An updated meta-analysis targeting the prevalence of left ventricular hypertrophy (LVH), a cardinal marker of hypertensive heart disease (HHD), over the last 15 years is lacking. Thus, we analyzed the literature in order to provide a comprehensive information on LVH prevalence, as assessed by echocardiography, in the hypertensive setting.

The PubMed, OVID-MEDLINE, and Cochrane Library databases were analyzed to search English-language articles published from 1 January 2011 up to 31 December 2025. Studies were identified by using MeSH terms and crossing the following search items: 'left ventricular hypertrophy', 'left ventricular mass', 'hypertensive heart disease', 'echocardiography', 'hypertension', and 'subclinical cardiac damage'.

A total of 51 studies including 74 632 hypertensive patients were considered. Overall, the prevalence of LVH in the pooled cohort, defined according to criteria recommended by echocardiographic guidelines, was 36.6% (95% CI: 33.4-40%). Data provided by 18 studies (n = 40 108 patients) showed that the probability of having LVH was lower in men than in women (OR = 0.62, CI: 0.48-0.80, P < 0.0001). Among patients with LVH (17 studies), the risk of concentric LVH was almost twice as high as eccentric (OR = 1.94, CI: 1.52-2.49, P < 0.0001).

Our meta-analysis suggests that the high contemporary prevalence of LVH reflects the failure of therapeutic strategies worldwide in the prevention and treatment of HHD. From a clinical perspective, these data imply the need for a more aggressive treatment of hypertension and related cardiovascular risk factors leading to LVH, especially in women.

Vascular cognitive impairment (VCI), the second leading cause of dementia, is characterized by heterogeneous pathophysiology and a potentially reversible early phase, underscoring the need for timely identification. This review synthesizes advances across four complementary domains - targeted cognitive assessments, imaging biomarkers, molecular fluid biomarkers, and ecological behavioral characteristics - conceptualized as the TIME framework. Emerging markers, including the peak width of skeletonized mean diffusivity (PSMD), oxygen extraction fraction, brain-derived extracellular vesicles, and digital gait metrics, enable the detection of microvascular injury before overt cognitive decline. Given the limitations of single modalities, we advocate for multimodal integration via machine learning to capture the disease continuum from vascular insult to clinical impairment. Establishing a standardized, pathophysiologically anchored classification system, analogous to the AT(N) framework in Alzheimer's disease, is essential to advance precision risk stratification and early intervention in VCI.

Qingxin Tongmai Yin (QXTMY), a classic traditional Chinese medicine (TCM) formula widely used for cardiovascular and cerebrovascular diseases, has unclear multitarget mechanisms against atherosclerosis (AS). This study integrated network pharmacology with experimental validation to investigate these mechanisms. Network pharmacology identified 128 bioactive compounds and 135 potential targets of QXTMY, highlighting key anti-AS targets such as TNF, IL6, insulin (INS), IL1B, MMP9, CCL2, and ALB, with the AGE-RAGE signaling pathway as a central mechanism; principal active ingredients included quercetin, kaempferol, luteolin, and cryptotanshinone. In vitro experiments using THP-1-derived macrophages induced with phorbol-12-myristate-13-acetate (PMA) and oxidized low-density lipoprotein (ox-LDL) showed that QXTMY significantly suppressed inflammatory responses, inhibited foam cell formation, and downregulated the AGE-RAGE signaling pathway, as measured by Western blot, ELISA, cholesterol quantification, and Nile Red staining. These findings suggest that QXTMY may exert protective effects against AS, potentially via suppression of the AGE-RAGE-mediated inflammatory axis. However, in vivo validation is still required to support these preliminary conclusions.

Heart failure with preserved ejection fraction (HFpEF) is a highly prevalent and clinically heterogeneous syndrome characterized by substantial variability in pathophysiology, disease progression, therapeutic response, and clinical outcomes. Although conventional echocardiography remains central to diagnosis, traditional imaging parameters incompletely capture the biological complexity of HFpEF. Growing recognition of distinct disease phenotypes has stimulated interest in echocardiographic phenomapping as a strategy to improve patient characterization and support future precision medicine approaches.

