Frontiers in Cardiovascular Medicine最新文献

Paravalvular leak (PVL) following Bentall surgery in patients with Marfan syndrome is exceedingly rare. A 38-year-old Marfan patient underwent Bentall + Sun's procedure for Stanford type A aortic dissection with severe aortic regurgitation. On the third month after surgery, the patient was readmitted due to exertional dyspnea. Echocardiography revealed a paravalvular leak with significant left-to-right shunting, leading to symptoms including exertional dyspnea, hepatomegaly, and heart failure. After adequate preparation, the leak was successfully closed using a symmetric VSD occluder. Post-procedural imaging showed near-complete resolution of the leak, significant reduction in the pseudoaneurysm size, and improvement in heart failure symptoms. The patient was discharged in stable condition.

Background: Foreign-body-related aortoesophageal fistula (AEF) is rare and fatal without rapid hemostasis and infection control.

Case: A 74-year-old woman presented with hematemesis and shock after suspected fish-bone ingestion. Emergency TEVAR with a 32 mm covered stent-graft (proximal landing in the distal third of the left subclavian artery) controlled bleeding. Endoscopic clip-and-line closure of an approximately 15 mm esophageal defect was performed. Despite broad-spectrum antimicrobial therapy, the patient developed recurrent fever and later rebleeding associated with mediastinal sepsis.

Conclusion: TEVAR and endoscopic repair require an integrated, early source-control strategy. A stepwise algorithm prioritizing timely mediastinal drainage is essential to prevent graft contamination, infectious relapse, and rebleeding.

Objective: This study evaluates the impact of early oral anticoagulant (OAC) initiation at hospital discharge on functional and safety outcomes in atrial fibrillation (AF)-related acute ischemic stroke (AIS) patients undergoing endovascular therapy (EVT).

Methods: AF patients undergoing EVT of symptom onset in AIS were included in this study. Patients were grouped by postoperative anticoagulation status. The patients were regularly followed up 90 days and 1 year after discharge. The primary outcome measure for assessing prognosis is the modified Rankin Scale (mRS) score. The secondary evaluation indicators were the occurrence of recurrent ischemic stroke/systemic embolism (IS/SE) outcomes, safety outcomes, and all-cause mortality outcomes within 1 year. The differences in prognostic indicators between the two groups were compared by combining PSM.

Results: Among the 296 eligible patients, 113 (38.18%) received anticoagulation at discharge, while 183 (61.82%) did not. Before PSM, the anticoagulation cohort exhibited markedly elevated rates of favorable functional outcomes at 90 days post-discharge (mRS 0-2: 60.18% vs. 25.14%, P < 0.001) and at 1 year (mRS 0-2: 64.60% vs. 30.05%, P < 0.001), along with a lower all-cause mortality rate within 1 year (16.81% vs. 44.26%, P < 0.001). After PSM, the results demonstrated that the anticoagulation group had elevated rates of favorable functional outcomes at 90 days (55.81% vs. 27.91%, P < 0.001) and at 1 year (60.47% vs. 30.23%, P < 0.001). The anticoagulation group had a lower all-cause mortality rate at both 90-day (11.63% vs. 40.70%, P < 0.001) and 1-year follow-up (17.44% vs. 50%, P < 0.001). Statistical analysis revealed no significant intergroup differences in terms of IS/SE recurrence rates, safety outcomes. Multivariate logistic regression modeling identified OAC therapy upon discharge as an independent predictor of improved 90-days (OR = 4.478, 95% CI: 1.122-17.874, P = 0.034) and 1 year (OR = 4.168, 95% CI: 1.118-5.542, P = 0.033) functional recovery among patients.

Conclusion: In patients with AF complicated by stroke who underwent EVT and were at no high risk for severe bleeding, OAC therapy is associated with improved functional and mortality outcomes compared with those not receiving OAC. The benefit remained statistically significant following PSM to adjust for intergroup disparities.

Objective: This study aimed to investigate the association between serum fibroblast growth factor 23 (FGF23) and soluble α-Klotho levels with left ventricular hypertrophy (LVH) in hypertensive patients undergoing peritoneal dialysis (PD). We also sought to evaluate their potential as biomarkers of left ventricular remodelling and to analyze potential non-linear relationships with the left ventricular mass index (LVMI), including subgroup differences.

