ObjectiveTo construct and validate a risk prediction model of in-hospital mortality using machine learning (ML) algorithm in a retrospective cohort of acute type A aortic dissection (ATAAD) patients undergoing surgical treatment.MethodsPatients with ATAAD undergoing surgical treatment between January 2014 and December 2022 were enrolled to predict in-hospital mortality. To address class imbalance and overfitting, we developed a robust Random Forest (RF)-based classification framework using a nested stratified 5-fold cross-validation (NCV). This was a single-center, retrospective study with internal validation only; no external validation was performed. Performance was evaluated via ROC-AUC, Precision-Recall Area Under the Curve (PR-AUC), sensitivity, brier score and calibration metrics, with Shapley Additive exPlanations (SHAP) utilized for feature interpretation.ResultsA total of 639 ATAAD patients were included in the analytical cohort, with an in-hospital mortality rate of 5.6% (36/639). The calibrated full RF model (50 preoperative clinical variables) achieved an ROC-AUC of 0.666, PR-AUC of 0.145, brier score of 0.051, and calibration slope of 0.836, with a sensitivity of 0.694 at an optimized threshold. A parsimonious 15-feature model maintained robust performance (ROC-AUC: 0.752, PR-AUC: 0.207, brier score: 0.050 and calibration slope: 0.934). SHAP analysis identified Creatine Kinase-MB, Myoglobin, and Fibrinogen Concentration as the top mortality predictors.ConclusionWe developed and internally validated an explainable RF model to predict in-hospital mortality after ATAAD surgery. Given the low positive predictive value and high negative predictive value, the model is best regarded as a promising preliminary rule-out/triage tool that requires multicenter external validation before clinical use.

[This corrects the article DOI: 10.3389/fcvm.2025.1647188.].

Atherosclerosis is the most recognized pathological basis of cardiovascular disease, and the rupture of vulnerable atherosclerotic plaque is one of the most important factors leading to the end-stage event, myocardial infarction. Nanomedicine has emerged as a stratedgy to improve the diagnositic and therapeutic efficacy. The microenvironment has attracted great interest as the target of an intelligent drug delivery system to alter the pathological process. This review summarizes microenvironment-targeted nanomedicine for diagnosis and treatment of atherosclerosis. The pathological processes share similar characteristics of microenvironment, including high endogenous reactive oxygen species levels, acidic pH values, and high enzyme activity. Target cell population may include endothelial cells, vascular smooth muscle cells, macrophages, and foam cells. Lesion neovascularization also represents a potent target. Nanomaterials have been applied in fluorescence imaging, magnetic resonance imaging, single-photon emission computed tomography/computed tomography imaging, and multimodal imaging for detecting atherosclerosis. The nanomaterial-based treatment approaches of atherosclerosis include microRNA-based therapy, photodynamic therapy, anti-inflammatory therapy, antioxidant therapy, and immunotherapy. Although nanomedicine expanded a promising avenue for more detailed diagnosis procedure and efficient treatment of atherosclerosis, the biosafety concerns still remain awaiting further investigation. The clinical application of microenvironment-targeted nanomedicine in atherosclerosis still represents a challenge.

The design of bioresorbable vascular scaffolds (BVSs) with integrated therapeutic and imaging functions remains a significant challenge in cardiovascular biomaterials, primarily due to the lack of bioactivity and intrinsic radiopacity in existing biodegradable polymer systems. A multifunctional biodegradable composite was created by blending poly(epsilon-caprolactone) (PCL) with 3,5-diiodoaspirin (DIA), a halogenated aspirin derivative that preserves anti-inflammatory and antiplatelet properties while introducing intrinsic radiopacity through molecular iodination. The key mechanism underlying this dual functionality lies in the molecular iodination of aspirin, which enhances X-ray attenuation without disrupting the polymer matrix, while enabling sustained release of bioactive aspirin moieties from the biodegradable composite. The resulting PCL/DIA films exhibited homogeneous morphology, favorable processability, and dose-dependent X-ray visibility. Spectroscopic and thermal analyses confirmed successful incorporation of DIA without compromising the polymer matrix's structural integrity, ensuring effective molecular integration. In vitro studies demonstrated sustained DIA release over 30 days, excellent cytocompatibility, minimal hemolysis, and significant reduction in platelet adhesion. Additionally, the DIA-loaded polymer mitigated lipopolysaccharide (LPS)-induced inflammatory responses and reactive oxygen species (ROS) production in endothelial cells and macrophages, in line with aspirin's known antiinflammatory effects. Subcutaneous implantation in rats showed lasting radiopacity and reduced fibrous capsule formation over 30 days. Notably, PCL/aspirin controls exhibited similar bioactivity but lacked radiographic contrast, highlighting the dual functionality of DIA. These findings suggest that DIA incorporation enables a biodegradable polymer platform that combines therapeutic action with imaging capability, offering a promising foundation for the future development of image-guided vascular biomaterials.

