Cardiovascular Therapeutics最新文献

{"title":"Prasugrel Outperforms Ticagrelor in Acute Coronary Syndrome: A Real-World Analysis","authors":"Septi Melisa,&nbsp;Christianus Heru Setiawan,&nbsp;Chun-Yao Huang,&nbsp;Tian-Hsing Chen,&nbsp;Wei-Ting Chang,&nbsp;Wei-Pin Chang,&nbsp;Min-Huei Hsu,&nbsp;Christine Y. Lu,&nbsp;Jason C. Hsu","doi":"10.1155/cdr/2457933","DOIUrl":"https://doi.org/10.1155/cdr/2457933","url":null,"abstract":"<p>Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor is standard for patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI), yet real-world comparisons of ticagrelor and prasugrel remain limited. We evaluated their relative effectiveness and safety using the TriNetX Global Collaborative Network (2010–2024). Adult ACS patients receiving prasugrel or ticagrelor within 24 h post-PCI were included. The primary endpoint was a 1-year composite of all-cause mortality, myocardial infarction (MI), and cerebral infarction; secondary endpoints included individual components, major bleeding, and repeat revascularization. Propensity score matching balanced baseline characteristics, with subgroup and sensitivity analyses assessing robustness. Among 14,895 matched pairs (<i>n</i> = 29,790) from 126,273 patients, prasugrel was associated with lower risk of the composite endpoint (HR 0.641; 95% CI 0.613–0.671), all-cause mortality (HR 0.557; 95% CI 0.487–0.637), and MI (HR 0.648; 95% CI 0.616–0.680), without increased bleeding (HR 0.945; 95% CI 0.824–1.084). Repeat revascularization was higher with prasugrel (HR 1.791; 95% CI 1.639–1.957). Effects were consistent across subgroups. In this real-world setting, prasugrel demonstrated superior effectiveness over ticagrelor in reducing mortality and ischemic events without increasing the risk of bleeding, although higher rates of repeat revascularization warrant further study. These findings support prasugrel as a potentially preferred P2Y12 inhibitor in selected ACS patients undergoing PCI.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/2457933","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Logistic Regression Prediction Model for Post-PCI In-Hospital Major Adverse Cardiovascular Events in Patients With Acute ST-Segment Elevation Myocardial Infarction: Construction and Internal Validation","authors":"Jun Li,&nbsp;Geng Pan,&nbsp;Na Wang,&nbsp;Mei Wu","doi":"10.1155/cdr/3618662","DOIUrl":"https://doi.org/10.1155/cdr/3618662","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The incidence of in-hospital major adverse cardiovascular events (MACE) remains high in patients with acute ST-segment elevation myocardial infarction (STEMI) after emergency percutaneous coronary intervention (PCI). Existing risk prediction tools mostly focus on preoperative baseline indicators and ignore intraoperative interventional parameters, lacking comprehensive postprocedural risk assessment tools for STEMI patients after PCI. This study is aimed at developing and internally validating a logistic regression prediction model for post-PCI in-hospital MACE in STEMI patients based on multidimensional perioperative clinical indicators, so as to realize accurate postoperative risk stratification and guide individualized perioperative management.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;We retrospectively included 1195 STEMI patients who underwent emergency PCI at the Chest Pain Center of Lu′an People′s Hospital from January 2019 to October 2024. Patients were randomly divided into training (&lt;i&gt;n&lt;/i&gt; = 837) and validation (&lt;i&gt;n&lt;/i&gt; = 358) sets at a 7:3 ratio. The primary endpoint was in-hospital MACE (composite of cardiogenic shock, malignant arrhythmias, acute heart failure, reinfarction, or all-cause death). A prediction model was constructed using least absolute shrinkage and selection operator (LASSO) regression combined with multivariate logistic regression. Model discrimination was evaluated via the area under the receiver operating characteristic curve (AUC). Head-to-head discriminative comparison with the widely used GRACE and TIMI risk scores was performed using AUC values and the DeLong test to quantify the incremental predictive value of the novel model. Model calibration and clinical utility were assessed via calibration plots, the Hosmer–Lemeshow test, and decision curve analysis (DCA), with internal validation performed in the validation set.