Cardiovascular Drugs and Therapy最新文献

{"title":"In-Hospital SGLT-2 Inhibitor Initiation in Acute Heart Failure: Clarifying Event Timing, Mechanisms, and Safety Boundaries.","authors":"Xiaoxue You","doi":"10.1007/s10557-026-07953-9","DOIUrl":"https://doi.org/10.1007/s10557-026-07953-9","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918140","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":"Liraglutide Ameliorates Atrial Fibrillation in Association with Enhanced Adiponectin Signaling in Epicardial Adipose Tissue.","authors":"Xinning Li, Yanmeng Liu, Fan Wang, Feifei Zhang, Lina Zhang, Yi Dang, Xiaoyong Qi","doi":"10.1007/s10557-026-07958-4","DOIUrl":"https://doi.org/10.1007/s10557-026-07958-4","url":null,"abstract":"<p><strong>Purpose: </strong>Atrial fibrillation (AF) is associated with obesity and epicardial adipose tissue (EAT) dysfunction. Although glucagon-like peptide-1 receptor agonists (GLP-1 RAs), such as liraglutide, exert cardiovascular benefits, the underlying mechanisms, particularly those related to EAT and adipokine signaling remain unclear.</p><p><strong>Methods: </strong>AF rat model was established using acetylcholine-CaCl₂ infusion. Model rats were treated with liraglutide or saline, and cardiac functions were assessed using electrocardiography (ECG) and echocardiography. Myocardial and EAT morphology was examined histologically. The levels of adiponectin (ADPN), inflammatory factors, and lipids were measured using enzyme-linked immunosorbent assay, and the protein levels of ADPN and its receptor were evaluated through western blotting. In vitro, 3T3-L1 adipocytes were treated with TNF-α to simulate a model of dysregulated lipid metabolism and inflammation. Subsequently, HL-1 cells were treated with the conditioned medium from 3T3-L1 cells. The interaction between adipocytes and cardiomyocytes was evaluated by assessing HL-1 cell proliferation, apoptosis, and levels of ADPN and inflammatory factors.</p><p><strong>Results: </strong>Liraglutide significantly reduced the duration of AF, improved cardiac function (decreased E/E', increased ejection fraction and LAACF), ameliorated myocardial fibrosis, and restored EAT morphology. Mechanistically, liraglutide specifically enhanced ADPN secretion and upregulated AdipoR1 expression in EAT, reduced interleukin (IL)-6 and IL-1β levels, and decreased free fatty acid (FFA) and triglyceride content. Notably, using an ADPN-neutralizing antibody in vitro, we demonstrated that ADPN mediates the protective effects of liraglutide on cardiomyocytes, suggesting the role of EAT-derived ADPN signaling.</p><p><strong>Conclusion: </strong>Liraglutide alleviates AF by increasing ADPN secretion and AdipoR1 expression in the EAT, improving local lipid metabolism, and attenuating inflammation. These findings establish a correlational association between liraglutide treatment, favorable modulation of the EAT phenotype, and AF amelioration, and propose a testable hypothesis that adiponectin signaling is involved in liraglutide-mediated cardioprotection.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001335","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":"Efficacy and Safety of Fixed-Dose Combination Therapy with Cilostazol and Rosuvastatin in Patients with Symptomatic Lower Extremity Peripheral Artery Disease: A Multicenter Randomized Controlled Trial.","authors":"Adelin Dhivi Kemalasari, Dong Woo Suh, In Tae Jin, Seung-Jun Lee, Chul-Min Ahn, Donghoon Choi, Ji Yong Jang, Cheol Woong Yu, Osung Kwon, Han Young Ryu, Ung Kim, Jong Kwon Park, Ki Hyuk Park, Jang Yong Kim, Young-Guk Ko","doi":"10.1007/s10557-026-07951-x","DOIUrl":"https://doi.org/10.1007/s10557-026-07951-x","url":null,"abstract":"<p><strong>Purpose: </strong>To evaluate whether combined cilostazol and rosuvastatin therapy improves health-related quality of life, walking performance, and lipid profiles compared with rosuvastatin alone in patients with symptomatic lower extremity peripheral artery disease (PAD).</p><p><strong>Methods: </strong>This multicenter, double-blind, randomized placebo-controlled trial enrolled 260 patients with chronic lower extremity PAD (Rutherford category 2 or 3) at 52 sites in Korea. Participants were randomly assigned (1:1) to receive cilostazol 200 mg plus rosuvastatin or a matching placebo plus rosuvastatin for 24 weeks. The primary endpoint was the change in the Korean Peripheral Artery Questionnaire (KPAQ) summary score from baseline to week 24.