary atherosclerosis. To assess the association of reduced retinal vascular density and subclinical coronary atherosclerosis in asymptomatic individuals. This cross-sectional cohort study included asymptomatic individuals with elevated cardiovascular risk who self-referred for a health screening program involving coronary computed tomography angiography (CTA) at Asan Medical Center in Seoul, South Korea, and subsequently underwent OCTA as part of ophthalmic evaluations. This study was conducted from October 2015 to December 2020, and data analysis was conducted from January 2021 to May 2025. The primary outcome was the association between OCTA parameters and coronary CTA parameters. A total of 1286 eyes from 1286 participants were analyzed (mean [SD] age, 64.2 [9.9] years; 482 female participants [37.5%]). Coronary artery calcium score (CACS), presence of plaque and its subtypes, obstructive coronary artery disease (CAD), severe CAD, segment stenosis score (SSS), and segment involvement score (SIS) were significantly increased across the quartiles of superficial and deep parafoveal vascular density (PFVD). When modeled as continuous variables, superficial capillary plexus (SCP) and deep capillary plexus (DCP) PFVD were the most significant metrics and correlated with CACS, number of coronary vessels involved, SSS, and SIS. The lowest quartile of SCP PFVD was associated with significantly higher odds of obstructive CAD (adjusted odds ratio [aOR], 2.91; 95% CI, 1.83-4.73), severe CAD (aOR, 3.30; 95% CI, 1.55-7.91), and elevated SSS and SIS scores compared to the highest quartile. Similar but attenuated associations were observed for DCP PFVD. Continuous variable analysis for ORs for unit increase supported a linear inverse association between PFVD and CAD burden. Incorporating PFVD into models with cardiovascular risk factors improved area under the curve (AUC) for identifying severe CAD (AUC, 0.79; 95% CI, 0.75-0.82), obstructive CAD (AUC, 0.78; 95% CI, 0.76-0.81), and SSS of 10 or higher (AUC, 0.77; 95% CI, 0.74-0.80), with SCP yielding superior performance over DCP. In this cross-sectional cohort study, reduced retinal PFVD was independently associated with subclinical coronary atherosclerosis in a population with elevated vascular risk. In this context, decreased PFVD may reflect greater subclinical coronary atherosclerotic burden and help identify individuals who could benefit from further coronary evaluation, beyond traditional risk factors.

Background: While sleep duration’s association with stroke is established, the combined influence of sleep onset time and duration on stroke subtypes remains inadequately explored. Since circadian biology links sleep onset timing to vascular risk via mechanisms operating independently of sleep duration, we quantified their joint contributions to the risk of stroke. Methods: In this population-based cross-sectional study, from 31 December 2021 to 31 March 2022, we recruited 8168 ischemic stroke cases, 3172 intracerebral hemorrhage cases, and 13,458 control participants across 152 survey centers in 28 counties in Hunan Province, China. Standardized computer-assisted interviews collected sleep parameters. Conjoint analysis identified protective sleep profiles. Results: Short sleep duration (<6 h) was consistently associated with elevated ischemic risk across all sleep onset times (p < 0.05 in all cases, i.e., sleep before 10 p.m. [odds ratio (95%CI): 1.886(1.606, 2.214)], 10–11 p.m. [1.740(1.336, 2.265)], 11 p.m.–12 a.m. [2.335(1.190, 4.581)], and after 12 a.m. [2.834(1.193, 6.728)]). A sleep duration of 6–8 h with a sleep onset time between 10 p.m. and 12 a.m. was associated with the lowest ischemic risk (p < 0.001 in all cases). Conversely, prolonged sleep (>8 h) with an early sleep onset time (<10 p.m.) increased ischemic risk (OR 1.194, 95% CI 1.090–1.308, p < 0.001), whereas a late sleep onset time (11 p.m.–12 a.m.) in long sleepers was protective (OR 0.580, 95% CI 0.352–0.956, p < 0.001). Similar trends were observed for ICH, though the effect sizes were attenuated. Conclusion: Sleep duration and onset time interact to influence stroke risk. Optimal cerebrovascular protection requires ≥6 h of sleep, ideally initiated between 10 p.m. and 11 p.m. These findings highlight sleep optimization as a potential modifiable target for high-risk populations.

