Cardiovascular Drugs and Therapy最新文献

{"title":"Therapeutic Potential of GLP-1 Receptor Agonists in Diabetes and Cardiovascular Disease: Mechanisms and Clinical Implications.","authors":"Xinyu Zhang, Chao Cao, Fei Zheng, Chang Liu, Xiuqing Tian","doi":"10.1007/s10557-025-07670-9","DOIUrl":"https://doi.org/10.1007/s10557-025-07670-9","url":null,"abstract":"<p><strong>Background: </strong>Glucagon-like peptide-1 (GLP-1) is a crucial incretin hormone secreted by intestinal endocrine L cells. Given its pivotal physiological role, researchers have developed GLP-1 receptor agonists (GLP-1 RAs) through structural modifications. These analogues display pharmacological effects similar to those of GLP-1 but with augmented stability and are regarded as an effective means of regulating blood glucose levels in clinical practice.</p><p><strong>Objective: </strong>This review aims to comprehensively summarize the role of GLP-1 RAs in the management of diabetes mellitus (DM) and cardiovascular disease (CVD), with a particular emphasis on the underlying signal transduction pathways and their therapeutic potential.</p><p><strong>Methods: </strong>A comprehensive review was carried out through literature research.</p><p><strong>Results and discussion: </strong>In pancreatic β-cells, GLP-1 RAs regulate the secretion of insulin and glucagon in a glucosedependent manner by influencing signaling pathways such as cAMP, PI3K, and MAPK. They also contribute to the regulation of blood glucose levels by promoting the proliferation of β-cells and inhibiting apoptosis in these cells. Recent comprehensive studies have also demonstrated the favorable impact of GLP-1 RAs on cardiovascular wellbeing. In addition to the cardiovascular protection afforded by glucose metabolism regulation, a large body of evidence from animal and cellular studies has corroborated the beneficial effects of GLP-1 RAs on conditions such as heart failure (HF), hypertension, and ischemic cardiomyopathy. These benefits are mainly attributed to the alleviation of inflammatory responses, reduction of oxidative stress, and prevention of cell apoptosis. Clinical data shows that GLP-1 RAs can reduce the risk of major adverse cardiovascular events (MACE) in diabetic patients.</p><p><strong>Conclusion: </strong>GLP-1 RAs play an important role in the management of both diabetes and cardiovascular diseases. They show potential therapeutic value through the modulation of multiple signal transduction pathways. However, there may still be some issues in practical applications that require further research and resolution.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001068","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":"Novel Protective Role for Gut Microbiota-derived Metabolite PAGln in Doxorubicin-induced Cardiotoxicity.","authors":"Jie Huang, Xingyuan Hou, Ni Zhou, Nan Su, Shanshan Wei, Yuanying Yang, Taoli Sun, Guangdi Li, Wenqun Li, Bikui Zhang","doi":"10.1007/s10557-024-07665-y","DOIUrl":"https://doi.org/10.1007/s10557-024-07665-y","url":null,"abstract":"<p><strong>Purpose: </strong>Doxorubicin (Dox) is a classic anthracycline chemotherapy drug with cause cumulative and dose-dependent cardiotoxicity. This study aimed to investigate the potential role and molecular mechanism of phenylacetylglutamine (PAGln), a novel gut microbiota metabolite, in Dox-induced cardiotoxicity (DIC).</p><p><strong>Methods: </strong>DIC models were established in vivo and in vitro, and a series of experiments were performed to verify the cardioprotective effect of PAGln. RNA sequencing (RNA-seq) was employed to explore the mechanism of PAGln in DIC. Subsequently, the differentially expressed genes (DEGs) were subjected to comprehensive analysis using diverse public databases, and RT-PCR was used to confirm the expression levels of the candidate genes. Finally, molecular docking techniques were used for validation.</p><p><strong>Results: </strong>PAGln effectively prevented both in vivo and in vitro Dox-induced myocardial injury and cell apoptosis. RNA-seq results showed that 40 genes were up-regulated and 54 down-regulated in the Dox group compared to the Con group, displaying opposite changes in the Dox + PAGln group. Enrichment analysis highlighted several mechanisms by which PAGln alleviated Dox-induced cardiotoxicity, including the lipid metabolic process, calcium-mediated signaling, positive regulation of store-operated calcium channel activity, and hypertrophic cardiomyopathy. In vitro and in vivo experiments confirmed that PAGln treatment could reverse the changes in the expression levels of Klb, Ece2, Nmnat2, Casq1, Pak1, and Apob in Dox. Molecular docking results showed that these genes had good binding activity with PAGln.