Circulation最新文献

{"title":"Outcomes of Transcatheter Aortic Valve Replacement in Low-Risk Patients in the United States: A Report From the STS/ACC TVT Registry.","authors":"Andrew M Vekstein, Zachary K Wegermann, Pratik Manandhar, Michael J Mack, David J Cohen, G Chad Hughes, J Kevin Harrison, Tsuyoshi Kaneko, Samir R Kapadia, Konstantinos Stathogiannis, William F Fearon, Suzanne Arnold, Andrzej S Kosinski, Martin B Leon, Wayne B Batchelor, Vinod H Thourani, Sreekanth Vemulapalli","doi":"10.1161/CIRCULATIONAHA.124.071838","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.124.071838","url":null,"abstract":"<p><strong>Background: </strong>Real-world low-risk transcatheter aortic valve replacement (TAVR) outcomes in the United States have not been assessed comprehensively versus pivotal trials, which is a key component of measuring the quality of clinical technology adoption.</p><p><strong>Methods: </strong>We identified heart team-designated low-risk patients undergoing TAVR for trileaflet severe, symptomatic aortic stenosis in the Society of Thoracic Surgeons/American College of Cardiology Transcatheter Valve Registry, as well as a subset of patients who met low-risk trial inclusion and exclusion criteria, from January 2020 to March 2024. Outcomes (mortality, stroke, new pacemaker, and \"alive and well,\" defined as alive at 1 year with Kansas City Cardiomyopathy Questionnaire score ≥60 and ≤10-point decrease from baseline) at 30 days and 1 year were assessed. Multivariable models were developed to assess predictors of death within 1 year after TAVR.</p><p><strong>Results: </strong>Among 383 030 patients who underwent TAVR during the study period, 108 407 (28%) were designated low risk by the heart team, and 68 194 (18%) met other study inclusion and exclusion criteria. Of these, 62% (n=42 093) would have been eligible for the low-risk trials. In the overall heart team-designated low-risk population, 30-day outcomes included 0.8% mortality, 1.5% stroke, and 8.4% new permanent pacemaker requirement; 1-year outcomes included 4.6% mortality, 2.6% stroke, and 90% alive and well. In the trial-eligible population, 0.6% mortality, 1.4% stroke, and 8.0% new permanent pacemaker requirement had occurred by 30 days; values at 1 year included 3.1% mortality, 2.4% stroke, and 92% alive and well. Notable multivariable predictors of 1-year mortality were atrial fibrillation, nontransfemoral access, and lower baseline Kansas City Cardiomyopathy Questionnaire score.</p><p><strong>Conclusions: </strong>One-year outcomes among real-world trial-eligible patients are excellent, but adverse events are higher compared with published clinical trial data, likely because of greater comorbidity burden and lower baseline Kansas City Cardiomyopathy Questionnaire score. These data can help inform expected outcomes and health status after low-risk TAVR.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":35.5,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771464","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":"METTL4-Mediated Mitochondrial DNA N6-Methyldeoxyadenosine Promoting Macrophage Inflammation and Atherosclerosis.","authors":"Longbin Zheng, Xiang Chen, Xian He, Huiyuan Wei, Xinyu Li, Yongkang Tan, Jiao Min, Minghong Chen, Yunjia Zhang, Mengdie Dong, Quanwen Yin, Mengdie Xue, Lulu Zhang, Da Huo, Hong Jiang, Tingyou Li, Fei Li, Xin Wang, Xuesong Li, Hongshan Chen","doi":"10.1161/CIRCULATIONAHA.124.069574","DOIUrl":"10.1161/CIRCULATIONAHA.124.069574","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Mitochondrial dysfunction is a key factor in the development of atherogenesis. METTL4 (methyltransferase-like protein 4) mediates N6- methyldeoxyadenosine (6mA) of mammalian mitochondrial DNA (mtDNA). However, the role of METTL4-mediated mitoepigenetic regulation in atherosclerosis is still unknown. This study aims to investigate the potential involvement of METTL4 in atherosclerosis, explore the underlying mechanism, and develop targeted strategies for treating atherosclerosis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Expression