Cerebral amyloid angiopathy (CAA) is a leading cause of intracranial hemorrhage and cognitive decline in the elderly. This study seeks to investigate the quantitative MRA features as new markers of CAA. In this cross-sectional study, consecutive patients with CAA, along with controls, who underwent 3DTime-of-flight-MRA were included. Demographic and clinical data, including sex, age, diabetes, smoking, hypertension, and atrial fibrillation, were collected. Radiologic features, including the microhemorrhage classification, siderosis, and Fazekas scale, were also collected. Using in-house developed semi-automated software (VesselVoyager), quantitative MRA features, including total arterial length, number of branches, and tortuosity, were extracted. Univariable and multivariable logistic regression analyses were then performed to compare the CAA and non-CAA cohorts. Seventy-four patients were included: 43 with CAA and 31 controls. Quantitative MRA analysis showed that patients with CAA had significantly reduced total arterial length (1900±1240 mm vs. 2880±1540 mm, p=0.006). Univariable logistic regression identified total arterial length (p=0.009), age (p=0.012), and total branch number (p=0.107) as relevant predictors of CAA. In multivariable analysis, total arterial length (OR = 0.95; 95% CI: 0.92-0.99; p=0.014) and age (1.06; 1.01-1.12; p=0.023) remained independently associated with CAA diagnosis. Quantitative MRA total arterial length is inversely independently and significantly associated with CAA diagnosis. This could potentially serve as an imaging marker of CAA diagnosis and potentially further elucidate vascular segment involvement in CAA patients. CAA = Cerebral amyloid angiopathy; TOF-MRA = Time-of-flight MRA; LDL = Low-density lipoprotein; BMI = Body mass index.

C-reactive protein (CRP) is well-known marker of inflammation and immune response. Its potential role in Alzheimer's disease (AD) pathophysiology remains unclear, particularly in relation to central AD biomarkers, including beta-amyloid (Aβ), tau, and neurodegeneration. To investigate the associations between circulating CRP levels and central AD biomarkers-including Aβ deposition, tau, and AD-signature neurodegeneration-in nondemented older adults. This cross-sectional observational study analyzed data from a Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer Disease conducted from 2014 to 2020. A total of 417 nondemented older adults underwent comprehensive evaluations, including blood sampling and multimodal neuroimaging for measuring of Aβ and AD-signature neurodegeneration. A subset of participants (N = 123) also underwent tau positron emission tomography (PET) scan. The primary outcomes were A/T/N biomarkers of AD, including brain Aβ and tau deposition measured via amyloid and tau PET, as well as AD-signature neurodegeneration measured by fluorodeoxyglucose (FDG)-PET. Associations between CRP levels and these biomarkers were analyzed while adjusting for CRP-decreasing allele scores, as well as other confounders, including age, sex, vascular risk score, body mass index, nonsteroidal anti-inflammatory drug (NSAID) usage, smoking status, and APOE ε4 carrier status. The mean (SD) age of participants was 70.57 (8.00) years, with 179 (42.9 %) females. Circulating CRP levels showed non-linear associations with A/T/N biomarkers of AD, showing a U-shaped relationship with Aβ and tau deposition and an inverted U-shaped association with neurodegeneration. Threshold effect analyses revealed that CRP was inversely associated with Aβ deposition (B = -0.081; 95 % CI, -0.153 to -0.007; p = 0.031) below 0.63 mg/L, after adjusting for all confounding variables. In contrast, higher CRP levels were associated with lower cerebral glucose metabolism in AD-signature regions, indicative of greater AD-related neurodegeneration, when above 2.15 mg/L (B = -0.056; 95 % CI, -0.112 to -0.001; p= 0.042). Our study revealed differential associations between circulating CRP levels and central AD biomarkers that varied according to the CRP concentration. Further studies are necessary to elucidate the mechanisms underlying the inverse relationship between circulating CRP and brain Aβ within the clinically normal range, as well as potential aggravating effects of elevated CRP on Aβ-independent neurodegeneration.