</p><p><strong>Conclusions: </strong>PAGln shows potential in alleviating Dox-induced cardiotoxicity, with Ece2 identified as key regulatory molecules related to endothelial dysfunction.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142977729","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":"Impact of Warfarin and Dual Antiplatelet Therapy on Graft Failure After Coronary Endarterectomy: A Retrospective Cohort Study.","authors":"Jianfan Zhen, Xiang Luo, Jie Liu, Zerui Chen, Jinlin Wu, Tucheng Sun","doi":"10.1007/s10557-024-07667-w","DOIUrl":"https://doi.org/10.1007/s10557-024-07667-w","url":null,"abstract":"<p><strong>Purpose: </strong>Coronary endarterectomy combined with coronary artery bypass grafting (CE-CABG) effectively achieves coronary revascularization in patients with diffuse atherosclerotic coronary artery disease (CAD). However, the loss of the subendothelial tissue at the CE-CABG coronary artery accelerates local thrombosis, leading to CE-CABG graft failure. Dual antiplatelet therapy (DAT) and warfarin plus aspirin (WPA) are the two most common anticoagulation strategies post CE-CABG. This retrospective study compares the clinical outcomes and graft failure rates associated with these two approaches.</p><p><strong>Methods: </strong>This study is a retrospective cohort study. Between July 2016 and April 2024, 102 patients with diffuse CAD underwent CE-CABG. Six patients were excluded. In total, 96 patients (mean age 59.8 ± 7.7 years) enrolled in the study (43 in DAT group and 53 in WPA group). The DAT group received aspirin (100 mg, qd) and clopidogrel (75 mg, qd) for 1 year postoperatively, transitioning to aspirin (100 mg, qd) after 1 year. The WPA group received warfarin (international normalized ratio, INR remained at 1.8-2.5) and aspirin (100 mg, qd) for 3 months postoperatively, followed by DAT after 3 months, changed to aspirin monotherapy after 1 year. The primary endpoint was graft failure of the CE-CABG graft.</p><p><strong>Results: </strong>Four patients died during the perioperative period (1 in DAT group, 3 in WPA group), resulting in an overall perioperative mortality rate of 4.2%. Five patients were lost for follow-up. Mean follow-up time was 38 months. Three patients died during the follow-up period (1 in DAT group, 2 in WPA group). The CE-CABG graft patency of the WPA group was significantly higher compared to the DAT group (88.1% vs. 50.0%, P < 0.001). Kaplan-Meier analysis showed that the median graft failure time was significantly longer in the WPA group (77 months, 95% CI 69-85) compared to the DAT group (73 months, 95% CI 17-129, P = 0.017). A higher proportion of the DAT group was classified as NYHA III-IV compared to the WPA group (26.2% vs. 10.2%, P = 0.046). One patient of the WPA group had a gastrointestinal bleeding event, and the overall incidence of bleeding events was not statistically different between the two groups.</p><p><strong>Conclusion: </strong>Using the WPA strategy after CE-CABG significantly reduces the rate of graft failure and improves cardiac function without increasing the risk of bleeding events.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142977699","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":"Therapeutic Potential of Curcumin in Diabetic Cardiomyopathy: Modulation of Pyroptosis Pathways.","authors":"Fei Wang, Lehan Liu, Jiaxin Wang, Yizhu Zhou, Xiaochun Feng, Kun Liu","doi":"10.1007/s10557-024-07644-3","DOIUrl":"https://doi.org/10.1007/s10557-024-07644-3","url":null,"abstract":"<p><strong>Purpose: </strong>Cardiac inflammation is a basic pathological process of diabetic cardiomyopathy (DCM). Inflammatory response is closely related to pyroptosis, which is a recently identified programmed cell death type. Curcumin (CUR) is a polyphenol extracted from turmeric and has been reported to be crucial in alleviating pyroptosis in DCM. However, the exact mechanism by which CUR improves pyroptosis remains unclear. Therefore, we aimed to investigate the effect of CUR on pyroptosis in DCM and explore the potential mechanisms.</p><p><strong>Methods: </strong>The molecular docking (MOD) analysis was performed using AutoDock Tools to evaluate the binding patterns and affinities between CUR and tripartite motif containing 21 (TRIM21), as well as between TRIM21 and gasdermin D (GSDMD). Subsequently, DCM models were established in Sprague-Dawley (SD) rats (in vivo) by administering streptozotocin (STZ) and feeding them a high-fat diet. In addition, H9C2 cells were cultured in a high glucose and palmitate environment to construct in vitro models of DCM. Rats or cells were treated by CUR directly. Subsequently, body weight (BW), heart weight (HW)/BW ratio, fasting blood glucose level, and lipid metabolism were measured. Pathological changes were analyzed using hematoxylin and eosin (H&E) and Masson staining. Small interfering RNA (si-RNA) was used to knockdown TRIM21 expression, and the pyroptosis protein expression and cellular activity were evaluated in different groups.