Methods: In this cross-sectional study, 124 hypertensive PD patients were enrolled. Serum concentrations of FGF23 and soluble α-Klotho were measured via enzyme-linked immunosorbent assay (ELISA). Echocardiography was used to assess left ventricular structure and define LVH. Multivariate logistic regression analysis was performed to evaluate the independent associations of these biomarkers with LVH. A restricted cubic spline (RCS) model was employed to explore non-linear relationships with LVMI.

Results: The prevalence of LVH was 62.9%. After adjusting for gender, systolic blood pressure C-reactive, protein, haemoglobin, serum calcium, ejection fraction, serum phosphorus, and parathyroid hormone, multivariate analysis identified soluble α-Klotho as an independent protective factor against LVH (OR = 0.415, 95% CI: 0.247-0.643, P < 0.001), whereas FGF23 was an independent risk factor (OR = 1.260, 95% CI: 1.079-1.501, P = 0.005). RCS analysis revealed a significant non-linear relationship between FGF23 and LVMI (P < 0.001), with an inflection point at approximately 39.8 pg/mL. This association was more pronounced in patients aged >61 years and in males. The overall association between soluble α-Klotho and LVMI was not statistically significant.

Conclusion: Among hypertensive PD patients, serum soluble α-Klotho is an independent protective biomarker for LVH, while elevated FGF23 levels are associated with an increased risk of LVH, suggesting an interaction between the two. FGF23 demonstrates a non-linear association with LVMI, which is modified by age and gender. Concurrent measurement of FGF23 and soluble α-Klotho may help identify patients at high risk for cardiovascular remodelling, thereby informing risk stratification and personalized management strategies.

Objective: Dilated cardiomyopathy (DCM) is a major cause of heart failure (HF). In this study, we aimed to explore potential autophagy-related biomarkers associated with DCM with HF.

Methods: The GSE17800 dataset was downloaded from GEO, and differentially expressed genes (DEGs) were identified. Autophagy-related DEGs (AR-DEGs) were obtained by merging DEGs with autophagy-related genes (ARGs) from HADb and HAMdb databases. Gene function enrichment analysis was performed using GO and KEGG. Hub genes were identified via protein-protein interaction (PPI) network analysis, with their expression and diagnostic values validated using the GSE21610 dataset. A doxorubicin (DOX)-induced cardiomyocyte injury model was established to evaluate hub gene expression in vitro and in vivo studies. Potential therapeutic small molecules targeting hub genes were screened via L1000FWD, and their binding affinity to targets was assessed by molecular docking.

Results: In the GSE17800 dataset, a total of 45 AR-DEGs were identified by intersecting with ARGs from HADb and HAMdb. Through PPI network analysis, 7 hub genes were extracted: CDKN1A, CTSD, DDIT3, EP300, FN1, PKM, and SOD2. Further validation using the GSE21610 dataset showed that receiver operating characteristic (ROC) curve analysis confirmed CTSD and SOD2 had high diagnostic value for DCM with HF. Moreover, in both in vitro and in vivo DOX-induced cardiomyocyte injury models, DOX treatment resulted in upregulated CTSD expression and downregulated SOD2 expression. Additionally, small molecules targeting CTSD and SOD2 (e.g., QL-XII-47 and tipifarnib-P2) were identified as potential therapeutic candidates for DCM with HF.

Conclusion: This study provides novel evidence that CTSD and SOD2 potently contribute to autophagy regulation in DCM with HF. These findings highlight their diagnostic potential for DCM with HF and lay a foundation for exploring targeted small-molecule therapies (e.g., QL-XII-47, tipifarnib-P2) to improve the disease's clinical management.

Background: Apoptosis and inflammation are the key pathological mechanisms of heart failure after myocardial infarction (MI-HF). Wenxin Granules (WXG), an effective compound that has been used clinically for more than 20 years, could improve cardiac function, lipids and blood rheology in patients with MI and delay the occurrence of HF. However, the exact mechanism is still unclear.

