Artificial Intelligence is increasingly embedded in stroke care, yet clear guidance on the competencies required for its safe and ethical use in vascular neurology is lacking.

To map the literature on Artificial Intelligence applications across the stroke care continuum and to synthesize the technical, ethical-legal, and humanistic competencies needed for Artificial Intelligence-augmented clinical practice.

PubMed/MEDLINE, Embase, Scopus, Google Scholar, and targeted gray literature from professional and regulatory bodies.

Peer-reviewed studies, reviews, and consensus statements or guidance documents addressing Artificial Intelligence in stroke care or related ethicallegal and humanistic competencies. Case reports, exclusively preclinical studies, and non-scholarly publications were excluded.

A scoping review was conducted according to PRISMA-ScR and JBI guidance, with independent screening and narrative thematic synthesis.

From 1,426 records, 74 studies were included. Validated Artificial Intelligence applications were identified in hyperacute imaging (e.g., automated ASPECTS and large-vessel occlusion detection), prognostication, complication prediction, and rehabilitation monitoring, with improvements in speed and precision. Key gaps included limited external validation, insufficient bias assessment, and weak implementation governance. Three competency domains emerged: technical (data literacy and model evaluation), ethical-legal (accountability, privacy and equity), and humanistic (empathy, communicationand shared decision-making). We propose "clinical-Artificial Intelligence correlation" as a core competency integrating algorithmic outputs with clinical judgment.

Artificial Intelligence can enhance stroke care when combined with rigorous clinical oversight and strong ethical and humanistic foundations.

10.17605/OSF.IO/G4W9J.

Death from cardiovascular diseases (CVD) represents an essential marker for evaluating the progress and limitations of public policies, especially in territories with greater vulnerability.

To analyze mortality from CVD, hypertensive diseases (HD), ischemic heart disease (IHD), and cerebrovascular diseases (CEVD) by sex, in Brazil, its regions, and Federative Units, between 2010 and 2023.

Time series study with mortality data obtained from DATASUS. Rates were standardized by age, and the temporal trend was assessed using the Joinpoint regression model, with the calculation of annual percent change (APC) and the Average Annual Percentage Change (AAPC) for the entire period. A 95% confidence interval and a significance level of 5% were considered.

Between 2010 and 2023, there were 4,991,937 deaths from CVD in Brazil (52.50% in men). Mortality from CVD decreased in men (Federal District: -3.58%, p<0.001; South: -2.23%, p<0.001), but increased in Amazonas (1.04%, p<0.01) and Amapá (1.54%, p<0.01). IHD increased in men in Amapá (5.21%, p<0.001) and Roraima (2.61%, p=0.03). HD increased in Bahia (men: 1.38%, p=0.03; women: 1.50%, p=0.04) and Rio Grande do Sul (men: 1.93%, p<0.001; women: 1.86%, p<0.01). CEVD mortality shows a downward trend in most states. Premature mortality from HD increased among men in the South (+1.61%, p<0.001).

In Brazil, despite advances in the prevention and treatment of CVD, improvements have not been equitable: strong regional and socioeconomic inequalities persist, with higher mortality rates among vulnerable populations.

Left ventricular outflow tract diameter (LVOTd) is essential for estimating stroke volume and aortic stenosis severity, but technical limitations may affect its accuracy. A predicted LVOTd may overcome these issues, though it has not been validated in large populations. We studied the participants of the representative random sample and with ≥ 60 y-o from the Elsa-Brasil study with echocardiogram performed (n=3,267), divided into a derivation (70%) and a validation subgroup (30%). In the derivation cohort, independent determinants of LVOTd were identified, and a regression equation was derived. In the validation cohort, the performance of LVOTELSA was evaluated and compared with previously published formulas. In our derivation sample (n= 1,822; 58.9 ± 9.5 y-o; 52% females), the mean measured LVOTd was 19.5 ± 2.5 mm. The strongest predictors of LVOTd were sex, height, aortic root diameter (AoDiam), and LV end-diastolic diameter (LVEDD), deriving the equation LVOTELSA = 0.03 + [0.59 x male] + [0.04 x height] + [0.22 x AoDiam] + [0.13 x LVEDD]. In the validation sample (n=739), LVOTELSA showed a high correlation (r=0.63) with measured LVOTd with similar agreement to LVOTPestelli (r=0.61), but worse with LVOTBSA(r=0.47). These differences are reflected in relevant differences in stroke volumes. LVOTELSA showed good performance in a general adult population and may be used as an alternative when direct echocardiographic measurement of LVOTd is not feasible.