BACKGROUND Vertebral artery dissection (VAD) is an important cause of ischemic stroke in young adults and is often associated with mechanical stressors such as trauma, sudden neck movements, or intense physical activity. While video games are not traditionally recognized as a risk factor, the increasing popularity of interactive fitness games calls for attention to their potential health implications. CASE REPORT We present the case of a 25-year-old sedentary woman with no vascular risk factors who developed acute left-sided neck pain while performing repetitive overhead pushing and pulling movements using a resistance-based controller during gameplay with Ring Fit Adventure (Nintendo Co., Ltd.), a home fitness video game. Two days later, she experienced sudden-onset left-sided numbness and visual disturbance. Neurological examination revealed left homonymous hemianopia and hemisensory deficits. Brain MRI revealed an acute infarct in the right occipital lobe, and magnetic resonance angiography showed right posterior cerebral artery occlusion and dissection of the left vertebral artery with intramural thrombus. She underwent successful endovascular thrombectomy and intra-arterial thrombolysis, followed by dual antiplatelet therapy. Her symptoms improved markedly, and she was discharged with only mild visual field defect. Imaging at follow-up demonstrated vascular remodeling. No underlying vasculopathy or prothrombotic condition was identified. CONCLUSIONS This case highlights that even a seemingly benign fitness video game may exert sufficient mechanical stress to trigger VAD, particularly in untrained individuals. While the temporal association suggests a potential link, causality cannot be definitively established. As home fitness gaming becomes increasingly popular, it is important for both clinicians and the general public to be aware of rare but serious vascular complications that may arise from sudden, strenuous activity in previously sedentary individuals.

Ultrasound Guidance for Botulinum Toxin Injection of Muscles Innervated by the Facial Nerve: A Systematic Review of Anatomical Precision, Safety, and Outcomes.

Background and ObjectivesIndividual MRI markers of cerebral small vessel disease (CSVD) are associated with impaired cognition and dementia but may not reflect the overall burden of CSVD. In addition, it is unclear whether these markers provide additional value in dementia risk assessment beyond vascular risk factors alone. Thus, we studied the association between the additive burden of multiple CSVD markers and incident dementia and determined whether this relationship remains independent of the Framingham Stroke Risk Profile (FSRP), a tool used commonly used for stroke risk prediction.MethodsA total of 1,152 MRI scans from participants in the Original and Offspring cohorts of the Framingham Heart Study, a large observational cohort study, were included. Participants were older than 55 years and free of prevalent dementia, stroke, or other neurologic conditions at the time of MRI. A multimarker score capturing CSVD burden was defined as the sum of CSVD features detected in the MRI: cerebral microbleeds, covert brain infarcts, extensive white matter hyperintensities, high-burden perivascular spaces, and cortical superficial siderosis. Multivariate Cox regression models examined the association between the multimarker CSVD score and incident all-cause dementia, Alzheimer dementia (AD), and vascular dementia.ResultsThe mean age was 70.9 years (SD 8.7) (527 [46%] were male), and 211 (18%) had a CSVD score of ≥2. Over a median follow-up time of 7.4 years (interquartile range 4.6–11.3), participants with a score ≥2 had significantly elevated risk of all-cause dementia compared with those with no CSVD markers after adjustment for the FSRP (hazard ratio [HR] 1.67; 95% CI 1.05–2.66) and vascular risk factors (HR 1.76; 95% CI 1.10–2.81). The multimarker CSVD score demonstrated similar model performance metrics to the FSRP (Harrell c-statistics 0.82–0.83).DiscussionWe found a significant association between all-cause dementia and multimarker CSVD scores, which was independent of the FSRP as well as its individual components. Our results support the use of a multimarker CSVD score as an indicator for incident all-cause dementia risk and suggest that it may be as robust as the FSRP. Further studies are necessary to validate the use of a multimarker CSVD score in dementia risk prediction.

New nicotine products and vascular risk.

