Journal of Cardiovascular Pharmacology最新文献

{"title":"Oltipraz ameliorates pressure overload-induced pathological cardiac hypertrophy in mice.","authors":"Junmou Hong, Huang Cao, Yan Wang","doi":"10.1097/FJC.0000000000001704","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001704","url":null,"abstract":"<p><p>Oltipraz (OPZ), a synthetic dithiothiol, is regarded as a novel agonist of nuclear factor erythroid-2 (Nrf-2). Recent studies revealed that Nrf-2 activation could suppress the pathological cardiac hypertrophy in mice. However, the therapeutic role of OPZ in the pathological cardiac hypertrophy remains incompletely understood. Thus, we evaluated the cardioprotective effects of OPZ in vivo and in vitro. Transverse aortic constriction (TAC) surgery was performed to induce the pathological cardiac hypertrophy in mice. In addition, the H9c2 cells were treated with angiotensin II (Ang II) to induce cardiomyocyte hypertrophy in vitro experiments. Our data revealed that OPZ relieved the TAC-induced pathological cardiac hypertrophy and myocardial damage in mice. Similarly, OPZ mitigated the increase in cardiomyocyte size induced by Ang II, indicating its ability to counteract cardiomyocyte hypertrophy. In addition, OPZ reduces cardiomyocyte oxidative stress, inflammation and apoptosis by activating Nrf-2 signaling in vivo and in vitro. Interestingly, our results also demonstrated that Nrf-2 knockdown abolished the protective effects of OPZ in vitro. Taken together, these data revealed that OPZ ameliorates the pathological cardiac hypertrophy via activating Nrf-2 signaling.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143981104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contemporary Analysis of cardiac Tamponade Etiologies, Treatments, and Outcomes: the CATEO Study.","authors":"Marco Giuseppe Del Buono, Mattia Brecciaroli, Gianluigi Saponara, Alessia D'Aiello, Daniela Pedicino, Gaetano Pinnacchio, Lorenzo Genuardi, Rocco Antonio Montone, Simone Filomia, Giulia La Vecchia, Ilaria Poli, Francesca Rigoli, Mariantonietta Di Salvatore, Michela Quirino, Jacopo Lenkowicz, Edoardo Pompei, Laura Antenucci, Giovanna Liuzzo, Carlo Trani, Giampaolo Tortora, Francesco Burzotta, Tommaso Sanna","doi":"10.1097/FJC.0000000000001702","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001702","url":null,"abstract":"<p><p>Cardiac tamponade is a critical condition resulting from various etiologies, including malignancies, inflammatory conditions and iatrogenic causes. With advances in treatments and changing epidemiology, there is a need to reassess the prevalence, management, and outcomes of pericardial tamponade. This study aimed to evaluate the current prevalence of different etiologies of tamponade, the management, and the clinical outcomes in a cohort of patients admitted to a high-volume Cardiac Intensive Care Unit (CICU). We conducted a retrospective analysis of 87 patients diagnosed with cardiac tamponade (median age 70 years; 51% male). Data on patient demographics, clinical characteristics, etiologies, treatment strategies, and outcomes were collected and analyzed. Malignant tamponade was the predominant etiology, observed in 47% of cases, with lung cancer being the most common. Other etiologies included inflammatory (22%), iatrogenic (20%), idiopathic (9%), and congestive heart failure-related (2%) effusions. The majority of patients (94%) underwent urgent percutaneous pericardiocentesis. Anti-inflammatory therapy was administered in 67% of cases, including NSAIDs (22%), colchicine (46%), steroids (24%) and IL-1 inhibitors (3%), with some patients receiving combination therapy. The 3-month all-cause mortality rate was 29%, with significantly higher mortality observed in patients with malignant effusions compared to non-malignant causes (49% vs. 11%, p<0.001). This study provides valuable insights into the clinical characteristics, management, and outcomes of patients with cardiac tamponade at a high-volume cancer center. Neoplastic pericardial effusion, particularly due to lung cancer, is the leading cause of tamponade in this cohort. Anti-inflammatory therapies were frequently used, but their role in improving outcomes requires further investigation. Mortality remains high, especially among those with malignancy-related effusions.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143992405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Muscarinic Acetylcholine Receptors in Oxytocin-Induced Cardioprotection Against Ischemia-Reperfusion Injury in Rats.","authors":"Mahdieh Faghihi, Mohammadreza Ahmadi-Beni, Fariba Houshmand","doi":"10.1097/FJC.0000000000001701","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001701","url":null,"abstract":"<p><p>Oxytocin (OT) has been shown to provide myocardial protection against ischemia-reperfusion (I/R) injury. This study investigates the involvement of muscarinic receptors in the OT-induced cardioprotection, focusing on its potential mechanisms and effects on myocardial infarction (MI) and ischemic arrhythmias. Male rats anesthetized with