Understanding the geometry and thus the possibility of repairing the aortic valve (AV) has evolved over time thanks to the integration of historical insights and technological advances. The aortic root geometry has proven to be central to understanding valve function. Today, with modern finite element models and flow studies supported by four-dimensional magnetic resonance imaging, we have provided a better understanding of the importance of the sinuses of Valsalva in blood flow dynamics. Their presence reduces cusp stress, improves repair durability, and promotes the adoption of valve prostheses with incorporated sinuses. Looking to the future, the scientific community must push towards a better fusion of currently available technologies to address AV repair, towards personalizing procedures to fit the unique anatomy of each patient. New technologies, including artificial intelligence, can provide personalized surgical simulations. The goal is to make techniques more standardized, reproducible and accessible, while maintaining flexibility to address anatomical variability. Additionally, new materials and tools are being explored to further improve outcomes.

Hypertension is a major contributor to the development of cardiovascular disease, and effective blood pressure control is a critical intervention for reducing cardiovascular events. While age-adjusted awareness rates among women surpass those of their male counterparts, gender-specific control rates remain suboptimal. A rigorous pharmacological assessment and evidence-based prescription of antihypertensive agents, meticulously aligned with their distinct mechanistic and therapeutic profiles, constitute a cornerstone of clinical practice. This review examines the distinct epidemiological, pathophysiological, and clinical characteristics of hypertension in women, highlighting gender-specific differences across various life stages. Key topics addressed include hormonal influences, risk factors, pregnancy-related hypertensive disorders, menopause-associated hypertension, and sex-specific responses to treatment. The review emphasizes the importance of tailored management strategies and individualized antihypertensive therapy to improve outcomes in women.

Chronic lung diseases (CLDs) include a variety of disorders of the pulmonary vasculature and alveolar compartments, and they have become a considerable global health challenge due to their high morbidity and limited therapeutic options. Increasing evidence shows that cellular senescence, an irreversible cell-cycle arrest accompanied by altered secretory activity and resistance to apoptosis, plays a crucial role in the onset and progression of CLDs. One of the major consequences of senescence-associated secretory phenotype activity in senescent cells is the further exacerbation of CLD pathogenesis through the maintenance of chronic inflammation, tissue remodeling, and structural vascular changes. Although individual CLDs exhibit distinct pathological features, they share common mechanisms, including persistent inflammation and dysregulated tissue repair. Experimental models and new methods have advanced, demonstrating the promise of targeted approaches, such as senolytics and regulators of senescence-associated traits, for treating these diseases. This review evaluates how cell senescence is involved with pulmonary arterial hypertension, pulmonary fibrosis and chronic obstructive pulmonary disease, highlights both shared and different pathologic routes, and discusses using seno-therapeutic methods within precision medicine plans.

Clinical decision-making for individuals undergoing valvular and aortic surgery remains challenging, particularly in young patients facing lifelong risk and repeated interventions. As predictive technologies such as artificial intelligence and advanced statistical modelling evolve, the surgical community must ensure that key foundational elements, namely data governance, including data standardization, and regulation, are firmly in place. Without high-quality, standardized, and ethically governed data, predictive models risk offering misleading guidance rather than meaningful personalization. While data governance ensures the scientific robustness of predictive technologies, shared decision-making (SDM) ensures these innovations remain closely aligned with the lived experiences, values, and preferences of individual patients. This perspective emphasizes that advancing decision-making in aortic surgery requires deliberate investment in building data ecosystems and fostering SDM communication practices, ensuring that innovation is both scientifically sound and truly responsive to patient needs.

