Flavio L Ribichini, Gabriele Pesarini, Giuseppe Tarantini
{"title":"FFR-guided revascularization in patients undergoing TAVI: insights on the FAITAVI trial.","authors":"Flavio L Ribichini, Gabriele Pesarini, Giuseppe Tarantini","doi":"10.1093/eurheartj/ehag259","DOIUrl":"10.1093/eurheartj/ehag259","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":"5320-5321"},"PeriodicalIF":45.3,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147987173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Leaders in cardiology: Donna Fitzsimons.","authors":"Judith Ozkan","doi":"10.1093/eurheartj/ehag347","DOIUrl":"10.1093/eurheartj/ehag347","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":"5228-5229"},"PeriodicalIF":45.3,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148162416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ioannis D Laoutaris,Athanasios Dritsas,Stamatis Adamopoulos
{"title":"Training the diaphragm as a pillar of cardiac rehabilitation in heart failure","authors":"Ioannis D Laoutaris,Athanasios Dritsas,Stamatis Adamopoulos","doi":"10.1093/eurheartj/ehag789","DOIUrl":"https://doi.org/10.1093/eurheartj/ehag789","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"13 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ke Chen,Zhen-Zhen Chen,Jin-Wei Tian,Jun-Zhuo Wang,Lun Xiao,Hai-Zeng Zhang,Wen-Bin Wang,Dong-Ming Zhou,Xiao-Qiang Li,Jun Xie,Wen-Dong Li
{"title":"Deep vein thrombosis exacerbated by syndecan-4 shedding and piezo1-dependent endothelial-mesenchymal transition","authors":"Ke Chen,Zhen-Zhen Chen,Jin-Wei Tian,Jun-Zhuo Wang,Lun Xiao,Hai-Zeng Zhang,Wen-Bin Wang,Dong-Ming Zhou,Xiao-Qiang Li,Jun Xie,Wen-Dong Li","doi":"10.1093/eurheartj/ehag775","DOIUrl":"https://doi.org/10.1093/eurheartj/ehag775","url":null,"abstract":"Abstract Background and Aims Deep vein thrombosis (DVT) remains a major health burden with incompletely understood mechanisms and limited therapeutic options. This study aims to investigate the role of key molecules in DVT and to explore the feasibility of treatment strategies based on this mechanism. Methods Plasma proteomic profiling (LC-MS/MS) was performed on DVT patients and healthy controls, identifying syndecan-4 (SDC4) as a differentially expressed protein. Functional investigations utilized SDC4 knockout mice, endothelial cell (EC)-specific lineage tracing models, and single-cell RNA sequencing to assess endothelial-to-mesenchymal transition (EndMT) during DVT progression. In vitro EndMT models were established in human umbilical vein endothelial cells. Protein interactions were confirmed by co-immunoprecipitation. Piezo1 was pharmacologically inhibited in vivo, and network pharmacology was used to seek a potential therapeutic agent. Results SDC4 levels were elevated in DVT patients. SDC4 deficiency exacerbated thrombus formation and promoted EndMT, as evidenced by reduced EC markers and increased mesenchymal markers. Single-cell sequencing revealed a specific EC subpopulation (C1) driving EndMT, with Piezo1 identified as a downstream mediator of SDC4. Co-IP confirmed direct SDC4–Piezo1 interaction. Piezo1 upregulation activated the PI3K/Akt pathway, Piezo1 knockdown attenuated EndMT and reduced thrombus burden. Quercetin directly bound Piezo1, reduced its expression in a dose-dependent manner, and significantly decreased thrombus size in DVT mice. Conclusions SDC4 shedding exacerbates DVT by promoting Piezo1-dependent EndMT via PI3K/Akt signalling. Quercetin shows therapeutic potential as a Piezo1 inhibitor.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"1 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mahmoud H Elbatreek,Zhen Li,Xiaoman Yu,Natalie D Gehred,Tatiana Gromova,Jingshu Chen,Miguel Huerta,Naoto Muraoka,Martin Borch Jensen,Vinay Kartha,Chris Carrico,Timothy D Allerton,Xinheng Zhang,Hsin-Jung R Yang,Michael E Bowdish,Sanjiv J Shah,Kathleen C Woulfe,Timothy A McKinsey,Edwin Yoo,David J Polhemus,Thomas M Vondriska,David J Lefer,Traci T Goodchild
{"title":"Semaglutide, independent of weight loss, attenuates cardiac and hepatic remodelling in experimental heart failure with preserved ejection fraction","authors":"Mahmoud H Elbatreek,Zhen Li,Xiaoman Yu,Natalie D Gehred,Tatiana Gromova,Jingshu Chen,Miguel Huerta,Naoto Muraoka,Martin Borch Jensen,Vinay Kartha,Chris Carrico,Timothy D Allerton,Xinheng Zhang,Hsin-Jung R Yang,Michael E Bowdish,Sanjiv J Shah,Kathleen C Woulfe,Timothy A McKinsey,Edwin Yoo,David J Polhemus,Thomas M Vondriska,David J Lefer,Traci T Goodchild","doi":"10.1093/eurheartj/ehag732","DOIUrl":"https://doi.org/10.1093/eurheartj/ehag732","url":null,"abstract":"Abstract Background and Aims Heart failure with preserved ejection fraction (HFpEF) remains a significant therapeutic challenge. While GLP-1 receptor agonists (GLP-1RAs) show clinical promise, it remains unknown if their benefits are driven solely by weight loss or involve weight loss-independent mechanisms. We investigated the weight loss-independent