Methods: MI-HF mice model were established by permanent ligation of the left anterior descending, and the protective effects of WXG on cardiac function and fibrosis were evaluated by Elisa, echocardiography, Masson staining and HE staining. The core components of WXG and its targets and mechanisms of action in MI-HF were clarified by UPLC-MS/MS, network pharmacology and bioinformatics. The association of potential genes with HF was further clarified genetically using Mendelian Randomization Analysis (MR). Molecular docking was utilized to clarify the docking energies between the core components of WXG and the key pathogenic targets of MI-HF. Immunofluorescence, Tunel staining, Elisa, Quantitative real-time polymerase chain reaction (RT-qPCR) and Western blot (WB) were used to evaluate cardiomyocyte apoptosis and inflammatory response, and to validate key proteins on the MAPK pathway and its downstream effect proteins.

Results: The animal experiments showed that WXG significantly improved cardiac function, inhibited myocardial fibrosis, inhibited cardiomyocyte apoptosis and reduced the expression of inflammatory factors in MI-HF mice. Network pharmacology and bioinformatics analyses revealed that WXG may exert its cardioprotective effects through the MAPK signaling pathway. MR further confirmed the high correlation between the apoptotic protein MAPK3 and HF. Molecular docking results showed that Astragaloside IV, Paeoniflorin, Liquiritin, Albiflorin, Ononin, and Pratensein 7-O-beta-D-glucopyranoside, the core components of WXG, were well docked to key pathogenic targets of MI-HF. WB, RT-qPCR and Elisa results showed that pro-apoptotic proteins and pro-inflammatory factors were significantly elevated in the Model group, which was inhibited by WXG.

Conclusion: WXG may reduce inflammatory response and enhance cardioprotection and anti-fibrosis by inhibiting the expression of MAPK signaling pathway and its downstream effect proteins. The cardioprotective effects of WXG may be attributed to its core components, including Astragaloside IV, Paeoniflorin, Liquiritin, Albiflorin, Pratensein 7-O-beta-D-glucopyranoside and Ononin.

Objective: Systematic review and meta-analysis of the incidence and risk factors for 30-day unplanned readmissions in patients with chronic heart failure(CHF).

Methods: We searched PubMed, Embase, Web of Science, Scopus, Medline, CINAHL, and Chinese databases up to February 2025. Data were analyzed by using Stata 17.0.

Results: Among 4,040 screened publications, 21 studies were included. The incidence of 30-day unplanned readmission in CHF patients was 17.7% (95% CI: 13.9%-21.5%). Age ≥65 years (OR = 1.35, P = 0.024), diagnosed with chronic kidney disease (CKD) (OR = 1.26, P = 0.000), diabetes (OR = 1.49, P = 0.001), atrial fibrillation (AF) (OR = 1.12, P = 0.005), coronary heart disease (CHD) (OR = 5.28, P = 0.000), cardiomyopathy (OR = 1.44, P = 0.000), NYHA class ≥Ⅲ or Ⅳ (OR = 1.64, P = 0.000), use of beta blockers (OR = 1.25, P = 0.000), loop diuretics (OR = 1.41, P = 0.004), thiazides (OR = 1.22, P = 0.000), LVEF < 40% (OR = 1.44, P = 0.000), and length of stay (LOS) (OR = 1.16, P = 0.000) were risk factors for 30-day unplanned readmission in CHF patients.

Conclusions: The incidence of 30-day unplanned readmissions in patients with CHF is moderate but concerning. Accurate identification of identified risk factors for targeted interventions to reduce the need for readmissions.

Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/view/CRD42024610843, PROSPERO CRD42024610843.

Background: Antiphospholipid antibodies (aPL) and systemic rheumatic-immune inflammation (RII) may be associated with angiographic in-stent restenosis (ISR) after drug-eluting stent (DES) implantation. We prospectively evaluated these associations in a large Chinese cohort of DES recipients.

Methods: In this prospective cohort, we enrolled 2,503 consecutive adults who received at least one new-generation DES between May 2022 and January 2024. Preprocedural blood samples were assessed for antiphospholipid antibodies (anticardiolipin IgG/IgM, anti-β2-glycoprotein I IgG/IgM, and lupus anticoagulant) and inflammatory biomarkers [RII; high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), erythrocyte sedimentation rate (ESR), complement C3/C4, rheumatoid factor, and anti-cyclic citrullinated peptide (anti-CCP) antibodies]. At 12 months, invasive coronary angiography or coronary CT angiography (CCTA) was used to assess ISR. All ISR analyses were restricted to participants who completed 12-month imaging (the imaging-complete cohort). Multivariable logistic regression adjusted for prespecified clinical/lesion/stent covariates and imaging modality. Model performance was compared for a Clinical model vs. an immune-enhanced model (clinical  +  aPL  +  IL-6) with internal bootstrap validation. ICA-only analyses were prespecified. Clinically driven target-lesion revascularization (TLR) was evaluated with Cox models in all enrolled patients.