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;A total of 260 patients (21.8%) experienced in-hospital MACE. After LASSO regression screening and multivariate logistic regression analysis, eight independent predictors were identified: admission systolic blood pressure, Killip classification, intervention duration, contrast volume, postprocedural TIMI flow grade, culprit vessel occlusion, serum creatinine, and serum potassium. The training set AUC was 0.84 (95% CI: 0.80–0.87) with a sensitivity of 77.7% and specificity of 78.2%; the validation set AUC was 0.826 (95% CI: 0.782–0.870). Comparative discriminative analysis showed that the traditional GRACE and TIMI risk scores exhibited moderate predictive performance. The training set AUC of the GRACE score was 0.763 (","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/3618662","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149206096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a Risk Prediction Model for Arteriovenous Fistula Restenosis Following Percutaneous Transluminal Angioplasty in Maintenance Hemodialysis Patients Using SMOTE Algorithm","authors":"Jianping Yang,&nbsp;Yamei Zhu,&nbsp;Xiaoqing Zhu,&nbsp;Zhuangzhuang Guo,&nbsp;Mi Wang,&nbsp;Chensi Dong,&nbsp;Xueqiang Xu,&nbsp;Xianrong Xu","doi":"10.1155/cdr/5807867","DOIUrl":"10.1155/cdr/5807867","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Arteriovenous fistula (AVF) restenosis after percutaneous transluminal angioplasty (PTA) affects hemodialysis in maintenance hemodialysis (MHD) patients. Data imbalance limits predictive model accuracy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To identify risk factors and develop a SMOTE-based risk prediction model for AVF restenosis within 12 months after PTA.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This retrospective cohort study enrolled 241 consecutive MHD patients with AVF stenosis undergoing PTA between July 2022 and July 2025. Each patient contributed one index PTA. Patients were divided into restenosis (45 cases) and nonrestenosis (196 cases) groups according to whether AVF restenosis occurred within 12 months after PTA. Univariate and multivariate logistic regression identified risk factors. The SMOTE algorithm addressed data imbalance. Model performance was evaluated by ROC curves, calibration curves, and decision curve analysis (DCA).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Original-data multivariate analysis identified multisegmental stenosis, cannulation method, platelet count, and C-reactive protein (CRP) as independent risk factors. After SMOTE, intradialytic hypotension and serum albumin also became significant; however, these variables should be interpreted as exploratory because SMOTE does not create additional independent clinical information. The SMOTE-based model (P2) achieved AUC of 0.934 (training set) and 0.868 (validation set), outperforming the original model (P1).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The SMOTE-based model may help predict AVF restenosis within 12 months after PTA, but it is an exploratory internally validated tool and requires external validation before clinical use.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Esmolol Alleviates Sepsis-Associated Myocardial Injury by Acting on the APAF1 and JAK2/STAT3 Inflammatory Pathways","authors":"Lei Zhao,&nbsp;Hua Dong,&nbsp;Shimin Dong","doi":"10.1155/cdr/2843754","DOIUrl":"10.1155/cdr/2843754","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>The aim of this study is to explore the protective effect of esmolol against sepsis-associated myocardial injury (SAMI) and its underlying molecular mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>SAMI-related differentially expressed genes were identified from the Gene Expression Omnibus database (GSE267388). Potential targets of esmolol were predicted using PharmMapper. Overlapping genes were used for enrichment and molecular docking analyses. H9C2 cells were treated with LPS to establish an injury model, followed by esmolol treatment. Cell viability, apoptosis, oxidative stress, and mitochondrial function were also assessed. The expressions of apoptotic protease activating factor 1 (APAF1) and JAK2/STAT3 pathway molecules were detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting. A rat model of sepsis was used to verify cardiac function, inflammation, oxidative stress, and related protein expression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Six core targets were screened, and esmolol showed the strongest binding to APAF1. Esmolol increased cell viability; reduced apoptosis, ROS, and MDA; restored mitochondrial membrane potential; downregulated APAF1, Bax, cleaved-caspase-9/3; and suppressed JAK2/STAT3 phosphorylation. Esmolol reversed APAF1 overexpression-induced injury. In vivo, esmolol alleviated myocardial pathological injury, decreased the concentrations of myocardial markers and inflammatory factors, and inhibited the APAF1 and JAK2/STAT3 pathways.