pentobarbital sodium were subjected to 25-min ischemia followed by 120-min reperfusion after intraperitoneal administration of OT (0.01 μg), atropine (1.5 µg/kg), or saline. Cardioprotection was evaluated by monitoring lactate dehydrogenase (LDH), malondialdehyde (MDA), and cardiac creatine kinase isoenzyme (CK-MB) levels, infarct size, arrhythmia severity, ventricular fibrillation, and mortality. OT markedly reduced infarct size, oxidative stress, and the severity of ischemic arrhythmias, including ventricular tachycardia and ventricular fibrillation, compared with saline-treated I/R animals. OT also significantly improved survival rates. Pretreatment with atropine abolished most protective effects of OT but did not significantly alter its suppression of ventricular fibrillation, suggesting the involvement of muscarinic receptor-independent mechanisms. These findings highlight that the OT-induced cardioprotection, mediated in part by acetylcholine (ACh) locally released in the left ventricle, extends beyond infarct limitation to include potent anti-arrhythmic effects. The dual impact of OT on MI and arrhythmias provides insights into the mechanisms underlying its preconditioning effect and its potential application in MI management.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aprocitentan for Treatment-Resistant Hypertension: Pharmacology Concepts and Clinical Insights.","authors":"Apryl N Peddi, Sarah E Wheeler, Keerthana Akkisetty, John D Bucheit","doi":"10.1097/FJC.0000000000001700","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001700","url":null,"abstract":"<p><p>Treatment resistant hypertension (TRH) occurs in nearly 20% of patients with a diagnosis of hypertension despite receiving three or more antihypertensives and places individuals at an increased risk of morbidity and mortality compared to essential hypertension. Numerous pathophysiological factors underlie TRH, including endothelin-1, which until recently no approved treatments targeted. Endothelin-1 exhibits multiple actions through binding to ETA and ETB receptors. Vasoconstriction of the vascular smooth muscle occurs when endothelin-1 binds ETA and ETB, however; vasodilation of endothelial cells also occurs through activation of ETB. Currently available endothelin receptor antagonists (ERA) were only approved for pulmonary hypertension until 2024 when the Food and Drug Administration approved aprocitentan as the first ERA for hypertension treatment in combination with other antihypertensives. The approval of aprocitentan occurred following the publication of the phase 3 PRECISION trial that compared aprocitentan versus placebo for patients with \"true\" TRH. Aprocitentan 12.5 mg exhibited a placebo-adjusted reduction in sitting systolic and diastolic blood pressure of 3.8/3.9 mmHg at 4 weeks of treatment. A dose-dependent increase in peripheral edema and a small reduction in hemoglobin due to hemodilution were greater in the aprocitentan-treated patients. Animal study data from past endothelin receptor antagonists showed this class of agents may lead to birth defects and was the basis for aprocitentan's black-box warning. Overall, clinical trial data supports aprocitentan's use as an effective agent for the TRH, but clinicians will need to individualize patient treatment selection and consider the safest and most efficacious options currently available.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Observation of the therapeutic effect of dapagliflozin on atherosclerosis in mice and preliminary exploration of the mechanism of action.","authors":"Fangfang Chen, Xu Wang, Yang Ma, Sihua Liu, Hongfei Sang","doi":"10.1097/FJC.0000000000001696","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001696","url":null,"abstract":"<p><p>In recent years, the incidence of Atherosclerosis (AS) has been increasing and has gradually become a major disease threatening human health. In this study, we analyzed the effect of dapagliflozin on AS and preliminarily explore the mechanism of action. First, apolipoprotein E (ApoE) knockout C57Bl/6J mice were used to establish an AS model in vitro. An intervention group treated with dapagliflozin and a model group treated with normal saline, both administered by gavage, were set up. The effects of dapagliflozin on macrophage polarization, blood lipids, inflammation, oxidative stress, and vascular adhesion of AS mice were observed, we found that compared with the model group, macrophages in the intervention group of mice were polarized from M2 to M1 type, the levels of inflammatory factors in the intervention group decreased, and the oxidative stress reaction and vascular adhesion were inhibited. Subsequently, the aorta tissues of mice were stained with HE and oil red O to observe their histopathological changes. We observed a significant improvement in aortic pathologic damage in the intervention group, converging to normal mice. Finally, autophagy in mouse aortic cells was determined, found the intervention group showed markedly increase Beclin-1 and LC3-II expression in the aorta than the model group. In conclusions, dapagliflozin can ameliorate the progression of AS, and its mechanism is related to the activation of aortic cell autophagy.