Cardiovascular surgery involves complex clinical scenarios and high demands on clinical judgment. This study aimed to evaluate the effectiveness of an artificial intelligence (AI)-enabled personalized teaching model in cardiovascular surgery training. From February to June 2025, 158 trainees in the department of cardiovascular surgery at our hospital were randomly assigned to an experimental group (n = 79) or a control group (n = 79). The control group received conventional teaching, including lectures, bedside teaching, and case discussions. The experimental group received a personalized teaching model integrating an intelligent question bank, staged case-based teaching, and AI-based standardized patient training. Outcomes included theoretical examination scores, the Chinese version of the California Critical Thinking Disposition Inventory (CTDI-CV), clinical interview performance, and teaching satisfaction. The experimental group achieved significantly higher theoretical examination scores than the control group (84.56 ± 5.07 vs. 77.95 ± 9.04, P < 0.001). CTDI-CV results showed significantly higher total scores and higher scores in truth-seeking, open-mindedness, analyticity, systematicity, and inquisitiveness in the experimental group (all P < 0.05). In the clinical interview assessment, the experimental group scored significantly higher in completeness of information collection, communication skills, diagnostic reasoning, and overall performance (all P < 0.001), while the between-group difference in empathy was not significant (P = 0.328). Teaching satisfaction in the experimental group was high, with an overall satisfaction score of 4.68 ± 0.39. The AI-enabled personalized teaching model may represent a feasible and effective approach for cardiovascular surgery education. It was associated with higher theoretical examination scores, better critical thinking disposition, higher scores in several dimensions of simulated clinical interview performance, and high learner satisfaction. Further studies are needed to confirm its broader applicability and long-term educational value.

Background The heterogeneous etiology and limited therapeutic options of pediatric restrictive cardiomyopathy (RCM)underscore the urgent need to elucidate its molecular mechanisms and identify potential treatment targets. Methods We performed integrated transcriptomic and proteomic analyses on myocardial tissues from 7 pediatric RCM patients and 3 control donors. Differentially expressed genes (DEG) were detected, with log(2) transformed fold change (log2FC)>1 or log2FC < -1 as well as P < 0.05 after the correction of false discovery rates (FDR) as the threshold. Then, the same proteins as DEGs were identified from the proteomic profiling for the further analysis. The t-test was adopted and the differentially expressed proteins (DEPs) with P < 0.05 after FDR correction and an FC > 1.5 or <0.67 were labeled as significant dysregulation. Furthermore, pathway enrichment was further conducted based on DEGs and DEPs, respectively. RNA and protein validation studies (including real-time polymerase chain reaction and western blot) were conducted to confirm key molecular alterations. Finally, bioinformatic approaches were employed to predict potential therapeutic candidates targeting the identified pathways. Results Multi-omics integration revealed 23 consistently dysregulated genes/proteins central to RCM pathogenesis (FDR adjusted P < 0.05). RNA validation confirmed significant expression changes in most hub genes, while protein-level assays demonstrated marked downregulation of CKB, PGAM2, and TPM2 in RCM myocardium (P < 0.05). Functional enrichment analysis highlighted the involvement of these molecules in critical pathways, including muscle contraction, sarcomere organization, and extracellular matrix remodeling. Drug prediction analysis identified several repurposed candidates, including phenytoin, diazepam, and paricalcitol, which may target these aberrant pathways. Conclusions This study elucidates the fundamental molecular mechanisms underlying muscle contraction and energy metabolism in RCM, while simultaneously translating these insights into clinically actionable strategies. Specifically, it identifies the downregulation of key proteins as potential biomarkers and proposes drug repurposing strategies informed by pathway analysis. These findings offer a novel perspective on the pathophysiology of RCM and establish an evidence-based foundation for the development of targeted diagnostic and therapeutic tools.