Endovascular recanalization has revolutionized the treatment of peripheral artery disease (PAD), offering minimally invasive alternatives to open surgery. However, permanent metallic stents, while effective in restoring blood flow, are associated with long-term complications such as chronic inflammation, restenosis, and stent thrombosis. Bioresorbable scaffolds (BRS) have emerged as an innovative solution, providing temporary mechanical support while delivering antiproliferative drugs before fully degrading, thus eliminating the risks associated with permanent implants. Significant advancements in bioresorbable materials have led to the development of new-generation scaffolds with improved radial strength, controlled degradation rates, and enhanced drug-eluting properties. Several BRS platforms, including polymer- and magnesium-based designs, are undergoing clinical and preclinical evaluation for peripheral applications. Early trials suggest that BRS may offer comparable short-term patency rates to conventional stents while potentially reducing late adverse events. However, challenges such as scaffold thrombosis, mechanical integrity in large and calcified vessels, and long-term efficacy remain under investigation. This narrative review explores the evolution of BRS technology, the mechanisms of scaffold resorption, current clinical evidence, and future prospects for their use in peripheral endovascular interventions. As research progresses, BRS may represent a paradigm shift in the treatment of PAD, offering a balance between structural support and vascular restoration.

In this special interview, Professor Barry A. Franklin shared key experiential and research-based insights on professional success, exercise-based cardiovascular therapy, and the impactful role of cardiorespiratory fitness in promoting long-term health outcomes. (a) Professional success is built on clearly defined written goals, consistent daily action, personal responsibility, a mindset of happiness, optimism, and gratitude, and exemplary service to others; (b) Outstanding academic and clinical careers require effective mentorship, strong communication skills, advanced training and continuing education, disciplined work habits, and proactive management of stress and health; (c) Aerobic and resistance training provide complementary benefits in combating cardiovascular disease, with aerobic exercise contributing most strongly to long-term survival; (d) Cardiorespiratory fitness or VO₂max (maximum volume of oxygen uptake), expressed as metabolic equivalents (METs), is a powerful, independent, and additive predictor of survival, with each 1-MET (one metabolic equivalent) increase associated with a mortality reduction of ~ 15%-17%; (e) Higher fitness levels significantly reduce the risk and improve the prognosis of heart failure with preserved ejection fraction and heart failure with reduced ejection fraction, independent of body mass index and traditional risk factors; (f) Although aerobic fitness declines rapidly with detraining, it is reversible, while muscle strength can be largely maintained with one resistance training session per week; (g) To date, no pharmacologic therapy can elicit the increases in metabolism needed to improve fitness, as well as the associated favorable adaptations, and safe, accessible activities such as stair climbing and daily walking provide substantial cardiovascular risk reduction.

We read with great interest a recent study investigating the role of nuclear receptor coactivator 7 (NCOA7) as a critical regulator of lysosomal function, oxysterol, and bile acid metabolism, and its link to endothelial cells (ECs) inflammation and immune activation in pulmonary artery hypertension (PAH). The study demonstrated that NCOA7 deficiency exacerbated lysosomal dysfunction, leading to inflammatory sterol accumulation and immune activation, which subsequently triggers endothelial immune responses. Translationally, NCOA7 activation emerges as a promising therapeutic strategy, while plasma oxysterol and bile acid levels offer potential prognostic biomarkers for PAH severity and mortality.

Aim: Pulmonary vascular endothelial cells (ECs) comprise functionally distinct subpopulations, including arterial, venous, general capillary (gCap), and aerocyte capillary (aCap) ECs, that are essential for the maintenance of lung function. SMAD family member 4 (SMAD4) signaling is a critical contributor to vascular homeostasis. This study aims to elucidate how SMAD4 affects individual endothelial subpopulations in the lung.

Methods: We curated a previously published single-cell RNA sequencing (scRNA-seq) dataset from Smad4-deficient (Smad4^fl/fl; Rosa26CreER^T2) and control (Smad4^fl/fl) mouse lungs, using a unified bioinformatic pipeline. Integrated analyses of cell clustering, differential gene expression, high-dimensional weighted gene co-expression network analysis (hdWGCNA), and chromatin immunoprecipitation sequencing were applied to resolve subpopulation-specific transcriptomic shifts and regulatory modules in the pulmonary endothelial compartment.

