Paravalvular leak (PVL) is a serious complication following heart valve replacement. Percutaneous closure is an effective alternative to reoperation, but it is particularly challenging in patients with mechanical tilting-disc prostheses due to the risk of device-disc interference. We report a 61-year-old female presenting with severe symptomatic PVL 33 years after aortic valve replacement with a tilting disc prosthetic valve. Echocardiography revealed multiple paravalvular jets, with a dominant 5-mm leak at the 7 o’clock position. Given her high surgical risk, percutaneous closure was selected. Using a retrograde femoral approach, an 8-mm Amplatzer Vascular Plug II was deployed to occlude the dominant leak. The device was positioned with iterative adjustments, followed by a push-pull stability test and systematic pre-release safety checks under fluoroscopy and echocardiography to ensure unimpeded disc motion. At the 1-year follow-up, the patient demonstrated sustained clinical recovery with preserved valve function. In tilting-disc prostheses, percutaneous PVL closure is feasible but carries a uniquely high risk of fatal device-disc interference. Rigorous, structured pre-release safety checks are mandatory to prevent device interference.
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2, is now recognized as a multisystem disease with substantial cardiovascular involvement contributing to both acute and long-term morbidity. Cardiovascular manifestations range from myocardial injury and arrhythmias to thromboembolic disease, acute coronary syndromes, and heart failure, affecting both adult and pediatric populations. This narrative review provides a clinically oriented synthesis of the major cardiovascular manifestations associated with COVID-19. Current evidence indicates that myocardial injury, myocarditis, heart failure, arrhythmias, thromboembolic events, ischemic stroke, acute coronary syndromes, and pericardial disease arise through interconnected mechanisms involving endothelial dysfunction, systemic inflammation, immune dysregulation, and hypercoagulability. Older age, male sex, and pre-existing cardiovascular disease are consistently associated with worse outcomes. Although children generally experience milder disease, cardiovascular complications may occur, particularly in the setting of multisystem inflammatory syndrome in children. Emerging evidence also suggests persistent cardiovascular sequelae following acute infection, underscoring the importance of long-term surveillance and multidisciplinary follow-up, particularly among high-risk individuals. COVID-19 should be regarded as a multisystem disease with important short- and long-term cardiovascular implications. Recognizing shared pathophysiologic mechanisms may facilitate early risk stratification, targeted diagnostic evaluation, and appropriate longitudinal follow-up, particularly among high-risk populations. Further studies are needed to clarify long-term cardiovascular outcomes and optimize preventive and therapeutic strategies.
Snail family transcriptional repressor 2 (SNAI2), also known as SLUG, is a canonical driver of epithelial-mesenchymal transition (EMT). While its oncogenic roles are well-established, emerging evidence underscores its pivotal involvement in cardiovascular diseases (CVDs). This review systematically summarizes the multifaceted functions of SNAI2 in the cardiovascular system, highlighting its role in mediating endothelial-to-mesenchymal transition (EndMT) and vascular smooth muscle cell (VSMC) phenotypic reprogramming. We detail the involvement of SNAI2 across a spectrum of pathologies, including atherosclerosis, aortic aneurysm, valvular heart disease, myocardial fibrosis, and pulmonary arterial hypertension. By acting as a critical nexus in signaling networks such as TGF-β, Notch, and Wnt, SNAI2 regulates cellular fate and extracellular matrix remodeling under pathological stress. Finally, we discuss the potential of SNAI2 as a diagnostic biomarker and a novel therapeutic target, offering prospective insights for the clinical management of CVDs.
This study aimed to identify potential biomarkers associated with ruptured plaques in carotid artery stenosis (CAS) using bioinformatics and machine learning approaches and to elucidate the underlying molecular mechanisms of symptomatic CAS. Three GEO datasets related to symptomatic CAS were analyzed. Key genes were identified using LASSO, SVM-RFE, and random forest algorithms. Diagnostic performance was assessed using ROC analysis. A miRNA-mRNA regulatory axis was constructed with Cytoscape, and interactions were validated by dual-luciferase reporter assays. An ox-LDL-induced endothelial cell injury model was established to explore molecular mechanisms. The expression of inflammatory cytokines, adhesion molecules, apoptosis-related genes, and Wnt1/β-catenin pathway components was detected by qRT-PCR and Western blotting. Validation analysis confirmed OLFML2A as a potential biomarker for symptomatic CAS and as a regulatory target of miR-331-3p. OLFML2A was confirmed to directly interact with miR-331-3p. Silencing OLFML2A increased the expression of pro-inflammatory cytokines (IL-6, TNF-α, MCP-1), adhesion molecules (VCAM-1, ICAM-1), and the pro-apoptotic gene Bax, while decreasing the anti-apoptotic gene Bcl-2. Moreover, OLFML2A knockdown suppressed activation of the Wnt1/β-catenin signaling pathway. This study identifies OLFML2A as a novel biomarker and potential regulator of endothelial injury in symptomatic CAS. OLFML2A may promote ox-LDL-induced endothelial dysfunction by modulating the Wnt/β-catenin pathway.