To critically review the contemporary role of echocardiography in HFpEF phenomapping, evaluate the strengths and limitations of emerging imaging biomarkers, and propose a conceptual echocardiographic framework for phenotype-oriented classification.

A comprehensive narrative review was conducted using PubMed/MEDLINE, Scopus, and Web of Science. Contemporary evidence addressing myocardial mechanics, left atrial and right ventricular function, stress echocardiography, artificial intelligence, machine learning, and multimodal phenotyping was narratively reviewed, critically appraised, and synthesized, with emphasis on clinical applicability, methodological limitations, and future research directions.

Contemporary echocardiography enables multidimensional assessment of myocardial structure, ventricular mechanics, atrial function, right ventricular performance, pulmonary vascular interactions, and exercise physiology, providing information beyond conventional diagnostic parameters. Advanced imaging biomarkers, including global longitudinal strain, myocardial work indices, left atrial strain, right ventricular strain, and right ventricular-pulmonary arterial coupling, demonstrate incremental diagnostic and prognostic value in selected patient populations, although their routine clinical implementation remains limited by incomplete standardization, inter-vendor variability, and the need for external validation. Exercise echocardiography further uncovers latent hemodynamic abnormalities and impaired cardiovascular reserve. Artificial intelligence and machine learning have identified candidate HFpEF phenogroups in research settings and may facilitate integration of multidimensional imaging data, although prospective validation and demonstration of clinical utility remain necessary before widespread adoption. Based on the current evidence, we propose a conceptual echocardiographic phenomapping framework encompassing myocardial-dominant, atrial-myopathy, pulmonary vascular-right ventricular, and obesity-metabolic phenotypes.

HFpEF should be regarded as a heterogeneous spectrum of overlapping biological phenotypes rather than a single clinical entity. Modern echocardiography provides a comprehensive platform for multidimensional phenotyping and risk stratification that extends beyond conventional diagnostic assessment. However, important challenges - including biomarker standardization, external validation of proposed phenotypes, and demonstration of incremental value over existing clinical frameworks - must be addressed before phenotype-guided management can be routinely incorporated into clinical practice. Future integration of advanced imaging biomarkers with artificial intelligence, exercise physiology, and biological profiling may further refine individualized approaches to HFpEF management.

Emerging evidence implicates the gut microbiota (GM) in the pathogenesis of ischemic stroke (IS). However, systematic evaluations synthesizing evidence on microbial shifts, functional alterations, and clinical correlations are lacking. This study aimed to comprehensively analyze GM characteristics in IS patients versus healthy controls (HC).

A systematic search of PubMed, Web of Science, and Embase was conducted from inception to April 2025. Observational studies comparing GM in IS patients and HC were included. Data on alpha/beta diversity, relative microbial abundance (phylum to species), predicted functional pathways, and microbiota-clinical indicator correlations were extracted. A narrative synthesis summarized the direction and consistency of reported findings.

Twenty-four studies involving 1,957 participants (1,159 IS, 798 HC) were included. The qualitative synthesis revealed no consistent differences in alpha diversity indices between IS and HC, while significant beta diversity separation was frequently reported (18/22 studies). At the phylum level, an increased relative abundance of Proteobacteria and a decreased abundance of Firmicutes were the most consistent findings in IS patients. Key genera frequently enriched in IS included Lactobacillus, Streptococcus, and Parabacteroides, while Faecalibacterium, Agathobacter, and Blautia were commonly depleted. LEfSe analysis confirmed these discriminative taxa. Predicted functional analysis suggested enrichment of pro-inflammatory pathways (e.g., lipopolysaccharide biosynthesis) and depletion of metabolic and neuroprotective pathways in IS. Clinically, Faecalibacterium abundance correlated negatively with NIHSS and mRS scores, while Lactobacillus and Streptococcus showed positive correlations with stroke severity and inflammatory markers.

