{"title":"Evaluating the Role of Andexanet Alfa in Managing Intracranial Hemorrhage in Patients on Vascular-Dose Rivaroxaban: A Clinical Dilemma.","authors":"Matija Zupan, Pawel Kermer, Senta Frol","doi":"10.1007/s10557-025-07772-4","DOIUrl":"https://doi.org/10.1007/s10557-025-07772-4","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944081","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}
Efstratios Koutroumpakis, Juhee Song, Jorge A Irizarry-Caro, Cezar Iliescu, Nicolas Palaskas, Anita Deswal
{"title":"Response to: Concerns Regarding Midodrine Utilization in Cancer Patients with Heart Failure.","authors":"Efstratios Koutroumpakis, Juhee Song, Jorge A Irizarry-Caro, Cezar Iliescu, Nicolas Palaskas, Anita Deswal","doi":"10.1007/s10557-025-07763-5","DOIUrl":"https://doi.org/10.1007/s10557-025-07763-5","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944033","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}
Jueqian Yan, Ke Lin, Shanshan Dai, Yucong Zhang, Ruihan Zheng, Si Shi, Zhixuan Tang, Xianhui Lai, Weijian Huang, Lan Su
{"title":"Class Effect of SGLT2 Inhibitors Against Doxorubicin-Induced Cardiotoxicity via Regulating Adenosine Kinase Mediated-Cardiac Oxidative Stress.","authors":"Jueqian Yan, Ke Lin, Shanshan Dai, Yucong Zhang, Ruihan Zheng, Si Shi, Zhixuan Tang, Xianhui Lai, Weijian Huang, Lan Su","doi":"10.1007/s10557-025-07769-z","DOIUrl":"https://doi.org/10.1007/s10557-025-07769-z","url":null,"abstract":"<p><strong>Purpose: </strong>Doxorubicin-induced cardiotoxicity (DIC) limits its clinical application. While individual SGLT2 inhibitors have shown cardioprotective effects, it remains unclear whether this is a class effect and whether the underlying mechanisms are shared.</p><p><strong>Methods: </strong>A mouse model of DIC was established through the administration of six weekly intraperitoneal injections of doxorubicin at a dose of 2.5 mg/kg. To compare the protective effects, three different SGLT2 inhibitors were administered orally. Cardiac function, cardiac fibrosis, and markers of oxidative stress were assessed. Target prediction, cardiac adenosine ELISA assays, cardiac expression of adenosine kinase (ADK) and ADK siRNA and plasmid were conducted to identify potential targets of SGLT2 inhibitors. In another cohort, DIC mice were treated with the selective ADK inhibitor ABT-702, and cardiac function, fibrosis, and oxidative stress markers were similarly assessed.</p><p><strong>Results: </strong>All three SGLT2 inhibitors provided similar protection against doxorubicin-induced cardiotoxicity, improved ejection fraction (EF%), reduced left ventricular internal diameter in diastole (LVIDd), and attenuated cardiac fibrosis and oxidative stress. ADK was identified as the potential target. SGLT2 inhibitors reduced the overexpression of ADK in DIC and restored adenosine levels in heart tissues. Knockdown and overexpression of ADK revealed that SGLT2i regulated cellular oxidative stress in an ADK-dependent manner. Additionally, ABT-702 similarly protected against doxorubicin-induced cardiotoxicity by modulating oxidative stress in vivo.</p><p><strong>Conclusion: </strong>These findings support a class effect of SGLT2 inhibitors in protecting against DIC, likely via inhibition of ADK-mediated oxidative stress. ADK may represent a promising therapeutic target for DIC management.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944064","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}
Mohamed Nasser, Hazem E Mohammed, Mohamed E Haseeb, Mohamed Khalafalla Darwish, George Hanen, Nada A Abdelaziz, Anas Hussien Heiba, Abdelrahman Shata, Mohamed Salem Abdelkader
{"title":"Lomitapide, a Microsomal Triglyceride Transfer Protein Inhibitor, in Homozygous Familial Hypercholesterolemia: A Systematic Review and Meta-Analysis of Efficacy and Safety.","authors":"Mohamed Nasser, Hazem E Mohammed, Mohamed E Haseeb, Mohamed Khalafalla Darwish, George Hanen, Nada A Abdelaziz, Anas Hussien Heiba, Abdelrahman Shata, Mohamed Salem Abdelkader","doi":"10.1007/s10557-025-07764-4","DOIUrl":"https://doi.org/10.1007/s10557-025-07764-4","url":null,"abstract":"<p><strong>Purpose: </strong>Homozygous Familial Hypercholesterolemia (HoFH) is a rare and life-threatening genetic disorder characterized by elevated low-density lipoprotein cholesterol (LDL-C) and early-onset atherosclerotic cardiovascular disease. Lomitapide, a microsomal triglyceride transfer protein (MTP) inhibitor, decreases LDL-C independent of LDL receptor function, providing an alternative treatment in this population. We aimed to evaluate the efficacy and safety of lomitapide in patients with HoFH through a systematic review and meta-analysis of available clinical evidence.