Cardiovascular Therapeutics最新文献

{"title":"Atorvastatin Safety Reappraised: From Pharmacogenomic Mechanisms to Personalized Risk Management","authors":"Hanyu Wang,&nbsp;Yue Pan,&nbsp;Yiming Li,&nbsp;Pan Zhai","doi":"10.1155/cdr/4127131","DOIUrl":"10.1155/cdr/4127131","url":null,"abstract":"<p>Atorvastatin remains a cornerstone of lipid-lowering therapy and cardiovascular prevention, but concerns about adverse effects continue to undermine adherence and long-term clinical benefit. This structured narrative review critically reappraises its safety profile by integrating evidence from randomized trials, meta-analyses, observational studies, pharmacovigilance analyses, case reports, and preclinical models. Evidence is interpreted according to study design, with controlled and synthesized human data guiding clinical conclusions and lower level evidence treated as supportive or hypothesis-generating. Overall, atorvastatin provides substantial cardiovascular protection, whereas serious adverse reactions are uncommon. The principal clinical concerns are statin-associated muscle symptoms, hepatic laboratory abnormalities, drug–drug interactions, and a small dose- and susceptibility-dependent increase in new-onset diabetes. Safety is shaped by dose, comorbidities, interacting medicines, pharmacokinetic variability, and transporter variants, particularly SLCO1B1, although the clinical actionability of other pharmacogenomic markers remains limited. We, therefore, emphasize individualized risk assessment, interaction review, appropriate monitoring, dechallenge and rechallenge, dose adjustment, alternative statins, and nonstatin combination therapy when needed. Experimental delivery systems and mechanistic findings may inform future strategies but do not yet establish improved clinical safety. Taken together, the evidence supports a benefit-centered, evidence-stratified framework that addresses genuine toxicity without overstating uncertain safety signals or unnecessarily discontinuing effective therapy.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13633432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103530","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":"Is Oral Anticoagulation an Independent Predictor of Mortality in STEMI and High-Risk NSTEMI Patients After Primary PCI? A Propensity Score-Matched Retrospective Analysis","authors":"Recep Polat,&nbsp;Fuat Polat,&nbsp;Yalçın Velibey,&nbsp;Osman Bolca,&nbsp;Göktürk İpek","doi":"10.1155/cdr/1295386","DOIUrl":"10.1155/cdr/1295386","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Managing STEMI and high-risk NSTEMI-equivalent patients on chronic oral anticoagulation (OAC) undergoing primary PCI poses competing ischaemic and bleeding risks.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This single-centre retrospective study enrolled 604 consecutive STEMI/high-risk NSTEMI patients undergoing primary PCI (2012–2023). OAC users (<i>n</i> = 100) were compared with propensity score–matched controls (<i>n</i> = 203). Primary endpoints included all-cause mortality, bleeding, stroke, recurrent MI and rehospitalisation over a mean 3-year follow-up.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>OAC users had a higher prevalence of prior ischaemic stroke/TIA (19% vs. 3%, <i>p</i> &lt; 0.001) and known coronary artery disease (33% vs. 20%, <i>p</i> = 0.015). In-hospital mortality was comparable (7% vs. 5.9%, <i>p</i> = 0.80). Postdischarge long-term mortality was significantly higher in OAC users (31% vs. 14.8%, <i>p</i> = 0.001), as were access-site haematoma (8% vs. 2%, <i>p</i> = 0.02) and minor bleeding (7% vs. 1.5%, <i>p</i> = 0.03). On multivariable Cox regression, OAC use was not an independent mortality predictor (HR 0.81, 95% CI 0.47–1.37, <i>p</i> = 0.43); age, reduced ejection fraction and chronic kidney disease were the principal determinants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Despite higher postdischarge mortality and bleeding, OAC use was not independently associated with mortality after adjustment. Comorbidity burden drives prognosis, emphasising comprehensive risk stratification in this population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13627984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103603","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":"Comparing Transcatheter Mitral Valve Replacement to Transcatheter Edge-to-Edge Repair in Mitral Regurgitation: A Systematic Review","authors":"Rama A. Safadi,&nbsp;Alaa Dean A. Esmail,&nbsp;Lauren E. DeProfio,&nbsp;Ahmed Adham R. Elsayed,&nbsp;Marc D. Basson","doi":"10.1155/cdr/7522199","DOIUrl":"https://doi.org/10.1155/cdr/7522199","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Mitral regurgitation affects 2% of the population globally, with a widely increasing prevalence. Although mitral regurgitation is most commonly corrected by open surgery, there has been a recent shift toward less invasive transcatheter approaches, including both transcatheter edge-to-edge repair (TEER) and transcatheter mitral valve replacement (TMVR).