The in vivo performance of tissue-engineered heart valves remains constrained by a persistent early failure triad at the blood-material interface, namely thrombosis, unresolved inflammation, and slow endothelialization. Here, a bioinstructive multilayer valve scaffold is engineered to address these interfacial barriers through spatially integrated structural and biological functions. The scaffold comprises a digitally programmable 3D-printed framework, a silk fibroin wrapping layer, and a hydrogel biointerface incorporating Arg-Gly-Asp/GelMA adhesive cues together with H2S-releasing microgels. This layered design endows the construct with valve-relevant tensile properties while simultaneously programming the immune-endothelial microenvironment. The hydrogel biointerface promotes endothelial migration, proliferation, and angiogenic activity, whereas sustained H2S delivery biases macrophages toward a pro-resolving M2-like phenotype and suppresses inflammatory activation. Transcriptomic analysis further reveals coordinated upregulation of endothelial programs related to endothelial repair, migration, and proliferation, accompanied by attenuation of stress- and inflammation-associated responses. In vivo, the scaffold mitigates thromboinflammatory reactions, shows preliminary anti-calcification performance, and supports endothelialization under blood-contacting conditions. Together, this work establishes a layered bioactive engineering approach that converts a passive 3D-printed structural scaffold into a regenerative, hemocompatible, and immunoregulatory biofunctional valve scaffold. This strategy offers a promising design principle for the further development of regenerative valve scaffolds.

OBJECTIVE:Cardiac reverse remodeling (RR) after pressure unloading has been widely studied using abdominal aortic banding (AB) and debanding (DB) models. However, the DB procedure is technically challenging and associated with high postoperative mortality, limiting broader use. Here, we aim to develop a modified, film-supported ligature technique for AB and DB to improve procedural feasibility and survival and to generate a reproducible RR model. METHODS:A rat cardiac RR model was established using medical film-supported abdominal AB followed by DB. Rats underwent 4  weeks of AB and then 2  weeks of DB. Echocardiography and blood pressure measurement were performed to confirm successful establishment of pressure overload and subsequent unloading. RR was assessed by echocardiographic structural and functional parameters, cardiac histology and serum levels of BNP, ANP and GDF-15. RESULTS:The modified DB procedure yielded a postoperative survival rate of 93.33%. AB induced significant hemodynamic changes at the constriction site and led to progressive cardiac remodeling and diastolic dysfunction from 4 to 6  weeks. After 2  weeks of DB, cardiac function showed substantial improvement; serum BNP, ANP and GDF-15 levels, as well as cardiac hypertrophy and fibrosis returned close to baseline. CONCLUSION:The film-supported AB and DB model is a technically streamlined and reproducible rat approach that markedly reduces postoperative mortality and enables consistent induction and reversal of cardiac remodeling. This model provides a useful experimental platform for studies of RR.

Valvular endothelial cells (VECs) derived from induced pluripotent stem cells (iPSCs) serve as a promising source for cardiovascular research, yet their application is limited by suboptimal differentiation efficiency and functional immaturity. The extracellular matrix (ECM) influences stem cell differentiation, with the valvular ECM being unique compared to other tissues, and our understanding of its role in VECs differentiation is limited. The proteomic analysis comparing the protein composition of decellularized human heart valve ECM (dhECM) and Matrigel found that type V collagen (Col V) was uniquely present in dhECM and localized beneath the endothelium in the ventricular layer of valves. Subsequent investigations into the role of Col V in the differentiation of iPSC-derived valvular endothelial-like cells (iVECs) demonstrated that Col V significantly enhanced differentiation efficiency from 18.2% to a peak of 69.6%. Moreover, Col V promoted the proliferation, adhesion, migration, tube formation, and low-density lipoprotein (LDL) uptake functions of iVECs in vitro, showing a closer alignment with the functionality of primary VECs. Overall, this study indicates that Col V directs the differentiation of iPSCs into valvular endothelial-like cells with improved differentiation efficiency and functionality, which is instrumental for the development and application of tissue-engineered heart valves, drug screening, and the future of regenerative medicine.