BACKGROUND:The estimated glucose disposal rate (eGDR) is a validated surrogate marker of insulin resistance. However, its association with stroke and dementia in nondiabetic populations remains insufficiently investigated.METHODS:This prospective cohort study included nondiabetic participants from the UK Biobank. The outcomes in this study were stroke, ischemic stroke, hemorrhagic stroke, all-cause dementia, vascular dementia, and Alzheimer disease. Multivariable Cox regression and restricted cubic splines were used to examine the associations between eGDR and outcomes. Polygenic risk score analyses were applied to investigate interactions between eGDR and genetic risk.RESULTS:Overall, 430 093 participants were included. During a follow-up of around 13.5 years, 10 307 stroke cases and 11 137 all-cause dementia cases were recorded. Restricted cubic splines analyses indicated nonlinear associations between eGDR and the risks of stroke and vascular dementia. Below specific thresholds (<7.64 for stroke, <7.60 for ischemic stroke, <7.75 for hemorrhagic stroke, and <8.31 for vascular dementia), eGDR levels were not significantly associated with these outcomes except a modest inverse association with overall stroke risk (hazard ratio [HR] 0.97 [95% CI, 0.95–0.99]; P=0.012). In contrast, above these thresholds, higher eGDR levels were associated with significantly reduced risks of stroke (HR, 0.80 [95% CI, 0.78–0.82]; P<0.001), ischemic stroke (HR, 0.80 [95% CI, 0.78–0.81]; P<0.001), hemorrhagic stroke (HR, 0.81 [95% CI, 0.78–0.84]; P<0.001), and vascular dementia (HR, 0.89 [95% CI, 0.84–0.94]; P<0.001). A linear inverse relationship was observed between eGDR and all-cause dementia and Alzheimer disease. The HR in the highest versus lowest quartile was 0.81 (95% CI, 0.75–0.88) for all-cause dementia and 0.73 (95% CI, 0.64–0.84) for Alzheimer disease. Stratified polygenic risk score analyses revealed a synergistic interaction between reduced eGDR and elevated genetic susceptibility.CONCLUSIONS:eGDR exhibited nonlinear associations with stroke and vascular dementia risk and linear inverse associations with all-cause dementia and Alzheimer disease in nondiabetic populations.

PurposeTo determine the impact of 24-hour post-reperfusion glycemic control on 90-day functional outcomes in acute large vessel occlusion (ALVO) patients after successful recanalization.Materials and MethodsThis multi-center retrospective study analyzed 2056 ALVO patients (male: 1488; female: 568) from three cerebrovascular centers achieving successful reperfusion via mechanical thrombectomy with/without bridging thrombolysis. Using 1:1 propensity score matching (covariates: gender, age, Diabetes mellitus, hypertension, hyperlipidemia, cardiac disease, smoking status, glucose measurement timing, baseline NIHSS, and preoperative mRS), 194 matched pairs (mean age 63[IQR 55–71] years; male: 278) were stratified by 90-day modified Rankin Scale (mRS) outcomes into favorable (mRS 0–2) and poor prognosis (mRS 3–6) cohorts.ResultsThe poor prognosis cohort demonstrated significantly elevated mean fasting blood glucose (MFBG) levels (7.22 mmol/L [6.66–8.50] vs 6.86 mmol/L [6.28–7.58], P<0.001). Multivariable logistic regression adjusted for sex, age, vascular risk profile, and baseline NIHSS (adjusted OR=0.819, 95% CI 0.714–0.940, P=0.004) confirmed MFBG elevation as an independent risk factor for unfavorable outcomes.ConclusionSustained hyperglycemia during the initial 24-hour post-recanalization period independently predicts impaired 90-day functional recovery in ALVO patients. These findings highlight the imperative for standardized glucose monitoring protocols during the hyperacute post-thrombectomy phase, while optimal glycemic targets (<7.0 mmol/L vs individualized thresholds) and therapeutic windows for neuroprotection warrant validation through prospective multicenter RCTs.

Effects of vascular disease risk factors on brain metabolism in multiple sclerosis.

Vascular sites have distinct susceptibility to atherosclerosis and aneurysm, yet the epigenomic and transcriptomic underpinning of vascular site-specific disease risk is largely unknown. Here, we performed single-cell chromatin accessibility (scATACseq) and gene expression profiling (scRNAseq) of mouse vascular tissue from three vascular sites. Through interrogation of epigenomic enhancers and gene regulatory networks, we discovered key regulatory enhancers to not only be cell type, but vascular site-specific. We identified epigenetic markers of embryonic origin including developmental transcription factors such as Tbx20, Hand2, Gata4, and Hoxb family members and discovered transcription factor motif accessibility to be vascular site-specific for smooth muscle, fibroblasts, and endothelial cells. We further integrated genome-wide association data for aortic dimension, and using a deep learning model to predict variant effect on chromatin accessibility, ChromBPNet, we predicted variant effects across cell type and vascular site of origin, revealing genomic regions enriched for specific TF motif footprints—including MEF2A, SMAD3, and HAND2. This work supports a paradigm that cell type and vascular site-specific enhancers govern complex genetic drivers of disease risk.