</p><p><strong>Methods: </strong>A comprehensive search was conducted in PubMed, Scopus, and Web of Science through March 2025. Observational studies and clinical trials reporting on lipid profile changes and safety outcomes in HoFH patients receiving lomitapide were included. Outcomes were pooled using random-effects models, and heterogeneity was assessed using the I<sup>2</sup> statistic.</p><p><strong>Results: </strong>Eight studies comprising both adult and pediatric patients (n = 209) were included. Lomitapide significantly reduced LDL-C levels by 49.27%, total cholesterol by 46.05%, and apolipoprotein B by 51.01%. Reductions were also observed in triglycerides, VLDL-C, and non-HDL-C. HDL-C remained relatively unchanged. Adverse events were mostly gastrointestinal, with a 14% discontinuation rate. The overall quality of studies ranged from fair to good.</p><p><strong>Conclusions: </strong>Lomitapide demonstrates substantial efficacy in reducing LDL-C and other atherogenic lipids in HoFH patients, with an acceptable safety profile. These findings support its role as an adjunctive therapy in this population, though further randomized controlled trials are warranted to validate long-term safety and effectiveness.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144943992","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}
Ali Al-Ramadan, George G Kidess, Abdul Rasheed Bahar, Yasemin Bahar, Mohammad Hazique, MChadi Alraies
{"title":"Morbidity and Mortality of Ondansetron in Patients with Non-congenital Long QT Syndrome: A Review Article.","authors":"Ali Al-Ramadan, George G Kidess, Abdul Rasheed Bahar, Yasemin Bahar, Mohammad Hazique, MChadi Alraies","doi":"10.1007/s10557-025-07766-2","DOIUrl":"https://doi.org/10.1007/s10557-025-07766-2","url":null,"abstract":"<p><p>Selective 5-hydroxytryptamine type 3 (5-HT3) receptor antagonists are widely used for managing chemotherapy-induced, post-operative, and radiation-induced nausea and vomiting. The 5-HT3 receptor, a ligand-gated ion channel in the nervous system, regulates vomiting and gastrointestinal motility. Selective antagonists like ondansetron, granisetron, and tropisetron treat chemotherapy and post-surgical nausea, while non-selective antagonists include metoclopramide and prochlorperazine. Despite their efficacy, a critical safety concern is the potential for prolonging the QT interval, which can predispose patients to life-threatening arrhythmias such as torsades de pointes, particularly in those with congenital long QT syndrome. This risk has led to FDA dosing recommendations and an emphasis on cardiac monitoring, particularly in patients with predisposing factors such as electrolyte imbalances, cardiac conditions, or concurrent QT-prolonging drugs. This review explores the underlying mechanisms of QT-interval prolongation associated with the selective 5-HT3 receptor antagonist ondansetron, evaluates its impact on morbidity and mortality in at-risk populations, and discusses risk mitigation strategies.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944038","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":"Letter to \"Short-Course Potent P2Y12 Inhibitor-Based DAPT Versus Clopidogrel-Based DAPT After PCI: A Propensity-Matched Real-World Study\".","authors":"Peng Zhao, Shanshan Liang","doi":"10.1007/s10557-025-07762-6","DOIUrl":"https://doi.org/10.1007/s10557-025-07762-6","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944074","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":"Comment on: \"Moderate-Intensity Atorvastatin and Ezetimibe Combination Therapy Versus High-Intensity Atorvastatin in Patients with Angina Pectoris Who Underwent Percutaneous Coronary Intervention\".","authors":"Shaoxiang Huang, Xueyu Wang, Peili Zhang","doi":"10.1007/s10557-025-07761-7","DOIUrl":"https://doi.org/10.1007/s10557-025-07761-7","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944020","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}
Muzamil Akhtar, Rayyan Nabi, Sheema Saadia, Danish Ali Ashraf, Syed Muhammad Hassan, Mehmood Akhtar, Muhammad Ali Zia, Raheel Ahmed
