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Not an allergy: Iodine contrast-induced acute sialadenitis after coronary angiography 不是过敏:冠状动脉造影术后碘造影剂诱发的急性浆膜炎。
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-01 DOI: 10.1016/j.repc.2024.06.002
Victor Vallejo-Garcia , Óscar Fabregat-Andrés , Ana Lainez-Nuez
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引用次数: 0
Tuberculous submitral aneurysm: A rare cardiac presentation of a common pathogen 结核性腹膜下动脉瘤:一种常见病原体的罕见心脏表现。
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-01 DOI: 10.1016/j.repc.2024.03.002
Usnish Adhikari , Harikrishnan Sivadasanpillai , Bineesh K. Radhakrishnan , Mohamed Iliyas
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引用次数: 0
Acknowledgement Reviewers 确认评论者
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-12-01 DOI: 10.1016/j.repc.2024.11.004
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引用次数: 0
Beyond clinical trials – The cost saving associated with dapagliflozin use in Portugal hospital clinical practice 临床试验之外 - 在葡萄牙医院临床实践中使用达帕格列净可节省成本。
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-12-01 DOI: 10.1016/j.repc.2024.04.012
Dulce Brito , Cândida Fonseca , Fátima Franco , Vanessa Lopes , Sara Gonçalves , Rui Baptista , Joana Sequeira , Irene Marques , Rita Rego , Joana Pimenta , José Silva-Cardoso , Margarida Lopes , Mário Almeida

Introduction and objectives

Heart failure (HF) is a clinical syndrome associated with substantial morbidity, mortality, and healthcare costs. Dapagliflozin has proven efficacy in reducing the risk of death and hospitalization in HF patients, regardless of left ventricular ejection fraction (LVEF). This paper aimed to project the potential impact of dapagliflozin on healthcare costs related to HF subsequent hospitalizations (HFHs) in Portuguese hospitals.

Methods

The total number of HF-related hospitalizations (hHF), HFHs, and the average length of stay for patients with a primary diagnosis of HF from six Portuguese hospitals, between January 2019 and December 2021, were collected and aggregated by hospital classification. Costs associated with HFHs were calculated according to Portuguese legislation and considering conservative, average, and complex approaches. Cost-saving projections were based on extrapolations from hHF risk reductions reported in dapagliflozin clinical trials.

Results

Considering a 26% risk reduction in hHF reported on pooled-analysis of DAPA-HF and DELIVER as the expected reduction in HFHs, the use of dapagliflozin would be associated with cost savings ranging from EUR 1 612 851.54 up to EUR 6 587 360.09, when considering all hospitals and the different approaches, between 2019 and 2021. A similar projection is observed based on 24% RRR derived by weighting DAPA-HF and DELIVER sub-analyses and PORTHOS epidemiological data.

