Circulation最新文献

{"title":"Correction to: Development and Validation of the American Heart Association's PREVENT Equations.","authors":"Sadiya S Khan, Kunihiro Matsushita, Yingying Sang, Shoshana H Ballew, Morgan E Grams, Aditya Surapaneni, Michael J Blaha, April P Carson, Alexander R Chang, Elizabeth Ciemins, Alan S Go, Orlando M Gutierrez, Shih-Jen Hwang, Simerjot K Jassal, Csaba P Kovesdy, Donald M Lloyd-Jones, Michael G Shlipak, Latha P Palaniappan, Laurence Sperling, Salim S Virani, Katherine Tuttle, Ian J Neeland, Sheryl L Chow, Janani Rangaswami, Michael J Pencina, Chiadi E Ndumele, Josef Coresh","doi":"10.1161/CIR.0000000000001491","DOIUrl":"https://doi.org/10.1161/CIR.0000000000001491","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179861","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: Infective Endocarditis: Diagnosis, Antibiotic Therapy, and Management: A Scientific Statement From the American Heart Association.","authors":"Daniel C DeSimone, Laura Marks, Mark J Dayer, Zerelda Esquer Garrigos, David Messika-Zeitoun, Patrick T O'Gara, Gosta B Pettersson, Emily M Bucholz, Lindsey S Andrews, Vance G Fowler, Jose M Miro, Larry M Baddour","doi":"10.1161/CIR.0000000000001485","DOIUrl":"https://doi.org/10.1161/CIR.0000000000001485","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 15","pages":"e620"},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165866","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":"Infective Endocarditis: Diagnosis, Antibiotic Therapy, and Management: A Scientific Statement From the American Heart Association.","authors":"Daniel C DeSimone, Laura Marks, Mark J Dayer, Zerelda Esquer Garrigos, David Messika-Zeitoun, Patrick T O'Gara, Gosta B Pettersson, Emily M Bucholz, Lindsey S Andrews, Vance G Fowler, Jose M Miro, Larry M Baddour","doi":"10.1161/CIR.0000000000001466","DOIUrl":"10.1161/CIR.0000000000001466","url":null,"abstract":"<p><p>Since the publication of the 2015 American Heart Association scientific statement on infective endocarditis, its incidence has increased, its epidemiology has changed, and novel diagnostic and treatment options have become available. Updated case definitions, non-culture-based pathogen identification methods, and advanced multimodality imaging techniques have emerged. A randomized controlled trial of partial oral therapy published in 2019 may change the treatment landscape for the foreseeable future. Percutaneous mechanical aspiration of right-sided vegetations is being used in select patients with uncontrolled infection despite appropriate antimicrobial therapy. The importance of an endocarditis team has become increasingly recognized in the management of this life-threatening syndrome. Therefore, multidisciplinary experts in cardiovascular infections were commissioned to develop this updated scientific statement on the diagnosis and management of infective endocarditis.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"e593-e619"},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905268","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":"Impact of Prolonged Spaceflight on Cardiac Structure and Function: An Exploratory Longitudinal Observational Study.","authors":"Vinesh Appadurai, Kazuaki Negishi, Allen G Borowski, Zoran B Popović, Neil L Greenberg, David S Martin, Michael W Bungo, Benjamin D Levine, James D Thomas","doi":"10.1161/CIRCULATIONAHA.125.078665","DOIUrl":"10.1161/CIRCULATIONAHA.125.078665","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Gravitational gradients, ranging from the surface of the Earth (1 G) to the microgravity of spaceflight (0 G), including intermediate gravitational fields such as those on Mars (⅜ G), directly affect cardiovascular hemodynamics. We sought to track changes in cardiac structure and function over the course of long-duration spaceflight and compare them with responses to specific gravitational loads measured preflight and postflight in a uniquely simulated Martian gravitational load.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We performed a prospective, within-subject, repeated-measures observational study of astronauts during flights to the International Space Station, with acquisition of echocardiographic variables during preflight supine rest and upright tilt at specific gravitational loads, including simulated Martian gravity (22° tilt; 0.38 G). Data were subsequently acquired during spaceflight onboard the International Space Station, upon landing on Earth, and after landing during exposure to simulated Martian gravity. Offline analyses of echocardiographic images were performed according to standardized methods, including myocardial deformation measurements.