High-field MRI (1.5-3 T) delivers excellent images but requires costly, energy-intensive infrastructure. Emerging low-field systems (<1 T) cut equipment and operating costs and consume far less power, making them attractive for low- and middle-income countries (LMICs). We conducted a narrative review of human studies from LMICs that reported clinical, economic or environmental outcomes of low-field MRI, paying special attention to cardiovascular applications and implementation issues in Pakistan. Across included papers, low-field scanners lowered capital expenditure, energy consumption and siting requirements while maintaining diagnostic performance comparable to high-field units in several settings, notably musculoskeletal imaging and intra-operative guidance. Evidence for cardiovascular imaging remains scarce, and key barriers-lower spatial resolution, limited local expertise and infrastructure gaps-persist. Nonetheless, low-field MRI offers Pakistan a feasible, environmentally sustainable option for clinical imaging more broadly; direct evidence for cardiovascular applications, however, remains limited and largely indirect, so routine cardiovascular use will require dedicated validation and further technical refinement before it can be recommended.

Chronic inflammation is a pathological mechanism of central importance that underpins a wide range of diseases, including neurodegenerative, cardiovascular, respiratory, gastrointestinal, and dermatological disorders. Ginkgo biloba extract (GBE), a standardized formulation derived from Ginkgo biloba leaves, has attracted growing attention due to its anti-inflammatory, antioxidant, and neuroprotective properties. This review comprehensively summarizes the current preclinical and clinical evidence regarding the therapeutic potential of GBE and its active constituents in inflammation-related diseases. GBE has been shown to attenuate pro-inflammatory cytokine production, suppress nuclear factor kappa B (NF-κB) activation, restore redox homeostasis, and modulate disease-relevant pathways in models of Alzheimer's disease, Parkinson's disease, multiple sclerosis, atherosclerosis, asthma, chronic obstructive pulmonary disease, inflammatory bowel disease, inflammatory skin conditions and rheumatoid arthritis. While these findings highlight the promising multi-targeted anti-inflammatory actions of GBE, limitations remain regarding the identification of specific active compounds, standardization of formulations, and the availability of robust clinical evidence. Further research is warranted to clarify the mechanisms of action and optimize delivery of GBE, and to validate the efficacy and safety of GBE in large-scale clinical trials.

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as pivotal agents in the treatment of type 2 diabetes (T2D) and obesity, with well-established metabolic and cardiovascular benefits that translate into improvement in quality of life and life expectancy. While a potential benefit may also be hypothesized in patients with metabolic disorders and malignancy, robust clinical evidence is still lacking. In recent years, attention has turned to their potential impact on cancer risk, although current evidence remains limited and, in some cases, conflicting. Several biological pathways, such as improvements in insulin sensitivity, reductions in chronic inflammation, modulation of cellular signaling, and changes in the tumor microenvironment, have been proposed as possible mechanisms through which GLP-1RAs might influence cancer development or progression. However, available data derive from preclinical or observational studies, and high-quality prospective clinical evidence is still lacking. While some reports suggest possible protective associations in specific cancer types, others raise concerns about potential risks, particularly in hormonally sensitive or receptor-expressing tissues. This position paper synthesizes available data on the oncologic safety and potential antitumor effects of GLP-1RAs, highlights key knowledge gaps, and discusses clinical implications, underscoring the need for further research to clarify their role in cancer prevention and treatment.

The Osaka Prognostic Score (OPS), which is based on C‑reactive protein (CRP), total lymphocyte count (TLC), and albumin (ALB), has been reported to have prognostic value in several types of cancer. Recent studies have revealed a relationship between the OPS and cardiovascular diseases. The aim of this study was to evaluate the relationship between the OPS and paroxysmal atrial fibrillation (AF), a significant rhythm disorder.

A total of 941 individuals, including 198 patients with a history of AF and 743 patients without AF as the control group, were included in the study. These groups were compared in terms of demographic characteristics and laboratory findings.