Background:Complex congenital heart disease (CHD) has long been a significant cause of infant mortality and severe morbidity. However, pediatric cardiac rehabilitation (CR) is gaining recognition, and evidence regarding postoperative ICU phase CR for infants with CHD remains scarce. Methods:This was a retrospective case series, we reviewed clinical data for 10 infants with complex CHD who received an early, individualized CR program during the postoperative ICU phase. The rehabilitation was initiated between postoperative days 5-15 (median 9). The program was based on an exercise prescription, and integrated multidimensional interventions, including respiratory training, gross motor function training, nutritional support, and developmental care. Results:All infants were critically ill postoperatively requiring various forms of life-support therapy in the ICU. No serious adverse events related to rehabilitation occurred; transient fluctuations in vital signs resolved promptly with temporary pauses in therapy. Eight infants were discharged home after recovery, and two were transferred to other institutions. Functional improvements were observed across respiratory, feeding, neuromotor, and circulatory domains during the ICU stay. Conclusion:For infants with complex CHD, early initiation of a cardiac rehabilitation program during the ICU phase appears safe and feasible when implemented under multidisciplinary assessment and close clinical monitoring. This approach may support functional recovery across cardiopulmonary and neuromotor domains during a critical developmental window.

The Fontan procedure improves survival in single-ventricle patients, but some progress to Fontan circulatory failure (FCF) with limited treatment options. Fontan-associated liver disease (FALD) further complicates management and raises uncertainty regarding the choice between isolated heart transplantation (HT) and combined heart-liver transplantation (CHLT). Data from Asian populations are limited, and this study aimed to provide additional evidence on transplantation outcomes in this population. A single-center retrospective study in China, describing the clinical characteristics, surgical procedures, and outcomes of six consecutive HT patients and one CHLT patient with FCF. The study was conducted between August 2017 and October 2025. There were no perioperative deaths and 30‑day survival was 100

Arrhythmia is a clinically common cardiovascular disorder characterized by high incidence and a strong association with sudden cardiac death, posing a significant threat to patient survival and quality of life. The pathogenesis of arrhythmia is complex, and abnormal autonomic nervous system (ANS) modulation, as one of the causes, offers new perspectives and therapeutic targets for arrhythmia treatment. This review discusses the mechanisms by which abnormal ANS modulation leads to arrhythmias and strategies for treating arrhythmias through ANS modulation.

The global burden of valvular heart disease (VHD) is increasingly burdensome, and precise early diagnosis combined with accurate risk stratification constitutes the core strategy for improving patient prognosis. As the first-line imaging modality for VHD assessment, echocardiography is constrained by interobserver variability and cumbersome, time-consuming data processing workflows, which prevent it from fully meeting the demands of precision medicine. In recent years, breakthroughs in artificial intelligence (AI), particularly deep learning (DL) technologies, have been reshaping the paradigm of imaging-based evaluation for VHD. This review systematically summarizes the latest advances in AI applications across the entire workflow of echocardiographic assessment in VHD: from the precise segmentation of valvular anatomical structures and identification of lesions using convolutional neural networks, to the automated grading of hemodynamic severity achieved through end-to-end learning. More importantly, this article explores how AI can surpass the limitations of traditional imaging indicators by leveraging unsupervised clustering to unearth potential high-risk phenotypes and integrating multimodal data to predict adverse outcomes. Finally, the paper critically analyzes the current challenges in data standardization, model interpretability, and clinical translation, and offers perspectives on future directions in the intersection of clinical medicine and engineering.

[This corrects the article DOI: 10.1016/j.bioactmat.2024.11.018.].

Calcific aortic valve disease (CAVD), the most common human valve disease on a global scale, ranks and persists as an unaddressed clinical challenge. This is primarily attributed to the absence of efficacious pharmacological approaches. The Nuclear Receptor Subfamily 4 Group A Member 1 (NR4A1), intricately associated with the pathogenesis of multiple cardiovascular diseases, has emerged as a pivotal target for the diagnosis and treatment of numerous ailments. However, the specific molecular mechanisms and the functional significance of NR4A1 in the pathogenesis of CAVD are yet to be comprehensively elucidated. By performing in-depth analyses on human aortic valve tissues and carrying out functional investigations using primary valvular interstitial cells (VICs), we were able to demonstrate that NR4A1 significantly facilitated cellular proliferation and intensifies the osteogenic differentiation process of VICs. Evidently, this is reflected in the elevated expression of key osteogenic markers, namely runt-related transcription factor 2 (RUNX2) and alkaline phosphatase (ALP). Mechanistically, the pro-calcific effects were achieved via NR4A1-dependent modulation of the cell cycle regulatory protein Cyclin D2 (CCND2). Significantly, in vivo investigations employing ApoE-/- mice maintained on a high-fat Western diet demonstrated that pharmacological suppression of NR4A1 efficiently mitigated the advancement of aortic valve calcification. These discoveries not merely determine NR4A1 to be a crucial modulator in cellular proliferation, thereby accelerating valvular calcification, but also present compelling evidence advocating for targeting NR4A1 may represent a potential therapeutic strategy for CAVD.