Ischemic heart disease (IHD) remains the leading global cause of mortality. Although IHD mortality has declined in China over recent decades, incidence has not declined in parallel. At the same time, the global IHD risk-factor profile is shifting from traditional behavioral and environmental exposures toward metabolic drivers. We analyzed IHD burden using Global Burden of Disease (GBD) 2021 estimates, comparing mortality, incidence, disability-adjusted life years (DALYs), and attributable risk factors across China, the United States, and global averages. We then analyzed a large national health examination cohort of 186,838 adults; among 5,597 participants with atherosclerotic coronary heart disease and complete AMI information, AMI status was modeled using multiple logistic regression and Extreme Gradient Boosting (XGBoost). China’s age-standardized IHD mortality decreased by 32.1
Acute myocardial infarction (AMI) strikes suddenly and progresses rapidly, yet early recognition remains difficult. This study explores combining miR-660-3p with echocardiography for noninvasive assessment of AMI, plus cell experiments to clarify its role in cardiomyocyte damage. A total of 105 non-cardiogenic chest pain cases and 127 AMI cases were enrolled, with clinical data, echocardiographic parameters, and serum miR-660-3p levels collected from all participants. Multivariate logistic regression identified independent factors associated with AMI, and ROC curves assessed the diagnostic value of individual and combined indicators. In vitro, H₂O₂ was used to induce injury in H9c2 cardiomyocytes, followed by transfection with a miR-660-3p inhibitor to evaluate changes in cell viability (CCK-8) and inflammatory cytokines (ELISA). Compared with controls, the AMI group exhibited markedly lower left ventricular ejection fraction and fractional shortening, along with a larger left ventricular end-diastolic diameter and significantly elevated serum miR-660-3p levels. Multivariate logistic regression identified miR-660-3p as an independent risk factor. ROC analysis showed an AUC of 0.815 for miR-660-3p alone, which increased to 0.944 when combined with echocardiographic parameters. In vitro, suppressing miR-660-3p alleviated H₂O₂-induced cardiomyocyte injury, improved cell viability, and reduced inflammatory cytokine release. miR-660-3p levels are significantly correlated with AMI, and incorporating this marker into echocardiography may enhance noninvasive diagnostic accuracy. The molecule may mediate cardiomyocyte injury via inflammatory pathways, suggesting its potential clinical value.
Right heart thrombi are rare but life-threatening, with particularly high mortality when accompanied by pulmonary embolism (PE). Cardiac surgery may predispose to in-situ thrombus formation via suture lines or patch material, yet thromboembolic risk and preventive strategies following Ventricular Septal Defect (VSD) repair remain unclear. Here, we report a case of a young patient with a massive right atrial (RA) thrombus with PE one year after VSD repair in the absence of any known hypercoagulable state. A 17-year-old male with a history of surgical VSD repair one year earlier, who was not taking any antithrombotic therapy prior to presentation, presented with acute dyspnea, tachycardia, and severe hypoxia. Transthoracic echocardiography revealed a large, freely mobile RA mass. Subsequent CT pulmonary angiography and cardiac magnetic resonance confirmed a massive right pulmonary artery embolus and characterized the RA mass as an intracardiac thrombus. Because of clinical deterioration despite therapeutic anticoagulation, he underwent a successful urgent cardiac surgery with RA mass excision and pulmonary embolectomy. Postoperative histopathology confirmed the mass to be a thrombus. Our case highlights a rare late RA thrombus with PE one year after surgical VSD repair, requiring urgent surgery. Further research is needed to clarify post–VSD closure surveillance and thromboprophylaxis strategies.
The Ascyrus Medical Dissection Stent (AMDS) is an adjunctive hybrid prosthesis designed to support true lumen expansion following type A aortic dissection repair. While early series demonstrate favourable aortic remodelling in selected patients, emerging data suggest a risk of central stent collapse. The authors present a case of early post-operative central collapse of an AMDS stent following emergency Type A aortic dissection repair. Subsequent successful rescue treatment with a thoracic aortic endograft demonstrated a successful endovascular salvage strategy in this patient. This case emphasises careful anatomical selection, early post-operative CTA surveillance and timely consideration of supportive TEVAR when collapse is identified.