</p><p><strong>Results: </strong>MOD analysis revealed that CUR had a strong binding affinity with TRIM21, and TRIM21 showed a robust interaction with GSDMD. STZ-induced diabetic SD rats showed metabolic abnormalities, structural changes in the ventricle, and the expression of TRIM21 and pyroptosis markers, including nod-like receptor protein-3 (NLRP3), Caspase-1, and GSDMD, were upregulated. CUR reduced cardiac remodeling and improved cardiac function in vivo. CUR inhibited pyroptosis by regulating TRIM21 through in vivo and in vitro studies.</p><p><strong>Conclusion: </strong>CUR improves DCM by regulating TRIM21 expression to inhibit pyroptosis. Furthermore, this study provides novel approaches and experimental evidence for the research and treatment of DCM and presents new insights into its potential mechanisms.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945195","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":"Novel Selective Cardiac Myosin-Targeted Inhibitors Alleviate Myocardial Ischaemia-Reperfusion Injury.","authors":"Nur Liyana Mohammed Yusof, Derek M Yellon, Sean M Davidson","doi":"10.1007/s10557-024-07663-0","DOIUrl":"https://doi.org/10.1007/s10557-024-07663-0","url":null,"abstract":"<p><strong>Purpose: </strong>Reperfusion of the ischaemic heart is essential to limit myocardial infarction. However, reperfusion can cause cardiomyocyte hypercontracture. Recently, cardiac myosin-targeted inhibitors (CMIs), such as Mavacamten (MYK-461) and Aficamten (CK-274), have been developed to treat patients with cardiac hypercontractility. These CMIs are well tolerated and safe in clinical trials. We hypothesised that, by limiting hypercontraction, CMIs may reduce hypercontracture and protect hearts in the setting of ischaemia and reperfusion (IR).</p><p><strong>Methods: </strong>We investigated the ability of MYK-461 and CK-274 to inhibit hypercontracture of adult rat cardiomyocytes (ARVC) in vitro following ATP depletion. A suitable dose of CMIs for subsequent in vivo IR studies was identified using cardiac echocardiography of healthy male Sprague Dawley rats. Rats were anaesthetized and subject to coronary artery ligation for 30 min followed by 2 h of reperfusion. Prior to reperfusion, CMI or vehicle was administered intraperitoneally. Ischaemic preconditioning (IPC) was used as a positive control group. Infarct size was assessed by tetrazolium chloride staining and extent of hypercontracture was assessed by histological staining.</p><p><strong>Results: </strong>Treatment with CMIs inhibited ARVC hypercontracture in vitro. MYK-461 (2 mg/kg) and CK-274 (0.5 mg/kg to 2 mg/kg) significantly reduced infarct size vs. vehicle. IR caused extensive contraction band necrosis, which was reduced significantly by IPC but not by CMIs, likely due to assay limitations. GDC-0326, an inhibitor of PI3Kα, abrogated CK-274-mediated protection following IR injury. GDC-0326 reduced phosphorylation of AKT when administered together with CK-274.</p><p><strong>Conclusion: </strong>This study identifies CMIs as novel cardioprotective agents in the setting of IR injury.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926757","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 Finerenone in Cardiovascular and Renal Outcomes: A Systematic Review and Meta-analysis.","authors":"Juan Carlos Rivera-Martinez, Michael Sabina, Aqeel Khanani, Andrew Lurie, Amanda Rigdon, Waiel Abusnina, Luis Daniel Lugo Rosado, Anas Bizanti, Timir K Paul","doi":"10.1007/s10557-024-07666-x","DOIUrl":"https://doi.org/10.1007/s10557-024-07666-x","url":null,"abstract":"<p><strong>Purpose: </strong>Heart failure (HF) management is well-defined for reduced ejection fraction (HFrEF) but less so for mildly reduced (HFmrEF) or preserved ejection fraction (HFpEF). This meta-analysis evaluates the impact of Finerenone, a nonsteroidal mineralocorticoid receptor antagonist, on cardiovascular and renal outcomes in these patient populations.