Background Tobacco exposure (TS) is a globally prevalent environmental toxicant associated with increased cardiovascular morbidity. Serum cotinine, a robust biomarker of TS, provides an objective measure of internal dose. However, the inflammatory pathways linking TS to peripheral artery disease (PAD), and the potential contribution of cotinine-related signaling to this relationship, remain insufficiently defined. Methods This study combined epidemiologic analyses of NHANES data with network toxicology, two-sample Mendelian randomization, molecular docking and dynamics, and single-cell transcriptomic profiling to explore cotinine-related inflammatory pathways associated with PAD. Results Elevated cotinine levels were linearly associated with higher PAD prevalence both before and after propensity score matching. Network toxicology and MR analyses consistently identified IL6 and STAT3 as inflammation-related mediators with genetically predicted effects on PAD susceptibility. Molecular docking and dynamics suggested possible transient interactions between cotinine and IL6/STAT3, providing hypothesis-generating toxicological insights. Single-cell RNA sequencing revealed IL6 and STAT3 expression among vascular-associated immune and stromal cell populations, offering cellular context for cotinine-related inflammatory responses. Conclusion Our findings support a positive association between TS-related cotinine exposure and PAD. Integrative analyses suggest that IL6/STAT3 signaling may represent a cotinine-related pathway that potentially partially mediates the association between TS and PAD. This multidisciplinary work provides new insights into the environmental determinants of vascular injury and underscores the importance of reducing TS as a public health priority.

Background:Recent studies have identified a co-occurrence of chronic obstructive pulmonary disease and congestive heart failure in ICU patients. Abnormal red cell distribution width (RDW) frequently manifests in critically ill patients, but its clinical significance remains a subject of debate. This study aims to investigate the relationship between RDW and in-hospital mortality in patients with concurrent congestive heart failure and chronic obstructive pulmonary disease. Methods:We conducted a retrospective cohort study using the Medical Information Mart for Intensive Care (MIMIC) IV version 2.0 database. RDW levels were assessed within 24 h of admission. The impact of RDW at ICU admission on in-hospital mortality was analyzed through multivariable logistic regression models, generalized additive models, and subgroup analysis. Results:We enrolled 6,309 patients with congestive heart failure and concomitant chronic obstructive pulmonary disease, with an in-hospital mortality rate of 12.4% (783/6,309). The fully adjusted model revealed a positive association between RDW and in-hospital mortality in congestive heart failure patients with concurrent chronic obstructive pulmonary disease, even after accounting for confounding factors (OR = 1.07, 95% CI: 1.03-1.12, p < 0.001). When comparing the highest quartile (Q4) to the lowest quartile (Q1), the odds ratio (OR) was 1.62, with a 95% confidence interval (CI) of 1.17-2.22, p = 0.003. We observed a linear relationship between RDW and in-hospital mortality, which remained consistent in subgroup analysis. Conclusions:Our data suggest that RDW is positively associated with in-hospital mortality in patients with both congestive heart failure and chronic obstructive pulmonary disease. At the same time, large prospective research and longer follow-up time are required to further validate the findings of this study.

