Circulation: Heart Failure最新文献

{"title":"Microcurrent Therapy in Cardiac Repair: Bridging Mechanistic Biology and Clinical Evidence.","authors":"Jesus Eduardo Rame, Dipthi Bachamanda Somesh, David Lanfear, Marat Fudim, Stavros Drakos, Daniel Burkhoff, Rob S MacLeod, Javed Butler, Arantxa González Miqueo, Faouzi Kallel, Stefan D Anker","doi":"10.1161/CIRCHEARTFAILURE.126.014407","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.126.014407","url":null,"abstract":"<p><p>Cardiovascular disease remains a major cause of morbidity and mortality, with heart failure representing the common and often irreversible end stage, for which current therapies are largely palliative rather than restorative. Cardiac microcurrent therapy delivers a low-intensity, nondepolarizing direct current across the myocardium and has been proposed to modulate fibrosis, inflammation, and remodeling in heart failure with reduced ejection fraction. In Cardiac Microcurrent I (New York Heart Association III nonischemic heart failure with reduced ejection fraction), left ventricular ejection fraction increased by 12.6% at 6 months, 6-minute walk distance improved by 191 m, and 8 of 10 patients improved to New York Heart Association I within 2 weeks. In the randomized Cardiac Microcurrent II trial, patients showed further improvements, including a 5.1% increase in left ventricular ejection fraction, a reduction in New York Heart Association class (up to 69%), and a 38 m increase in 6-minute walk distance. However, NT-proBNP (N-terminal pro-B-type natriuretic peptide) levels did not show a consistent corresponding reduction. In vitro, microcurrent altered the myofibroblast phenotype and reduced the expression of transforming growth factor-β1, collagen, α-smooth muscle actin, and fibronectin. Transcriptomics revealed downregulation of inflammatory and immune pathways, while cardiomyocytes from spontaneously hypertensive rats exhibited enhanced survival and stress resistance. This review combines early clinical observations and preclinical findings to examine potential mechanisms of action and bioelectrical effects of cardiac microcurrent therapy. Given the limited clinical evidence and largely in vitro nature of the data, the current mechanistic findings should be considered preliminary. We highlight key knowledge gaps and propose future studies to define molecular mechanisms, discover biomarkers, analyze key signaling pathways, and evaluate clinical outcomes in adequately powered, sham-controlled trials, which could further validate this therapeutic approach.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014407"},"PeriodicalIF":8.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788940","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":"Combined Post- and Precapillary Pulmonary Hypertension in Patients With Advanced Heart Failure.","authors":"E Ashley Hardin, Adi Dewanjee, Parker Davis, Ryan J Tedford, Nick Hendren, Mark H Drazner, Teresa De Marco, Kelly M Chin","doi":"10.1161/CIRCHEARTFAILURE.126.014787","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.126.014787","url":null,"abstract":"<p><p>Pulmonary hypertension associated with left heart disease, or group 2 pulmonary hypertension, is common in patients with advanced heart failure. In at least a third of these patients, the pulmonary pressures are disproportionately elevated relative to left heart filling pressures and are classified as combined post- and precapillary pulmonary hypertension (CpcPH). CpcPH is thought to result not only from chronically elevated left heart filling pressures but also from neurohormonal activation, a genetic predisposition, and other risk factors. Traditional pulmonary vasodilator therapies are not efficacious and may be harmful in CpcPH. For patients with advanced heart failure, higher-risk CpcPH hemodynamics, particularly significantly elevated or nonreversible pulmonary vascular resistance and transpulmonary gradient, may preclude isolated heart transplantation, while acute vasodilator testing may identify patients who can proceed with acceptable risk. Strategies to minimize posttransplant risk in recipients with CpcPH based on donor selection, for example, oversizing of the donor by relative predicted heart mass or selecting donors with preexisting PH, remain unproven. This review serves to (1) highlight new insights into the pathophysiology and epidemiology of CpcPH; (2) summarize the existing literature surrounding indications for, and interpretation of response to, acute pulmonary vasodilator testing; (3) provide recommendations for management of patients with heart failure and CpcPH, with a particular focus on advanced therapies; and (4) identify knowledge gaps and future research priorities.