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Esmolol protects against SAMI by dual inhibition of the APAF1 mitochondrial apoptotic and JAK2/STAT3 inflammatory pathways, with APAF1 likely serving as a key downstream target of esmolol.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13656344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiopulmonary Fitness and Exercise-Based Cardiac Rehabilitation in Patients With Myocarditis","authors":"Si-Si Zhang,&nbsp;Lu-Ying Jiang,&nbsp;Hou-Juan Zuo,&nbsp;Wan-Jun Liu","doi":"10.1155/cdr/3611934","DOIUrl":"10.1155/cdr/3611934","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Cardiorespiratory fitness (CRF) is a powerful predictor of cardiovascular morbidity and mortality. The cardiopulmonary exercise test (CPET) is considered a gold standard in assessing CRF. Patients with myocarditis are recommended to abstain from exercise because of the risk of sudden cardiac death (SCD). Therefore, the clinical benefit of exercise-based cardiac rehabilitation (CR) has not been previously established in this population.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Objective&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The aim of this study is to assess the CRF of myocarditis and the safety and effectiveness of an exercise-based CR program in these populations.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Method&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;A total of 70 consecutive patients with a diagnosis of myocarditis admitted to Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology between October 2021 and December 2024 were enrolled in the current study. CPET was performed within 3–6 months of hospital discharge. The exercise-based CR program was performed for 3 months. The protocol included biomarker analysis, CPET, and standard-of-care echocardiography (including resting left ventricular ejection fraction and global longitudinal strain [GLS]). Data were collected at admission and 3 months after discharge.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;A total of 70 patients with myocarditis were enrolled. Among them, 47 patients completed the rehabilitation program and had complete follow-up assessments, including cardiopulmonary exercise testing, and were included in the final analysis. In comparison with NFM, patients with FM were more often female, and had higher levels of creatine kinase (CK), lactate dehydrogenase (LDH), urea nitrogen (UN), N-terminus probrain natriuretic peptide (NT-proBNP), fasting blood glucose (FBG), and white blood cell (WBC). For FM, echocardiography revealed more frequently signs of left ventricular (LV) dysfunction in the form of a reduced ejection fraction (&lt;i&gt;p&lt;/i&gt; &lt; 0.01), and lower GLS (&lt;i&gt;p&lt;/i&gt; &lt; 0.01) in contrast to NFM. CPET results showed that FM patients had markedly lower exercise capacity, impaired ventilatory efficiency, and pulmonary function (&lt;i&gt;p&lt;/i&gt; &lt; 0.05). After the 3-month exercise-based CR program, both groups demonstrated significant improvements in peak VO&lt;sub&gt;2&lt;/sub&gt;, peak workload, and MVV. However, no significant between-group differences were observed in the magnitude of improvement in CRF.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13656339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardioprotective Effect of Metformin Treatment in Mouse Model of Experimental Autoimmune Myocarditis","authors":"Magdalena Czepiec,&nbsp;Katarzyna Fryt,&nbsp;Agnieszka Jaźwa-Kusior,&nbsp;Andrea Laimbacher,&nbsp;Gabriela Kania,&nbsp;Maciej Siedlar,&nbsp;Małgorzata Tyszka-Czochara,&nbsp;Przemysław Błyszczuk","doi":"10.1155/cdr/6615227","DOIUrl":"10.1155/cdr/6615227","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Metformin is a well-established treatment for Type 2 diabetes. Beyond its role in glycemic control, metformin has gained attention for its pleiotropic effects, including cardioprotective properties. However, its role in autoimmune myocarditis and subsequent postinflammatory dilated cardiomyopathy remains poorly understood.