BackgroundStroke is a leading cause of death and disability globally, with frequent cognitive sequelae affecting up to 60% of stroke survivors. Despite the high prevalence of post-stroke cognitive impairment (PSCI), early detection remains underemphasized in clinical practice, with limited focus on broader neuropsychological and affective symptoms. Stroke elevates dementia risk and may act as a trigger for progressive neurodegenerative diseases. However, the underlying neurobiological mechanisms and the interaction between vascular and degenerative pathways are poorly understood. The ICTUSCOG study aims to address these gaps by determining the incidence, predictors and progression factors of PSCI in a prospective, multicenter cohort of nondisabling stroke patients. The work will explore distinct patient profiles, evaluate the role of biomarkers, and develop a predictive model to identify at risk individuals.MethodsICTUSCOG is a five-year observational project involving four Spanish centres. Recruitment began in 2022 and includes consecutive patients aged 18–75 with no prior cognitive impairment and nondisabling stroke. Participants undergo detailed neuropsychological, functional, and neuroimaging assessments at baseline, 3, 6, and 12 months, and annually thereafter. Key data include stroke characteristics, vascular risk factors, advanced neuroimaging metrics, and biological biomarkers. Neuropsychological assessments incorporate domain-specific validated tools tailored for stroke patients.DiscussionThe study will quantify the incidence of early and late PSCI, identify predictors of progression, and characterise cognitive profiles. Multivariate models and clustering techniques will explore interactions among clinical, biological and imaging data. A predictive model will be developed and validated for clinical use. ICTUSCOG will provide critical insights into the mechanisms and trajectories of PSCI, informing prevention, early intervention, and rehabilitation strategies. The work aims to establish predictive tools and care pathways to mitigate the burden of cognitive impairment in stroke survivors.

Background: Ischemic stroke is a leading cause of morbidity and mortality worldwide. Despite established prevention strategies, many patients present with previously undiagnosed vascular risk factors (URFs) at the time of their first-ever ischemic stroke, suggesting missed opportunities for early detection. In Canada, particularly in Quebec, access to primary care is inconsistent, and a substantial proportion of the population lacks attachment to a family doctor (FD). Objective: This study aimed to determine the prevalence of URFs among patients with first-ever ischemic stroke and to evaluate the relationship between URFs, geographic region, and access to primary care in Quebec, Canada. We hypothesized that patients without an FD would have a higher prevalence of URFs. Methods: We conducted a retrospective chart review of 610 patients admitted with first-ever ischemic stroke to the McGill University Health Center (MUHC) between 2014 and 2017. Data collected included demographics; known and undiagnosed stroke risk factors such as hypertension (HTN), diabetes mellitus (DM), hyperlipidemia (HLD), and atrial fibrillation (AF); FD status; and geographic location based on postal code. Results: Among the 610 patients, 136 (22.3%) had at least one URF. The most common URF was HLD (14.3%), followed by HTN (6.2%), AF (1.6%), and DM (0.1%). Of 609 patients with available data, 146 (23.97%) lacked an FD. Patients without an FD were significantly more likely to have undiagnosed HTN (7.6% vs. 2.1%, p = 0.008). No significant differences were observed for the other URFs. Geographic variation was noted in both URF prevalence and FD access, but regional differences were not statistically significant. Conclusions: Our findings support the hypothesis that a lack of an FD is associated with a higher prevalence of undiagnosed HTN in ischemic stroke patients. Targeted screening and improved access to primary care, particularly in underserved regions, may help to reduce the burden of preventable stroke by facilitating the earlier identification and management of modifiable risk factors.