Conclusions

In this projection, dapagliflozin use in all eligible hHF patients is associated with a significant reduction in direct costs. Our data support that, in addition to the improvements in HF-related outcomes, dapagliflozin may have a significant economic impact on healthcare costs in Portuguese hospitals.
导言和目标:心力衰竭(HF)是一种与大量发病率、死亡率和医疗成本相关的临床综合征。事实证明,无论左心室射血分数(LVEF)如何,达帕格列净都能有效降低心力衰竭患者的死亡和住院风险。本文旨在预测达帕格列净对葡萄牙医院与高血压后续住院(HFHs)相关的医疗费用的潜在影响:收集了2019年1月至2021年12月期间葡萄牙六家医院的HF相关住院总人数(hHF)、HFHs以及初诊为HF患者的平均住院时间,并按医院分类进行汇总。根据葡萄牙法律,并考虑到保守、平均和复杂方法,计算了与高频心房颤动相关的成本。成本节约预测基于达帕格列净临床试验中报告的高血压风险降低的推断:结果:如果将 DAPA-HF 和 DELIVER 的汇总分析所报告的 HFH 风险降低 26% 作为 HFHs 的预期降低率,那么考虑到所有医院和不同的方法,在 2019 年至 2021 年期间,使用达帕格列净可节约成本 1 612 851.54 欧元至 6 587 360.09 欧元不等。通过加权 DAPA-HF 和 DELIVER 子分析以及 PORTHOS 流行病学数据得出的 24% 的 RRR 也得出了类似的预测结果:在这一预测中,所有符合条件的 hHF 患者使用达帕格列净可显著降低直接费用。我们的数据证明,除了改善心房颤动相关预后外,达帕格列净还可能对葡萄牙医院的医疗成本产生重大经济影响。
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引用次数: 0
One more piece in the puzzle of stem cell therapy in cardiovascular diseases 干细胞治疗心血管疾病的拼图又多了一块。
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-12-01 DOI: 10.1016/j.repc.2024.08.007
Rita Nogueira-Ferreira , Adelino F. Leite-Moreira
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引用次数: 0
Orbital atherectomy: An expanded toolbox for coronary calcium management 眼眶动脉粥样硬化切除术:冠状动脉钙化治疗的扩展工具箱。
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-12-01 DOI: 10.1016/j.repc.2024.10.001
Luís Leite
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引用次数: 0
Dapagliflozin: Improving heart failure outcomes does not necessarily mean increasing costs Dapagliflozin:改善心衰预后并不一定意味着增加成本。
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-12-01 DOI: 10.1016/j.repc.2024.08.008
António Valentim Gonçalves
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引用次数: 0
Customizing solutions: Ventricular tachycardia and implantable cardioverter-defibrillator programming 定制解决方案:室性心动过速和植入式心律转复除颤器编程。
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-12-01 DOI: 10.1016/j.repc.2024.04.008
Tatiana Pavlenko , Pedro Silva Cunha , Mário Martins Oliveira
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引用次数: 0
Pulmonary arterial hypertension: Navigating the pathways of progress in diagnosis, treatment, and patient care 肺动脉高压:引领诊断、治疗和患者护理的进步之路。
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-12-01 DOI: 10.1016/j.repc.2024.03.004
Miguel Azaredo Raposo , Daniel Inácio Cazeiro , Tatiana Guimarães , Nuno Lousada , Céline Freitas , Joana Brito , Susana Martins , Catarina Resende , Peter Dorfmüller , Rita Luís , Susana Moreira , Pedro Alves da Silva , Luís Moita , Mário Oliveira , Fausto J. Pinto , Rui Plácido
Pulmonary arterial hypertension (PAH) is a form of precapillary pulmonary hypertension caused by a complex process of endothelial dysfunction and vascular remodeling. If left untreated, this progressive disease presents with symptoms of incapacitating fatigue causing marked loss of quality of life, eventually culminating in right ventricular failure and death. Patient management is complex and based on accurate diagnosis, risk stratification, and treatment initiation, with close monitoring of response and disease progression. Understanding the underlying pathophysiology has enabled the development of multiple drugs directed at different targets in the pathological chain. Vasodilator therapy has been the mainstay approach for the last few years, significantly improving quality of life, functional status, and survival. Recent advances in therapies targeting dysfunctional pathways beyond endothelial dysfunction may address the fundamental processes underlying the disease, raising the prospect of increasingly effective options for this high-risk group of patients with a historically poor prognosis.
肺动脉高压(PAH)是一种毛细血管前肺动脉高压,由内皮功能障碍和血管重塑的复杂过程引起。如果不及时治疗,这种渐进性疾病会出现使人丧失能力的疲劳症状,导致生活质量明显下降,最终导致右心室衰竭和死亡。患者管理非常复杂,需要准确诊断、风险分层、开始治疗并密切监测反应和疾病进展。通过对基本病理生理学的了解,针对病理链中的不同靶点开发出了多种药物。过去几年来,血管扩张剂治疗一直是主流方法,大大改善了患者的生活质量、功能状态和存活率。针对内皮功能障碍以外的功能障碍通路的疗法的最新进展可能会解决该疾病的基本过程,为这一预后历来较差的高危患者群体提供越来越有效的选择。
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引用次数: 0
Mesenchymal stem cells may alleviate angiotensin II-induced myocardial fibrosis and hypertrophy by upregulating SFRS3 expression 间充质干细胞可通过上调 SFRS3 的表达,缓解血管紧张素 II 诱导的心肌纤维化和心肌肥厚。
IF 1.6 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2024-12-01 DOI: 10.1016/j.repc.2024.04.010
Ling Gu, Xin Wan, Ying Liu, Zhenbin Gong, Rijin Huang, Yundi Shi, Huogen Liu

Introduction and objectives

The development of cardiac fibrosis (CF) and hypertrophy (CH) can lead to heart failure. Mesenchymal stem cells (MSCs) have shown promise in treating cardiac diseases. However, the relationship between MSCs and splicing factor arginine/serine rich-3 (SFRS3) remains unclear. In this study, our objectives are to investigate the effect of MSCs on SFRS3 expression, and their impact on CF and CH. Additionally, we aim to explore the function of the overexpression of SFRS3 in angiotensin II (Ang II)-treated cardiac fibroblasts (CFBs) and cardiac myocytes (CMCs).

Methods

Rat cardiac fibroblasts (rCFBs) or rat cardiac myocytes (rCMCs) were co-cultured with rat MSCs (rMSCs). The function of SFRS3 in Ang II-induced rCFBs and rCMCs was studied by overexpressing SFRS3 in these cells, both with and without the presence of rMSCs. We assessed the expression of SFRS3 and evaluated the cell cycle, proliferation and apoptosis of rCFBs and rCMCs. We also measured the levels of interleukin (IL)-β, IL-6 and tumor necrosis factor (TNF)-α and assessed the degree of fibrosis in rCFBs and hypertrophy in rCMCs.