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;To investigate the role of metformin in autoimmune-mediated cardiac disease, we employed the experimental autoimmune myocarditis mouse model. Six to eight weeks old Balb/c mice were immunized twice with an &lt;i&gt;α&lt;/i&gt;-myosin heavy chain peptide emulsified in complete Freund′s adjuvant to induce myocarditis and progression toward dilated cardiomyopathy. Metformin was administered in two approaches: a preventive (from Days 0 to 21 or 40) and a therapeutic (from Days 21 to 40). Cardiac function and disease progression were evaluated at two time points: Day 21 (inflammatory phase) and Day 40 (fibrotic phase), using echocardiography, histopathological assessment, and molecular analyses.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Treatment with metformin resulted in activation of the AMP-activated protein kinase-dependent signaling pathway during the inflammatory phase of myocarditis. This treatment was associated with activation of apoptosis-related pathways and a moderate reduction in inflammatory cell infiltration. Mice receiving metformin in the preventive approach exhibited preserved cardiac function. This was accompanied by decreased cardiomyocyte cross-sectional area and altered expression of hypertrophy-associated genes (&lt;i&gt;Acta1&lt;/i&gt; and &lt;i&gt;Myh6&lt;/i&gt;). In contrast, neither preventive nor therapeutic administration of metformin significantly reduced the extent of myocardial fibrosis.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Our findings suggest that metformin provides cardioprotective effects during the early inflammatory stages of autoimmune myocarditis and, to a lesser extent, during the later fibrotic remodeling phase.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Significance Statement&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Untreated acute myocarditis can lead to functional decline and postinflammatory dilated cardiomyopathy. Using an autoimmune myocarditis mouse model, we demonstrate that preventive metformin treatment reduces cardiac inflammation and preserves cardiac function. These findings suggest that metformin, in addition to its applications in diabetes, could be used to prevent infla","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Naringenin Attenuates Diabetic Cardiac Injury via SIRT1 Activation in Streptozotocin-Induced Rats","authors":"Baolan Wang,&nbsp;Dandan Zhang,&nbsp;Fudan Zhang,&nbsp;Xue Meng,&nbsp;Li Zhang,&nbsp;Zhenzuo Li,&nbsp;Amirabas Bostani","doi":"10.1155/cdr/9581618","DOIUrl":"10.1155/cdr/9581618","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Diabetic cardiomyopathy (DCM) lacks targeted therapies. This study investigated naringenin (NAR), a citrus flavonoid, in a streptozotocin (STZ)-induced diabetic rat model with cardiac complications, focusing on SIRT1-mediated mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Rats (<i>n</i> = 8/group) included control, NAR, DCM, DCM + NAR, and DCM + NAR + EX-527 (SIRT1 inhibitor). After 8 weeks, metabolic profiles, cardiac function, histopathology, oxidative stress (Nuclear Factor Erythroid–Related Factor 2 [Nrf2], MDA, SOD, and GSH), inflammation (nuclear factor kappa B [NF-<i>κ</i>B], TNF-<i>α</i>, and IL-6), apoptosis (Bax/Bcl-2 and Caspase-3), fibrosis (transforming growth factor beta [TGF-<i>β</i>] and Smad2), and SIRT1 signaling were analyzed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>NAR exhibited hypoglycemic effects, stimulated the release of insulin, and enhanced the lipid profile, thus maintaining the structural integrity of cardiomyocytes and preventing an increase in heart weight, while also restoring the histomorphology in DCM rats. Moreover, NAR influenced both systolic and diastolic blood pressure; reduced serum levels of CK-MB, BNP, and troponin T; downregulated the activity of TGF-<i>β</i>, Smad2, and Caspase-3; and decreased the Bax/Bcl-2 ratio. Crucially, NAR upregulated SIRT1 and modulated the levels of Nrf2, NF-<i>κ</i>B, Smad2, and Forkhead Box Protein O1 (FOXO1) in the cardiac tissues of the DCM group. These findings were associated with a significant reduction in oxidative stress and inflammation, alongside diminished NF-<i>κ</i>B activity, while promoting Nrf2 activity and Bcl-2. Importantly, the effects of NAR were counteracted by EX-527.