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Thirteen astronauts (9 male) with a mean age of 49±4 years were included. The median spaceflight duration was 164 days (interquartile range, 126 to 169 days; median absolute deviation, 21 days). Significant reductions occurred in left ventricular (LV) end-diastolic volume, stroke volume, and myocardial deformation measures from preflight supine to early in-flight (14 days) measures in microgravity. These early in-flight values were similar in magnitude to those observed in the preflight upright Earth posture, with the exception of an increase in LV longitudinal strain magnitude (-14.5%±1.79% versus -16.9%±2.03%; &lt;i&gt;P&lt;/i&gt;=0.006) and a reduction in LV global circumferential strain (-26.09%±1.76% versus -23.3%±3.22%; &lt;i&gt;P&lt;/i&gt;=0.016). Throughout the subsequent duration of spaceflight, LV end-diastolic volume and LV stroke volume increased toward preflight supine values. After ≈6 months in space, when astronauts were exposed to simulated Martian gravity (⅜ G), no volumetric or hemodynamic measure evinced greater load or hemodynamic stress than upright posture on Earth before flight.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;In this small exploratory study, initial changes in LV chamber volumes, myocardial mechanics, cardiac output, and stroke volume with transition from Earth's gravitational loads to microgravity were transient and stabilized during flight. Given current countermeasures, prolonged spaceflight of up to 6 months does not result in large changes in cardiac structure or function within the context of normal posture variations on Earth. These adaptations generally return to baseline upon return to Earth, with no large changes in cardiac volumes or function relative to the upright posture on Earth in a simulated Martian gravity landing, s","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1444-1455"},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966874","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 Munir et al to Letter Regarding Article, \"CXCR6⁺ T Cells Drive Immune Checkpoint Inhibitor Myocarditis\".","authors":"Amir Z Munir, Paul Gougis, Javid J Moslehi, Joe-Elie Salem","doi":"10.1161/CIRCULATIONAHA.126.081477","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.081477","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 15","pages":"e591-e592"},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165819","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":"Definition and Prognosis of Mitral Regurgitation in Transthyretin Amyloid Cardiomyopathy: A Multicenter International Cohort Study.","authors":"Laurenz Hauptmann, Christina Kronberger, Stéphanie K Schwarting, Daniela Tomasoni, Lara S Schlender, Sophia Koschatko, Maximilian Autherith, Charlotte Jantsch, Caglayan Demirel, Franz Duca, Andreas Kammerlander, Luca Bordignon, Gabriele Guidi Colombi, Nora Schwegel, Matteo Serenelli, Aldostefano Porcari, Steven A Muller, Nicolas Verheyen, Marish I F J Oerlemans, Maria Papathanasiou, Christian Hengstenberg, Marco Merlo, Jörg Hausleiter, Marianna Adamo, Philipp E Bartko, Christian Nitsche","doi":"10.1161/CIRCULATIONAHA.125.079085","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.125.079085","url":null,"abstract":"<p><strong>Background: </strong>In transthyretin amyloid cardiomyopathy, mitral regurgitation (MR) severity may be underestimated by conventional (semi-)quantitative echocardiographic criteria due to restrictive low-flow hemodynamics. We sought to define and validate disease-specific MR risk thresholds and compare their prognostic performance with guideline definitions.</p><p><strong>Methods: </strong>In a multicenter cohort study (8 centers, 4 countries), 1101 patients with newly diagnosed transthyretin amyloid cardiomyopathy (derivation, n=722; validation, n=379) underwent standardized echocardiography with blinded core laboratory analysis, including MR measures (vena contracta width, effective regurgitant orifice area, regurgitant volume, and regurgitant fraction). All-cause mortality and time to first heart failure hospitalization (HFH) served as end points. Prognostic thresholds were derived from spline analysis, validated externally, and compared with American Heart Association/American College of Cardiology, European Society of Cardiology/European Association for Cardiothoracic Surgery, and American Society of Echocardiography definitions.