Background Recurrent implantation failure (RIF) and recurrent pregnancy loss (RPL) are major causes of pathological early pregnancy, yet their mechanisms remain poorly understood. This study aimed to identify shared molecular mediators and their roles in endometrial dysfunction and immune regulation.Methods Gene expression datasets for RIF and RPL were analyzed for differentially expressed genes (DEGs), functional enrichment, and protein-protein interaction (PPI) networks. Key regulators were identified using CytoHubba and Random Forest, and receiver operating characteristic (ROC) analysis evaluated their diagnostic performance. Endometrial stromal cells (ESCs) from RIF or RPL patients were used for in vitro functional assays, and in vivo murine models with in situ uterine PTN knockdown and IGF-2 rescue were established to assess pregnancy outcomes. RT-qPCR, immunoblotting, immunofluorescence, and flow cytometry were performed to assess decidualization markers and immune cell compositions.Results PPI network and machine learning analysis identified PTN as a central hub gene shared by RIF and RPL. ROC curves showed that PTN had the highest diagnostic value among all candidate genes. Immunofluorescence confirmed that PTN is mainly expressed in ESCs and downregulated in RIF and RPL patients. In vitro, PTN promoted decidualization markers (IGFBP1, PRL, IGF-2, WNT4, and LIF) and modulated immune cell composition via IGF-2. In vivo, uterine PTN knockdown impaired implantation, reduced embryo numbers, and increased embryo resorption rates, while IGF-2 supplementation partially rescued these defects. These results indicate that PTN regulates ESC decidualization and endometrial immune tolerance and serves as a highly predictive biomarker for pathological pregnancies in RIF and RPL.Discussion The PTN/IGF-2 axis promotes ESC decidualization and a tolerogenic immune microenvironment, supporting endometrial receptivity. Dysregulation of this pathway may underlie pathological pregnancies (including RIF and RPL), highlighting PTN as a potential therapeutic target for early pregnancy loss.