Results: SMAD4 deficiency induced markedly asymmetric transcriptomic changes across pulmonary vascular endothelial subpopulations. Upon Smad4 loss, arterial ECs largely preserved their core transcriptomic identity, whereas venous and gCap ECs transitioned into a vulnerable state characterized by aberrant proteostasis and reduced survival. Smad4-null gCap ECs also exhibited disrupted vascular homeostatic and morphogenic processes. Smad4-null aCap ECs displayed a distinct transcriptomic shift, manifested as gas-exchange dysregulation and immune activation, alongside shared defects in translation/protein folding and vascular morphogenic capacity. Regulatory modules and putative hub genes associated with venous/gCap EC vulnerability and aCap-specific transcriptomic shift upon SMAD4 deficiency were further identified.

Conclusion: These findings define a lineage-resolved framework for SMAD4 signaling in the pulmonary endothelium and uncover molecular vulnerabilities that may inform EC subpopulation-targeted vascular interventions.

Aim: Cardiovascular-kidney-metabolic (CKM) syndrome accelerates aging and increases mortality. We evaluated whether Triglyceride-Glucose-Waist-to-Height Ratio (TyG-WHtR), a marker of insulin resistance, predicts mortality in CKM and whether age acceleration mediates this association.

Methods: This investigation enrolled 16,145 individuals diagnosed with CKM syndrome. The relationships between TyG-WHtR and mortality were examined using multivariable Cox proportional hazards models, threshold effect analysis, and restricted cubic splines. Besides, the mediating role of age acceleration was investigated through mediation analysis. Risk within different populations was assessed using interaction tests and subgroup analysis.

Results: In multivariate Cox proportional hazards analyses, TyG-WHtR showed a positive association with mortality outcomes. Per one standard deviation (1-SD) increase, the hazard of cardiovascular death was 18% higher (hazard ratio (HR): 1.180; 95% confidence interval (CI): 1.08-1.29), while all-cause mortality risk rose by 8.6% (HR: 1.086, 95%CI: 1.01-1.17). Both cardiovascular and all-cause mortality showed a strong U-shaped association with TyG-WHtR. Mediation analysis revealed that PhenoAge acceleration and Klemera-Doubal Method age acceleration mediated 19.7% and 15.8% of the association between TyG-WHtR and all-cause mortality, respectively, and 20.7% and 16.8% of the association between TyG-WHtR and cardiovascular mortality, respectively.

Conclusion: TyG-WHtR is associated with mortality in patients with CKM syndrome, partly through accelerated aging. It is positively associated with age acceleration and exhibits a U-shaped relationship with mortality. Targeting the metabolic-aging crosstalk may help reduce mortality in CKM patients.

Panvascular aging-related diseases, including coronary artery disease, ischemic stroke, and peripheral artery disease, are leading global causes of death and disability, yet their management remains fragmented. Emerging technologies offer solutions to this challenge. Big data integration across imaging, multi-omics, wearables, and environmental exposures provides opportunities for cross-organ insights but faces issues of heterogeneity and privacy. Artificial intelligence enables early detection and refined risk prediction by recognizing subtle vascular changes and integrating biomarkers, though adoption is limited by interpretability and bias. Foundation models, through cross-modal learning, offer a unifying framework for mechanism discovery, personalized management, and digital twin applications. By linking technological innovation with clinical practice, these approaches can transform panvascular aging management and promote healthy longevity. Importantly, translating these innovations into policy and practice will be essential for advancing equitable vascular health and achieving population-level impact.

The integrity of the vascular endothelium is fundamental to its barrier function, maintaining vascular homeostasis and microenvironmental stability, and serves as a prerequisite for preventing certain vascular diseases. After vascular integrity is compromised, endothelial progenitor cells (EPCs), a diverse population of progenitor cells with the capacity to develop into endothelial cells, can reconstruct blood vessels. This occurs primarily through two mechanisms: (1) direct integration into existing vessels for repair; and (2) paracrine secretion of proangiogenic factors to promote EPC mobilization and migration, regulate immune functions, and inhibit endothelial hyperplasia. This review aims to elucidate the mechanisms by which EPCs participate in vascular remodeling, and to discuss the latest advances in clinical translation strategies such as cell therapy, EPC-derived exosome therapy, and EPC functional modulation, as well as the current challenges in standardization and clinical application.