effects of semaglutide in two preclinical models of cardiometabolic HFpEF: the ZSF1 Obese rat and the Göttingen HFpEF minipig. Methods Male ZSF1 Obese rats (n = 12/group) and female Göttingen minipigs with ‘two-hit’ induced HFpEF (early intervention: n = 5/group; delayed intervention: n = 4/group) were treated with semaglutide at doses empirically determined to be non-weight-loss inducing. Comprehensive assessments included invasive hemodynamic (LVEDP, PCWP), echocardiography, and histological quantification of fibrosis and lipid burden. Delayed intervention utilized Cardiac MRI to quantify subcutaneous and ectopic fat depots. In rats, advanced multi-omics (NULISA plasma proteomics, single-cell RNA sequencing and tissue proteomics) were utilized to explore molecular mechanisms. Results In ZSF1 Obese rats, semaglutide significantly improved diastolic function (reducing LVEDP by ∼60%) and attenuated cardiac hypertrophy (by ∼30%), interstitial fibrosis, and cardiac lipid deposition in the absence of a significant weight loss. These functional benefits were conserved in the minipig HFpEF model, where treatment attenuated cardiac hypertrophy, left ventricular E/e′, normalized pulmonary capillary wedge pressure (PCWP) and reversed advanced hepatic bridging fibrosis. Delayed intervention in established HFpEF minipigs reversed diastolic dysfunction and significantly reduced ectopic lipid depots (intramyocardial, epicardial, and hepatic fat) without affecting subcutaneous fat or total body weight. Mechanistically, multi-omics analyses in the rat heart revealed that these benefits were driven by suppression of pro-fibrotic and hypertrophic signals and up-regulation of branched-chain amino acid (BCAA) catabolism and fatty acid oxidation pathways in cardiomyocytes. Conclusions Semaglutide attenuates cardiac and hepatic remodelling in preclinical models of obesity-associated cardiometabolic HFpEF in the absence of profound weight loss. The conservation of these effects across male rodents and female swine supports their translational relevance, while future studies are needed to define dose equivalence and confirm GLP-1 receptor engagement in cardiac and hepatic tissues. These findings support further mechanistic investigation of weight loss-independent GLP-1 receptor agonist signalling in this HFpEF phenotype.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"24 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Congenital heart disease in adults: evolving health systems and lifelong outcomes","authors":"Gerhard-Paul Diller,Curt Daniels,Ariane Marelli","doi":"10.1093/eurheartj/ehag616","DOIUrl":"https://doi.org/10.1093/eurheartj/ehag616","url":null,"abstract":"Abstract Over the past decades, advances in the diagnosis and treatment of congenital heart disease have reshaped its epidemiology. Congenital heart disease is now increasingly a chronic, lifelong disorder, with adult survivors outnumbering affected children in many countries. This demographic transition has shifted the focus from preventing early mortality towards optimizing long-term health and managing comorbidities. Adult congenital heart disease (ACHD) experience acquired cardiovascular and systemic complications that challenge traditional models of care. As the lifelong burden of disease in ACHD patients continues to rise globally, advanced training pathways in ACHD have spearheaded the content expertise required to deliver high quality of care. The well-established hub-and-scope model has been recommended in the last two decades to improve ACHD care by expanding the number of specialized centres that allow ACHD specialists to reach underserved regions more effectively. However, the advent of technology, digital health, and artificial intelligence–enhanced decision-making provides an opportunity to imagine a different approach, to coordinate advances in research, clinical care, and health system design, with particular emphasis on scalable models that align expertise, data, and delivery across the life course. Networked care structures, workforce redesign, and digitally enabled learning health systems offer a pathway to close persistent gaps in care access and quality. Ultimately, the future of ACHD care will depend on our ability to integrate these innovations into routine practice, ensuring that extended survival is matched by preserved function, quality of life, and equitable outcomes at the population scale.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"31 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"European funding for cardiovascular research: room for improvement for the ERC track.","authors":"Reza Parvan, Cecilia M Linde, Rudolf A de Boer","doi":"10.1093/eurheartj/ehag415","DOIUrl":"10.1093/eurheartj/ehag415","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":"5230-5233"},"PeriodicalIF":45.3,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148162340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}