CirculationPub Date : 2025-09-25DOI: 10.1161/cir.0000000000001377
Dhruv S Kazi,Abdul R Abdullah,Suzanne V Arnold,Anirban Basu,Brandon K Bellows,Khadijah Breathett,Derek S Chew,David J Cohen,Colette DeJong,Paul A Heidenreich,Susan Hennessy,Inmaculada Hernandez,Nicolas Isaza,Karen E Joynt Maddox,Ann Marie Navar,Ankur Pandya,Kendra D Sims,Merilyn S Varghese,Liesl Zühlke
{"title":"2025 AHA/ACC Statement on Cost/Value Methodology in Clinical Practice Guidelines (Update From 2014 Statement): A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.","authors":"Dhruv S Kazi,Abdul R Abdullah,Suzanne V Arnold,Anirban Basu,Brandon K Bellows,Khadijah Breathett,Derek S Chew,David J Cohen,Colette DeJong,Paul A Heidenreich,Susan Hennessy,Inmaculada Hernandez,Nicolas Isaza,Karen E Joynt Maddox,Ann Marie Navar,Ankur Pandya,Kendra D Sims,Merilyn S Varghese,Liesl Zühlke","doi":"10.1161/cir.0000000000001377","DOIUrl":"https://doi.org/10.1161/cir.0000000000001377","url":null,"abstract":"AIMThe \"2025 AHA/ACC Statement on Cost/Value Methodology in Clinical Practice Guidelines (Update From 2014 Statement)\" describes a systematic approach for consistent implementation of \"economic value statements\" across ACC/AHA guidelines. It updates the cost-effectiveness threshold and proposes a new level of certainty framework that summarizes the strength of the available evidence. Additionally, it describes how cost-effectiveness analyses (CEAs) can help advance equity in population cardiovascular health.METHODSA focused literature search was conducted from January 9, 2024, to February 2, 2024, encompassing English-language publications related to CEA methodology in PubMed, EMBASE, and the Cochrane Library, with publication dates ranging from 1973 to the present. Additional relevant studies published during the writing process (through June 25, 2024) were also considered by the writing committee.STRUCTUREThis Cost/Value Methodology Statement updates prior guidance regarding the incorporation of evidence from published CEAs into clinical guidelines. It provides guidance for identifying and synthesizing relevant high-quality evidence, developing economic value statements, and communicating level of certainty in such statements. It defines the US cost-effectiveness threshold as $120 000 per quality-adjusted life year gained, highlights special considerations related to cardiovascular drugs and devices, emphasizes health equity considerations when interpreting CEAs, and defines a reference case for future CEAs.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"38 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145140359","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":"PYGM Protects Against Myocardial Infarction by Enhancing Glycogenolysis and Facilitating Autophagic Flux.","authors":"Jing Gan,Ruyi Zhao,Dong Zheng,Yue Peng,Maolan Wu,Feifan Sun,Ruike An,Aimin Xu,Maohua Chen,Yulin Li,Wei Lei,Zhuofeng Lin,Fan Wu","doi":"10.1161/circulationaha.124.072312","DOIUrl":"https://doi.org/10.1161/circulationaha.124.072312","url":null,"abstract":"BACKGROUNDPYGM (muscle glycogen phosphorylase), the rate-limiting enzyme in glycogenolysis, plays an indispensable role in maintaining cardiac energy metabolism. However, the role of PYGM in the pathogenesis of myocardial infarction (MI) remains unclear.METHODSThe expression profiles of PYGM in cardiac tissues and plasma samples from subjects with MI were assessed using immunoblotting. The role of PYGM in MI was determined by evaluating the effects of PYGM deficiency and its replenishment through adeno-associated virus-mediated PYGM expression in mice with MI.RESULTSWe found that circulating PYGM levels and their cardiac contents were significantly decreased in patients with MI, which was associated with impaired cardiac function. Loss of PYGM significantly exacerbated MI-induced cardiac dysfunction and damage in mice, and replenishment of PYGM profoundly reversed these adverse effects. Mechanistically, PYGM enhanced glycogenolysis by activating glycolysis and the pentose phosphate pathway, thereby improving cardiac energy homeostasis and mitigating oxidative stress. In addition, PYGM improved MI-induced autophagic flux obstacles and alleviated MI-induced cardiac damage by suppressing the expression of Thbs1 (thrombospondin-1). Moreover, genetic deficiency or pharmacological blockage of autophagy attenuated the protective effects of PYGM against MI-induced cardiac injury, and cardiac-specific knockdown of Thbs1 substantially improved the adverse impact of MI on cardiac dysfunction and damage in PYGM-null mice.CONCLUSIONSPYGM safeguards against MI-induced myocardial injury by stimulating glycogenolysis and promoting autophagic flux, thus preserving myocardial energy homeostasis.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"156 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145127141","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}