Aim: This study examines the learning curve for vein-to-aorta anastomosis in minimally invasive coronary artery bypass grafting (MICS CABG) and develops a virtual reality (VR) simulation model for this procedure, with validation to confirm its clinical relevance.

Methods: We analyzed 132 consecutive off-pump MICS CABG procedures with multi-vessel grafting performed by a single surgeon (January 2017-January 2020). Proximal anastomosis time was plotted against case sequence, and the learning curve was quantified using cumulative summation analysis. A VR simulation platform was developed to reproduce key clinical challenges, using hierarchical geometric modeling and real-time physics simulation of tissue-instrument interactions with haptic feedback. Cardiac surgery experts evaluated the VR simulator via a structured questionnaire.

Results: The learning curve for proximal anastomosis followed a three-phase progression, with proficiency achieved after 52 cases (model fit R² (the coefficient of determination) = 0.994). The VR simulation accurately replicated key surgical scenarios, focusing on bimanual suturing mechanics and needle-vessel interactions. Expert validation yielded an overall validity index of 0.78 (exceeding the 0.7 threshold), confirming good construct validity and clinical relevance of the simulator.

Conclusion: Proficiency in MICS CABG proximal anastomosis is achieved after 52 cases, marking the inflection point of the learning curve. Our physics-validated VR simulator, supported by expert evaluation, has potential to accelerate surgical skill acquisition and shorten the learning curve.

Aim: Reliable prognostic tools remain limited for patients with ST-segment elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI) more than 48 h after symptom onset. This study aimed to develop and externally validate a nomogram based on routinely available in-hospital clinical variables to predict post-discharge adverse outcomes in this population.

Methods: We retrospectively analyzed data from Tongji Hospital between June 2019 and August 2022 and identified 198 STEMI patients who underwent delayed PCI as the training cohort. Independent predictors of composite adverse events, defined as all-cause mortality, nonfatal myocardial infarction, and New York Heart Association class IV heart failure, were identified using multivariate Cox proportional hazards regression. A nomogram was subsequently constructed and internally validated using bootstrap resampling. External validation was performed in an independent cohort of 599 patients treated at the Second Hospital of Lanzhou University, with a median follow-up duration of 20 months.

Results: Four variables were identified as independent predictors of adverse outcomes and incorporated into the nomogram: (1) heart rate > 83 beats per minute (hazard ratio [HR] 2.786, 95% confidence interval [CI]: 1.226-6.32, P = 0.014); (2) absence of statin therapy (HR 0.213, 95%CI: 0.064-0.71, P = 0.012); (3) intraoperative slow-flow/no-reflow phenomenon (HR 2.889, 95%CI: 1.247-6.69, P = 0.013); and (4) requirement for mechanical ventilation (HR 7.469, 95%CI: 2.57-21.70, P < 0.001). The nomogram demonstrated good discrimination and calibration in the training cohort, with a concordance index of 0.782. External validation confirmed its robust predictive performance. Patients classified as high risk exhibited significantly lower event-free survival compared with those at low risk (P < 0.0001).

Conclusion: This validated nomogram, derived from routinely collected clinical variables, provides reliable prediction of adverse outcomes in STEMI patients undergoing delayed PCI and may facilitate individualized risk stratification and optimized post-discharge management.

Aim: To evaluate the long-term impact of obstructive sleep apnea (OSA) risk profile on atrial fibrillation (AF) recurrence after catheter ablation in patients with paroxysmal AF.

Methods: This prospective study enrolled 161 patients with paroxysmal AF undergoing initial ablation. Patients were stratified by the Berlin Questionnaire (BQ) into high-risk (n = 94) and low-risk (n = 67) OSA groups. Atrial tachyarrhythmias occurring within the initial three months were defined as early recurrence, whereas recurrence beyond three months was defined as late recurrence. A subgroup of 71 patients with recurrence underwent a redo ablation.