This study conducted a bibliometric analysis to outline the publication landscape, identify key contributors, and map the evolution, interactions, and future directions of the therapeutic paradigms for sclerotherapy, an established primary treatment for lower limb varicose veins. This bibliometric study utilized data from the Web of Science Core Collection, analyzed with VOSviewer, the R package bibliometrix, and CiteSpace. High-frequency keywords were manually categorized into three thematic groups: Comprehensive Therapy; Perioperative Management Outcomes and Minimally Invasive Therapy. Annual group intensity was calculated to track the evolving research focus on these therapeutic paradigms. A total of 352 publications were included. The USA was the leading nation in research contributions, with institutions such as the University of Birmingham and University of California System at the forefront. Key journals, including Phlebology and the European Journal of Vascular and Endovascular Surgery, were pivotal in disseminating knowledge. Influential authors such as Bradbury A. W., Bate G. R. and Darvall K. A. L. significantly shaped the research landscape. Keyword cluster analysis identified six distinct thematic groups, focusing on patient-centered outcomes, complication management and evidence-based guidelines. Burst analysis highlighted “high ligation”, “randomized clinical trial” and “endovenous laser ablation”. Under the proposed keyword taxonomy, the relative distribution of the three thematic paradigms showed an apparent tendency toward greater balance after 2020. This bibliometric study maps the evolution and current frontiers of lower limb varicose vein sclerotherapy research. These findings suggest that future research may further examine combination strategies, individualized risk-stratified protocols, and interdisciplinary collaboration in the management of lower limb varicose vein sclerotherapy.
Lower extremity peripheral arterial disease (LEPAD) is a major atherosclerotic condition in ageing populations, contributing to mobility loss, disability, and excess cardiovascular risk. Using modelled estimates from the Global Burden of Disease (GBD) 2021 study, we assessed global, regional, and national LEPAD burden from 1990 to 2021 and projected age-standardised trends to 2040. Modelled estimates of LEPAD prevalence, incidence, deaths, and disability-adjusted life years (DALYs) were extracted from the GBD 2021 study for 204 countries and territories and stratified by age, sex, and socio-demographic index (SDI). Unless otherwise stated, all rates are age-standardised using the GBD world standard population and are reported per 100,000 population with 95
Adverse distal aortic remodeling after type A aortic dissection (TAAD) repair is the principal cause of late aneurysm formation, rupture, and reintervention, significantly compromising long-term survival in patients with TAAD. This study is a systematic review. A comprehensive search of Chinese and English databases up to December 10, 2025 was performed to systematically identify imaging-based risk factors for adverse distal aortic remodeling after TAAD repair and to summarize the efficacy and limitations of current endovascular intervention strategies. After systematically searching CNKI, Wanfang Data, VIP, PubMed, Embase, the Cochrane Library, and Web of Science, a total of 31 studies involving 5330 patients were included. Imaging-based risk factors for adverse distal aortic remodeling include early postoperative descending aortic diameter ≥ 40 mm, a patent or partially thrombosed false lumen, and distal anastomotic new entry (DANE). Endovascular techniques, including false lumen occlusion, aortic true lumen stenting, and adjunctive intimal fenestration, can effectively improve patient outcomes. Early identification of high-risk patients and individualized intervention are key to enhancing the long-term prognosis of individuals with TAAD.