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143998766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flavin adenine dinucleotide ameliorates pressure overload-induced heart failure by activating the short-chain acyl-CoA dehydrogenase.","authors":"Chunyu Chen, Xue Qin, Yuhong Cao, Liyuan Qing, Zhichao Ma, Qingping Xu, Huan Peng, Guifang Jin, Zhicheng Yang, Jieyu Xing, Sigui Zhou","doi":"10.1097/FJC.0000000000001698","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001698","url":null,"abstract":"<p><p>Flavin adenine dinucleotide (FAD), a cofactor that catalyzes the reaction of flavin protein, participates in fatty acid β-oxidation, which has been shown to inhibit pathological cardiac hypertrophy and fibrosis in spontaneously hypertensive rats. However, the therapeutic advantage of FAD for heart failure treatment has not been investigated. This study aimed to explore the effects and underlying mechanisms of FAD in a transverse aortic constriction (TAC)-induced heart failure mouse model and in vitro tert-Butyl hydroperoxide (tBHP)-induced cardiomyocyte apoptosis model experiments. FAD considerably inhibited tBHP-induced cardiomyocyte apoptosis. In addition, FAD significantly increased the activity and expression of the short-chain acyl-CoA dehydrogenase (SCAD) enzyme and ATP content while reducing the content of free fatty acids and reactive oxygen species both in vitro and in vivo. Meanwhile, FAD increased the mitochondrial membrane potential, suppressed mitochondrial membrane swelling, and decreased myocardial fibrosis and TUNEL-positive apoptosis cells in the TAC-induced heart failure mice. In conclusion, our results indicate that FAD plays a positive role in preventing and treating heart failure, which can be attributed in part to the activation of SCAD.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Factor XI as a Drug Target for the Prevention and Treatment of Thrombosis.","authors":"Nathaniel B Wayne, Sarah B Schaidle, Craig J Beavers","doi":"10.1097/FJC.0000000000001699","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001699","url":null,"abstract":"<p><p>The optimal anticoagulation therapeutic intervention balances preventing or treating thrombosis, depending on the clinical scenario, and bleeding. A novel drug target, factor eleven (FXI), may theoretically represent a way to prevent thrombosis in the clotting cascade, without increasing the risk of bleeding. Several mechanisms for inhibiting FXI or its activated form are being studied and include antisense oligonucleotides, monoclonal antibodies, small molecules, natural peptides, and aptamers. Many of the drugs that have been developed have been studied in clinical trials evaluating their use in secondary prevention of acute coronary syndromes, prevention of venous thromboembolism after orthopedic surgery, and stroke and systemic embolism prevention. Ongoing areas of interest include special patient populations such as patients with end stage renal disease (ESRD), cancer, and COVID-19 infection. FXI inhibition is a novel concept with many drug mechanisms that exist and are in varying stages of clinical study for a number of clinical uses.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roxadustat has beneficial effects on the vascular tone of the rat thoracic aorta.","authors":"Keisuke Nakagawa, Yoriko Oshiba, Reo Sukita, Ayaka Hosomi, Masashi Tawa, Mamoru Ohkita","doi":"10.1097/FJC.0000000000001697","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001697","url":null,"abstract":"<p><p>Roxadustat, an agent for renal anemia, may have beneficial effects on the cardiovascular system, but its direct effects on the vasculature system have not been clarified. Therefore, in this study, the effect of roxadustat on vascular tone was examined using rat thoracic aortas and superior mesenteric arteries according to the organ chamber method. Roxadustat relaxed the thoracic aorta in the presence or absence of vascular endothelium, but the degree of vascular relaxation was attenuated by endothelium denudation, indicating that the majority of vasorelaxation caused by roxadustat is endothelium-dependent. Pretreatment with a nitric oxide (NO) synthase inhibitor (i.e., NG-nitro-L-arginine-methyl ester), a soluble guanylate cyclase (sGC) inhibitor (i.e., 1H-[1,2,4] oxadiazolo-[4,3-a]quinoxaline-1-one), and a bradykinin B2 receptor inhibitor (i.e., icatibant) significantly weakened roxadustat-induced vasorelaxation. In addition, roxadustat treatment of endothelium intact vascular rings increased mildly NO metabolites. When the direct effects of roxadustat on vascular smooth muscle were examined, various selective potassium channel inhibitors markedly diminished roxadustat-induced vasorelaxation in vascular endothelium-denuded rings. Moreover, roxadustat significantly inhibited angiotensin Ⅱ- and phenylephrine-induced vasocontraction, regardless of the presence of vascular endothelium. Not only the thoracic aorta, roxadustat relaxed the superior mesenteric artery, a smaller vessel. These results suggest that roxadustat-induced vasorelaxation of the thoracic aorta involves activation of endothelial NO synthase through bradykinin B2 receptors and the subsequent NO/sGC pathway. Furthermore, roxadustat probably inhibited vasocontraction by activating potassium channel opening.