Introduction Coronary artery bypass grafting (CABG) is a standard treatment for coronary artery disease, particularly in patients with multivessel disease. Connecting the saphenous vein graft (SVG) to the right internal mammary artery (RIMA) instead of the aorta has been proposed as an alternative approach to minimise aortic manipulation and potentially improve graft patency. This study aims to determine whether the RIMA-SVG technique is non-inferior to the conventional Aorta (Ao)-SVG approach in terms of 1-year graft patency, while also comparing perioperative complications and short-term clinical outcomes.Methods and analysis This non-inferiority, single-centre, prospective, double-blind, randomised clinical trial will enrol 300 patients undergoing CABG. Participants will be randomised into two surgical groups (RIMA-SVG vs Ao-SVG). The primary outcome is the 1-year SVG patency rate, assessed using coronary CT angiography. Secondary outcomes include perioperative complications, all-cause mortality, major adverse cardiovascular and cerebrovascular events (MACCE), and surgical site infections occurring during hospitalisation and up to 1 year postoperatively. Randomisation will be computer-generated, and all procedures will be performed by experienced surgeons. Patients will be followed up 12 months post-surgery. Non-inferiority will be established if the upper bound of the one-sided 97.5% CI for the difference in graft occlusion rates is less than the prespecified non-inferiority margin of 10%.Ethics and dissemination This study has been approved by the Ethics Committee of the Second Hospital of Jilin University (No. 460) and registered at ClinicalTrials.gov (NCT06787651). All participants will provide written informed consent before enrolment. To ensure data integrity and minimise bias, randomisation details will be concealed from researchers until surgery, and data analysts will remain blinded to group assignments. The findings will be disseminated through academic journals and conference presentations to promote knowledge sharing and clinical application in the field of cardiovascular surgery.Trial registration number NCT06787651.

Background:Renal failure and dysfunction remain one of the most significant morbidities impacting patient's life. Effective treatments still lack in the context of an increasing number of patients with renal failure. This study aims to investigate the impact of growth differentiation factor 15 (GDF15) in treating renal dysfunction and to explore its therapeutic potential. Methods:Renal injury was induced with a murine ischemia reperfusion injury (IRI) model. Mice overexpressing GDF15 (GDF15 transgenic (GDF15TG) mice, GDF15 knock out (GDF15 KO) mice and wild type (WT) mice all underwent IRI to test the effects of GDF15 on renal injury. Renal function and histopathological changes were measured 24 h after reperfusion. Cell apoptosis was detected by TUNEL and tissue inflammation was detected by myeloperoxidase (MPO) activity. qRT-PCR was conducted to determine the expression of genes and circular RNAs. Results:Overexpression of GDF15 reduced mortality of mice with lethal renal IRI whereas GDF15 deficiency increased the mortality. GDF15TG mice had better renal function with the lower levels of blood creatinine and blood urea nitrogen (BUN). Over-expression of GDF15 reduced kidney pathological changes, cell apoptosis, neutrophil infiltration and mortality. Over-expression of GDF15 also decreased the expression of apoptotic genes (high mobility group 1, HMGA1 and Bax), inflammatory genes IL-1β, IL-6, tumor necrosis factor (TNF-α), chemokine 1 (CK1), and senescent gene p21 whereas increases Bcl-XL, Importin 11 and CRIM1. IRI upregulated circular RNA Smad3 and reduced circular RNA Hipk3 and circular RNA Crim1, which was offset by GDF15. Conclusion:Over-expression of GDF15 protects renal function and prevents renal failure, highlighting its potential in treating renal failure.

Type A aortic dissection (TAAD) is a lethal cardiovascular disease characterized by the separation of the layers within the aortic wall. The underlying pathological mechanisms of TAAD requires further elucidation to develop effective prevention and pharmacological treatment strategies. Inflammation plays a crucial role in TAAD pathogenesis. Disulfidptosis, an emerging type of cell death, may shed light on disease mechanisms. This study investigates the role of disulfidptosis-related genes in immune infiltration in TAAD. TAAD gene expression datasets were obtained from the Gene Expression Omnibus (GEO) database. Immune cell infiltration analysis assessed immune cell dysregulation in TAAD. Differentially expressed genes (DEGs) between TAAD samples and controls were identified and intersected with known disulfidptosis-related gene sets to obtain relevant DEGs. Hub genes were identified using machine learning algorithms. A diagnostic model was constructed using Least Absolute Shrinkage and Selection Operator (LASSO) regression on 25 TAAD samples. Consensus clustering classified TAAD samples based on disulfidptosis-related gene expression. Functional enrichment analyses, including Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, elucidated associated biological processes and pathways. A total of 13,316 DEGs were identified, among which 11 disulfidptosis-related genes were screened: INF2, CD2AP, PDLIM1, ACTN4, MYH10, MYH9, FLNA, FLNB, TLN1, MYL6, ACTB, CAPZB, DSTN, and IQGAP1. Most of these genes exhibited lower expression levels in TAAD samples, except CAPZB, and were correlated with immune cell infiltration. Cluster-specific DEGs were found in one cluster, involving several immune response processes. Co-clustering analysis based on disulfidptosis-related genes classified TAAD samples into two clusters, with higher gene expression levels observed in cluster C2 compared to cluster C1. Three key hub genes were identified, and potential therapeutic mechanisms for TAAD were explored. Immuno-infiltration results revealed significant differences in immune profiles, with higher immunological scores and more extensive immune infiltration in TAAD. Disulfidptosis occurs in TAAD and is associated with immune cell infiltration and metabolic activity, influencing immune cell function and responses. These findings suggest that disulfidptosis may promote TAAD progression through the induction of immune responses and metabolic activities. This research provides new insights into the pathogenesis and identifies potential therapeutic targets for TAAD.