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A comprehensive literature search was conducted using four databases: PubMed, Cochrane Library, Virtual Health Library (VHL), and Web of Science (WOS), following the PRISMA guidelines. Relevant observational studies were assessed for reporting using STROBE guidelines, whereas case reports were assessed using CARE guidelines. Independent reviewers evaluated studies based on eligibility criteria and analyzed relevant studies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Postoperative complications observed in patients undergoing either technique (TMVR or TEER) included acute kidney injury, stroke, access site complications, and postoperative bleeding. These complications were generally more frequent in patients after TMVR. Myocardial infarction, prosthesis malposition, and valve migration were reported exclusively after TMVR, whereas ischemic cardiomyopathy was associated with TEER. Regarding hemodynamic outcomes, TMVR patients were associated with greater MR reduction to ≤ 1, frequently observed complete MR resolution, near-laminar blood flow, and marked improvement in left ventricular function (assessed using LVEDVI and LVESVI). TMVR was associated with significantly higher 30-day mortality, whereas pooled 1-year mortality did not differ significantly between TMVR and TEER.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Although TEER remains the safer option in appropriately selected patients, TMVR offers greater efficacy in MR resolution at the cost of higher procedural risk. However, findings should be interpreted with caution, given that patient selection between TMVR and TEER patients may influence observed outcomes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/7522199","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149048564","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":"Comparison of Hybrid Strategy With Drug-Coated Balloons Versus Stent-Only Strategy for Coronary Bifurcation Lesions: A Systematic Review and Meta-Analysis","authors":"Yuyang Cao,&nbsp;Hao Li,&nbsp;Jiayu Zhang,&nbsp;Queyun Sun,&nbsp;Zhao Ma,&nbsp;Sida Jia,&nbsp;Na Xu,&nbsp;Jinqing Yuan,&nbsp;Ying Song","doi":"10.1155/cdr/7598895","DOIUrl":"10.1155/cdr/7598895","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;Coronary bifurcation lesions (CBLs) account for approximately 15%–20% of all percutaneous coronary interventions and remain a therapeutic challenge. A hybrid strategy combining drug-coated balloons (DCBs) for the side branch with drug-eluting stents (DESs) for the main vessel has emerged as a novel therapy aimed at mitigating complications associated with permanent implants. This study was aimed at systematically evaluating the efficacy and safety of the hybrid strategy compared with a DES-only strategy (including single- and double-stent strategies) in CBLs.&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;Following the PRISMA 2020 guidelines, we systematically searched major databases for randomized controlled trials (RCTs) and observational studies comparing the DES + DCB hybrid strategy with a DES-only strategy for CBLs. The primary endpoint was major adverse cardiovascular events (MACE). Secondary endpoints included target lesion revascularization (TLR), target vessel revascularization (TVR), late lumen loss (LLL), myocardial infarction (MI), and restenosis rate. Statistical analyses were performed using RevMan 5.4 and StataMP.&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;We included 13 studies, comprising five RCTs and eight observational studies, with a total of 2186 patients (1030 in the hybrid strategy group and 1156 in the DES-only group). Compared with the DES-only strategy, the hybrid strategy was associated with a lower incidence of MACE (OR 0.75; 95% CI 0.57–0.99; &lt;i&gt;p&lt;/i&gt; = 0.04) and a lower risk of TLR (OR 0.46; 95% CI 0.26–0.79; &lt;i&gt;p&lt;/i&gt; = 0.005); however, the MACE benefit was of borderline statistical significance. Regarding angiographic endpoints, the hybrid strategy substantially lowered the risk of side branch restenosis (OR 0.13; 95% CI 0.05–0.34; &lt;i&gt;p&lt;/i&gt; &lt; 0.0001). Side branch LLL was consistently lower with the hybrid strategy across all contributing studies; however, extreme between-study heterogeneity (&lt;i&gt;I&lt;/i&gt;&lt;sup&gt;2&lt;/sup&gt; = 96&lt;i&gt;%&lt;/i&gt;) precluded meaningful pooling. Subgroup analysis indicated a more pronounced reduction in MACE risk for left main lesions (OR 0.50; 95% CI 0.31–0.81; &lt;i&gt;p&lt;/i&gt; = 0.005), with extremely low heterogeneity (&lt;i&gt;I&lt;/i&gt;&lt;sup&gt;2&lt;/sup&gt; = 0&lt;i&gt;%&lt;/i&gt;). No statistically significant differences were observed between the two groups with respect to MI or TVR.