Cardiovascular Drugs and Therapy最新文献

{"title":"Low-Dose Rivaroxaban vs. Aspirin in Addition to Clopidogrel After Percutaneous Coronary Intervention in Coronary Atherosclerotic Heart Disease Patients with Gastrointestinal Disease.","authors":"Yue Li, Tienan Zhou, Yan Liu, Junxian Qi, Lei Zhang, Ruoxi Gu, Dongyuan Sun, Xiaozeng Wang","doi":"10.1007/s10557-025-07682-5","DOIUrl":"https://doi.org/10.1007/s10557-025-07682-5","url":null,"abstract":"<p><strong>Purpose: </strong>Dual antiplatelet therapy (DAPT) is the cornerstone for patients with coronary atherosclerotic heart disease (CHD) undergoing percutaneous coronary intervention (PCI) while increasing the risk of bleeding, particularly when combined with gastrointestinal disease (GID). Rivaroxaban 10 mg once daily is widely used in Asia. This study compared the effects of low-dose rivaroxaban (10 mg daily) plus clopidogrel vs. DAPT in CHD patients with GID undergoing PCI.</p><p><strong>Methods: </strong>In this prospective, single-center, randomized controlled trial, eligible CHD patients with GID undergoing PCI were randomized (1:1) to either the dual pathway inhibition (DPI) group (rivaroxaban 10 mg plus clopidogrel 75 mg daily) or the DAPT group (aspirin 100 mg plus clopidogrel 75 mg daily). The primary outcome was Bleeding Academic Research Consortium (BARC) type 2-5 bleeding. The secondary outcome was major adverse cardiovascular or cerebrovascular events (MACCE), which included cardiac death, nonfatal myocardial infarction, ischemia-driven target vessel revascularization, all-cause death, stent thrombosis, and stroke during the 6-month follow-up.</p><p><strong>Results: </strong>A total of 1042 patients were enrolled and analyzed (DPI, 522; DAPT, 520). Low-dose rivaroxaban (10 mg daily) plus clopidogrel was non-inferior to DAPT in BARC type 2-5 bleeding [8 (1.5%) vs. 6 (1.2%), absolute risk difference 0.38%, 95% confidence interval (CI) (- 1.02-1.78), p < 0.0001 for non-inferiority]. Abdominal pain was significantly lower in the DPI group (p = 0.009). Other abdominal discomforts, gastrointestinal bleeding, or MACCE were similar.</p><p><strong>Conclusions: </strong>In CHD patients with GID undergoing PCI, low-dose rivaroxaban (10 mg daily) plus clopidogrel was non-inferior to DAPT.</p><p><strong>Trial registration: </strong>Chinese Clinical Trial Registry ChiCTR2100044319. Registered on March 16, 2021.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143673249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Verapamil on Blood Glucose in Type 1 and Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis.","authors":"Shiqi Tu, Ruiqi Zhang, Qiyue Zheng, Jiaojiao Wang, Yun Chen, Xiaosi Li, Jieyu He, Zhaokai Zhou, Qiong Lu","doi":"10.1007/s10557-025-07683-4","DOIUrl":"https://doi.org/10.1007/s10557-025-07683-4","url":null,"abstract":"<p><strong>Purpose: </strong>Verapamil, an L-type calcium channel blocker treating hypertension, arrhythmia, and other cardiovascular diseases, has emerged as a potential drug for lowering blood glucose by regulating cellular calcium homeostasis and affecting expression of apoptosis-related proteins in pancreatic β-cells. However, this promising effect must be weighed against potential risks, including cardiovascular adverse effects of this drug.</p><p><strong>Methods: </strong>We conducted a systematic review and meta-analysis and included randomized controlled trials (RCTs) assessing verapamil in individuals with type 1 or type 2 diabetes. The primary outcomes were glycated hemoglobin (HbA1c) and serum glucose concentration. The secondary outcomes were area under the curve (AUC) values for C-peptide level, body weight, changes in HbA1c and blood glucose concentration pre- and post-intervention, and adverse drug reactions.</p><p><strong>Results: </strong>A total of eight RCTs involving 1100 patients were included in the analysis. Meta-analysis showed that verapamil effectively lowered blood glucose levels (weighted mean difference [WMD] -6.38, 95% CI -12.52, -0.25 mg/dL, P = 0.04; 6 trials), decreased HbA1c (WMD -0.45, 95% CI -0.66, -0.23%, P < 0.001; 7 trials), and increased C-peptide AUC (WMD 0.27, 95% CI 0.21, 0.32 pmol/mL, P < 0.0001; 2 trials) in patients with both type 1 and type 2 diabetes, without significant trial-related adverse events (OR 1.33, 95% CI 0.85, 2.09, P = 0.21).</p><p><strong>Conclusion: </strong>The adjunctive use of verapamil to standard hypoglycemic therapy is a safe and effective means of improving glycemic control in diabetic patients. However, the limited scale of RCTs and heterogeneity of basic glucose-lowering regimens across studies might constrain generalizability of these findings. Future high-quality research is warranted to further elucidate the role of verapamil in diabetes management.