Ischemic stroke is associated with distinct gut microbial dysbiosis characterized by a pro-inflammatory, opportunistic pathogen-enriched, and butyrate-producer-depleted profile. These alterations correlate with disease severity and are linked to predicted disruptions in microbial metabolic functions. However, whether this dysbiosis is a cause, consequence, or exacerbating factor of IS remains to be determined. The gut microbiota may serve as a potential biomarker and therapeutic target in ischemic stroke.

https://www.crd.york.ac.uk/PROSPERO/view/CRD420251117510, identifier CRD420251117510.

Among the immune mechanisms underlying the pathogenesis of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), B-lineage cells play crucial roles by producing ANCA, presenting antigens to T cells, and secreting proinflammatory cytokines. The upregulated signaling pathways of the B-cell activation factor of tumor necrosis factor family (BAFF) and a proliferation-inducing ligand (APRIL), which are broadly produced by several types of myeloid cells, contribute to the activation and survival of autoreactive B cells, leading to disease onset and relapse. Furthermore, elevated levels of soluble BAFF and APRIL persist even in patients who achieve clinical remission following conventional induction therapies such as cyclophosphamide and rituximab (RTX), resulting in the cause of relapse. Active AAV is characterized by expansions of specific phenotypes in circulating B-cell lineages, including plasmablasts and plasma cells. Conversely, reductions in transitional, memory, and regulatory B cells are observed. Significant expressions of affinity receptors binding to secreting BAFF/APRIL, including decreased BAFF receptor expression on memory B cells and transitional B cells or increased transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI) expression on transitional B cells and plasmablasts/plasma cells, are also observed during acute and remission AAV. Enhanced BAFF and APRIL signaling through these receptors, especially TACI, activates the intracellular nuclear factor-κB pathway in B cells, promoting their proliferation and ANCA production. B-cell depletion therapy using RTX is effective; however, it requires repeated administration to maintain remission, which can occasionally lead to infection. Belimumab, a BAFF-inhibiting monoclonal antibody, alone has shown limited efficacy in preventing relapse of AAV. Targeting BAFF/APRIL signaling pathways and their binding receptors, along with the downstream molecular pathways in targeted B cells, is essential for developing novel therapeutic strategies aimed at achieving complete and sustained AAV remission.

Ischemic heart disease (IHD) remains the leading cause of mortality and disability in the G20, yet member states exhibit heterogeneous epidemiological transitions. Comparative assessments with long-term projections are essential to inform cardiovascular strategies.

To comprehensively evaluate the temporal trends, regional disparities, risk factors, and future projections of ischemic heart disease burden across G20 countries using GBD 2023 estimates.

Using Global Burden of Disease (GBD) 2023 estimates, we quantified IHD incidence, mortality, and disability-adjusted life years (DALYs) across G20 members from 1990 to 2023. Temporal patterns were evaluated using estimated annual percentage change (EAPC) and Joinpoint regression. Modifiable risks were assessed using population attributable fractions. ARIMA and Bayesian age-period-cohort (BAPC) models projected IHD burden through 2050. Determinants of DALYs were examined using XGBoost with SHAP interpretability.

In 2023, the G20 reported 8.52 million IHD cases and 5.81 million deaths. Age-standardized incidence (ASIR) and mortality (ASMR) declined overall (EAPC -1.61 and -1.49), although incidence increased in women aged 15-49 years, and mortality rebounded modestly after prior declines. The absolute burden was largest in India and China, while Russia had the highest ASIR, ASMR, and age-standardized DALY rates. High systolic blood pressure was the dominant modifiable risk, while particulate matter and lead exposure emerged as prominent environmental contributors. Projections indicate continued ASIR declines overall, though Japan is projected to experience a peak again around 2032. Age was the strongest determinant of DALYs, with a consistent male disadvantage.

The G20 has achieved substantial but uneven reductions in IHD burden, with early signs of reversal, demographic pressures, and expanding environmental risks. Targeted, stage-specific cardiovascular strategies will be required to sustain progress and reduce disparities through mid-century.