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014787"},"PeriodicalIF":8.3,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788976","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":"Elevated Endogenous Insulin and Insulin Resistance Are Associated With Progressive Diastolic Dysfunction and Worse Cardiovascular Outcomes.","authors":"Fadi W Adel, Benjamin Gochanour, Christopher Scott, Jasraj Singh, J C Malsawmzuali, Xiaoyu Ma, Horng H Chen","doi":"10.1161/CIRCHEARTFAILURE.126.014410","DOIUrl":"10.1161/CIRCHEARTFAILURE.126.014410","url":null,"abstract":"<p><strong>Background: </strong>Although diabetes is a known driver of heart failure with preserved ejection fraction, whether antecedent hyperinsulinemia drives preclinical diastolic dysfunction (DD) progression before overt hyperglycemia remains unknown. Therefore, we investigated whether elevated endogenous insulin and insulin resistance independently predict longitudinal DD progression and adverse cardiovascular outcomes.</p><p><strong>Methods: </strong>In a community-based cohort study, we evaluated 1191 participants from the Olmsted County Heart Function Study (median age, 58.7 [interquartile range, 52.4-66.6 years]) who underwent echocardiography at baseline and after 4 years. Fasting insulin and homeostatic model assessment of insulin resistance were assessed. The primary end point was DD progression. Secondary outcomes (mortality, heart failure) were assessed in 2030 participants followed for a median of 10.97 (95% CI, 10.90-11.05) years for heart failure and a median of 18.1 (95% CI, 18.0-18.2) years for mortality.</p><p><strong>Results: </strong>DD progression occurred in 7.5% of participants. Baseline fasting insulin and homeostatic model assessment of insulin resistance strongly predicted progression (<i>P</i><0.001). In multivariable analysis, every 1-SD increase in log-transformed insulin was associated with 65% increased odds of progression (odds ratio, 1.65 [95% CI, 1.33-2.07]; <i>P</i><0.001), adjusting for age, creatinine, and NT-proBNP (N-terminal pro-B-type natriuretic peptide). Similar results were observed for homeostatic model assessment of insulin resistance (odds ratio, 1.66 [95% CI, 1.34-2.08]; <i>P</i><0.001). In secondary analyses, elevated insulin independently predicted all-cause (hazard ratio, 1.11 per 1-SD [95% CI, 1.02-1.21]) and cardiovascular mortality (hazard ratio, 1.16 [95% CI, 1.02-1.33]). Homeostatic model assessment of insulin resistance was similarly predictive of all-cause (hazard ratio, 1.11 [95% CI, 1.03-1.20]) and cardiovascular mortality (hazard ratio, 1.16 [95% CI, 1.02-1.32]).</p><p><strong>Conclusions: </strong>Elevated endogenous insulin and insulin resistance are predictors of progressive DD and long-term mortality, even after accounting for body mass index. Metabolic dysregulation may drive myocardial stiffening before diabetes onset, identifying a potential early therapeutic window for heart failure with preserved ejection fraction prevention.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014410"},"PeriodicalIF":8.3,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148701003","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":"Utility of ECG-Vision for Surveillance of Left Ventricular Dysfunction in Patients With Hypertrophic Cardiomyopathy Initiated on Mavacamten.","authors":"Aakash Bavishi, John Fritzlen, Marybeth Soutar, Kutaiba Nazif, Margaret Kurnides, Heather Speer, Glenda Oyarce, Karen Richards, Cara Flahive, Matthew W Martinez","doi":"10.1161/CIRCHEARTFAILURE.126.014177","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.126.014177","url":null,"abstract":"<p><strong>Background: </strong>Frequent transthoracic echocardiograms (TTEs) are required to monitor for left ventricular systolic dysfunction (LVSD) in patients with obstructive hypertrophic cardiomyopathy receiving myosin inhibitors. This requirement may be cumbersome and limit access in underserved and rural areas. The objective of this study was to evaluate the performance of an artificial intelligence (AI)-enabled ECG tool in predicting LVSD in hypertrophic cardiomyopathy patients on mavacamten.