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>NAR protects against DCM primarily through SIRT1 activation, integrating hypoglycemic, antioxidant, anti-inflammatory, antifibrotic, and antiapoptotic actions. SIRT1 represents a promising target for flavonoid-based DCM therapy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9581618","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of the C-Reactive Protein–Triglyceride–Glucose Index With All-Cause and Cardiovascular Mortality in U.S. Adults: Insights From NHANES 1999–2010","authors":"Xin Wang,&nbsp;Siyuan Ma,&nbsp;Xinrui Hai,&nbsp;Ali Ma,&nbsp;Peng Wu,&nbsp;Xiaolan Liang,&nbsp;Yu Hao,&nbsp;Libo Yang,&nbsp;Ning Yan","doi":"10.1155/cdr/4209201","DOIUrl":"10.1155/cdr/4209201","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;CTI combines C-reactive protein with the triglyceride–glucose index and may capture concurrent inflammatory and insulin–resistance-related metabolic disturbance. Emerging cohort evidence has linked higher CTI values to all-cause and CVD mortality, but the robustness, dose–response characteristics, and predictive relevance of these associations remain uncertain. This study evaluated the associations of CTI with all-cause and CVD mortality among U.S. adults.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Participants were selected from NHANES survey cycles conducted from 1999 through 2010, yielding an analytic sample of 10,528 adults aged 18 years or older. The CTI was computed using the formula: CTI = 0.412 × ln [CRP (mg/L)] + ln {[triglycerides (mg/dL) × fasting glucose (mg/dL)]/2}. We used weighted Cox proportional hazards models to investigate the relationships of CTI with all-cause and CVD mortality. Restricted cubic spline analyses were used to assess nonlinearity, followed by exploratory two-piecewise Cox regression to examine possible changes in slope. Beyond the primary analysis, the robustness and potential heterogeneity of these associations were further assessed using sensitivity, subgroup, and interaction analyses.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;During a survey-weighted mean follow-up of 164.29 ± 50.47 months, the primary survey-weighted analytic sample included 10,528 participants. In the primary DAG-informed Cox models, each 1-unit increase in CTI was associated with higher risks of all-cause mortality (HR = 1.24, 95% CI: 1.18–1.31, &lt;i&gt;p&lt;/i&gt; &lt; 0.001) and CVD mortality (csHR = 1.35, 95% CI: 1.20–1.53, &lt;i&gt;p&lt;/i&gt; &lt; 0.001). Compared with Q1, participants in Q4 had higher risks of all-cause mortality (HR = 1.54, 95% CI: 1.29–1.84, &lt;i&gt;p&lt;/i&gt; &lt; 0.001) and CVD mortality (csHR = 1.78, 95% CI: 1.27–2.49, &lt;i&gt;p&lt;/i&gt; &lt; 0.001). These associations remained significant after additional clinical adjustment. Exploratory two-piecewise analysis estimated an inflection point of 8.165 for all-cause mortality (conventional likelihood-ratio &lt;i&gt;p&lt;/i&gt; = 0.002); because the breakpoint was selected using a data-driven procedure, this comparison was interpreted cautiously. For CVD mortality, the estimated inflection point was 8.070 and the two-piecewise model did not clearly improve fit over the linear model (&lt;i&gt;p&lt;/i&gt; = 0.067). Time-dependent AUCs for CTI were approximately 0.60–0.62 at 5, 10, and 15 years, indicating modest discrimination.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;After adjustment for presp","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/4209201","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircIdh2 Attenuates Endothelial-to-Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential","authors":"Yanjia Chen,&nbsp;Xinai Meng,&nbsp;Tian Liu,&nbsp;Yuchen Zhang,&nbsp;Xingfu Huang","doi":"10.1155/cdr/2005876","DOIUrl":"10.1155/cdr/2005876","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Endothelial-to-mesenchymal transition (EndMT) contributes to myocardial fibrosis after cardiac injury. Circular RNAs (circRNAs) have been implicated in the regulation of EndMT, but whether circRNAs participate in this process through translational potential remains unclear. This study investigated the role of circIdh2 in EndMT and examined whether its coding capacity may contribute to its biological effects.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Rat endothelial progenitor cells (rEPCs) were treated with TGF-&lt;i&gt;β&lt;/i&gt;1 (5 ng/mL) for 7 days to induce EndMT. The expression of circSorbs1, circIdh2, and circSntb2 was measured by qRT-PCR. EndMT-related markers, including VE-cadherin, vimentin, and N-cadherin, were detected by western blotting. Cell migration was assessed using Transwell and scratch wound healing assays. The translational potential of circIdh2 was examined using an Idh2-IRES luciferase reporter assay, FLAG immunoprecipitation followed by western blotting, and mass spectrometry. A circIdh2 mutant construct and a rat model of acute myocardial infarction (AMI) were used to further evaluate the contribution of circIdh2 and its putative circIdh2-derived product.