Background:Covert cerebrovascular disease (CCD), comprising covert brain infarction (CBI) and white matter disease (WMD), is common in older adults and linked to increased risk of stroke and dementia. While most CCD research relies on MRI, CT remains the predominant imaging modality in clinical care. The influence of imaging modality on detection and prognosis of incidentally discovered CCD remains unclear.Methods:We identified 18,626 patients aged ≥50 years from Kaiser Permanente Southern California who underwent both CT and MRI brain scans within 30 days between 2009–2022. Patients with known prior stroke or dementia were excluded. Natural language processing algorithms were applied to radiology reports to identify CBI and WMD status and WMD severity (none, mild, moderate, severe). We assessed prevalence, cross-modality agreement (Cohen’s kappa), and reclassification patterns. Prognostic associations with incident stroke or dementia were estimated using Cox Proportional Hazards regression adjusted for vascular and cognitive risk factors.Findings:CBI prevalence was similar for CT (6.3%) and MRI (6.1%), but agreement was modest (κ=0.27). WMD was reported far more often on MRI (60.5%) than CT (24.4%). Among 15,551 patients with classifiable severity on both modalities, 47.9% (n=7,441) had discordant grades, with 92.3% upgraded on MRI. The incidence rates of stroke or dementia per 1,000 person-years were 12.7 (95% CI 11.5 – 14.0) for patients without WMD on either modality (36.3% of the cohort), 22.6 (21.0 – 24.2) for WMD detected on MRI only (39.2% of the cohort), and 52.2 (48.69 to 55.95) for WMD detected on both CT and MRI (21.2% of the cohort). In adjusted Cox models, WMD detected on MRI only was associated with a 23% higher hazard of stroke or dementia (HR=1.23, 95% CI 1.07–1.41) compared with no WMD on either modality, while WMD detected on both CT and MRI was associated with an 82% higher hazard (1.82, 1.58–2.11).Interpretation:MRI detects substantially more WMD than CT; however, WMD visible on CT has stronger prognostic significance, despite CT’s low sensitivity. These findings emphasize modality-based diagnostic and prognostic differences and support the need for modality-specific approaches when translating CCD research into clinical risk assessment and patient counselling.

Interactive effects of arterial stiffness and Alzheimer's disease risk on cognitive decline in older adults without dementia

Recent studies in stroke patients from predominantly Asian populations have underscored the significance of trimethylamine N-oxide (TMAO) as a valuable blood biomarker for predicting incident strokes and major adverse cardiovascular events (MACE). However, its prognostic role after ischemic stroke in other populations is not yet comprehensively investigated. We measured plasma TMAO levels in 1726 acute ischemic stroke patients (within 24 h from symptom onset) from the multicenter BIOSIGNAL cohort. Using cox and logistic regression models adjusting for demographic and vascular risk factors, we investigated the association of TMAO with recurrent stroke, MACE within 365 days and functional outcome at 90 days after stroke. TMAO levels were not associated with any risk of recurrent stroke (n = 108, unadj. HR per unit increase of log (TMAO) 1.15, 95% CI 0.88-1.51, adjust. HR 1.07, 95% CI 0.78-1.47) or MACE (n = 309, unadj. HR of log (TMAO) 1.10,95% CI 0.91-1.3, adjust. HR 0.90, 95% CI 0.74-1.09). There was an univariable positive association between higher TMAO plasma levels and unfavorable functional outcome, this association remained statistically significant in the multivariable analysis (unadj. OR of log (TMAO) 1.56, 95% CI 1.34-1.81, adjust. OR 1.28, 95% CI 1.04-1.57). In this large cohort of acute stroke patients from a predominantly White population, TMAO had no independent association with either recurrent stroke, or MACE or death. In univariable, and multivariable analysis, there was a significant association between TMAO and unfavorable functional outcome, which might not be clinically significant due to its low effect size. Therefore, TMAO seems not to be a clinically relevant biomarker for risk stratification after stroke.