levels of mtDNA 6mA and METTL4 were determined in atherosclerotic lesions. We explored the mechanism of METTL4 involvement in atherosclerosis using &lt;i&gt;Mettl4&lt;/i&gt;&lt;sup&gt;&lt;i&gt;Mac&lt;/i&gt;&lt;/sup&gt;&lt;sup&gt;&lt;i&gt;-KO&lt;/i&gt;&lt;/sup&gt;-&lt;i&gt;Apoe&lt;/i&gt;&lt;sup&gt;&lt;i&gt;-/&lt;/i&gt;-&lt;/sup&gt; and &lt;i&gt;Mettl4&lt;/i&gt;&lt;sup&gt;&lt;i&gt;MUT&lt;/i&gt;&lt;/sup&gt;-&lt;i&gt;Apoe&lt;/i&gt;&lt;sup&gt;&lt;i&gt;-/&lt;/i&gt;-&lt;/sup&gt; mice and cell models, as well as bone marrow transplantation. Natural compound libraries were screened to identify potent METTL4 antagonists. In addition, bioinspired proteolysis targeting chimera technology targeting macrophages within plaques was used to increase the efficacy of the METTL4 antagonist.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The expression levels of mtDNA 6mA and METTL4 were significantly increased in plaque macrophages. &lt;i&gt;Mettl4&lt;/i&gt;&lt;sup&gt;&lt;i&gt;Mac-KO&lt;/i&gt;&lt;/sup&gt;-&lt;i&gt;Apoe&lt;/i&gt;&lt;sup&gt;&lt;i&gt;-/&lt;/i&gt;-&lt;/sup&gt; mice displayed suppressed mtDNA 6mA levels and atherosclerotic progression, which were reversed by METTL4 restoration through bone marrow transplantation (n=6). Mechanistically, elevated METTL4 expression reduces mitochondrial ATP6 (MT-ATP6) expression by suppressing its transcription, thereby impairing the activity of mitochondrial respiration chain complex V. This disruption leads to the accumulation of excess protons in the mitochondrial intermembrane space, causing mitochondrial dysfunction. Consequently, mtDNA is released into the cytoplasm, ultimately triggering inflammasome activation. All results were reversed by the mutation in the METTL4 methyltransferase active site. &lt;i&gt;Mettl4&lt;/i&gt;&lt;sup&gt;&lt;i&gt;MUT&lt;/i&gt;&lt;/sup&gt;-&lt;i&gt;Apoe&lt;/i&gt;&lt;sup&gt;&lt;i&gt;-/&lt;/i&gt;-&lt;/sup&gt; mice showed suppressed mtDNA 6mA levels and atherosclerotic progression and repaired mitochondrial function of macrophage, which were reversed by METTL4 restoration through bone marrow transplantation (n=6). Pemetrexed was identified as the first METTL4 antagonist to effectively alleviate atherosclerotic progression. Furthermore, we generated a proteolysis targeting chimera drug based on pemetrexed that specifically targeted METTL4 in macrophages within plaques, showing a promising therapeutic effect on atherosclerosis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;This study revealed a novel mechanism by which mtDNA 6mA orchestrated mitochondrial function-related gene expression in macrophages, thereby promoting atherosclerosis. Through various experimental techniques, such as gene manipulation, pharmacological inhibition, and proteolysis targeting chimera, this study","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"946-965"},"PeriodicalIF":35.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11952693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142834247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Olmesartan Restores <i>LMNA</i> Function in Haploinsufficient Cardiomyocytes.","authors":"Eric J Kort, Nazish Sayed, Chun Liu, Gema Mondéjar-Parreño, Jens Forsberg, Emily Eugster, Sean M Wu, Joseph C Wu, Stefan Jovinge","doi":"10.1161/CIRCULATIONAHA.121.058621","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.121.058621","url":null,"abstract":"<p><strong>Background: </strong>Gene mutations are responsible for a sizeable proportion of cases of heart failure. However, the number of patients with any specific mutation is small. Repositioning of existing US Food and Drug Administration-approved compounds to target specific mutations is a promising approach to efficient identification of new therapies for these patients.