</p><p><strong>Results: </strong>A total of 257 patients were included in the full analysis set. The combination therapy group showed significantly greater improvement in the KPAQ summary score than in the rosuvastatin monotherapy group (least-squares mean change: 15.4 vs. 10.3 points; between-group difference 5.1 points, 95% confidence interval 1.5-8.7; P = 0.005). The treatment effect became statistically significant at week 12 and continued to increase through week 24. Treadmill walking distances improved in both groups; improvements were numerically greater with combination therapy but between-group differences were not significant at weeks 12 or 24. Compared with rosuvastatin monotherapy, combination therapy resulted in greater reductions in triglycerides and smaller increases in ApoB, together with greater increases in HDL cholesterol. Adverse events, adverse drug reactions, and discontinuations due to adverse events were numerically more frequent in the combination therapy group. Diarrhea was the only adverse event that occurred significantly more frequently, whereas no unexpected safety signals were observed.</p><p><strong>Conclusion: </strong>In patients with symptomatic PAD, the addition of cilostazol to rosuvastatin significantly improved patient-reported health status and provided additional favorable effects on atherogenic lipid profiles beyond rosuvastatin therapy alone.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov, NCT07600385.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905149","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":"From Genetic Prioritization to Therapeutic Validation: Interpreting C4B in Calcific Aortic Valve Stenosis.","authors":"Güney Sarıoğlu","doi":"10.1007/s10557-026-07952-w","DOIUrl":"https://doi.org/10.1007/s10557-026-07952-w","url":null,"abstract":"<p><p>Li et al. identified C4B as a potential therapy target for calcific aortic valve stenosis using genetic and histological analyses. However, genetic target prioritization isn't the same as pharmacological validation. Lifelong genetic differences in C4B may not replicate therapeutic inhibition effects, especially given the complex C4A/C4B locus. Increased C4B in calcified valves supports biological relevance but doesn't prove causality. C4B is a promising candidate needing further functional and pharmacological validation.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896482","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":"Spatiotemporal Nanotherapy After Myocardial Infarction: Targeting the Inflammatory-to-reparative Transition With Extracellular Vesicles and Engineered Nanoparticles.","authors":"Xuesi Chen, Yingchun Bao, Qijun Zhang","doi":"10.1007/s10557-026-07950-y","DOIUrl":"https://doi.org/10.1007/s10557-026-07950-y","url":null,"abstract":"<p><strong>Purpose: </strong>Post-myocardial infarction (MI) healing is a moving sequence of injury, inflammatory clearance, resolution, vascular repair, and scar maturation. This review evaluates how extracellular vesicles (EVs), cell-derived nanovesicles, and engineered nanoparticles can be matched to these changing biological requirements.</p><p><strong>Methods: </strong>A critical narrative synthesis was organized around four approximate post-MI windows: minutes to 24 h, days 1-3, days 3-7, and after day 7. Representative mechanistic, rodent, porcine, and human studies were compared by target cell, cargo, material, release profile, route, quantitative delivery evidence, efficacy, and translational liability.</p><p><strong>Results: </strong>Early oxidative and microvascular injury favors brief cytoprotection and vascular targeting; the inflammatory peak favors calibrated control of recruited leukocytes while preserving debris removal; resolution favors efferocytosis, reparative immune signaling, angiogenesis, and local immunomodulation; and later remodeling favors selective rather than global antifibrotic therapy. Directly generated nanovesicles and modified-mRNA lipid nanoparticles expand the design space. However, human evidence remains sparse, and most preclinical studies use fixed schedules, young non-comorbid rodents, qualitative biodistribution, and incompletely defined potency assays.</p><p><strong>Conclusion: </strong>A credible spatiotemporal product must demonstrate phase-dependent target availability, controlled exposure, target-cell cargo engagement, and reduced benefit or emerging harm with a deliberately mismatched schedule. Translation requires quantitative pharmacokinetics and biodistribution, route-specific safety, mechanism-linked potency, scalable manufacturing, and validation in reperfused comorbid large-animal models.