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial to \"A Plant-Powered Remedy: Hyperoside's Potential Against Trastuzumab-Induced Cardiotoxicity\" by Bullock et al.","authors":"Zaniqua N Bullock, Xander H T Wehrens, Damian W Young","doi":"10.1007/s10557-025-07684-3","DOIUrl":"https://doi.org/10.1007/s10557-025-07684-3","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143662567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GLP-1 Receptor Agonists and Cardiac Health: Insights from a Systematic Review.","authors":"Mauricio Reis Pedrosa, Arnaldo Alves da Silva, Virginia Fernandes Moça Trevisani","doi":"10.1007/s10557-025-07680-7","DOIUrl":"https://doi.org/10.1007/s10557-025-07680-7","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-TEVAR Type A Aortic Dissection: Insights and Future Directions.","authors":"Jessica K Wang, Xander H T Wehrens, K Jane Grande-Allen","doi":"10.1007/s10557-025-07681-6","DOIUrl":"10.1007/s10557-025-07681-6","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143582187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.","authors":"Yanna Sun, Lili Xiao, Linlin Chen, Xiaofang Wang","doi":"10.1007/s10557-025-07673-6","DOIUrl":"https://doi.org/10.1007/s10557-025-07673-6","url":null,"abstract":"<p><strong>Background: </strong>The therapeutic prowess of doxorubicin in oncology is marred by its cardiotoxic consequences, manifesting as cardiac remodeling. Pathophysiological alterations triggered by doxorubicin include inflammatory cascades, fibrotic tissue deposition, vascular and valvular changes, and finally cardiomyopathy. These multifarious consequences collectively orchestrate the deterioration of cardiac architecture and function.</p><p><strong>Method: </strong>By charting the molecular underpinnings and remedial prospects, this review aspires to contribute a novel perspective using latest publications to the ongoing quest for cardioprotection in cancer therapy.</p><p><strong>Results and discussion: </strong>Experimental analyses demonstrate the pivotal roles of oxidative stress and subsequent necrosis and apoptosis of cardiomyocytes, muscle cells, endothelial cells, and small muscle cells in different parts of the heart. In addition, severe and unusual infiltration of macrophages, mast cells, and neutrophils can amplify oxidative damage and subsequent impacts such as chronic inflammatory responses, vascular and valvular remodeling, and fibrosis. These modifications can render cardiomyopathy, ischemia, heart attack, and other disorders. In an endeavor to counteract these ramifications, a spectrum of emerging adjuvants and strategies are poised to fortify the heart against doxorubicin's deleterious effects.</p><p><strong>Conclusion: </strong>The compendium of mitigation tactics such as innovative pharmacological agents hold the potential to attenuate the cardiotoxic burden.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143499249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biochanin A Mitigates Pressure Overload-Induced Cardiac Hypertrophy Through Modulation of the NF-κB/Cbl-b/NLRP3 Signaling Axis.","authors":"Lina Ba, Nan Wu, Xiang Feng, Ruixuan Wang, Zhichao Zhao, Rui Wang, Renling Liu, Pilong Shi, Hongli Sun, Hanping Qi","doi":"10.1007/s10557-025-07677-2","DOIUrl":"https://doi.org/10.1007/s10557-025-07677-2","url":null,"abstract":"<p><strong>Purpose: </strong>The purpose of this study was to investigate the protective effects of biochanin A (BCA) on cardiac hypertrophy and to elucidate the underlying molecular mechanisms. The research question was whether BCA can reverse heart dysfunction and attenuate cardiomyocyte hypertrophy induced by pressure overload and AngII, respectively, and how it interacts with the NLRP3 pyroptosis pathway to achieve these effects.</p><p><strong>Methods: </strong>We employed an animal model of pressure overload-induced cardiac hypertrophy and an in vitro model of AngII-induced cardiomyocyte hypertrophy to assess the effects of BCA. The expression of NLRP3 and its related signaling molecules was analyzed by western blotting, and the activity of the NLRP3 pathway was measured using pyroptosis assays. The role of Cbl-b, an E3 ubiquitin ligase, in BCA-mediated NLRP3 inhibition was also investigated.</p><p><strong>Results: </strong>BCA was found to reverse heart dysfunction and attenuate cardiomyocyte hypertrophy induced by pressure overload and AngII. Mechanistically, BCA mitigated cardiac hypertrophy by targeting the NLRP3 pyroptosis pathway. The reduction in NLRP3 expression by BCA was predominantly mediated through the upregulation of Cbl-b, which enhanced the ubiquitination and subsequent degradation of NLRP3. Additionally, BCA facilitated the upregulation of Cbl-b expression by interacting with NF-κB, preventing NF-κB binding to the promoter region of Cbl-b and reversing its suppressive action on Cbl-b expression.</p><p><strong>Conclusion: </strong>This study provides initial evidence that BCA can protect against cardiac hypertrophy. Its mechanism of action involves interacting with NF-κB to promote the expression of Cbl-b, which facilitates the ubiquitination and degradation of NLRP3, ultimately inhibiting pyroptosis. This finding suggests that BCA may be a potential therapeutic agent for the treatment of cardiac hypertrophy.