Results: After 16.1 ± 0.4 years, multivariable models revealed that a BQ-defined high OSA risk was independently associated with early recurrence (odds ratio [OR] 1.99, 95% confidence interval [CI] 1.02-3.86, P = 0.043), whereas it was not independently associated with late recurrence after the initial procedure (hazard ratio [HR] 1.05, 95%CI: 0.70-1.57, P = 0.810). Cox regression identified early recurrence (HR 2.95, 95%CI: 1.99-4.39, P < 0.001) and baseline high-sensitivity C-reactive protein (hs-CRP; HR 1.02, 95%CI: 1.00-1.03, P = 0.022) as independent predictors of late recurrence after the initial procedure. Following redo ablation, early recurrence remained a strong independent predictor (HR 5.93, 95%CI: 2.13-16.50, P < 0.001).

Conclusions: The BQ-defined high OSA risk was an independent predictor of early recurrence; however, it was not significantly associated with late recurrence after AF ablation. Early recurrence was the strongest predictor of long-term outcome, highlighting the importance of management during the post-procedural blanking period.

Atherosclerosis research has been significantly advanced by mouse models, particularly genetically engineered strains such as apolipoprotein E-deficient mice and low-density lipoprotein receptor-deficient mice (Ldlr^-/-). These mouse models replicate the hyperlipidemia-driven plaque pathogenesis, providing critical insights into lipid metabolism, inflammation, and therapeutic responses. Classic models play an important role in validating the effects of lipid-lowering therapies such as statins and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. There are also some limitations, including species-specific lipoprotein profiles and incomplete replication of advanced human plaque complexity. Novel models have emerged to address these gaps, incorporating features such as hemodynamic stress, humanized lipid metabolism, and inducible gene regulation to complement the inadequacies of classic models, thereby better simulating the multifactorial complexity of atherosclerosis. For example, adeno-associated virus serotype 8 carrying the Pcsk9[D377Y] mutant gene and Ldlr-antisense oligonucleotide mice integrate hemodynamic stress, humanized lipid metabolism, and multifactorial comorbidities. However, there are still some shortcomings, including metabolic disparities, inadequate modeling of plaque rupture/thrombosis, and oversimplification of systemic disease interactions. Future directions prioritize next-generation models featuring humanized lipoprotein profiles, dynamic gene regulation, and combined with metabolic syndrome features. These approaches can be synergized with advanced phenotyping tools—including single-cell omics and intravital imaging—alongside artificial intelligence-driven multi-omics integration. By bridging translational gaps between murine pathophysiology and human disease complexity, these mouse models promise to accelerate the development of atherosclerosis therapies.

Heart failure (HF) is a syndrome of global concern with high morbidity and mortality, whose complex molecular regulatory mechanisms are not yet fully understood. Moving beyond the traditional research framework focused on microRNAs, long non-coding RNAs (ncRNAs), and circular RNAs, this review concentrates on the pivotal roles of emerging ncRNAs - specifically Piwi-interacting RNAs (piRNAs), transfer RNA-derived small RNAs (tsRNAs), and small nucleolar RNAs (snoRNAs) - in the pathological progression of HF. In the acute phase of HF, these molecules rapidly respond to stressors such as ischemia and hypoxia. They directly influence cardiomyocyte fate and acute injury outcomes by regulating processes including apoptosis, necroptosis, autophagy, and inflammatory responses. During the chronic phase, they are deeply involved in pathological myocardial remodeling. They precisely regulate cardiomyocyte hypertrophy, cardiac fibroblast activation, and interstitial fibrosis in a cell-specific manner, maintaining a fine-tuned balance between pro-pathological and protective functions. These discoveries significantly enrich the molecular regulatory map of HF and reveal the considerable potential of these ncRNAs as novel non-invasive biomarkers and promising therapeutic targets. Of particular note, strategies employing engineered exosomes to deliver specific snoRNAs have demonstrated therapeutic effects in preclinical models, such as reversing fibrosis and improving cardiac function. This marks a shift in the treatment paradigm for HF toward precise RNA-level regulation.