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896472","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":"Profiling Cardiovascular Disease-Associated Changes in the Composition of High-Density Lipoprotein Particles.","authors":"Tanith Fester, Carmelita Abrahams, Sandrine Lecour","doi":"10.1007/s10557-026-07949-5","DOIUrl":"https://doi.org/10.1007/s10557-026-07949-5","url":null,"abstract":"<p><p>Cardiovascular disease remains the leading cause of death worldwide, imposing significant morbidity and healthcare costs. While low serum high-density lipoprotein (HDL)-cholesterol levels have traditionally been linked to cardiovascular risk, most pharmacological interventions aimed at raising HDL-cholesterol levels have not consistently improved cardiovascular outcomes. Epidemiologic and genetic studies further suggest that circulating HDL-cholesterol levels may not directly determine cardiovascular risk, underscoring the complexity of HDL particles in cardiovascular health. HDL particles are dynamic, multifunctional complexes composed of diverse proteins and lipids, whose composition determines their cardioprotective properties. In cardiovascular disease, the composition of HDL particles is frequently remodeled, resulting in dysfunctional particles with impaired antioxidant, anti-inflammatory, and lipid transport functions. Consequently, the composition and functionality of HDL particles, rather than their cholesterol content, appear to be the primary determinants of their protective capacity. A deeper understanding of HDL particles' compositional changes in cardiovascular disease may guide therapies that restore their protective capacity, thus offering a more effective strategy to reduce cardiovascular risk. This review summarizes current knowledge on changes in the proteomic and lipidomic composition of HDL particles associated with cardiovascular disease, highlighting molecular alterations that may drive HDL particle dysfunction.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886610","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":"Empagliflozin Improves Atherosclerosis by Promoting Mitophagy in Endothelial Cells.","authors":"Longlong Yan, Jingjing Lu, Wendong Xu, Ruoyu Dong","doi":"10.1007/s10557-026-07938-8","DOIUrl":"https://doi.org/10.1007/s10557-026-07938-8","url":null,"abstract":"<p><strong>Purpose: </strong>To investigate whether empagliflozin (EMPA) delays the progression of atherosclerosis (AS) by promoting mitophagy in endothelial cells.</p><p><strong>Methods: </strong>In vivo and in vitro AS models were established using ApoE^-/- mice fed a high-fat diet (HFD) and HUVECs treated with oxLDL, respectively. Models received EMPA intervention alone or combined with the autophagy inhibitor 3-MA. To specifically confirm the pivotal role of Pink1, siRNA-mediated knockdown was performed in HUVECs. Aortic plaque area was evaluated by Oil Red O staining. Serum lipids, mitochondrial function, and endothelial markers were assessed. Mitophagy-related proteins were detected by Western blot, and the co-localization of TOM20 with LC3 and CD31 with LC3 was observed via immunofluorescence.</p><p><strong>Results: </strong>EMPA significantly reduced aortic plaque area and ameliorated lipid metabolism in mice, independent of hypoglycemic effects. In vitro, EMPA restored mitochondrial membrane potential and ATP levels while reducing ROS production. Furthermore, EMPA upregulated Pink1/Parkin expression and the LC3-II/LC3-I ratio, and promoted TOM20-LC3 co-localization. Critically, both 3-MA treatment and Pink1 knockdown reversed EMPA-induced improvements in endothelial viability and migration, abolished its inhibition of inflammatory cytokine release, and negated its regulatory effects on endothelial function, demonstrating that mitophagy is essential for EMPA's action.</p><p><strong>Conclusion: </strong>EMPA inhibits the progression of AS by activating Pink1/Parkin-mediated mitophagy, thereby improving mitochondrial function and alleviating endothelial injury. This finding provides a novel basis for the cardiovascular protective mechanisms of EMPA.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872994","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":"Berberine Attenuates Hypertrophic Phenotype in RAF1-Mutant Induced Pluripotent Stem Cell-Derived Cardiomyocytes through Suppression of ERK5-Cyclin D1 Signaling.","authors":"Hongfei Chen, Yule Zhang, Xiaoqi Lai, Shushui Wang","doi":"10.1007/s10557-026-07947-7","DOIUrl":"https://doi.org/10.1007/s10557-026-07947-7","url":null,"abstract":"<p><strong>Background: </strong>Noonan syndrome-associated hypertrophic cardiomyopathy (NS-HCM) occurs frequently in patients with RAF1 mutations, but the signaling mechanisms underlying the hypertrophic cardiomyocyte phenotype remain incompletely understood, and effective therapeutic targets remain to be defined. This study aimed to characterize MAPK signaling dysregulation in RAF1-mutant induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) and to determine whether berberine (BBR) attenuates the hypertrophic phenotype through modulation of ERK5-Cyclin D1 signaling.