CirculationPub Date : 2025-09-23Epub Date: 2025-09-22DOI: 10.1161/CIR.0000000000001384
Maya K Vadiveloo, Christopher D Gardner, Sara N Bleich, Neha Khandpur, Alice H Lichtenstein, Jennifer J Otten, Casey M Rebholz, Chelsea R Singleton, Miriam B Vos, Selina Wang
{"title":"Correction to: Ultraprocessed Foods and Their Association With Cardiometabolic Health: Evidence, Gaps, and Opportunities: A Science Advisory From the American Heart Association.","authors":"Maya K Vadiveloo, Christopher D Gardner, Sara N Bleich, Neha Khandpur, Alice H Lichtenstein, Jennifer J Otten, Casey M Rebholz, Chelsea R Singleton, Miriam B Vos, Selina Wang","doi":"10.1161/CIR.0000000000001384","DOIUrl":"https://doi.org/10.1161/CIR.0000000000001384","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"152 12","pages":"e264"},"PeriodicalIF":38.6,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124322","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}
CirculationPub Date : 2025-09-23Epub Date: 2025-08-05DOI: 10.1161/CIRCULATIONAHA.125.074737
Yaozhong Liu, Huilun Wang, Minzhi Yu, Lei Cai, Ying Zhao, Yalun Cheng, Yongjie Deng, Yang Zhao, Haocheng Lu, Xiaokang Wu, Guizhen Zhao, Chao Xue, Hongyu Liu, Ida Surakka, Anna Schwendeman, Hong S Lu, Alan Daugherty, Lin Chang, Jifeng Zhang, Ryan E Temel, Y Eugene Chen, Yanhong Guo
{"title":"Hypertriglyceridemia as a Key Contributor to Abdominal Aortic Aneurysm Development and Rupture: Insights From Genetic and Experimental Models.","authors":"Yaozhong Liu, Huilun Wang, Minzhi Yu, Lei Cai, Ying Zhao, Yalun Cheng, Yongjie Deng, Yang Zhao, Haocheng Lu, Xiaokang Wu, Guizhen Zhao, Chao Xue, Hongyu Liu, Ida Surakka, Anna Schwendeman, Hong S Lu, Alan Daugherty, Lin Chang, Jifeng Zhang, Ryan E Temel, Y Eugene Chen, Yanhong Guo","doi":"10.1161/CIRCULATIONAHA.125.074737","DOIUrl":"10.1161/CIRCULATIONAHA.125.074737","url":null,"abstract":"<p><strong>Background: </strong>Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease with no effective pharmacological treatments. The causal role of triglycerides (TGs) in AAA development remains unclear and controversial.</p><p><strong>Methods: </strong>Mendelian randomization was applied to assess causal relationships between lipoproteins, circulating proteins, metabolites, and the risk of AAA. To test the hypothesis that elevated plasma TG levels accelerate AAA development, we used <i>Lpl</i>-deficient, <i>Apoa5</i>-deficient, and human <i>APOC3</i> transgenic mice, which display varying degrees of hypertriglyceridemia. Mechanistic studies were performed using RNA sequencing and Western blot analysis of palmitate-treated vascular smooth muscle cells and validated in vivo by local overexpression of key mediator in the suprarenal abdominal aorta. Antisense oligonucleotides targeting <i>Angptl3</i> were administered to reduce TG levels and assess therapeutic potential in human <i>APOC3</i> transgenic and <i>Apoe</i>-deficient mice.</p><p><strong>Results: </strong>Mendelian randomization analyses integrating genetic, proteomic, and metabolomic data identified causal relationships between elevated TG-rich lipoproteins, TG metabolism-related proteins/metabolites, and AAA risk. In the angiotensin II infusion AAA model, most <i>Lpl</i>-deficient mice with severely elevated TG concentrations died of aortic rupture. Similarly, <i>Apoa5</i>-deficient mice with moderately elevated TG levels developed accelerated AAA, and human <i>APOC3</i> transgenic mice with dramatically elevated TG levels exhibited aortic dissection and rupture. Mechanistically, elevated TG and palmitate inhibited lysyl oxidase (LOX) maturation and reduced LOX activity. Locally overexpressing lysyl oxidase eliminated the proaneurysmal effect of hypertriglyceridemia in human <i>APOC3</i> transgenic mice. Moreover, an <i>Angptl3</i>-targeting antisense oligonucleotide profoundly attenuated AAA progression in both human <i>APOC3</i> transgenic and <i>Apoe</i>-deficient mice.</p><p><strong>Conclusions: </strong>These findings identify hypertriglyceridemia as a key contributor to AAA pathogenesis and suggest that targeting TG-rich lipoproteins may be a promising therapeutic strategy for AAA.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"862-881"},"PeriodicalIF":38.6,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12327802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783636","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}
CirculationPub Date : 2025-09-22DOI: 10.1161/circulationaha.124.073382
Suyin Feng,Ziheng Wang,Runfeng Sun