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143456935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating the Methodological Rigor and Recommendation Excellence of TAVR Guidelines: Insights from AGREE II and AGREE-REX Instruments.","authors":"Jianguo Xu, Qingyong Zheng, Yating Cui, Junfei Wang, Yafei Xie, Lin Li, Ya Gao, Ming Liu, Yu Qin, Jiaxuan Sun, Kang Yi, Jinhui Tian","doi":"10.1007/s10557-025-07679-0","DOIUrl":"https://doi.org/10.1007/s10557-025-07679-0","url":null,"abstract":"<p><strong>Purpose: </strong>Transcatheter aortic valve replacement (TAVR) has emerged as a critical innovation for managing severe aortic stenosis, prompting the development of numerous clinical practice guidelines worldwide. This study systematically evaluates the guideline development methodologies of major international TAVR guidelines using the AGREE II and AGREE-REX instruments, aiming to enhance understanding of current development processes.</p><p><strong>Methods: </strong>A comprehensive search was conducted in PubMed, Embase, Web of Science, and specialized guideline repositories. Twenty-four TAVR-specific guidelines were independently evaluated by four reviewers using the AGREE II and AGREE-REX instruments. The guidelines were categorized as evidence- or consensus-based, and statistical analysis was performed using SPSS to standardize scores and assess inter-rater reliability.</p><p><strong>Results: </strong>Systematic assessment revealed significant methodological variations across guidelines. The AGREE II evaluation showed the highest performance in scope and purpose (83.9 ± 10.0%) but lower scores in rigor of development (43.5 ± 29.0%) and applicability (42.4 ± 26.8%). The AGREE-REX analysis demonstrated stronger performance in implementability (78.6 ± 14.5%) while identifying gaps in the integration of values and preferences (35.7 ± 17.2%). Evidence-based guidelines consistently outperformed consensus-based ones across multiple domains, particularly in terms of methodological rigor and implementation planning.</p><p><strong>Discussion: </strong>This evaluation highlights key areas for improving guideline development methodology, including standardized evidence evaluation processes, systematic stakeholder engagement, and structured implementation planning. The considerable variability in methodological quality underscores the need for more standardized approaches.</p><p><strong>Conclusion: </strong>Current TAVR guidelines exhibit significant heterogeneity in methodological quality, with evidence-based guidelines demonstrating superior performance in development rigor and implementation planning. Systematic approaches to evidence synthesis and stakeholder engagement are crucial for high-quality guideline development.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulated TRIM35 Alleviates Doxorubicin-Induced Cardiotoxicity by Suppressing Oxidative Stress and Inflammation via Inhibiting TLR4/NF-κB Pathway.","authors":"Yewen Hu, Shiqi Wang, Chaoxia Zhang, Fuwei He, Yongxing Jiang, Ruoyu Chen, Jia Su, Caijie Shen, Xiaomin Chen, Huimin Chu","doi":"10.1007/s10557-025-07672-7","DOIUrl":"https://doi.org/10.1007/s10557-025-07672-7","url":null,"abstract":"<p><strong>Purpose: </strong>The use of doxorubicin (DOX), a potent chemotherapy drug, is limited by its detrimental effects on the heart. This cardiotoxicity is primarily driven by oxidative stress and inflammation. TRIM35 plays a key role in inflammatory responses; however, its exact function in DOX-induced cardiotoxicity (DIC) remains to be fully understood. This study investigates the effects of TRIM35 on DIC and explores the underlying biological mechanisms.</p><p><strong>Methods: </strong>To assess the role of TRIM35, we reduced the expression of TRIM35 in the heart tissues of mice using an adeno-associated virus 9 (AAV9) system, delivered through tail vein injection. We then administered weekly doses of DOX (4 mg/kg) to C57BL/6 mice for 4 weeks to induce DIC. Echocardiography, histopathological assessments, and molecular techniques were employed to examine the effects and mechanisms of TRIM35 on DIC.</p><p><strong>Results: </strong>Our research found that DOX treatment increases TRIM35 levels in the heart. By lowering TRIM35 expression, we observed an improvement in cardiac function and a decrease in myocardial damage in DOX-treated mice. Additionally, reduced TRIM35 expression lessened myocardial hypertrophy and fibrosis. It also mitigated the oxidative stress and inflammation caused by DOX. Furthermore, the down-regulation of TRIM35 expression resulted in the downregulation of TLR4 and phosphorylated P65 expression.</p><p><strong>Conclusion: </strong>Downregulated TRIM35 expression mitigates the oxidative stress and inflammation caused by DOX, likely through impacting the TLR4/NF-κB signaling pathway. These insights indicate that TRIM35 holds promise as a therapeutic target for managing heart damage induced by DOX.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Beta-Blocker Dilemma: Revisiting Their Role in Cardiovascular Disease.","authors":"Matthew Fordham, Radmila Lyubarova, Mandeep Sidhu","doi":"10.1007/s10557-025-07678-1","DOIUrl":"https://doi.org/10.1007/s10557-025-07678-1","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}