Aim: Maternal overnutrition predisposes offspring to an increased prevalence of cardiovascular disease, yet the specific underlying mechanisms remain elusive.

Methods: This study examined the roles of inflammation and ferroptosis in driving fetal cardiac structural and functional alterations following maternal overnutrition. Multiparous ewes were fed either a control diet [100% of National Research Council (NRC) recommended requirements] or an overnutrition diet (150% of NRC requirement) from 60 days preconception until gestational day 135. Cardiac geometry, histomorphology, immune cell infiltration, cardiomyocyte function, intracellular Ca²⁺ handling, and expression of inflammatory and ferroptotic markers were assessed in fetal hearts.

Results: Despite comparable fetal crown-rump lengths and organ weights (e.g., brain and liver), fetuses from overnourished ewes exhibited significantly lower body and heart weights. Maternal overnutrition induced marked cardiac atrophy, interstitial fibrosis, lipid deposition, and oxidative damage, coupled with increased neutrophil and monocyte infiltration. At the cellular level, cardiomyocytes from overnourished fetuses exhibited impaired contractile and intracellular Ca²⁺ properties. Molecular profiling revealed that maternal overnutrition significantly upregulated proinflammatory markers (CD14, CD68, IL1A, IL1B, IL6, TLR4, and iNOS), and increased IκB phosphorylation (indicating NFκB activation). Concurrently, overnutrition suppressed IL18 and M-CSF expression, alongside the ferroptosis-defense proteins GPX4 and SLC7A11.

Conclusion: These findings demonstrate that maternal overnutrition creates a proinflammatory and ferroptosis-prone myocardial environment, resulting in pathological structural remodeling and functional impairment of fetal hearts. Our data suggest that targeting the inflammation-ferroptosis signaling may help to mitigate the developmental programming of cardiovascular disease.

Small nucleolar RNAs (snoRNAs) are increasingly recognized as key regulatory factors in cardiovascular disease (CVD), with functions that extend far beyond the traditional scope of ribosomal RNA modification. This review synthesizes current knowledge regarding the biology of snoRNAs and their emerging roles in CVD, aiming to provide a clear theoretical framework for their pathogenic mechanisms and clinical significance. We first discuss the biogenesis, classification, and functional diversity of snoRNAs, covering both classical modification roles and non-classical functions such as the regulation of messenger RNA splicing, participation in the DNA damage response, and the generation of snoRNA-derived small RNAs. In CVD, snoRNAs exhibit spatiotemporal dysregulation and are extensively involved in pathological processes ranging from congenital heart defects and cardiomyopathy to coronary artery disease, myocardial infarction, arrhythmias, and heart failure. Specific gene clusters, particularly 14q32 snoRNAs, repeatedly emerge as key regulatory nodes in processes such as vascular remodeling and platelet activation. However, the majority of dysregulated snoRNAs remain orphaned with unknown targets, limiting our understanding of their mechanisms and clinical translation. We emphasize that combining computational modeling with multi-omics approaches can accelerate target identification and functional elucidation. Finally, we systematically examine the opportunities and challenges facing the clinical translation of snoRNA research, including their potential as dynamic biomarkers, limitations of detection technologies, and barriers to therapeutic delivery. By comprehensively reviewing existing evidence and future directions, this review highlights the significant potential of snoRNAs as novel biomarkers and therapeutic targets for the precision diagnosis and treatment of cardiovascular diseases.