&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;For CBLs, the DES + DCB hybrid strategy appears to offer favorable safety and efficacy compared with a stent-only strategy. The observed benefits likely reflect both the avoida","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/7598895","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036282","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":"Zhenwu Decoction Attenuates Water-Retention–Related Phenotypes and Multiorgan Injury in Rats With Doxorubicin-Induced Chronic Heart Failure","authors":"Weijun Li,&nbsp;Zhenyu Zhao,&nbsp;Xuefeng Lin,&nbsp;Guoliang Chen,&nbsp;Lin Li,&nbsp;Ge Fang,&nbsp;Zhixi Hu","doi":"10.1155/cdr/8444915","DOIUrl":"10.1155/cdr/8444915","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study is aimed at evaluating the effects of Zhenwu Decoction (ZWD) on cardiac dysfunction, water-retention–related phenotypes, and brain and kidney injury in rats with doxorubicin-induced chronic heart failure (CHF), and at examining whether these effects were accompanied by changes in AVP, V2R, PKA-C<i>α</i>, and AQP2-related markers.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Rats that met the prespecified CHF criteria after doxorubicin administration were rerandomized to the model, ZWD-L, ZWD-M, ZWD-H, or tolvaptan groups and treated once daily for 14 consecutive days. Cardiac function, biochemical and water balance–related outcomes, histopathology, brain AVP, and renal V2R, PKA-C<i>α</i>, and AQP2 expression were assessed. The animal was the experimental unit, and the number analyzed is reported for each outcome.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared with the control group, model rats showed impaired cardiac function; increased ascites and tissue water retention; reduced 24-h urine output; histological injury in the heart, brain, and kidney; and altered AVP, V2R, PKA-C<i>α</i>, and AQP2-related markers. ZWD treatment was associated with improvement in these measured outcomes, with the magnitude and statistical support varying across doses. Tolvaptan produced the expected aquaretic reference response. Adjusted <i>p</i> values and the number of animals analyzed are reported for each outcome.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In this doxorubicin-induced CHF model, ZWD improved cardiac function and water-retention–related phenotypes and was accompanied by changes in AVP, V2R, PKA-C<i>α</i>, and AQP2-related markers. These data support an association but do not establish pathway mediation, direct target engagement, or heart–brain–kidney crosstalk.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/8444915","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149012138","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":"Role of Circulating Microparticles in Impairing Endothelial Function and Activating Oxidative Stress Is Related to No-Reflow in STEMI","authors":"Wen-bo Li,&nbsp;Wei Zhang,&nbsp;Feng-Jun Chang,&nbsp;Zhe Li,&nbsp;Yu-Juan Yang,&nbsp;Gong Cheng,&nbsp;Xin Jiang","doi":"10.1155/cdr/9055462","DOIUrl":"10.1155/cdr/9055462","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Patients with ST-segment elevation myocardial infarction (STEMI) frequently experience no-reflow (NRF) during percutaneous coronary intervention (PCI). Nevertheless, the pathogenesis of NRF involves multiple factors and has not been fully elucidated to date. Given that endothelial dysfunction, inflammation, and oxidative stress are jointly implicated in both MP-related processes and NRF occurrence, this study was performed to explore the potential role of circulating microparticles (MPs) in the development of NRF.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>MPs were isolated from healthy subjects (<i>n</i> = 30), patients with angina and negative coronary angiography (control, <i>n</i> = 30), and STEMI patients with (<i>n</i> = 30) or without NRF (<i>n</i> = 30). The effects of MPs on endothelium-dependent vasodilatation, the expression of caveolin-1 and endothelial nitric oxide synthase (eNOS), and the production of nitric oxide (NO), superoxide anion (O₂^•−), and intercellular adhesion molecule 1 (ICAM-1) were detected in mice. Furthermore, we examined the effects of MPs on the proliferation and endothelial tube formation of human coronary artery endothelial cells (HCAECs), with or without <i>N</i>^G-nitro-L-arginine methyl ester (L-NAME) preincubation.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Compared with controls and healthy subjects, circulating MP levels were significantly higher in STEMI patients and were further elevated in STEMI patients with NRF. MPs isolated from NRF patients impaired endothelial-dependent vasodilatation, decreased the expression of phosphorylated eNOS at Ser1177, reduced NO production, HCAECs proliferation, and endothelial tube formation, but upregulated the expression of caveolin-1 and phosphorylated eNOS at Thr495, and increased the generation of O₂^•− and ICAM-1. The effects of MPs on HCAECs were partially blocked by L-NAME.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Circulating MPs are associated with NRF in the clinical context and induce endothelial dysfunction in experimental models. Our findings provide new insight into the underlying molecular mechanisms of NRF in STEMI in experimental models.