BACKGROUND: Metabolic remodeling, marked by maladaptive shifts in substrate use and energy production, is a hallmark of pathologic cardiac hypertrophy. Yet the mechanisms linking stress signaling to impaired myocardial glucose oxidation remain incompletely defined. Sam68 (Src-associated in mitosis, 68 kDa; also known as KHDRBS1 [KH domain-containing, RNA-binding, signal transduction-associated protein 1]), a STAR (signal transduction and activation of RNA) family RNA-binding protein, has not previously been implicated in cardiac metabolic control.METHODS: SAM68 expression was examined in failing human hearts and transcriptomic data sets. Cardiomyocyte-specific Sam68 knockout mice (Sam68cKO) and AAV9 (adeno-associated virus serotype 9)-cTnT (cardiac troponin T)-mediated cardiomyocyte Sam68 overexpression (Sam68OE) were studied in transverse aortic constriction and angiotensin II models. Mechanistic studies included RNA sequencing, targeted metabolomics, in vivo [U-13C]-glucose tracing, coimmunoprecipitation, and protein-protein docking. Therapeutic relevance was tested with a PDK4 (pyruvate dehydrogenase kinase 4) inhibitor and the Sam68-Src interface blocker YB-0158, including pharmacokinetics, target engagement, and validation in Sam68cKO mice.RESULTS: Sam68 was increased in failing human cardiomyocytes and in murine hypertrophic hearts. Sam68cKO markedly attenuated angiotensin II- and transverse aortic constriction-induced hypertrophy, whereas Sam68OE aggravated remodeling and dysfunction. In vivo [U-13C]-glucose flux analysis showed that transverse aortic constriction caused sustained uncoupling of glycolysis from glucose oxidation, with increased glycolytic labeling but reduced 13C incorporation into tricarboxylic acid cycle intermediates at 3 days and 4 weeks. Sam68 deletion restored glucose-derived carbon entry into the tricarboxylic acid cycle, enhanced PDH (pyruvate dehydrogenase)-dependent M+2 labeling, and improved oxidative-anaplerotic balance during pressure overload. Mechanistically, Sam68 served as a stress-activated scaffold that promoted Src-dependent STAT3 (signal transducer and activator of transcription 3) Tyr705 phosphorylation, nuclear accumulation, and transcriptional induction of PDK4, leading to PDH Ser293 phosphorylation and suppression of PDH activity. The PDK4 inhibitor blunted Sam68OE-driven remodeling while preserving PDH activity and mitochondrial respiratory programs. YB-0158 achieved cardiac exposure, disrupted Sam68-Src engagement in vivo, suppressed STAT3-PDK4-PDH signaling, and improved transverse aortic constriction remodeling; these effects were lost in Sam68cKO mice, supporting on-target dependence. In failing human hearts, the Src-SAM68-STAT3-PDK4 axis was activated, and SAM68 abundance increased in parallel with PDK4 and reduced left ventricular ejection fraction.CONCLUSIONS: Sam68 is a stress-activated cardiomyocyte scaffold that drives pathologic hypertrophy through a Src-STAT3-PDK4 program that inhibits PDH and suppresses glucose oxidation. Genetic or pharmacologic disruption of this axis restores PDH-dependent pyruvate oxidation and limits pressure-overload remodeling, identifying Sam68 as a druggable metabolic control node in heart failure.

Background: This study aimed to develop and validate a machine learning model to predict postoperative complications in pediatric simple congenital heart disease (CHD) patients undergoing right vertical infra-axillary incision (RVIAI). Methods: A retrospective dataset of 638 patients who underwent treatment for ventricular septal defect and/or atrial septal defect via RVIAI at our hospital between August 2020 and August 2023 was collected. A total of 35 preoperative and intraoperative variables were used to construct 190 machine learning models. The optimal model was selected based on the highest mean C-index. Independent risk factors identified by the optimal model were ranked according to their importance. Kaplan-Meier analysis was used to compare the incidence of postoperative complications between different risk groups. Model performance was evaluated using the area under the receiver operating characteristic curve (ROC). Results: The optimal model, which combined Elastic Net (alpha = 0) and Gradient Boosting Machine, identified 18 baseline variables associated with postoperative complications. The top five predictors were defect size, globulin, activated partial thromboplastin time, red blood cell count, and blood urea nitrogen. Kaplan-Meier curves showed that postoperative complication rates were significantly higher in the high-risk group than in the low-risk group (p < 0.0001). The model demonstrated good discrimination, with area under the curve (AUC) values on postoperative days 5, 10, 15, and 20 remaining above 0.78 in both the training and test sets. Conclusions: This machine learning model provides a potential predictive tool for assessing postoperative risk in simple CHD patients undergoing RVIAI and may support more targeted perioperative management.

IntroductionDramatic alterations of the extracellular matrix (ECM), which can regulate cell behavior by binding to adhesion molecules and are intrinsically linked to immune regulation, occur in decidualization during early pregnancy. Decidual macrophages (dMφ) are a group of tissue-resident cells with an affinity for adhesion. An interactive dialogue occurs between decidual stromal cells (DSCs) and dMφ, however it remains unclear whether this process is associated with ECM-adhesion molecules. This study was conducted to investigate the cross-talk of DSC and CD16+ dMφ via extracellular matrix-adhesion molecule interaction in early pregnancy.MethodsSingle-cell sequencing data from endometrial and decidual tissues were analyzed to elucidate the interactions between DSCs and dMφ. We assessed the levels of ECM components in the decidua at the tissue or cellular levels, and examined the expression of adhesion molecules and polarization molecules in CD16+ or CD16- dMφ. Then we validated DSC-CD16+ Mφ interactions using the co-culture system. Finally, we evaluated the levels of ECM components in decidua and the expression of molecules in dMφ in patients with recurrent miscarriage (RM).ResultsDSCs communicated with dMφ via ECM-adhesion molecules. Collagen IV, osteopontin (OPN) and hyaluronic acid (HA) derived from DSCs promoted the development of CD16+ dMφ and their differentiation toward an immunomodulatory phenotype via their receptors, which is beneficial for maintaining immune tolerance. In patients with RM, decidua exhibits weakened ECM-CD16+ dMφ regulatory link, which may be associated with the underlying pathogenesis.DiscussionThis study confirms that DSC can regulate the immune status of CD16+ dMφ through the ECM-adhesion molecule axis, further elucidating the regulatory mechanisms of Mφ during decidualization. Exploration of therapeutic strategies based on ECM-receptor-mediated stroma-immune interactions holds promise as novel treatment approaches for miscarriage.