</p><p><strong>Methods: </strong>The National Institutes of Health Library of Integrated Network-Based Cellular Signatures database was interrogated to identify US Food and Drug Administration-approved compounds that demonstrated the ability to reverse the transcriptional effects of <i>LMNA</i> knockdown. Top hits from this screening were validated in vitro with patient-specific induced pluripotent stem cell-derived cardiomyocytes combined with force measurement, gene expression profiling, electrophysiology, and protein expression analysis.</p><p><strong>Results: </strong>Several angiotensin receptor blockers were identified from our in silico screen. Of these, olmesartan significantly elevated the expression of sarcomeric genes and rate and force of contraction and ameliorated arrhythmogenic potential. In addition, olmesartan exhibited the ability to reduce phosphorylation of extracellular signal-regulated kinase 1 in <i>LMNA</i>-mutant induced pluripotent stem cell-derived cardiomyocytes.</p><p><strong>Conclusions: </strong>In silico screening followed by in vitro validation with induced pluripotent stem cell-derived models can be an efficient approach to identifying repositionable therapies for monogenic cardiomyopathies.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":35.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751368","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":"From the Literature.","authors":"Tracy Hampton","doi":"10.1161/CIRCULATIONAHA.125.074395","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.125.074395","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 13","pages":"966-967"},"PeriodicalIF":35.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751466","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":"Paternal Cardiac Lesion Induces Cardiac Adaptation in Offspring.","authors":"Benedetta Coppe, María Galardi-Castilla, Andrés Sanz-Morejón, Prateek Arora, Javier Lucas, Casie Iciek, Laura Lalaguna, Enrique Lara-Pezzi, Ignacio Flores, Nadia Mercader","doi":"10.1161/CIRCULATIONAHA.124.070323","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.124.070323","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 13","pages":"968-971"},"PeriodicalIF":35.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751470","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":"Response by Yu and Cheng to Letter Regarding Article, \"Effect of Colchicine on Coronary Plaque Stability in Acute Coronary Syndrome as Assessed by Optical Coherence Tomography: The COLOCT Randomized Clinical Trial\".","authors":"Miao Yu, Xiang Cheng","doi":"10.1161/CIRCULATIONAHA.124.073362","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.124.073362","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 13","pages":"e769-e770"},"PeriodicalIF":35.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751485","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":"2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.","authors":"Sunil V Rao, Michelle L O'Donoghue, Marc Ruel, Tanveer Rab, Jaqueline E Tamis-Holland, John H Alexander, Usman Baber, Heather Baker, Mauricio G Cohen, Mercedes Cruz-Ruiz, Leslie L Davis, James A de Lemos, Tracy A DeWald, Islam Y Elgendy, Dmitriy N Feldman, Abhinav Goyal, Ijeoma Isiadinso, Venu Menon, David A Morrow, Debabrata Mukherjee, Elke Platz, Susan B Promes, Sigrid Sandner, Yader Sandoval, Rachel Schunder, Binita Shah, Jason P Stopyra, Amy W Talbot, Pam R Taub, Marlene S Williams","doi":"10.1161/CIR.0000000000001309","DOIUrl":"10.1161/CIR.0000000000001309","url":null,"abstract":"<p><strong>Aim: </strong>The \"2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes\" incorporates new evidence since the \"2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction\" and the corresponding \"2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes\" and the \"2015 ACC/AHA/SCAI Focused Update on Primary Percutaneous Coronary Intervention for Patients With ST-Elevation Myocardial Infarction.\" The \"2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes\" and the \"2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization\" retire and replace, respectively, the \"2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease.\"</p><p><strong>Methods: </strong>A comprehensive literature search was conducted from July 2023 to April 2024. Clinical studies, systematic reviews and meta-analyses, and other evidence conducted on human participants were identified that were published in English from MEDLINE (through PubMed), EMBASE, the Cochrane Library, Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline.</p><p><strong>Structure: </strong>Many recommendations from previously published guidelines have been updated with new evidence, and new recommendations have been created when supported by published data.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"e771-e862"},"PeriodicalIF":35.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522756","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":"Withdrawal of Guideline-Directed Medical Therapy in Patients With Heart Failure and Improved Ejection Fraction.","authors":"Christian Basile, Felix Lindberg, Lina Benson, Federica Guidetti, Ulf Dahlström, Massimo Francesco Piepoli, Peter Mol, Raffaele Scorza, Aldo Pietro Maggioni, Lars H Lund, Gianluigi Savarese","doi":"10.1161/CIRCULATIONAHA.124.072855","DOIUrl":"10.1161/CIRCULATIONAHA.124.072855","url":null,"abstract":"<p><strong>Background: </strong>Limited evidence exists on the prognostic role of continuing medical therapy in patients with heart failure (HF) and an ejection fraction (EF) that has improved over time. This study assessed rates of, patient profiles, and associations with morbidity/mortality of renin-angiotensin inhibitors (RASi), angiotensin receptor-neprilysin inhibitors (ARNi), beta-blockers (BBL), and mineralocorticoid receptor antagonists (MRA) withdrawal in patients with HF with improved EF.</p><p><strong>Methods: </strong>Patients with a first recorded EF <40% and a later EF ≥40% from the Swedish HF registry between June 11, 2000, and December 31, 2023, were included in this retrospective observational study. Withdrawal was defined as a patient on treatment at the first (reduced) but not at the second (improved) registration. The association between withdrawal and time to first cardiovascular mortality/hospitalization for HF with censoring at 1 year was assessed by Cox regression model using overlap weighting.</p><p><strong>Results: </strong>Of 8728 patients with HF with improved EF (median age, 70 years [25th to 75th percentile, 61-78], 2611 [29.9%] women), 96%, 94%, and 46% received RASi/ARNi, BBL, and MRA, respectively, when EF was <40%. The withdrawal rates at the time of the improved EF registration were 4.4% for RASi/ARNi, 3.3% for BBL, and 17.2% for MRA. Predictors of withdrawal included lower use of other HF medications, higher EF at the later EF registration, and a longer time between the 2 EF assessments. After weighting, withdrawal was independently associated with a higher risk of cardiovascular mortality/hospitalization for HF by 38% for RASi/ARNi and 36% for MRA, but not for BBL. Withdrawal of BBL was associated with a higher risk of the primary outcome in the subgroup of patients with an improved EF of 40% to 49% versus ≥50% (<i>P</i>-interaction 0.03).</p><p><strong>Conclusions: </strong>In patients with HF with improved EF, HF therapy withdrawal was rare. Withdrawing RASi/ARNi and MRA was associated with higher mortality/morbidity at 1 year. No association was found for BBL withdrawal, albeit with a significant heterogeneity for EF at improvement, suggesting better outcomes with continuing BBL only until EF improves up to 50%. These results are hypothesis-generating and highlight the need for randomized controlled trials testing BBL withdrawal in patients with HF with improved EF.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"931-945"},"PeriodicalIF":35.