Congenital heart disease (CHD) is a common birth defect frequently requiring surgical repair with thymectomy. While transient neonatal lymphopenia is usually benign, persistent lymphopenia may increase susceptibility to infections and immune dysregulation. This study examines the prevalence and longitudinal course of lymphopenia after thymectomy in infants with CHD, contributory factors, and infection risk. This is a retrospective cohort study in which all children <2 years who underwent first congenital heart surgery with thymectomy between 2017–2022 for conotruncal defects were recruited. Baseline, post-operative, long-term lymphocyte counts, and episodes of infections for 3 years following the surgery were collected. The data were collected from 95 patients with median age at the time of surgery 9.0 (IQR 5.0, 12.0) months and median weight 5.0 (1.0, 25.0) Kg. Tetralogy of Fallot (TOF) represented 53.68
Total Anomalous Pulmonary Venous Return (TAPVR) is a rare congenital defect requiring surgical correction. Outcomes are influenced by associated anomalies and preoperative pulmonary venous obstruction, which increase morbidity, mortality, and postoperative pulmonary hypertension risk. This study reviews our institutional experience with pediatric TAPVR repair, emphasizing postoperative outcomes and prognostic determinants. This single-centre retrospective cohort (2006–2024) at Aga Khan University Hospital included pediatric TAPVR patients (< 18 years). Preoperative, intraoperative, and postoperative data were analyzed. Continuous variables summarized as mean/SD or median/IQR and categorical as frequencies, with appropriate statistical tests applied. Our cohort included 80 patients (65
Superior sinus venous atrial septal defect (SVASD) associated with partial anomalous pulmonary venous return (PAPVR) is a rare congenital heart disease that is predominantly diagnosed and surgically treated in childhood; however, sometimes the diagnosis is delayed and requires intervention in adulthood. A 69-year-old patient presented to the adult congenital heart disease (ACHD) clinic due to shortness of breath and recurrent syncopal episodes and was found to have significant right ventricular enlargement by echocardiogram of undetermined cause. Cardiac CT detected a large SVASD with PAPVR that required surgical intervention. The postoperative course was complicated by delirium tremens. ACHD patients often have many comorbidities that are not commonly seen in the pediatric population. Because of this, it is of utmost importance that pediatric surgical centers offering procedures for ACHD patients have established protocols to manage these comorbidities postoperatively, including substance withdrawal symptoms.
miR-511 is a well-known tumor suppressor in many tumor types. However, whether miR-511 directly regulates EREG in non-small cell lung cancer (NSCLC) and the functional consequences of this regulation have not been investigated. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to measure miR-511 expression. The proliferation, invasion and migration abilities of NSCLC cell lines A549 and H460 were determined by CCK-8, colony formation, and Transwell assays. RNA-seq was used to screen the target genes of miR-511. A xenograft mouse model was established to validate the tumor-suppressive role of miR-511 in vivo. The expression of miR-511 is significantly down-regulated in NSCLC tissues and cells. The inducing of miR-511 dramatically inhibit the proliferation, invasion and migration of NSCLC cells. TargetScan predicates that EREG might be a target gene of miR-511. Dual-luciferase reporter assay confirmed that miR-511 directly binds to the 3‘-UTR of EREG. Induction of MiR-511 significantly down-regulated the mRNA and protein levels of EREG, thus validating the prediction. Moreover, rescue experiments show that EREG overexpression impairs the effect of miR-511 on suppressing the malignant phenotype of NSCLC cells. Furthermore, in vivo xenograft experiments demonstrated that miR-511 overexpression significantly suppressed NSCLC tumor growth and reduced EREG expression in tumor tissues. miR-511 inhibits the proliferation and metastasis of NSCLC by down-regulating the expression of EREG. The miR-511-EREG axis may provide a potential basis for future therapeutic exploration in NSCLC.
Postoperative atrial fibrillation (POAF) is a common complication after coronary artery bypass grafting (CABG), leading to higher rates of morbidity and greater demands on healthcare resources. This study aimed to assess the relationship between the C-reactive protein to albumin ratio (CAR) and the development of POAF in patients undergoing CABG. A retrospective cohort study was conducted on 109 patients who underwent elective CABG. CAR was measured preoperatively. The primary outcome was the incidence of POAF within the first postoperative week. Logistic regression and receiver operating characteristic (ROC) curve analyses were used to evaluate the predictive value of CAR and other clinical variables. POAF occurred in 29 patients (26.6