The echocardiography is the first-line imaging modality in detecting the cardiac lipoma. Contrast-enhanced echocardiography improves its structural definition and characteristics of blood supply to exclude thrombus and malignant tumors. We introduced a case that large cardiac mass involving nearly the whole left ventricular cavity and papillary muscles without any complications. Multimodal imaging has confirmed lipoma before surgery. However, rather than recommending conservative treatment in accordance with guidelines, surgical intervention was performed to prevent future hemodynamic abnormalities. Combined with multimodal imaging, we showed a rare case on comprehensive evaluation of left ventricular silent lipoma and provided new clues for surgical strategy, which were different from guideline recommendations.

Background This study compared the clinical outcomes of right vertical infra-axillary incision (RVIAI) and median sternotomy approaches for treating pediatric simple congenital heart diseases, focusing on postoperative complications and associated risk factors. Methods A retrospective analysis was conducted on pediatric patients with simple congenital heart diseases who underwent surgical repair via median sternotomy incision (group A) or RVIAI (group B). Result A total of 805 patients were included in the study. Patients in group B had significantly shorter cardiopulmonary bypass time, surgery time, and intensive care unit stay, as well as lower chest drainage volumes on the first postoperative day compared to those in group A. Multivariable logistic regression analysis revealed that the probability of postoperative complications was lower with the group B compared to group A (OR: 0.42, 95% CI: 0.29-0.62). Conclusion RVIAI has a lower incidence of postoperative complications, higher safety, and better efficacy.

Myocardial ischemia–reperfusion injury (IRI) is the major cause of primary graft dysfunction in heart transplantation, which is characterized by mitochondrial dysfunction. Hyperoside is a bioactive compound that has been reported to have pharmacological potential for cardiac and mitochondrial protection. Here, we investigated the protective effect of hyperoside during myocardial IRI and identified the underlying mechanisms. In this study, we established IRI in an in vivo murine heterotopic heart transplantation model and an in vitro hypoxia–reoxygenation cell model. Inflammatory responses, oxidative stress level, mitochondrial function, and cardiomyocyte apoptosis were evaluated. We found that hyperoside pretreatment alleviated through reducing MDA content, LDH activity, TUNEL positive cells, serum cTnI level, Bax protein expression and the level of inflammatory cytokines, and increasing SOD activity and Bcl-2 protein expression. Furthermore, hyperoside pretreatment improved Opa1-mediated mitochondrial fusion, upregulated mitochondrial ATP content and downregulated NADP+/NADPH and GSSG/GSH ratios. Opa1 inhibitor blunted the protective effects of hyperoside. Mechanistically, Co-immunoprecipitation experiments showed the binding property between Tom70 and Opa1, siRNA knockdown, AAV-mediated loss-of-function and gain-of-function approaches suggested that hyperoside-promoted Opa1-mediated mitochondrial fusion required the upregulation of Tom70. Collectively, we demonstrated for the first time that hyperoside administration alleviates myocardial IRI by promoting Opa1-mediated mitochondrial fusion in vivo and in vitro. The Tom70-Opa1 pathway was essential for cardioprotective effects of hyperoside treatment. The results in our study indicated that hyperoside or promotion of mitochondrial fusion might be a new potential option for the prevention and treatment of IRI in heart transplantation.