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9055462","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988124","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":"Humanized hiPSC Platforms for I/R Injury: Advancing Toward Precision Cardioprotection","authors":"Mengyan Mi,&nbsp;Tzu-Yu Chen,&nbsp;Honghua Ye","doi":"10.1155/cdr/2729114","DOIUrl":"10.1155/cdr/2729114","url":null,"abstract":"<p>Myocardial ischemia–reperfusion (I/R) injury remains a major contributor to infarct expansion, adverse remodeling, and heart failure despite timely coronary revascularization. The repeated failure of cardioprotective interventions that were effective in animal models has exposed a persistent translational gap. Human induced pluripotent stem cell–derived cardiomyocytes (hiPSC-CMs) and engineered cardiac platforms preserve donor-specific human genetic backgrounds, provide scalable cell sources, and offer experimentally tractable systems for studying selected mechanisms of I/R injury. Recent advances in electrical, mechanical, metabolic, and endocrine maturation, together with engineered heart tissues (EHTs), cardiac organoids, and perfused heart-on-a-chip platforms, have improved the ability to model cardiomyocyte stress, calcium overload, mitochondrial dysfunction, oxidative injury, and multicellular crosstalk. Single-cell and spatial omics, CRISPR-based perturbation, and artificial intelligence (AI)–assisted high-content phenotyping further enable state-resolved and mechanistically testable analyses of vulnerable cardiac cell populations. In this narrative review, we synthesize recent progress in hiPSC-based myocardial I/R modeling, critically evaluate the strengths and limitations of current platforms, and discuss their use in mechanism-guided drug screening, cardiotoxicity assessment, and patient-specific preclinical modeling. We emphasize that these systems are not yet substitutes for clinical validation or whole-organ physiology. Their current value lies in providing controllable, human-relevant preclinical models that can prioritize mechanisms, identify candidate interventions, and support better-designed translational cardioprotection studies.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13577191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148975756","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":"Real-World Utilisation and Cost Trends of Mineralocorticoid Receptor Antagonists in England: A Population-Level Prescribing Analysis From 2022 to 2025","authors":"Chia Siang Kow,&nbsp;Syed Shahzad Hasan,&nbsp;Kaeshaelya Thiruchelvam,&nbsp;Abdullah Faiz Zaihan","doi":"10.1155/cdr/5473277","DOIUrl":"10.1155/cdr/5473277","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Mineralocorticoid receptor antagonists (MRAs) are a cornerstone in the management of cardiovascular and renal diseases. However, the introduction of newer agents and changes in drug pricing may influence prescribing patterns and healthcare expenditure.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>We aimed to evaluate temporal trends in utilisation, cost and cost per item of MRAs in England.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A retrospective observational study was conducted using publicly available prescribing data from OpenPrescribing, which reports NHS primary care prescribing in England for prescriptions dispensed in the community. Annual data from 2022 to 2025 were analysed for spironolactone, eplerenone and finerenone. Outcomes included total items dispensed, items per 100,000 population, total Actual Cost (£) and cost per item.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Spironolactone remained the most frequently dispensed MRA, with utilisation increasing from 3,140,245 items (5491 per 100,000 population) in 2022 to 4,060,648 (6902 per 100,000) in 2025. Eplerenone utilisation increased from 1,180,762 items (2065 per 100,000) to 1,963,447 (3337 per 100,000). Finerenone demonstrated rapid uptake following minimal initial use, reaching 35,484 items (60.3 per 100,000) in 2025. Total costs for spironolactone increased over the study period, whereas eplerenone costs declined in 2025 despite increased utilisation. Finerenone costs rose in parallel with uptake. Cost per item was lowest for spironolactone from 2022 to 2024, but eplerenone was lower in 2025 (£2.22 vs. £3.13); finerenone remained highest.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Spironolactone remained the most frequently dispensed MRA in England between 2022 and 2025. Eplerenone utilisation increased, whereas its cost per item declined markedly by 2025, and finerenone showed rapid uptake from a very low baseline while retaining the highest cost per item. These descriptive findings identify changing utilisation and expenditure patterns but do not establish indication-specific use, comparative effectiveness, safety, adherence or cost-effectiveness and should be considered hypothesis-generating.