</p><p><strong>Results: </strong>During a median follow-up of 24.9 months (interquartile range, 12.0-42.0), 314 patients (28.5%) died and 244 (22.2%) experienced HFH. All MR metrics independently predicted mortality and HFH (all <i>P</i><0.05). Spline-derived thresholds identified intermediate risk at vena contracta width ≥3.0 mm, effective regurgitant orifice area ≥0.10 cm², regurgitant volume ≥15 mL, and regurgitant fraction ≥20% and high risk at effective regurgitant orifice area >0.25 cm², regurgitant volume >38 mL, and regurgitant fraction >35%. Compared with guideline grading (≈12%-13%), the composite MR grading scheme classified a significantly higher proportion (21%) as severe MR and provided superior discrimination for clinical outcomes at 12 and 24 months in both the derivation and validation cohort. After multivariable adjustment, only the composite MR grading scheme remained strongly predictive for both mortality (hazard ratio, 1.20 [1.07-1.36]) and HFH (hazard ratio, 1.21 [1.05-1.38]).</p><p><strong>Conclusions: </strong>Quantitative MR thresholds in transthyretin amyloid cardiomyopathy are substantially lower than current guideline cutoffs. A validated, risk-based composite MR grading scheme improves prediction of both mortality and HFH, better reflecting the restrictive low-flow pathophysiology of transthyretin amyloid cardiomyopathy and supporting disease-specific MR grading.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT06836011.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179875","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":"Cardiovascular Complications of Chronic Liver Disease.","authors":"Seong Park, Deepak K Gupta, Manhal Izzy, Lisa B VanWagner","doi":"10.1161/CIRCULATIONAHA.126.079443","DOIUrl":"10.1161/CIRCULATIONAHA.126.079443","url":null,"abstract":"<p><p>Chronic liver disease is an increasingly prevalent and heterogeneous syndrome with important consequences for cardiovascular function. As the global burdens of chronic liver disease and cirrhosis continue to rise, cardiovascular disease has emerged as a major driver of overall morbidity and mortality in affected patients. Despite the growing recognition of the intersectionality between hepatology and cardiology care clinically, cardiovascular disease risk among patients with liver disease is underrecognized. This state-of-the-art review summarizes the current understanding of the bidirectional interactions between the liver and the cardiovascular system. Shared mechanisms-including inflammation, endothelial injury, and neurohormonal overactivation-that contribute to the development of adverse myocardial remodeling, atherosclerotic cardiovascular disease, heart failure, arrhythmias, pulmonary vascular syndromes, and cirrhosis-associated cardiovascular syndromes are reviewed. A specific focus is placed on metabolic dysfunction-associated steatotic liver disease, the most common form of chronic liver disease, while highlighting the distinct cardiovascular manifestations associated with other types of chronic liver disease. These include alcohol-associated liver disease and infiltrative diseases that affect the liver and heart with cardiovascular implications across the spectrum from early stages of liver disease through cirrhosis. We discuss practical approaches to detecting liver disease, including the assessment of liver fibrosis noninvasively in individuals at risk. We discuss the approach to assessing cardiovascular risk through cardiac imaging, biomarkers, and cardiac functional testing once chronic liver disease is detected. Management considerations for commonly encountered cardiovascular conditions and a critical appraisal of the evolving evidence supporting cardiometabolic therapies in patients with chronic liver disease are discussed to underscore potential cardiovascular and liver benefits. Critical evidence gaps and future research priorities are identified, including the development and evaluation of liver-informed cardiovascular risk models, incorporation of cardiovascular end points into liver disease trials, and implementation of integrated cardiohepatometabolic care pathways. Improved recognition of chronic liver disease and related cardiovascular disease risk represents a major opportunity to facilitate earlier disease detection, enhance risk stratification, and improve outcomes across the spectrum of chronic liver disease.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 15","pages":"1518-1536"},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13660431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166093","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":"Dual-Target Cardiac Regeneration: Controllable <i>Nfyb/Nr3c1</i> Cointervention Spurs Cardiomyocyte Cytokinesis After Myocardial Infarction.","authors":"Bingjun Lu, Wujian Liu, Ziyan Ge, Jiamin Zou, Yidan Xu, Zhuo Zhang, Lanlan Ma, Jiangcheng Shu, Yuyao Liu, Cong Chen, Juanjuan Zheng, Jia Li, Zhen Liu, Sisi Tian, Xuemei Chen, Yanli Guo, Donghui Zhang, Steven R Houser, Wei Eric Wang","doi":"10.1161/CIRCULATIONAHA.125.079049","DOIUrl":"10.1161/CIRCULATIONAHA.125.079049","url":null,"abstract":"<p><strong>Background: </strong>Myocardial infarction can cause a massive loss of functional cardiomyocytes, yet effective strategies to stimulate cardiac regeneration remain lacking. A key barrier to adult cardiomyocyte proliferation appears to be cytokinesis inhibition. This study aimed to determine whether combining proliferation stimulators with the removal of cytokinesis-inhibitory constraints could unlock regenerative potential after myocardial infarction.