BACKGROUND An anomalous origin of a coronary artery from the opposite sinus of Valsalva (ACAOS) is a rare congenital coronary abnormality that is usually asymptomatic throughout life. However, an anomalous coronary artery arising from an atypical aortic location can lead to myocardial ischemia, exertional symptoms, or even sudden cardiac death. Therefore, early recognition and risk stratification are essential. Clinical management of ACAOS should be highly individualized and guided by detailed anatomical features, clinical symptoms, and evidence of ischemia. This report describes an older woman who presented with new-onset chest pain as the first clinical manifestation of previously undiagnosed ACAOS. CASE REPORT A 70-year-old woman presented with 5 days of progressive chest tightness and 20 days of recurrent dizziness associated with poorly controlled hypertension. Initial conventional medical therapy provided inadequate symptom relief. Subsequent coronary angiography revealed an anomalous left circumflex artery originating independently from the right sinus of Valsalva, with 3 separate coronary ostia and concurrent clinically significant atherosclerotic stenosis. She underwent uncomplicated percutaneous coronary intervention of the right coronary artery, achieving successful revascularization and complete resolution of her presenting symptoms. CONCLUSIONS This report describes a rare case of ACAOS presenting with de novo chest pain in an older woman, highlighting the critical importance of accurate anatomical characterization and tailored, individualized management for optimal clinical outcomes.

Cerebral ischemia-reperfusion injury (CIRI) is a severe neurological condition. LncRNA-XIST is closely associated with CIRI; however, its underlying mechanism remains unclear. A middle cerebral artery occlusion/reperfusion (MCAO/R) rat model and an oxygen-glucose deprivation/reoxygenation (OGD/R) model in neuroblastoma cells (SH-SY5Y) were established. The expression of lncRNA-XIST, microRNA-532-5p, and PTEN was detected by qPCR. Binding sites between lncRNA-XIST and microRNA-532-5p, and between microRNA-532-5p and PTEN, were predicted using bioinformatic approaches and validated by dual-luciferase assays. Cell viability, apoptosis, and oxidative stress were assessed by CCK-8 assay, flow cytometry/Western blot, and MDA/SOD assay kits, respectively. LncRNA-XIST and PTEN were highly expressed in the MCAO/R rat brain tissues and the OGD/R cell model, whereas microRNA-532-5p was expressed at low levels. Knockdown of lncRNA-XIST attenuated OGD/R-induced cellular injury. Furthermore, lncRNA-XIST was found to target and inhibit microRNA-532-5p expression, while microRNA-532-5p in turn targeted and suppressed PTEN. The downregulation of PTEN expression and decrease in the apoptotic rate and oxidative stress levels induced by lncRNA-XIST knockdown in the OGD/R cell model were reversed by microRNA-532-5p knockdown. LncRNA-XIST promotes the development and progression of CIRI via the microRNA-532-5p/PTEN axis, offering potential therapeutic targets for CIRI.

Cardiovascular diseases (CVDs) involve complex, interrelated pathologies such as oxidative stress, inflammation, endothelial dysfunction, platelet aggregation, and dyslipidemia, for which single-target drugs remain constrained. As a multicomponent herbal medicine, Ginkgo biloba L. (G. biloba) contains diverse bioactive constituents, primarily flavonoids (e.g., quercetin, kaempferol, isorhamnetin, ginkgetin, and isoginkgetin) and ginkgolides (e.g., ginkgolide A, B, C, and J), which are proposed to exert synergistic effects against the multifaceted pathology of CVDs. This review systematically summarizes the pharmacokinetic characteristics and pharmacodynamic mechanisms of the major bioactive components in G. biloba, highlighting distinct mechanistic axes of Nrf2-mediated antioxidant defense, platelet-activating factor (PAF) receptor antagonism, and inflammasome inhibition. These preclinical findings collectively suggest the therapeutic potential of G. biloba extracts (GbE) for atherosclerosis, stable and unstable angina, myocardial infarction, heart failure, obesity-related and diabetic cardiomyopathy, as well as diabetic nephropathy, retinopathy, and non-alcoholic fatty liver disease. However, the clinical evidence remains limited and inconsistent, and G. biloba has not been established as a standard therapy for CVDs. This review evaluates the current clinical evidence and combination therapeutic strategies, aiming to provide a reference for the design of future clinical trials.