BackgroundCardiopulmonary bypass (CPB) remains an indispensable technique for open-heart surgery; however, it induces systemic inflammation and oxidative stress, leading to myocardial cell damage and compromised prognosis. Optimizing myocardial protection during CPB remains a critical objective. This study aimed to identify potential therapeutic targets for myocardial protection during CPB.MethodsWe performed weighted gene co-expression network analysis (WGCNA) on previously published datasets (GSE12486, GSE132176, GSE14956, and GSE38177) to identify CPB-related hub genes. An in vitro model of oxidative stress was established using H2O2-treated H9C2 cardiomyocytes to validate these hub genes. Through systematic validation, we identified the most representative hub gene. Subsequent functional studies, including gene knockdown and overexpression experiments, were conducted to elucidate its role and underlying mechanisms in oxidative stress-induced cardiomyocyte injury.ResultsIntegrated bioinformatics analysis and experimental validation identified MAFF as the most differentially expressed hub gene between pre- and post-CPB conditions. In the oxidative stress model, MAFF overexpression demonstrated cardioprotective effects by maintaining cell viability, significantly reducing reactive oxygen species (ROS) accumulation in both cytoplasm and mitochondria, and attenuating pyroptosis-mediated cell death.ConclusionOur findings demonstrate that MAFF exerts protective effects against oxidative stress-induced cardiomyocyte injury, positioning it as a promising therapeutic target for myocardial protection. These results provide novel insights into optimizing postoperative recovery and improving clinical outcomes for patients undergoing CPB-assisted cardiac surgery.

Background Switching from a contractile to a synthetic phenotype of pulmonary arterial smooth muscle cells (PASMCs) is known to play a crucial role in pulmonary arterial hypertension (PAH). We investigated how hypoxia and mechanical stress mediate the phenotypic switching of PASMCs. Methods Human PASMCs were used for experiments. Hypoxia treatment was done by culturing cells under 1% O₂. Mechanical stress was induced by loading cells to 50 mmHg hydrostatic pressure. We analyzed cell morphology, cell proliferation, phenotypic marker protein expression, cytokine release, and the activation of stress-related pathways at 24 h after treatment. Bulk and single-cell RNA-sequencing datasets were used to analyze heat shock protein family D member 1 (HSPD1) expression in PAH lungs and PASMCs. Heat shock protein 60 (HSP60) was knocked down in PASMCs by transfection of HSPD1-siRNA. Results Either hypoxia or mechanical stress alone induced the morphology change, increased cell proliferation, and promoted the phenotypic switching and inflammatory cytokines release of PASMCs. Interestingly, all those were dramatically enhanced under the combination of hypoxia and mechanical stress. Mechanistically, we found that the combination of hypoxia and mechanical stress not only significantly enhanced the mitochondrial HSP60 expression but also induced its partial redistribution to the cytosol. Bioinformatic analyses also confirmed the elevated HSPD1 expression in PAH lungs and PASMCs. HSP60 knockdown effectively attenuated the phenotypic switching of PASMCs induced by hypoxia and mechanical stress. Conclusion Hypoxia- and mechanical stress-induced upregulation of mitochondrial HSP60 is associated with phenotypic switching of PASMCs.