Results: Of the 2,503 enrolled participants, 2,388 completed 12-month imaging, with ISR occurring in 193 participants (8.1%; 95% CI 6.9-9.1). In adjusted analyses, any aPL positivity (OR 1.92, 95% CI 1.34-2.74) and IL-6 (per doubling) (OR 1.25, 95% CI 1.10-1.42) were independently associated with ISR. Adding aPL and IL-6 improved discrimination (AUC 0.79 vs. 0.72, Δ  =  0.07, p  =  0.008), calibration, and reclassification (categorical NRI 0.18, integrated discrimination improvement (IDI) 0.04). Optimism-corrected AUC was 0.78. The findings were consistent in the ICA-only cohort (aPL OR 1.95; IL-6 OR 1.27). Over 12 months, TLR occurred in 100/2,503 (4.0%). aPL positivity (HR 2.08, 95% CI 1.36-3.18) and IL-6 (per doubling; HR 1.29, 95% CI 1.11-1.50) were associated with higher TLR risk.

Conclusion: Baseline aPL seropositivity and higher IL-6 were associated with 12-month ISR and clinically driven TLR. Incorporating these immune markers improves risk discrimination beyond clinical and angiographic factors. External validation and interventional studies are warranted.

Artificial intelligence (AI) is revolutionizing cardiovascular imaging, with aortic computed tomography angiography (CTA) emerging as a prominent area of application. CTA imaging is essential for the diagnosis, risk stratification, and treatment planning of aortic diseases. However, conventional CTA techniques face limitations such as radiation exposure, contrast agent risks, and reliance on manual interpretation. The integration of AI into aortic CTA offers innovative solutions across multiple domains. AI can enhance image quality, automate anatomical segmentation, improve diagnostic accuracy for aortic emergencies, and provide quantitative tools for prognostic evaluation following interventions like endovascular aortic repair. Furthermore, this review provides the analysis of emerging techniques, including advanced image synthesis methods, Vision Transformer architectures, multi-task learning, weakly supervised learning, and the paradigm shift introduced by Foundation Models, emphasizing their potential for clinical application. This work comprehensively summarizes the current applications and nascent technological paradigms of AI in aortic CTA, along with existing challenges and future research directions.

Background: Hypertension prevalence is high in Saudi Arabia. Both lifestyle behaviors and biological intermediates influence blood pressure (BP); however, there is limited evidence from the Middle East on whether composite lifestyle scores that integrate both domains would capture BP variation better than behavioral metrics alone. This study aimed to examine associations of an overall lifestyle risk score (behavioral + biological) and a behavioral-only score with BP outcomes.

Methods: In a cross-sectional study of Saudi adults (n = 1,041), we constructed (i) an overall lifestyle score (BioBeh score), including waist circumference, total cholesterol, fasting glucose, smoking, sleep, physical activity, perceived stress, and diet quality, and (ii) a behavioral-only score (Beh score), including smoking, sleep, physical activity, perceived stress, and diet. We examined the association with BP [systolic/diastolic BP (SBP/DBP)], elevated BP, and hypertension using multivariable linear and logistic regression, adjusted for various confounders.

Results: Each 1-point higher BioBeh score was associated with lower SBP (-1.68 mmHg; 95% CI: -2.58, -0.79), lower DBP (-1.67 mmHg; 95% CI: -2.66, -0.68), and reduced odds of hypertension (OR 0.73; 95% CI: 0.63, 0.85), but not with elevated BP. No associations were found with the Beh score. Waist circumference was the strongest individual component [SBP -3.80 (-4.70, -2.91); DBP -3.31 (-4.30, -2.32) mmHg; hypertension OR 0.57; 95% CI: 0.49, 0.66].

Conclusions: In Saudi adults, a biologically enriched lifestyle score captures BP variation and hypertension risk more robustly than behavior-only metrics. These findings support risk stratification and prevention strategies that emphasize central adiposity alongside basic lipid and glucose profiles.