Univariable and multivariable binary logistic regression analyses revealed an independent relationship between the OPS and AF (odds ratio [OR]: 3.37, p < 0.001). In receiver operating characteristic (ROC) curve analysis, OPS above a cut-off level of 0.5 was associated with the presence of AF, with a sensitivity of 55.6% and a specificity of 77.4% (area under the ROC curve [AUC]: 0.682, p < 0.001).

This study found a relationship between the OPS and paroxysmal AF attacks. The OPS may provide additional information for the clinical evaluation of patients with paroxysmal AF in daily practice.

Daily apparel could enable continuous, noninvasive monitoring of cardiopulmonary health for the early detection and treatment of cardiopulmonary diseases, the leading causes of death and disability worldwide. Here we develop an all-fiber wireless auscultation system seamlessly integrated into garments. An ~150-μm-diameter fiber contact microphone is sewn, knitted or woven into clothing to capture deep-body acoustic signals while overcoming acoustic impedance mismatch and electromagnetic noise. An ~500-μm knitted fiber computer enables real-time signal processing and Bluetooth transmission to a mobile device. A clinical study in 10 patients with heart failure and 20 neonates demonstrated cardiopulmonary sound capture, including qualitative examples of pathological acoustic features such as cardiac murmurs, S3 gallops and crackles. Comparative validation against a digital stethoscope confirms the garment's ability to suppress environmental noise for high-fidelity cardiopulmonary sound capture. In addition, the fiber integrated within the garment array enables spatial sound mapping of cardiac and pulmonary abnormalities for localized diagnostics.

Gene-regulatory networks (GRNs) offer a mechanistic framework for dissecting the complex molecular and genetic architecture of coronary artery disease and for identifying new therapeutic opportunities. Here, we present a GRN-driven drug-repurposing strategy that integrates transcriptional signatures induced by silencing key drivers of the human arterial wall foam cell regulator GRN 42 with drug-induced gene expression profiles from the NIH LINCS program. In vitro screening of top candidate compounds validates the computational predictions, identifying candidate foam cell modulators and showing that auranofin, an FDA-approved gold salt used to treat rheumatoid arthritis, effectively reduces foam cell formation. In vivo, auranofin attenuates atherosclerosis and inflammation in both male mice and rabbits. Clinically, auranofin was associated with reduced cardiovascular risk in a retrospective cohort of patients with rheumatoid arthritis. Together, these findings show that a GRN-based drug-repurposing framework, coupled with preclinical and clinical validation, can uncover new therapeutic applications for existing drugs, including auranofin, in coronary artery disease.

Overactivation of Notch signaling in liver sinusoidal endothelial cells (LSECs) is an established driver of hepatic fibrosis, yet its precise upstream regulators and downstream effectors remain poorly defined, limiting therapeutic translation. Here, we demonstrate that FBXW7, the primary E3 ubiquitin ligase responsible for NOTCH1 degradation, serves as a critical suppressor of liver fibrosis. Using endothelial-specific Fbxw7 knockout mice subjected to three distinct fibrosis models, we show that FBXW7 loss exacerbates liver fibrosis, promotes LSEC capillarization, and enhances hepatic stellate cell activation. Transcriptomic analysis identified Sema3g as the top upregulated gene in FBXW7‑deficient LSECs, and conditioned medium from these cells stimulated HSC activation through SEMA3G‑dependent paracrine signaling. Moreover, nanoparticle-mediated delivery of Sema3g-targeting siRNA specifically to LSECs substantially ameliorated injury-induced liver fibrosis in Fbxw7 knockout mice. Mechanistically, FBXW7 loss stabilizes NOTCH1, leading to enhanced Sema3g transcription. Consistent with these findings, human cirrhotic samples and murine fibrotic livers exhibit reduced FBXW7 expression alongside elevated active NOTCH1 and SEMA3G in LSECs. Collectively, our results demonstrate that FBXW7 mitigates liver fibrosis by degrading NOTCH1 to transcriptionally silence SEMA3G, and suggest that targeting the FBXW7/NOTCH1/SEMA3G axis represents a promising therapeutic strategy for fibrotic liver disease.