{"title":"Reduced-Dose Versus Full-Dose Direct Oral Anticoagulants in the Extended Treatment of Venous Thromboembolism: A Systematic Review and Meta-Analysis.","authors":"Muzamil Akhtar, Rayyan Nabi, Sheema Saadia, Danish Ali Ashraf, Syed Muhammad Hassan, Mehmood Akhtar, Muhammad Ali Zia, Raheel Ahmed","doi":"10.1007/s10557-025-07759-1","DOIUrl":"https://doi.org/10.1007/s10557-025-07759-1","url":null,"abstract":"<p><strong>Purpose: </strong>The optimal dosing strategy for direct oral anticoagulants (DOACs) in extended treatment of venous thromboembolism (VTE) remains debated, particularly in balancing efficacy and bleeding risk.</p><p><strong>Methods: </strong>A systematic review and meta-analysis was performed to compare reduced-dose versus full-dose DOACs for extended VTE treatment. Databases including PubMed, Embase, and Cochrane Library were searched from inception to March 2025 for randomized controlled trials (RCTs) involving adult patients treated with different DOAC doses for VTE. Primary outcomes were recurrent VTE, major or clinically relevant non-major bleeding, and all-cause mortality. Subgroup analysis was conducted by DOAC type (apixaban vs. rivaroxaban).</p><p><strong>Results: </strong>Pooled data from 4 studies involving 8421 patients showed no statistically significant difference in recurrent VTE risk between reduced-dose and full-dose DOACs (RR = 0.94; 95% CI, 0.64-1.37; p = 0.75). Bleeding events were significantly lower in the reduced-dose group compared to the full-dose group (RR = 0.71; 95% CI, 0.61-0.82, p < 0.00001). All-cause mortality did not differ significantly between groups (RR = 0.80; 95% CI, 0.54-1.18; p = 0.25). Subgroup analysis showed consistent findings across DOAC type, with no significant interaction effects.</p><p><strong>Conclusion: </strong>Reduced-dose DOACs appear to be as effective as full-dose DOACs in preventing VTE, with a favorable safety profile due to reduced bleeding risk. These findings support reduced-dose DOACs as a viable option for extended anticoagulation in VTE patients.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944007","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":"Crocetin Attenuates Fibroblast-to-Myofibroblast Transition after Myocardial Infarction in Mice by Regulating Autophagy.","authors":"Ruhui Yang, Zhengyi Guo, Haili Jin, Chunli Liu, Jia Shuo Zhao, Bingjin Liu, Liping Zhou, Yinxiu Jin, Yinping Wang, Meifen Li, Songquan Wu","doi":"10.1007/s10557-025-07758-2","DOIUrl":"https://doi.org/10.1007/s10557-025-07758-2","url":null,"abstract":"<p><strong>Purpose: </strong>Myocardial infarction (MI) triggers pathological remodeling characterized by fibrosis and subsequent fibroblast-to-myofibroblast transition (FMT). Autophagy exerts a dual role in cardiac repair, balancing protective and detrimental effects. Crocetin, a carotenoid derived from saffron, exhibits anti-inflammatory and cardioprotective properties; however, its influence on autophagy-related FMT following MI remains unclear.This study aims to determine whether crocetin mitigates post-MI fibrosis and FMT by modulating autophagy in cardiac fibroblasts (CFs), while also evaluating its effects on cardiac function, infarct size, and autophagic flux.</p><p><strong>Methods: </strong>In vivo: Mice subjected to MI were administered crocetin (25-100 mg/kg). Cardiac function was assessed via echocardiography, and fibrosis was evaluated through Masson's trichrome staining and immunofluorescence analysis for α-SMA/LC3. In vitro: Hypoxic CFs were treated with crocetin or the autophagy inhibitor 3-methyladenine (3-MA). The effects on autophagic flux (GFP-RFP-LC3), protein expression (Beclin-1, LC3-II/I, P62), and mitochondrial membrane potential (JC-1) were analyzed.</p><p><strong>Results: </strong>Crocetin enhanced cardiac function, and reduced infarct size and fibrosis in a dose-dependent manner, while suppressing α-SMA expression. It promoted autophagic flux (as evidenced by increased LC3-II levels and autolysosome formation) and mitophagy (indicated by decreased mitochondrial membrane potential). Treatment with 3-MA negated the antifibrotic effects of crocetin.</p><p><strong>Conclusion: </strong>Crocetin attenuates post-MI pathological remodeling by enhancing autophagic flux to inhibit FMT, thereby identifying it as a promising candidate for antifibrotic therapy.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944009","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}