Circular RNA (circRNA) is becoming an increasingly popular field of study and topic of interest. With that, there is a renewed and heightened interest in generating circular RNA for both research and clinical use. CircRNA generation began in the 1990s using in vitro chemical ligation and has since expanded out to include in vitro enzymatic synthesis along with in vivo vector-based systems. Each of these methods has distinct advantages, limitations, and different function 1ality depending on application. Throughout this chapter, we explore and summarize different methods for generating pure circRNA constructs that can be readily utilized for different applications. We highlight the steps and aspects to be considered when selecting the method to synthesize circRNA based on yield, purity, and application. Overall, this chapter aims to provide the reader with an understanding of the current methods and applications of synthesizing circRNA both in vivo and in vitro for use in research and clinical settings.

OBJECTIVE:For type B aortic dissection (TBAD) involving the left subclavian artery (LSA), to secure sufficient proximal landing zones, the LSA can be intentionally covered during thoracic endovascular aortic repair (TEVAR). This study aimed to evaluate the midterm clinical outcomes of endovascular treatment for TBAD involving the LSA using the Castor single-branched stent graft. AIMS:The aim of this study was to evaluate the midterm efficacy and safety of Cator stent graft in the treatment of type B aortic dissection involving left subclavian artery. METHODS:From May 2018 to December 2022, 150 patients with TBAD involving the LSA were treated with the Castor single-branched stent graft (Micropart Corp, Shanghai, China). The data collected included technical success, incidences of Type I endoleak, retrograde type A dissection (RTAD), stroke, LSA patency, as well as follow-up mortality and morbidity, and reinterventions. RESULTS:The technical success rate was 97.3% (146/150). One patient experienced intraoperative RTAD, two patients had a small type I endoleak, and one patient suffered a stroke. Moreover, one patient developed RTAD on the third day after TEVAR. No in-hospital aorta-related mortality, paraplegia, or branch occlusion. During follow-up, one case (0.7%) of small endoleak, one case (0.7%) of branch occlusion, and two deaths were documented. Complete thrombosis of the false lumens was observed in 140 cases (99.3%). The true lumen diameter at the level of the aortic isthmus and pulmonary artery bifurcation increased significantly (13.3 ± 7.5 vs. 4.2 ± 2.1; 19.8 ± 5.7 vs. 5.4 ± 4.8, p < 0.01), and the ratio of the real lumen increased significantly (0.6 ± 0.2 vs. 0.9 ± 0.1; 0.4 ± 0.1 vs. 0.8 ± 0.1, p < 0.01). The median follow-up time was 36.0 months (IQR, 11.8 months) (range: 6-72 months). CONCLUSION:The Castor single-branched stent graft showed favorable midterm outcomes in the treatment of TBAD involving the LSA.

BackgroundDue to complications such as aortic root bleeding and high coronary tension with the conventional Bentall technique to treat aortic root aneurysms, new methods have been developed to enhance patient outcomes. This study aimed to describe a novel modification of the Bentall procedure for aortic root replacement and to report on its mid- and long-term follow-up outcomes.MethodsPatients diagnosed with aortic root aneurysm were enrolled in the study. The inclusion criteria included diameter of ascending aorta larger than 50 mm and the aortic valve with organic lesions. Data were collected including surgical time, aortic clamping time, cardiopulmonary bypass time, and pre-discharge computed tomography angiography findings.ResultsEighty-eight patients (nine with Marfan syndrome), including 69 men (78.4%) and 19 women (21.6%), underwent aortic root replacement using our new root reconstruction technique from 2011 to 2020 at our hospital. The patients’ mean age was 43.4 ± 11.7 years (range, 20–71 years). Of them, 35 (39.8%) had a Stanford type A aortic dissection (dissection group), while 53 (60.2%) had an aortic root aneurysm (aneurysm group). The patients’ in-hospital mortality rate was 2.3% (one case of multiple organ dysfunction syndrome, one case of arrhythmia). The mean aortic cross-clamp and cardiopulmonary bypass times were 120.9 ± 27.1 min and 159.2 ± 37.9 min, respectively. The follow-up rate was 94.2% (81/86) for a mean duration of 55 ± 23 months (range, 6–120 months). Follow-up mortality occurred in three cases (3.7%), including one death due to a traffic accident, one death due to cerebral hemorrhage, and one sudden death of unknown reasons. No patients required an aortic root re-operation during follow-up. The overall survival rate was 98.8%, 95.9%, and 95.9% after 48, 96, and 120 months, respectively.ConclusionsOur initial experience suggests that this technique is feasible and safe, with promising mid- and long-term outcomes in our series. These descriptive results justify further comparative studies to evaluate its role as a potential alternative for the treatment of aortic root aneurysms.