</p><p><strong>Methods: </strong>A systematic search in PubMed and Embase identified randomized controlled trials (RCTs) on Finerenone's cardiovascular and renal effects. Three RCTs were included-FIDELIO-DKD, FIGARO-DKD, and FINEARTS-HF-encompassing 19,027 participants. Primary outcomes included cardiovascular death, HF hospitalization, and renal failure. Secondary outcomes focused on safety and adverse events like acute kidney injury and hyperkalemia. Meta-analyses were performed using hazard ratios (HR), confidence intervals (CI), and Relative Risk (RR).</p><p><strong>Results: </strong>Finerenone was associated with a 20% reduction in HF hospitalization risk (HR 0.80, 95% CI: 0.72-0.90) and a 14% reduction in all-cause mortality (RR 0.86, 95% CI: 0.77-0.97). Finerenone did not significantly reduce cardiovascular death (HR 0.91, 95% CI: 0.82-1.01, p = 0.06). Renal failure rates were similar between Finerenone and placebo (RR 1.05, 95% CI: 0.65-1.68). Hyperkalemia incidence was significantly higher with Finerenone, with a RR of 2.31 (95% CI: 1.98-2.69).</p><p><strong>Conclusion: </strong>This meta-analysis shows that Finerenone significantly reduces HF hospitalizations and all-cause mortality in patients with chronic kidney disease and heart failure. Further studies are needed to clarify its effects on cardiovascular death and renal failure.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926744","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":"Recombinant dsAAV9-mediated Endogenous Overexpression of Macrophage Migration Inhibitory Factor Alleviates Myocardial Ischemia-Reperfusion Injury via Activating AMPK and ERK1/2 Signaling Pathways.","authors":"Xiao-Cui Chen, Min-Tao Gai, Chun-Hui He, Bang-Hao Zhao, Fen Liu, Xiang Ma, Yi-Tong Ma, Xiao-Ming Gao, Bang-Dang Chen","doi":"10.1007/s10557-024-07662-1","DOIUrl":"https://doi.org/10.1007/s10557-024-07662-1","url":null,"abstract":"<p><strong>Purpose: </strong>To investigate the protective effect and mechanism of enhanced expression of endogenous macrophage migration inhibitory factor (MIF) on cardiac ischemia-reperfusion (I/R) injury.</p><p><strong>Methods: </strong>A recombinant double-stranded adeno-associated virus serotype 9 with MIF or green fluorescent protein (GFP) genes (dsAAV9-MIF/GFP) was transduced into mice and neonatal rat ventricular myocytes (NRVMs). The models of cardiac 60 min ischemia and 24 h reperfusion and 12 h hypoxia/12 h reoxygenation (H/R) were established in mice and NRVMs, respectively. Infarct size, cardiac remodeling, and related signaling pathways were assessed.</p><p><strong>Results: </strong>The dsAAV9 vector demonstrated strong transduction efficacy and cardiac affinity. Cardiac overexpression of MIF led to a 35.3% reduction in infarct size and improved cardiac function following I/R injury. In the dsAAV9-MIF group, the AMP-activated protein kinase (AMPK) signaling pathway was activated, and autophagy was enhanced during the ischemic period. During reperfusion, the extracellular signal-regulated kinases 1 and 2 (ERK1/2) signaling pathway was upregulated, leading to reduced cardiac apoptosis. In vitro, transfection with MIF in NRVMs also upregulated AMPK and ERK1/2 signaling during hypoxia and reoxygenation, respectively. Furthermore, MIF overexpression significantly improved autophagy and mitochondrial function, evidenced by an increased LC3-II/I ratio and enhanced mitochondrial membrane potential (ΔΨm), with these effects reversed by the AMPK inhibitor compound C. Additionally, MIF overexpression led to a 60% reduction in the apoptosis rate of cardiomyocytes subjected to H/R and decreased the Bax/Bcl-2 ratio, partially through the ERK1/2 signaling pathway.</p><p><strong>Conclusion: </strong>Enhanced endogenous MIF expression via the dsAAV9 vector provides significant cardioprotection against I/R injury by activating the AMPK and ERK1/2 signaling pathways. Our findings suggest that targeting MIF may represent a viable therapeutic strategy for severe and prolonged I/R injury.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920869","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":"Dexmedetomidine Inhibits Ferroptosis to Alleviate Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Regulating the HDAC2/FPN Pathway.","authors":"Yueqi Fu, QingDong Wang, DongWei Wang, Yicong Li","doi":"10.1007/s10557-024-07664-z","DOIUrl":"https://doi.org/10.1007/s10557-024-07664-z","url":null,"abstract":"<p><strong>Purpose: </strong>Myocardial ischemia/reperfusion injury (MIRI) is closely associated with ferroptosis. Dexmedetomidine (Dex) has good therapeutic effects on MIRI. This study investigates whether dexmedetomidine (Dex) regulates ferroptosis during MIRI by affecting ferroportin1 (FPN) levels and elucidates the underlying mechanisms.