{"title":"Letter by Feng et al Regarding Article, \"Association of Coagulation Factor XI Level With Cardiovascular Events and Cardiac Function in Community-Dwelling Adults: From ARIC and CHS\".","authors":"Suyin Feng,Ziheng Wang,Runfeng Sun","doi":"10.1161/circulationaha.124.073382","DOIUrl":"https://doi.org/10.1161/circulationaha.124.073382","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"52 1","pages":"e239-e240"},"PeriodicalIF":37.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117138","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}
CirculationPub Date : 2025-09-22DOI: 10.1161/circulationaha.125.076354
Cameron M Cupp,Ignatius Gerardo E Zarraga
{"title":"Mechanism Behind QRS Widening With Faster Pacing.","authors":"Cameron M Cupp,Ignatius Gerardo E Zarraga","doi":"10.1161/circulationaha.125.076354","DOIUrl":"https://doi.org/10.1161/circulationaha.125.076354","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"11 1","pages":"899-901"},"PeriodicalIF":37.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117139","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}
CirculationPub Date : 2025-09-22DOI: 10.1161/circulationaha.125.075646
Yuekai Ji,Lin Yee Chen,Michael J Zhang
{"title":"Response by Ji et al to Letters Regarding Article, \"Association of Coagulation Factor XI Level With Cardiovascular Events and Cardiac Function in Community-Dwelling Adults: From ARIC and CHS\".","authors":"Yuekai Ji,Lin Yee Chen,Michael J Zhang","doi":"10.1161/circulationaha.125.075646","DOIUrl":"https://doi.org/10.1161/circulationaha.125.075646","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"16 1","pages":"e243-e244"},"PeriodicalIF":37.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117135","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}
CirculationPub Date : 2025-09-22DOI: 10.1161/circulationaha.125.074726
Rasha Al-Lamee,Shayna Chotai
{"title":"The Persistent Family Feud: CABG Versus PCI. Do We Even Need a Winner?","authors":"Rasha Al-Lamee,Shayna Chotai","doi":"10.1161/circulationaha.125.074726","DOIUrl":"https://doi.org/10.1161/circulationaha.125.074726","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"30 1","pages":"859-861"},"PeriodicalIF":37.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117141","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}
CirculationPub Date : 2025-09-22DOI: 10.1161/cir.0000000000001381
Glenn N Levine,Robert M Carney,Beth E Cohen,Susan L Dunn,Allison E Gaffey,Ian M Kronish,Erik M G Olsson,Jeff C Huffman,
{"title":"Post-Myocardial Infarction Psychological Distress: A Scientific Statement From the American Heart Association.","authors":"Glenn N Levine,Robert M Carney,Beth E Cohen,Susan L Dunn,Allison E Gaffey,Ian M Kronish,Erik M G Olsson,Jeff C Huffman, ","doi":"10.1161/cir.0000000000001381","DOIUrl":"https://doi.org/10.1161/cir.0000000000001381","url":null,"abstract":"The importance of psychological distress in patients with cardiovascular disease is increasingly recognized as both a contributing factor to the development and progression of cardiovascular disease and a consequence of the development of cardiovascular disease. Patients with acute myocardial infarction have increased risks for depression, anxiety, psychosocial stress, or posttraumatic stress disorder. Together, these negative psychological factors when occurring after myocardial infarction have been referred to as postmyocardial psychological distress. Up to half of patients after myocardial infarction may experience some form of psychological distress, and this postmyocardial psychological distress has been associated with an increased risk of future cardiac events. Biologically plausible mechanisms by which postmyocardial psychological distress may lead to increased future cardiac risk include lesser physical activity, smoking (and failure to stop smoking), excess alcohol consumption, poor diet, obesity, inadequate sleep, inadequate social support, decreased medication adherence, and poor attendance at cardiac rehabilitation. The data on whether treatment of postmyocardial psychological distress improves cardiac prognosis are mixed and of variable quality, and further studies, particularly in patients with anxiety, stress, and posttraumatic stress disorder, would be helpful. Regardless, multiple interventions can reduce psychological distress and thus lead to improved psychological health, a greater sense of emotional well-being, and a better quality of life. A goal of health care professionals should be to treat not only the disease but also the person as a whole in front of us.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"1 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145103391","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}