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13575777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966234","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":"FTH1 mRNA–Protein Discordance in Cardiac Ferroptosis: Multilayer Posttranscriptional and Degradative Control","authors":"Feng Zhou,&nbsp;Jia-Bin Zhou,&nbsp;Yi-Qing Yan,&nbsp;Tian-Peng Wei,&nbsp;Dan Wu,&nbsp;Yi-Fan Yang,&nbsp;Ru-Xing Wang","doi":"10.1155/cdr/8306021","DOIUrl":"10.1155/cdr/8306021","url":null,"abstract":"<p>Ferritin heavy Chain 1 (FTH1) is a key protective factor against ferroptosis in the heart, yet its protein abundance can diverge from transcript levels in cardiac ferroptosis contexts. Since resistance to ferroptosis depends on FTH1 protein abundance rather than transcript levels and its ferroxidase activity cannot be readily compensated by other ferritin subunits, this mismatch is functionally consequential. This review organizes the evidence into three regulatory layers acting downstream of transcription. Iron regulatory protein/iron-responsive element (IRP/IRE) signaling gates ribosome recruitment at the 5 ^′-untranslated region before translation begins. Epitranscriptomic marks and RNA-binding proteins (RBPs) then route the transcript toward decay or translation, with the N⁶-methyladenosine (m⁶A) reader YTHDF2 acting in opposite directions across cardiac contexts. Finally, nuclear receptor Coactivator 4 (NCOA4) delivers assembled ferritin for lysosomal degradation, depleting FTH1 protein independently of transcript level. Together, these mechanisms provide an integrated framework for understanding the mRNA–protein discordance of FTH1 and its contribution to cardiac ferroptosis susceptibility. We also discuss how this framework may inform layer-specific therapeutic strategies and identify the measurements that are missing (labile iron pool, ferritin iron loading, and ferritinophagic flux) before mechanistic insight can translate into clinical cardioprotection.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/8306021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929028","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":"Mechanistic Investigation of Salidroside Modulates Iron Overload to Mitigate Radiation-Induced Heart Disease","authors":"Jiaming Lai,&nbsp;Rong Wang,&nbsp;Shenglin Zhang,&nbsp;Li Li,&nbsp;Likun Qi,&nbsp;Zhenyao Dong,&nbsp;Ranran Yan,&nbsp;Bo Zhang,&nbsp;Guoquan Li,&nbsp;Hao Cai","doi":"10.1155/cdr/5141802","DOIUrl":"10.1155/cdr/5141802","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Radiation-induced heart disease (RIHD) severely compromises the long-term survival of cancer patients. Although ferroptosis has been implicated as a key contributor to RIHD pathogenesis, the underlying regulatory mechanisms remain incompletely defined. Prompted by clinical observations of elevated serum iron concentrations following thoracic radiotherapy, this study investigated iron-metabolic alterations during RIHD progression and evaluated the cardioprotective efficacy of salidroside in mitigating ferroptosis through restoration of iron homeostasis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In a retrospective cohort of 98 patients undergoing thoracic radiotherapy, clinical data were collected, and serum iron concentrations were measured before and after treatment. To elucidate the underlying mechanisms, an RIHD mouse model was established using single-dose precordial irradiation at 20 Gy, followed by salidroside administration. Cardiac function, mitochondrial integrity, and ferroptosis-related markers were systematically assessed. Mechanistic targets were identified using bulk and single-cell RNA sequencing and subsequently validated by molecular docking and Western blotting.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Clinical analysis revealed significantly elevated serum iron concentrations after radiotherapy (<i>p</i> &lt; 0.05). Consistent with this clinical phenotype, irradiated mice exhibited cardiac dysfunction, mitochondrial damage, and disrupted iron metabolism. Multiomics analyses identified the transferrin receptor 1 (TFRC) as a potentially critical regulator of these pathological processes. Salidroside treatment significantly ameliorated cardiac injury and attenuated ferroptosis-related alterations. KEGG pathway analysis further demonstrated enrichment of TFRC in the HIF-1 signaling pathway, and salidroside reduced HIF-1<i>α</i> expression, suggesting attenuation of irradiation-associated hypoxic-stress signaling.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Thoracic radiotherapy may promote RIHD pathogenesis by inducing disrupted iron homeostasis, thereby contributing to cardiomyocyte ferroptosis and mitochondrial injury. Salidroside effectively ameliorates myocardial damage by attenuating iron overload and ferroptosis. Collectively, these findings highlight the translational potential of salidroside as a promising adjunctive cardioprotective agent for patients undergoing thoracic radiotherapy.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2026 1","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5141802","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148918309","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}