Cardiovascular diseases are the leading cause of mortality and disease burden among the elderly, both in China and globally. This underscores the importance of cultivating medical professionals with a deep understanding of the unique characteristics of cardiovascular diseases in aging populations. Ideological and political education, a key component in fostering moral character and integrity, plays a vital role in cardiovascular surgery education within the context of an aging society. This article examines the application of the ideological and political education teaching model in cardiovascular surgery and identifies integration points within the teaching process. By embedding diverse ideological and political elements into cardiovascular surgery education, the approach ensures that students not only acquire specialized knowledge in the context of an aging population but also develop a well-rounded worldview and values. This strategy aims to cultivate comprehensive and ethically grounded cardiovascular surgery professionals equipped to address the challenges of an aging population.

Poly(lactide) has demonstrated significant potential in small-diameter vascular stents, particularly in coronary artery applications. However, its limited toughness and suboptimal biocompatibility hinder its use in high-stress regions such as the aorta. To overcome these limitations, we have designed and synthesized multi-arm poly(l-lactide-b-ε-caprolactone) (PLCL) copolymers with enhanced toughness and biocompatibility through copolymerization with polycaprolactone and multi-arm branching strategies. This study comprehensively evaluates the chemical structure, crystallization properties, mechanical properties, adhesion properties, biocompatibility and in vivo degradation profiles of multi-armed PLCLs. Results show that PLCLs exhibit substantial tensile strength and toughness, with tensile strength ranging from 1.43 MPa (2a-PLCL) to 42.45 MPa (6a-PLCL), and elongation at break from 3.07 % (2a-PLCL) to 31.49 % (6a-PLCL). Both of them were positively correlated with the number of arms. In vitro studies revealed enhanced cell adhesion and proliferation for multi-armed PLCLs. Animal model evaluations confirmed excellent histocompatibility and as the number of polymer arms increased, inflammation decreased, and the degradation rate accelerated. Notably, the 6a-PLCL exhibited the best overall performance, making it more favorable for promoting aortic remodeling. In summary, this study suggests that multi-armed PLCLs are promising candidates for cardiovascular tissue engineering and absorbable medical devices due to their enhanced mechanical properties and biocompatibility.

Background: Percutaneous atrial septal defect (ASD) closure is the preferred treatment for patients with suitable ASD anatomy. The safety and effectiveness of transcatheter closure have been established. However, reports on transesophageal echocardiography (TEE)-guided percutaneous closure of ASD via the right internal jugular vein (RIJV) are limited. The study aims to discuss the safety and effectiveness of percutaneous trans-jugular vein closure of ASD. Methods: We conducted a retrospective analysis of patients (n=103) with secondary ASD who underwent surgical treatment in the Department of Cardiovascular Surgery, the Second Hospital of Jilin University between July 2015 to July 2022. The article is a cross-sectional study. Clinical data, including age, gender, weight, defect diameter, tricuspid regurgitation, left atrial (LA) size, and the operation results, were collected and evaluated. Nonparametric rank sum tests were used to assess tricuspid regurgitation before and after surgery, while paired sample t-tests were used to compare LA size before and after surgery. Results: TEE-guided percutaneous closure of ASD via the RIJV was successfully performed in 97 out of 103 (94.2%) cases. The average procedure time was 34.48±13.06 min, and the mean age at the time of the procedure and ASD size were 36±18 years and 15.45±5.82 mm, respectively. On analyzing medical records and echocardiographic images, postoperative complications were found to occur in four (3.9%) patients. Among these, three patients had residual shunt as indicated by echocardiography during the operation, which subsequently disappeared at the three-month follow-up. One patient developed atrial fibrillation after surgery but returned to normal sinus rhythm with medication. Percutaneous closure of ASD via the RIJV was unsuccessful in 6 patients (5.8%), with 5 of them undergoing transthoracic ASD closure and achieving satisfactory results. One patient refused further surgical treatment. No pericardial effusion, thrombosis, atrioventricular block, or other complications were observed during the 3-month to 1-year follow-up period. Conclusions: ASD closure via the RIJV is a safe and effective therapeutic approach. The initial results are satisfactory, but further studies with large sample sizes and long-term follow-up are warranted to assess the long-term outcomes.