Cardiovascular diseases (CVDs) involve structural and functional abnormalities of the heart and blood vessels, in which genetic factor plays a significant role. Non-coding RNAs (ncRNAs), as important products of genetic material, are important contributors to CVDs. They mainly regulate the expression of targets and participate in various biological processes such as cell proliferation, cell apoptosis, and signal transduction. Genetic variation in ncRNAs can affect the expression levels of ncRNAs themselves and their downstream targets, leading to the dysregulation of biological processes and contributing to the occurrence and development of CVDs. This review aims to summarize the current research status of ncRNA genetic variation in CVDs and clarify the functions and biological mechanisms of ncRNA genetic variation involved in CVDs.

Aortic dissection (AD) is a rapidly progressive cardiovascular disease associated with high mortality. The core pathogenic mechanisms of AD include apoptosis and phenotypic switching of vascular smooth muscle cells (VSMCs), remodeling and degradation of the extracellular matrix (ECM), and vascular inflammation. However, the detailed molecular mechanisms remain incompletely understood. Noncoding RNAs (ncRNAs) are RNA molecules that do not encode proteins. Recent studies have confirmed that ncRNAs with aberrant expression exert critical regulatory functions in the pathogenesis and progression of AD, and several ncRNAs have shown significant application potential in the early diagnosis, conservative treatment, and prognostic assessment of AD. This review summarizes the latest research progress on the regulatory mechanisms of various ncRNAs in AD, and critically evaluates their potential clinical utility as clinical biomarkers and therapeutic targets for AD.

Heart failure (HF) is characterized by profound mitochondrial dysfunction, a central pathogenic mechanism driven by interconnected defects in metabolic dysregulation, excessive oxidative stress, impaired biogenesis, imbalanced dynamics, and defective mitophagy. This compromised mitochondrial fitness leads to bioenergetic deficiency, cardiomyocyte death, and progressive cardiac remodeling. MicroRNAs (miRNAs) have emerged as critical post-transcriptional regulators of mitochondrial homeostasis, capable of simultaneously modulating multiple components within these pathways. By fine-tuning the expression of key genes involved in fission/fusion, mitophagy, and biogenesis, miRNAs can either exacerbate or ameliorate HF progression, forming a complex and context-dependent regulatory network, and highlighting the potential of targeting the miRNA-mitochondria axis. However, clinical translation faces significant hurdles including target specificity, tissue-selective delivery and patient heterogeneity. Future research should focus on deciphering the mechanistic interplay between miRNA regulation and mitochondrial function in diverse HF contexts. This review aims to elucidate the molecular mechanisms by which miRNAs regulate mitochondrial dysfunction in HF, revealing novel therapeutic targets. A deeper understanding of this regulatory network is crucial for advancing HF management from symptom palliation toward mechanism-based precision medicine.

Aim: To identify factors associated with late atrial fibrillation (AF) recurrence after radiofrequency catheter ablation and to develop a nomogram for individualized risk prediction, followed by external validation in an independent cohort.

Methods: We conducted a retrospective cohort study of patients with AF who underwent catheter ablation at Tongji Hospital (training cohort, January 2020-December 2022) and the Second Hospital of Lanzhou University (validation cohort, June 2020-June 2023). Follow-up visits were scheduled at 1, 3, 6, 12, and 18 months after the procedure. Candidate predictors were identified using the Boruta algorithm and the least absolute shrinkage and selection operator. Selected variables were then entered into multivariable Cox proportional hazards models. Model performance was evaluated using Harrell’s C-index, time-dependent area under the receiver operating characteristic curve, calibration plots, and decision curve analysis.

Results: A total of 256 patients in the training cohort and 203 in the validation cohort were included, with a median follow-up of 12 months. Late AF recurrence occurred in 21.9% and 21.2% of patients, respectively. Six variables were included in the final model: early recurrence (HR = 7.616), left atrial diameter (HR = 1.684), intraoperative electrical cardioversion (HR = 1.423), serum creatinine (HR = 1.018), use of angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB)/angiotensin receptor-neprilysin inhibitor (ARNI) (HR = 0.426), and AF duration (HR = 1.003). The nomogram showed good discrimination, calibration, and clinical usefulness in both cohorts.

Conclusion: We developed and externally validated a six-variable nomogram for predicting late AF recurrence after catheter ablation. This model may support individualized risk stratification and guide post-ablation management.