Results

rMSCs induced SFRS3 expression and promoted cell cycle, proliferation, while reducing apoptosis of Ang II-treated rCFBs and rCMCs. Co-culture of rMSCs with these cells also repressed cytokine production and mitigated the fibrosis of rCFBs, as well as hypertrophy of rCMCs triggered by Ang II. Overexpression of SFRS3 in the rCFBs and rCMCs yielded identical effects to rMSC co-culture.

Conclusion

MSCs may alleviate Ang II-induced cardiac fibrosis and cardiomyocyte hypertrophy by increasing SFRS3 expression in vitro.
导言和目标:心脏纤维化(CF)和肥大(CH)的发展可导致心力衰竭。间充质干细胞(MSCs)已显示出治疗心脏疾病的前景。然而,间充质干细胞与剪接因子富精氨酸/丝氨酸-3(SFRS3)之间的关系仍不清楚。在本研究中,我们的目的是研究间充质干细胞对 SFRS3 表达的影响,以及它们对 CF 和 CH 的影响。此外,我们还旨在探索 SFRS3 在血管紧张素 II(Ang II)处理的心脏成纤维细胞(CFBs)和心肌细胞(CMCs)中过表达的功能:方法:将大鼠心脏成纤维细胞(rCFBs)或大鼠心肌细胞(rCMCs)与大鼠间充质干细胞(rMSCs)共同培养。通过在这些细胞中过表达 SFRS3,研究了 SFRS3 在 Ang II 诱导的 rCFBs 和 rCMCs 中的功能。我们评估了 SFRS3 的表达,并评价了 rCFBs 和 rCMCs 的细胞周期、增殖和凋亡。我们还测量了白细胞介素(IL)-β、IL-6 和肿瘤坏死因子(TNF)-α 的水平,并评估了 rCFBs 的纤维化程度和 rCMCs 的肥大程度。rMSCs 与这些细胞共培养还能抑制细胞因子的产生,减轻血管紧张素 II 引发的 rCFBs 纤维化和 rCMCs 肥大。在 rCFBs 和 rCMCs 中过表达 SFRS3 与 rMSC 共培养的效果相同:结论:间充质干细胞可通过增加体外 SFRS3 的表达,缓解 Ang II 诱导的心脏纤维化和心肌细胞肥大。
{"title":"Mesenchymal stem cells may alleviate angiotensin II-induced myocardial fibrosis and hypertrophy by upregulating SFRS3 expression","authors":"Ling Gu,&nbsp;Xin Wan,&nbsp;Ying Liu,&nbsp;Zhenbin Gong,&nbsp;Rijin Huang,&nbsp;Yundi Shi,&nbsp;Huogen Liu","doi":"10.1016/j.repc.2024.04.010","DOIUrl":"10.1016/j.repc.2024.04.010","url":null,"abstract":"<div><h3>Introduction and objectives</h3><div>The development of cardiac fibrosis (CF) and hypertrophy (CH) can lead to heart failure. Mesenchymal stem cells (MSCs) have shown promise in treating cardiac diseases. However, the relationship between MSCs and splicing factor arginine/serine rich-3 (SFRS3) remains unclear. In this study, our objectives are to investigate the effect of MSCs on SFRS3 expression, and their impact on CF and CH. Additionally, we aim to explore the function of the overexpression of SFRS3 in angiotensin II (Ang II)-treated cardiac fibroblasts (CFBs) and cardiac myocytes (CMCs).</div></div><div><h3>Methods</h3><div>Rat cardiac fibroblasts (rCFBs) or rat cardiac myocytes (rCMCs) were co-cultured with rat MSCs (rMSCs). The function of SFRS3 in Ang II-induced rCFBs and rCMCs was studied by overexpressing SFRS3 in these cells, both with and without the presence of rMSCs. We assessed the expression of SFRS3 and evaluated the cell cycle, proliferation and apoptosis of rCFBs and rCMCs. We also measured the levels of interleukin (IL)-β, IL-6 and tumor necrosis factor (TNF)-α and assessed the degree of fibrosis in rCFBs and hypertrophy in rCMCs.</div></div><div><h3>Results</h3><div>rMSCs induced SFRS3 expression and promoted cell cycle, proliferation, while reducing apoptosis of Ang II-treated rCFBs and rCMCs. Co-culture of rMSCs with these cells also repressed cytokine production and mitigated the fibrosis of rCFBs, as well as hypertrophy of rCMCs triggered by Ang II. Overexpression of SFRS3 in the rCFBs and rCMCs yielded identical effects to rMSC co-culture.</div></div><div><h3>Conclusion</h3><div>MSCs may alleviate Ang II-induced cardiac fibrosis and cardiomyocyte hypertrophy by increasing SFRS3 expression <em>in vitro</em>.</div></div>","PeriodicalId":48985,"journal":{"name":"Revista Portuguesa De Cardiologia","volume":"43 12","pages":"Pages 645-656"},"PeriodicalIF":1.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141581296","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}
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Revista Portuguesa De Cardiologia
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