</p><p><strong>Methods: </strong>A murine MIRI model was established using male C57BL/6 J mice subjected to 30 min of left anterior descending coronary artery ligation followed by 48 h of reperfusion. In vitro, cardiomyocyte hypoxia/reoxygenation (H/R) models were created with 16 h of hypoxia and 8 h of reoxygenation. Triphenyltetrazolium chloride (TTC) staining was employed to determine infarct size. The pathological changes in myocardial tissues were assessed using hematoxylin-eosin (HE) staining. Lipid reactive oxygen species (ROS) level was detected using BODIPY™ 581/591 C11, and ferrous iron (Fe²⁺) and malondialdehyde (MDA) levels were measured using the kits. Cardiomyocyte viability was examined using cell counting kit-8 (CCK8) assay. The histone H3 lysine 27 acetylation (H3K27Ac) level in the FPN promoter region was determined using DNA pulldown assay. Chromatin immunoprecipitation (ChIP) assay was used to investigate the relationship between histone deacetylase 2 (HDAC2) and FPN promoter.</p><p><strong>Results: </strong>Dex alleviated ferroptosis in cardiomyocytes by upregulating FPN levels, which mitigated H/R-induced oxidative damage. FPN knockdown abolished the protective effects of Dex, confirming its dependence on FPN expression. Additionally, HDAC2 knockdown alleviated I/R-induced myocardial injury and ferroptosis in mice. Moreover, H/R-induced HDAC2 upregulation transcriptionally inhibited FPN expression by reducing the H3K27Ac level in the FPN promoter region, but Dex therapy restored this impact via inhibition of HDAC2. As expected, HDAC2 overexpression partially reversed the inhibitory effect of Dex on H/R-mediated cardiomyocyte ferroptosis.</p><p><strong>Conclusion: </strong>Dex alleviated H/R-mediated cardiomyocyte ferroptosis through regulating the HDAC2/FPN axis. Our findings lend theoretical support to the use of Dex in MIRI therapy.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920867","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":"Control of Cardiac Output with Ivabradine or Beta-Blockers for Refractory Hypoxemia under Veno-Venous ECMO for Severe ARDS.","authors":"Paul Masi, Lionel Tchatat Wangueu, François Bagate, Alexandra Plesa, Thierry Folliguet, Armand Mekontso Dessap","doi":"10.1007/s10557-024-07650-5","DOIUrl":"https://doi.org/10.1007/s10557-024-07650-5","url":null,"abstract":"<p><strong>Purpose: </strong>Hypoxemia is a risk factor for mortality and long-term neuropsychological impairment during severe acute respiratory distress syndrome (ARDS). Veno-venous extracorporeal membrane oxygenation (VV-ECMO) is a potential treatment for such cases but may not suffice. We aimed to evaluate the effects of pharmacological interventions for cardiac output (CO) control using ivabradine or beta-blockers for refractory hypoxemia during VV-ECMO.</p><p><strong>Methods: </strong>The study involved retrospective analysis of consecutive patients with severe ARDS who underwent VV-ECMO at a tertiary university hospital between March 2020 and May 2022. Patients with refractory hypoxemia under VV-ECMO were included. Pharmacological interventions included ivabradine and/or short half-life beta-blockers. The primary endpoint was the change in ECMO flow/CO ratio and secondary endpoints were changes in macrocirculation (mean arterial pressure), oxygenation [arterial saturation (SaO₂) and oxygen transport (DO₂)] and tissue hypoxia (lactate levels).</p><p><strong>Results: </strong>Out of 70 patients on VV-ECMO, ten had refractory hypoxemia under VV-ECMO and received pharmacological interventions to control CO. The ECMO flow/CO ratio significantly increased with pharmacological intervention overall (from 60% [50-66] to 69% [61-81], p = 0.02), as well as with beta-blockers or ivabradine individually. However, DO₂ decreased, especially with beta-blockers and to some extent with ivabradine. There were no reported immediate adverse events, and lactate levels remained below the anaerobic threshold.</p><p><strong>Conclusion: </strong>Ivabradine and beta-blockers were clinically well-tolerated and improved the ECMO flow/CO ratio in patients with refractory hypoxemia during VV-ECMO. However, the improvement of arterial oxygenation was associated with decreased DO₂.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909478","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 Relationship Between Lansoprazole and Coronary Heart Disease Risk: Controversial Protective Effects and Cardiovascular Adverse Events.","authors":"Min Liu, De-Gang Mo","doi":"10.1007/s10557-024-07668-9","DOIUrl":"https://doi.org/10.1007/s10557-024-07668-9","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892073","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}