</p><p><strong>Methods: </strong>Transcriptomic profile from 5 regeneration models, including <i>Aurkb</i>-tdTomato cytokinesis reporter mice and <i>Myh6</i>-MerCreMer;mosaic analysis with double markers (MADM), and cross-species comparative analysis were used to explore the regulatory networks for cardiomyocyte proliferation. MADM mice were used to evaluate cardiac regeneration by quantifying after cytokinesis new cardiomyocytes and clonal clusters.</p><p><strong>Results: </strong>Integrative multimodel analysis revealed a dual regulatory control system for cardiomyocyte proliferation, along with key associated genes and transcriptional regulators. <i>Nfyb</i> was identified as an activator and <i>Nr3c1</i> as a repressor of cardiomyocyte proliferation. <i>Nfyb</i> overexpression enhanced cardiomyocyte proliferation and post-myocardial infarction cardiac repair through propelling cell-cycle gene transcription. <i>Nr3c1</i> inhibition promoted cardiomyocyte proliferation, improved cardiac function, and reduced infarct size. A spatiotemporally controlled adeno-associated virus 9 system combining drug-inducible <i>Nfyb</i> overexpression and CRISPR/enOsCas12f1-mediated <i>Nr3c1</i> deletion efficiently induces cardiomyocyte proliferation. Clonal analysis using MADM mice showed that the dual intervention synergistically increased new cardiomyocyte formation (28% clustered, >28-fold versus control). The enhanced regenerative effect of the dual intervention was demonstrated in post-myocardial infarction mice and human engineered heart tissues.</p><p><strong>Conclusions: </strong>This work documents a dual-control paradigm of cardiomyocyte proliferation and establishes <i>Nfyb</i>/<i>Nr3c1</i> cointervention as a putative new therapy to induce and control cardiac regeneration after injury.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1494-1509"},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13668044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812372","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":"Multidisciplinary Approach to Antiplatelet Management in Coronary Syndromes: A Scientific Statement From the American Heart Association.","authors":"Craig J Beavers, Paul P Dobesh, Mary Cushman, Robert J DiDomenico, Nkechinyere Ijioma, Ravi V Joshi, Jonathan Medina-Beckwith, Naveen Pereira, Marc Ruel, Rachel G Tabak","doi":"10.1161/CIR.0000000000001478","DOIUrl":"https://doi.org/10.1161/CIR.0000000000001478","url":null,"abstract":"<p><p>Antiplatelet therapy is a cornerstone of care for patients with acute coronary syndrome and chronic coronary disease, yet its optimal use requires careful balancing of thrombotic risk reduction with bleeding complications. Since the mid-2000s, advances in stent technology, antiplatelet pharmacotherapy, procedural technique, and risk stratification tools have led to increasingly individualized approaches to antiplatelet management. Current guidelines and evidence emphasize tailoring agent selection, intensity, and duration of therapy according to patient-, procedure-, and disease-specific factors rather than a uniform strategy. However, the growing complexity of evidence, frequent care transitions, social determinants of health, and variability in patient characteristics have increased the risk of inappropriate prescribing, nonadherence, and adverse outcomes. This scientific statement reviews contemporary evidence informing antiplatelet strategies and highlights the critical role of the multidisciplinary cardiovascular team (interventional cardiology, general cardiology, pharmacists, advanced practice nurses) and the importance of their collective expertise in ensuring antithrombotic stewardship in patients with acute coronary syndrome and chronic coronary disease.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179843","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":"Molecular Imaging of Thrombotic Sources of Ischemic Stroke.","authors":"Jamie W Bellinge, Graeme J Hankey","doi":"10.1161/CIRCULATIONAHA.126.082400","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.082400","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 15","pages":"1441-1443"},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164897","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}