Cardiovascular diseases (CVDs) are among the leading causes of global morbidity and mortality, placing a substantial burden on public health and socioeconomic development. Early and accurate diagnosis is essential for reducing CVDs mortality and optimizing individualized treatment strategies. Although conventional detection methods, such as enzymatic analysis and immunoassays, have reached a relative level of maturity in clinical applications, they are still constrained by high costs, complex procedures, and limited real-time capabilities. In recent years, electrochemical immunosensors have shown significant potential for detecting CVD-related biomarkers, owing to their advantages of high sensitivity, excellent selectivity, rapid response, and portability. In this review, we explore the latest advancements in electrochemical immunosensors for CVDs research, analyze innovative designs and fabrication techniques for various sensor types, and summarize their applications in detecting CVD-related biomarkers.

Aim: Atrial fibrillation and atrial flutter (AF/AFL) represent a growing public health challenge in China amid rapid population aging. This study aimed to comprehensively assess long-term trends, sex- and age-specific patterns, driving factors, and future projections of AF/AFL burden in China from 1990 to 2023.

Methods: Data were obtained from Global Burden of Disease 2023. Temporal trends, driving factors, and future projections were evaluated using joinpoint regression, age-period-cohort models, decomposition analysis, frontier analysis, and autoregressive integrated moving average (ARIMA) models.

Results: From 1990 to 2023, the absolute numbers of AF/AFL cases, deaths, and disability-adjusted life years (DALYs) increased substantially in China, whereas age-standardized mortality and DALY rates declined overall, with a recent upturn after 2020. Incidence and prevalence were generally higher in males, whereas females had higher mortality and DALYs at older ages. Population aging was the dominant contributor to increases in incidence, prevalence, mortality, and DALYs. Age-period-cohort models analyses showed that among individuals born after 1944, the burden of AF/AFL was higher in males than in females. Frontier analysis indicated that China still lags behind several high Socio-demographic Index regions in AF/AFL burden control. ARIMA projections suggested declining mortality and DALYs but heterogeneous future trends in incidence and prevalence by sex.

Conclusions: Despite improvements in age-standardized mortality and DALYs, the overall burden of AF/AFL in China continues to increase, primarily driven by population aging. Targeted prevention, early detection, and optimized management strategies - particularly among older adults and high-risk males - are urgently needed.

Aim: This study evaluated the association between postoperative body mass index (BMI) category at the 18 months postoperative follow-up and atrial fibrillation (AF) recurrence after radiofrequency catheter ablation (RCA).

Methods: From January to December 2023, 250 patients with AF who underwent single-operator RCA at the General Hospital of Northern Theater Command were enrolled. Baseline characteristics, BMI category at the 18 months postoperative follow-up (normal weight, overweight, obesity), and recurrence were collected. Kaplan-Meier survival analysis and multivariate Cox proportional hazards analysis were performed. The primary endpoint was AF recurrence confirmed by electrocardiogram (ECG) or Holter monitoring within 18 months.

Results: Among 110 patients with paroxysmal atrial fibrillation (PAF) and 140 patients with persistent atrial fibrillation (SAF). Multivariate Cox analysis showed that, among patients with PAF, postoperative obesity was associated with recurrence risk (P = 0.037). Among patients with SAF, postoperative overweight (P = 0.033), postoperative obesity (P = 0.003), and AF duration > 12 months (P = 0.002) were independently associated with recurrence. Kaplan-Meier analysis in patients with SAF showed 18 months recurrence-free rates of 88.2% for postoperative normal weight, 69.1% for postoperative overweight, and 55.3% for obesity (log-rank P = 0.006).

Conclusion: In this retrospective analysis, postoperative obesity was associated with a higher risk of recurrence after RCA for AF. Specifically, postoperative obesity was associated with recurrence in patients with PAF, whereas higher postoperative BMI grades and AF duration > 12 months were associated with recurrence in patients with SAF.