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;TGF-&lt;i&gt;β&lt;/i&gt;1 reduced the expression of circSorbs1, circIdh2, and circSntb2 in rEPCs. CircIdh2 showed the largest decrease in the initial qRT-PCR screen and was selected before any circIdh2-specific functional experiment. The Idh2 host gene supplied metabolic and redox context for the prespecified screen but was not used as evidence of circIdh2 function. CircIdh2 overexpression increased VE-cadherin expression, decreased vimentin and N-cadherin expression, and attenuated TGF-&lt;i&gt;β&lt;/i&gt;1–induced cell migration. In contrast, circIdh2 knockdown promoted EndMT-associated marker changes and cell migration. The Idh2-IRES reporter assay, FLAG immunoprecipitation, and mass spectrometry supported the translational potential of circIdh2 and detected a FLAG-tagged product derived from the circIdh2 expression construct. The FLAG-tagged circIdh2 expression construct modulated EndMT-related markers and reduced cell migration, whereas the coding-disrupted mutant construct did not reproduce the effects of wild-type circIdh2. In vivo, AAV-mediated delivery of circIdh2 or circIdh2-aa attenuated myocardial fibrosis and partly reversed EndMT-related marker changes after AMI.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusions&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;CircIdh2 attenuated EndMT-associated changes in rEPCs and was associated with reduced myocardial fibrosis ","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/2005876","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of Sodium–Glucose Cotransporter 2 Inhibitor Use With Outcomes in Patients Undergoing Transcatheter Aortic Valve Implantation: A Systematic Review and GRADE-Assessed Meta-Analysis","authors":"Ahmed Adel Mohamed,&nbsp;Batool Husain Husain,&nbsp;Tammam Khaled Dali,&nbsp;Mostafa Elsayed Ahmed,&nbsp;Ghaida Al Shawawreh,&nbsp;Ali Samir Galal,&nbsp;Mahmoud Abdelwahab Moussa,&nbsp;Abdallah M. Hibysh,&nbsp;Abdalrahman Salah Shehata,&nbsp;Youssef Ramadan,&nbsp;Osama M. Aldeeb,&nbsp;Tasneem Zanati Saeed,&nbsp;Mohammed Dibas","doi":"10.1155/cdr/8933859","DOIUrl":"10.1155/cdr/8933859","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Patients undergoing transcatheter aortic valve implantation (TAVI) remain at risk of adverse cardiovascular and renal outcomes despite procedural advancements. Sodium–glucose cotransporter 2 (SGLT2) inhibitors have demonstrated cardiovascular and renal benefits across various patient populations; however, their role in patients undergoing TAVI remains unclear. This study is aimed at evaluating the association between SGLT2 inhibitor use and clinical outcomes in this population.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We conducted a systematic review and meta-analysis comparing SGLT2 inhibitors versus non-SGLT2 inhibitors or standard care in patients undergoing TAVI. Major databases were searched through March 2026, with Embase updated through June 2026. Pooled analyses were performed using random-effects models to calculate risk ratios (RRs) and mean differences (MDs) with 95% confidence intervals (CIs).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Five studies involving 6111 patients (SGLT2 inhibitors: <i>n</i> = 2933; control: <i>n</i> = 3178) were included. In primary random-effects models, SGLT2 inhibitors were associated with lower all-cause mortality (RR 0.68, 95% CI 0.48–0.97, <i>p</i> = 0.03), heart failure (HF) hospitalization (RR 0.62, 95% CI 0.42–0.90, <i>p</i> = 0.01), and major adverse cardiovascular events (RR 0.68, 95% CI 0.48–0.96, <i>p</i> = 0.03). However, in REML/Hartung–Knapp sensitivity analyses, CIs crossed the null for all-cause mortality, HF hospitalization, MACE, and pooled hazard ratios. Mortality benefits were absent at 6 and 12 months and in the randomized trial but persisted in low left ventricular ejection fraction (RR 0.56, 95% CI 0.35–0.89, <i>p</i> = 0.01). No significant differences occurred in acute kidney injury, urinary tract infections, or echocardiographic parameters.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>SGLT2 inhibitor use was associated with lower all-cause mortality and HF hospitalization after TAVI, but the evidence is limited by observational designs, heterogeneity, and low certainty for several outcomes. Further randomized trials are required.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149104618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}