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647525","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":"Lymphatic Endothelial Branched-Chain Amino Acid Catabolic Defects Undermine Cardiac Lymphatic Integrity and Drive HFpEF.","authors":"Xiong Guo, Chong Huang, Ling Zhang, Guangyu Hu, Yunhui Du, Xiyao Chen, Fangfang Sun, Tongzheng Li, Zhe Cui, Congye Li, Yongzhen Guo, Wenjun Yan, Yunlong Xia, Shan Wang, Hui Liu, Zhiyuan Liu, Zhen Lin, Xinyi Wang, Zhengyang Wang, Fuyang Zhang, Ling Tao","doi":"10.1161/CIRCULATIONAHA.124.071741","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.124.071741","url":null,"abstract":"<p><strong>Background: </strong>Heart failure with preserved ejection fraction (HFpEF) has become the most prevalent type of heart failure, but effective treatments are lacking. Cardiac lymphatics play a crucial role in maintaining heart health by draining fluids and immune cells. However, their involvement in HFpEF remains largely unexplored.</p><p><strong>Methods: </strong>We examined cardiac lymphatic alterations in mice with HFpEF with comorbid obesity and hypertension, and in heart tissues from patients with HFpEF. Using genetically engineered mouse models and various cellular and molecular techniques, we investigated the role of cardiac lymphatics in HFpEF and the underlying mechanisms.</p><p><strong>Results: </strong>In mice with HFpEF, cardiac lymphatics displayed substantial structural and functional anomalies, including decreased lymphatic endothelial cell (LEC) density, vessel fragmentation, reduced branch connections, and impaired capacity to drain fluids and immune cells. LEC numbers and marker expression levels were also decreased in heart tissues from patients with HFpEF. Stimulating lymphangiogenesis with an adeno-associated virus expressing an engineered variant of vascular endothelial growth factor C (VEGFC^C156S) that selectively activates vascular endothelial growth factor receptor 3 (VEGFR3) in LECs restored cardiac lymphatic integrity and substantially alleviated HFpEF. Through discovery-driven approaches, defective branched-chain amino acid (BCAA) catabolism was identified as a predominant metabolic signature in HFpEF cardiac LECs. Overexpression of branched-chain ketoacid dehydrogenase kinase (encoded by the <i>Bckdk</i> gene), which inactivates branched-chain ketoacid dehydrogenase (the rate-limiting enzyme in BCAA catabolism), resulted in spontaneous lymphangiogenic defects in LECs. In mice, inducible <i>Bckdk</i> gene deletion in LECs to enhance their BCAA catabolism preserved cardiac lymphatic integrity and protected against HFpEF. BCAA catabolic defects caused ligand-independent phosphorylation of VEGFR3 in the cytoplasm by Src kinase, leading to lysosomal degradation of VEGFR3 instead of its trafficking to the cell membrane. Reduced VEGFR3 availability on the cell surface impeded downstream Akt (protein kinase B) activation, hindered glucose uptake and utilization, and inhibited lymphangiogenesis in LECs with BCAA catabolic defects.</p><p><strong>Conclusions: </strong>Our study provides evidence that cardiac lymphatic disruption, driven by impaired BCAA catabolism in LECs, is a key factor contributing to HFpEF. These findings unravel the crucial role of BCAA catabolism in modulating lymphatic biology, and suggest that preserving cardiac lymphatic integrity may present a novel therapeutic strategy for HFpEF.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":35.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751367","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":"Correction to: 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.","authors":"Sunil V Rao, Michelle L O'Donoghue, Marc Ruel, Tanveer Rab, Jaqueline E Tamis-Holland, John H Alexander, Usman Baber, Heather Baker, Mauricio G Cohen, Mercedes Cruz-Ruiz, Leslie L Davis, James A de Lemos, Tracy A DeWald, Islam Y Elgendy, Dmitriy N Feldman, Abhinav Goyal, Ijeoma Isiadinso, Venu Menon, David A Morrow, Debabrata Mukherjee, Elke Platz, Susan B Promes, Sigrid Sandner, Yader Sandoval, Rachel Schunder, Binita Shah, Jason P Stopyra, Amy W Talbot, Pam R Taub, Marlene S Williams","doi":"10.1161/CIR.0000000000001328","DOIUrl":"https://doi.org/10.1161/CIR.0000000000001328","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 13","pages":"e865"},"PeriodicalIF":35.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751370","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}