</p><p><strong>Methods: </strong>An in vitro NS-HCM cardiomyocyte model was established using induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) from a patient harboring the RAF1 p.Ser257Leu mutation. Wild-type iPSC-CMs were generated from healthy donors. Immunofluorescence was used to assess cardiomyocyte surface area, sarcomeric organization, and Ki-67/EdU-based cell-cycle activity. Transcriptomic analyses of public NS-HCM datasets were performed to identify differentially expressed genes and enriched pathways. Western blotting was performed to evaluate the activation of MEK1/2-ERK1/2 and ERK5 signaling pathways, downstream Cyclin D1 expression, and hypertrophic markers including ANP and BNP. RAF1^S257L/+ iPSC-CMs were treated with BBR, a MEK1/2 inhibitor (U0126), or a MEK5 inhibitor (BIX02189) to evaluate pathway modulation and hypertrophic phenotype.</p><p><strong>Results: </strong>RAF1^S257L/+ iPSC-CMs exhibited hallmark features of NS-HCM, including increased cell surface area, disrupted sarcomeric organization, and elevated expression of hypertrophic markers ANP and BNP. Transcriptomic analysis revealed significant enrichment of the MAPK pathway. Both MEK1/2-ERK1/2 and ERK5-Cyclin D1 pathways were markedly activated in RAF1^S257L/+ iPSC-CMs, and treatment with U0126 or BIX02189 attenuated this activation and reduced cardiomyocyte hypertrophy. BBR treatment suppressed ERK5 phosphorylation and Cyclin D1 expression, decreased Ki-67 positivity, and similarly attenuated the hypertrophic phenotype.</p><p><strong>Conclusion: </strong>RAF1-mutant iPSC-CMs exhibited concurrent activation of the MEK1/2-ERK1/2 and ERK5-Cyclin D1 signaling pathways. BBR attenuated the hypertrophic phenotype while reducing ERK5 phosphorylation and Cyclin D1 expression without significantly altering MEK1/2-ERK1/2 signaling. These findings suggest that ERK5-Cyclin D1 signaling contributes to the hypertrophic phenotype of RAF1-mutant cardiomyocytes and support further investigation of BBR as a potential therapeutic candidate for RAF1-associated NS-HCM.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148856998","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":"Correction to: Sotagliflozin: Two Birds with One Stone?","authors":"Juan Antonio Requena-Ibáñez, Kristine Mørk Kindberg, Carlos G Santos-Gallego, M Urooj Zafar, Juan J Badimon","doi":"10.1007/s10557-026-07948-6","DOIUrl":"https://doi.org/10.1007/s10557-026-07948-6","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857035","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":"Candidate Residual Inflammatory Risk in HFpEF: A Multiorgan Framework for Longitudinal Phenotyping, Trial Enrichment, and Therapeutic Evidence Appraisal.","authors":"Zhaoqi Yan, Xiangyi Pu, Tiantian Ren, Yongyuan Cai, Yifeng Xu, Jiamei Chen, Xing Chang, Yanli Wang, Zhiming Liu, Ruxiu Liu","doi":"10.1007/s10557-026-07941-z","DOIUrl":"https://doi.org/10.1007/s10557-026-07941-z","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome in which ejection fraction, natriuretic peptides, and resting diastolic indices do not fully explain disease initiation, progression, or treatment response. The dominant contemporary phenotype is frequently cardiorenal-metabolic, characterized by obesity, visceral and epicardial adiposity, insulin resistance, diabetes, hypertension, kidney dysfunction, endothelial dysfunction, and chronic low-grade inflammation. In this setting, candidate residual inflammatory risk (RIR) is best conceptualized not as an isolated elevation of C-reactive protein or interleukin-6, but as a persistent multiorgan immunometabolic state that may continue to drive symptoms, organ remodeling, and clinical events despite control of congestion and indication-appropriate management of comorbidities. Adipose-tissue expansion, immune-cell activation, endothelial adhesion and oxidative stress, impaired nitric oxide-cyclic guanosine monophosphate-protein kinase G signaling, cardiomyocyte stiffening, extracellular-matrix remodeling, renal amplification, skeletal-muscle bioenergetic failure, and gut-liver metabolic inputs form a self-reinforcing disease network. Biomarker, proteomic, imaging, and phenomapping studies indicate that inflammatory burden in HFpEF is layered rather than binary, ranging from obesity-linked high-CRP states to pan-inflammatory phenotypes with cardiorenal dysfunction, fibrosis signals, and worse outcomes. This framework may explain why broad anti-inflammatory therapy has produced limited benefit, whereas upstream phenotype-matched therapies, including sodium-glucose cotransporter-2 inhibitors, nonsteroidal mineralocorticoid receptor antagonism, obesity-directed incretin therapy, and structured lifestyle interventions, appear more effective in selected populations. Candidate RIR remains a research construct without a validated diagnostic cutoff or treatment-predictive biomarker. Framing cardiometabolic and cardiorenal HFpEF through candidate RIR may improve mechanistic stratification, longitudinal phenotyping, trial enrichment, and mechanism-matched therapy.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839459","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}