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder often complicated by vascular events, with or without antiphospholipid antibody syndrome (APS). This study aimed to explore subclinical venous involvement in SLE using biochemical and imaging modalities, focusing on vein wall thickness (VWT) and inflammation-related biomarkers. In this cross-sectional study, 68 SLE patients were categorized based on antiphospholipid antibody (APA) status and clinical APS. Results were compared with 22 rheumatoid arthritis (RA) patients and 20 healthy controls. Serum levels of P-selectin, growth differentiation factor 15 (GDF15), and citrullinated histone 3 (CH3) were measured using ELISA. Ultrasonographic assessments evaluated VWT at bilateral jugular veins, femoral veins, portal vein and femoral artery. Correlations and predictors of vascular changes were analyzed statistically. VWT was significantly increased in SLE patients compared with both control groups (p< 0.001), regardless of APA and APS status. Serum P-selectin, GDF15, and CH3 levels were elevated in SLE-APS patients. GDF15 levels correlated positively with VWT, and increased portal vein wall thickness was independently associated with thrombosis. Biomarkers showed significant associations with APS, suggesting their role as indicators of prothrombotic states. No significant associations were found between vascular parameters and disease activity score. Subclinical venous involvement appears to be a novel vascular feature of SLE, reflected by increased vein wall thickness (VWT) and its association with thrombosis and biomarkers. Increased portal vein thickness may indicate vascular risk. Whether these changes result from inflammation or vascular remodeling remains unclear, but their presence irrespective of disease activity highlights their clinical relevance.

Arterial stiffening is an independent risk factor forcardiovasculardiseases, particularly affecting organs with low vascular resistance,such as the brain and kidneys. Pulse wave velocity (PWV) is the clinicalgold standard for arterial stiffness assessment; however, conventionalequipment requires complex setups and trained operators, limitingreal-world and point-of-care monitoring. Here, we introduce a tactile-transparentwearable (TTW) sensor that preserves physicians’ tactile pulsepalpation abilities while providing quantitative cardiovascular riskassessment by integrating flexible Polydimethylsiloxane (PDMS) electrodesand ultrathin graphene oxide dielectric films. In a clinical studywith 20 healthy volunteers (aged 22–60 years), the TTW sensorshowed strong agreement with Doppler ultrasound for carotid-radialPWV (Pearson’s r = 0.88, p < 0.001; mean difference = – 0.084 m/s) and identifiedthat arterial stiffness is significantly correlated with age and BMI(both p < 0.001). High-fidelity waveform analysisfurther provided dynamic vascular risk indices (augmentation index,reflection index, stiffness index) not accessible by Doppler. ThisTTW sensor democratizes arterial stiffness assessment, providing transformativepotential for preventive cardiology and enabling widespread adoption,especially in resource-limited or community healthcare settings.

Young adults account for up to 15% of all ischemic strokes, yet data from Latin America remain scarce. Understanding their clinical profile and outcomes is essential to inform targeted interventions and public health strategies. We aimed to characterize demographics, vascular risk factors, stroke etiology, access to acute reperfusion therapies, and 90-day outcomes in Argentine patients aged 18-50 years with ischemic stroke. We conducted a retrospective multicenter cohort study including consecutive patients aged 18-50 years with ischemic stroke, enrolled between January 2015 and December 2023 across 26 centers in Argentina. Primary outcomes were functional dependence (modified Rankin scale (mRS) 3-5), stroke recurrence, and all-cause mortality at 90 days. Among 18,934 ischemic stroke patients, 1422 (7.5%) were young adults. Median age was 43 years (interquartile range (IQR) 36-47), and 53.7% (n = 763) were male. The most prevalent risk factors were hypertension (31.0% (n = 441)), smoking (29.3% (n = 417)), and obesity (18.8% (n = 267)). Median National Institute of Health Stroke Scale (NIHSS) on admission was 3 (IQR 1-8). Acute reperfusion therapy was administered in 18.9% (n = 269). Stroke etiology remained undetermined in 50.4% (n = 717) of cases; within this group, 26.1% (n = 312) fulfilled criteria for embolic stroke of undetermined source (ESUS), and 17.8% (n = 198) were cryptogenic strokes associated with patent foramen ovale. Arterial dissection accounted for 56.6% (n = 193) of other determined causes. At 90 days, functional dependence was observed in 12.1% (n = 110), stroke recurrence in 3.9% (n = 37), and mortality in 4.8% (n = 44). In Argentina, nearly 1 in 13 ischemic strokes occurs in young adults. Despite generally mild presentations, functional dependence and mortality remain substantial. The high rate of undetermined etiology underscores the need for standardized diagnostic protocols in this population, whose strokes carry a disproportionate individual and societal burden due to their early onset.