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronotropic Effects of Milrinone in a Guinea Pig Ex Vivo Model: A Pilot Study to Screen for New Mechanisms of Action.","authors":"Piero Pollesello, Jouko Levijoki, Zoltán Papp","doi":"10.1097/FJC.0000000000001675","DOIUrl":"10.1097/FJC.0000000000001675","url":null,"abstract":"<p><strong>Abstract: </strong>Positive inotropic responses upon administration of milrinone, an inhibitor of the phosphodiesterase enzyme (PDE), involve a well-pronounced positive chronotropic effect. Here, we tested whether milrinone evokes this chronotropic response solely by PDE inhibition or by a concerted action that involve additional pharmacological targets. Milrinone-stimulated increases in heart rate were studied in right atrial preparations of guinea pig in the presence or absence of inhibitors of putative ancillary molecular pathways or ion channels: ie, β receptor blockers with distinct selectivities (propranolol, metoprolol, and carvedilol), α1 receptor blocker (prazosin), inhibitor of the small conductance Ca 2+ activated K + (SK) channels (apamin), L-type Ca 2+ channel blockers (verapamil and diltiazem), and different Na + channel blockers (lidocaine, tetrodotoxin, and quinidine). Carvedilol, which inhibits β1, β2, α1, and 5-HT receptors, limited the positive chronotropic effects of milrinone to about 40%, ( P < 0.01). In the presence of another nonselective blocker of the β receptors, propranolol, and blockers of the l -type Ca 2+ channels, only nonsignificant trends toward reductions of the milrinone effects were seen. The α1 receptor blocker prazosin did not limit the milrinone-evoked positive chronotropy. Blockers of Na + channels, SK channels, or the β1 receptor blocker, metoprolol also did not affect the positive chronotropy evoked by milrinone. We conclude that milrinone increases heart rate in response to adrenergic signaling, which besides PDE inhibition, may involve a 5-HT receptor-dependent component. Our exploratory approach paves the way to more focused experiments with the use of selective 5-HT receptor antagonists to confirm or reject the involvement of a specific 5-HT receptor-dependent pathway.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"278-286"},"PeriodicalIF":2.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143028833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mineralocorticoid Receptor Antagonist versus Placebo in a Patient With End-Stage Kidney Disease Under Renal Replacement Therapy: A Systematic Review and Meta-Analysis.","authors":"Sagun Dawadi, Dhan Bahadur Shrestha, Prakash Raj Oli, Jurgen Shtembari, Sajog Kansakar, Suman Paudel, Kailash Pant","doi":"10.1097/FJC.0000000000001661","DOIUrl":"10.1097/FJC.0000000000001661","url":null,"abstract":"<p><strong>Abstract: </strong>The number of patients living with chronic kidney diseases is increasing, and so are the patients with end-stage renal disease (ESRD) undergoing renal replacement therapy. Although there is a common understanding that these patients face higher risks of fatal or nonfatal cardiovascular and cerebrovascular events, and mineralocorticoid receptor antagonists (MRAs) have been an essential pillar in managing heart failure, their use in this subset of patients has been overshadowed because of concerns of hyperkalemia. Patients with ESRD under renal replacement therapy have often been excluded from landmark trials. This meta-analysis was conducted based on the PRISMA guideline after registering the protocol with PROSPERO (CRD42024499835). A database search included articles until April 2024, and relevant data were extracted from the included studies. Analysis was done using RevMan web (version 5.4). A total of 15 studies among 1086 studies were included in the final analysis. Our meta-analysis revealed MRA significantly reduced all-cause mortality (odds ratio (OR) 0.35, confidence interval (CI), 0.23-0.54) and cardiovascular mortality (OR 0.37, 0.21-0.65). With some possible increase in the risk of hyperkalemia (OR 1.56, CI, 1.01-2.42), with no discernible difference in the occurrence of stroke (OR 0.57, CI, 0.25-1.28) or myocardial infarction (OR 0.63, CI, 0.08-4.72). The utilization of MRA in patients with ESRD under dialysis is linked to improved mortality outcomes, albeit with slight concerns for hyperkalemia. Although current evidence leans toward MRA usage, prospective randomized controlled trials involving a broader patient cohort are essential to establish robust guidance for MRA application in this subset of patients.</p>","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"270-277"},"PeriodicalIF":2.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}