To investigate the diagnostic value of the Residual Cholesterol Inflammatory Index (RCII) for assessing coronary artery disease severity in patients with premature coronary artery disease (PCAD) undergoing percutaneous coronary intervention (PCI), and to provide evidence for clinical risk stratification and individualized treatment. A retrospective study was conducted on 351 patients diagnosed with PCAD who underwent PCI at Nantong First People’s Hospital between January 2024 and December 2025. Patients were divided into four groups (low, medium, high, and extremely high RCII) based on RCII quartiles. Baseline characteristics, laboratory parameters, and coronary angiography data were collected. Coronary lesion severity was evaluated using the Gensini score. Associations between RCII and coronary lesion severity were analyzed using the Kruskal‑Wallis H test, χ² test, multiple linear regression, restricted cubic spline (RCS) analysis, and receiver operating characteristic (ROC) curves. With the increase in RCII levels, the Gensini score, the rate of three-vessel coronary artery disease, and the incidence of acute myocardial infarction (AMI) in PCAD patients undergoing PCI increased significantly (all P < 0.001). Multiple linear regression analysis, after adjustment for traditional cardiovascular risk factors, showed that RCII exhibited a significant non-linear (inverted U-shaped) association with Gensini score (P for nonlinearity < 0.001), with a positive linear relationship predominantly observed in the low-to-moderate RCII range (≤ 40, accounting for 94
Transcatheter aortic valve implantation (TAVI) for pure aortic regurgitation (AR) remains challenging, especially in bicuspid aortic valve (BAV) anatomy, which has been excluded from pivotal trials of dedicated AR devices. Whether cusp-engaging devices can be used in type 1 BAV with raphe is unknown. We report two East Asian male patients (aged 72 and 62 years) with severe pure AR and type 1 bicuspid aortic valve, confirmed by transthoracic echocardiography. Pre-procedural multidetector computed tomography (MDCT) demonstrated a raphe between the left and right coronary cusps in both patients, with relatively symmetric cusp sizes and minimal calcification. Self-expanding Taurus-Trio valves (27 mm and 25 mm, respectively) were successfully implanted under monitored anaesthesia care (MAC) with TTE guidance. Post-procedural TTE showed only trivial paravalvular leak (PVL). At 6-month follow-up, MDCT confirmed favourable valve performance, with all three locators appropriately engaged within the corresponding cusps, preserved leaflet morphology and motion, and no evidence of hypo-attenuated leaflet thickening (HALT). Neither patient developed new conduction disturbances requiring permanent pacemaker implantation. This case report demonstrates the feasibility of using a dedicated cusp-engaging transcatheter valve in carefully selected patients with type 1 BAV-AR, favourable cusp symmetry, and minimal calcification. These findings are hypothesis-generating and warrant further investigation; they should not be generalised to all BAV subtypes or to patients with significant calcification.
This study aims to investigate the clinical utility of serum lncRNA RHOXF1-AS1 combined with chest CT imaging features in distinguishing benign from malignant pulmonary nodules (PNs) and assessing prognosis in lung cancer patients. This study included 249 patients with pathologically confirmed PNs (100 benign, 149 malignant). The relative expression level of serum RHOXF1-AS1 was detected using RT-qPCR. Binary logistic regression analysis was performed to identify independent risk factors for malignant PNs. ROC curves assessed diagnostic performance. The association between RHOXF1-AS1 expression and prognosis was analyzed using Kaplan-Meier curves and Cox analysis. Serum RHOXF1-AS1 expression levels were significantly lower in the malignant nodule group compared to the benign nodule group. Low serum RHOXF1-AS1 expression, nodule diameter, spiculation, and nodule density were independent risk factors for predicting nodule malignancy. Among individual markers, serum RHOXF1-AS1 demonstrated the highest diagnostic curve AUC of 0.845. The AUC of the combined diagnostic model integrating all four markers increased to 0.900. Survival analysis indicated that patients with low serum RHOXF1-AS1 expression exhibited shorter survival times and represented an independent prognostic risk factor in multivariate analysis. Serum RHOXF1-AS1 serves as an effective biomarker for distinguishing benign from malignant PNs, and its low expression correlates with poor prognosis in lung cancer patients. Integrating serum RHOXF1-AS1 with key CT imaging features enables the construction of a combined model with superior diagnostic performance, offering a novel integrated strategy for early, precise diagnosis and prognostic assessment of PNs.
Postoperative atrial fibrillation (POAF) is a frequent complication after esophagectomy. The monocyte-to-high-density lipoprotein cholesterol ratio (MHR) integrates monocyte-related inflammatory burden with HDL-C-related anti-inflammatory and antioxidative capacity. We examined the association between preoperative MHR and POAF after radical esophagectomy for esophageal squamous cell carcinoma (ESCC). Consecutive patients with pathologically confirmed ESCC who underwent radical esophagectomy from January 2022 to December 2024 were screened, and 413 patients were included. MHR was calculated as monocyte count divided by HDL-C measured within 7 days before surgery. POAF was defined as new-onset atrial fibrillation lasting ≥ 30 s within 7 postoperative days. ROC/Youden analysis was used to derive an exploratory cut-off. Primary propensity score matching (PSM) based on sex, BMI, smoking, drinking, and diabetes mellitus yielded 147 matched pairs. An expanded PSM analysis was performed as a sensitivity analysis. The primary inferential analyses modeled MHR continuously, with additional exploratory categorical, quartile-based, restricted cubic spline, and Firth penalized logistic regression analyses. POAF occurred in 48 of 413 patients (11.6