</p><p><strong>Methods: </strong>At Morristown Medical Center/Atlantic Health, 147 patients initiated on mavacamten between June 2022 and June 2025 underwent ECGs and TTEs at baseline and clinically available follow-up visits. A validated AI-enabled ECG algorithm predicted the probability of LVSD. Sensitivity, specificity, negative predictive value, positive predictive value, and area under the curve were calculated for left ventricular ejection fraction <50%, with CIs accounting for repeated paired ECG-TTE observations within patients.</p><p><strong>Results: </strong>In 147 patients, mean age was 65±14 years; 44% were male. Among 453 paired ECG-TTE observations, 8 LVSD event observations occurred. At an AI probability threshold of 20%, sensitivity was 100% (95% CI, 68%-100%), specificity was 75% (95% CI, 69%-82%), positive predictive value was 7% (95% CI, 3%-11%), and negative predictive value was 100% (95% CI, 99%-100%). The area under the curve was 0.94 (95% CI, 0.90-0.98). Patient-level classifications between AI-enabled ECG and echo-confirmed LVSD were concordant in 127 of 147 patients (86%), inconclusive in 17 of 147 (12%), and discordant in 3 of 147 (2%).</p><p><strong>Conclusions: </strong>In this single-center exploratory cohort of patients with obstructive hypertrophic cardiomyopathy receiving mavacamten, ECG-Vision left ventricular demonstrated high observed sensitivity and negative predictive value for TTE-defined LVSD, although estimates were imprecise because LVSD events were infrequent. These findings support prospective multicenter validation of AI-enabled ECG as a potential adjunctive triage tool.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014177"},"PeriodicalIF":8.3,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700909","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":"MRAs and Race in Heart Failure: An Individual Participant Data Meta-Analysis of Randomized Trials.","authors":"Jawad H Butt, Pardeep S Jhund, Alasdair D Henderson, Atefeh Talebi, Orly Vardeny, Brian L Claggett, Muthiah Vaduganathan, Akshay S Desai, Marc A Pfeffer, Carolyn S P Lam, Michele Senni, Sanjiv J Shah, Adriaan A Voors, Dirk J van Veldhuisen, Subodh Verma, Eldrin F Lewis, Faiez Zannad, Bertram Pitt, Scott D Solomon, John J V McMurray, John J V McMurray","doi":"10.1161/CIRCHEARTFAILURE.125.014355","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.125.014355","url":null,"abstract":"<p><strong>Background: </strong>There are concerns that renin-angiotensin system inhibitors are less effective in Black patients than non-Black patients with heart failure (HF). We examined the efficacy and safety of mineralocorticoid-receptor antagonists (MRAs), compared with placebo, in patients with HF with reduced ejection fraction or HF with mildly reduced/preserved ejection fraction, according to self-reported race (Black or non-Black).</p><p><strong>Methods: </strong>This was a post hoc individual participant data meta-analysis of the 4 large placebo-controlled trials comparing MRAs to placebo in patients with HF with reduced ejection fraction (RALES [Randomized Aldactone Evaluation Study], EMPHASIS-HF [Eplerenone in Mild Patients Hospitalization and Survival Study in Heart Failure]) and HF with mildly reduced/preserved ejection fraction (TOPCAT [Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist], FINEARTS-HF [Finerenone Trial to Investigate Efficacy and Safety Superior to Placebo in Patients With Heart Failure]). The primary outcome was a composite of cardiovascular death or first HF hospitalization.</p><p><strong>Results: </strong>Of the 13 846 patients randomized in the 4 trials, 577 (4.2%) identified as Black. Despite being younger (64 versus 70 years), rates of HF hospitalizations and death were higher in Black than non-Black patients. The hazard ratio for MRA versus placebo for the primary composite outcome was 0.87 (95% CI, 0.66-1.15) in Black patients and 0.77 (95% CI, 0.72-0.82) in non-Black patients (<i>P</i>_interaction=0.34), with 3.9 and 2.7 fewer events per 100 person-years of treatment, respectively. For first HF hospitalization, the hazard ratios were 0.86 (95% CI, 0.63-1.17) and 0.73 (95% CI, 0.68-0.80) for Black and non-Black patients, respectively (<i>P</i>_interaction=0.36). The corresponding hazard ratios for cardiovascular death were 0.75 (95% CI, 0.48-1.17) and 0.81 (95% CI, 0.74-0.90), respectively (<i>P</i>_interaction=0.80). Adverse events with MRAs, compared with placebo, were not modified by race. The effects of MRAs in patients with HF with reduced ejection fraction and HF with preserved ejection fraction, individually, were not modified by race.</p><p><strong>Conclusions: </strong>There was no statistically significant evidence of heterogeneity in the absolute or relative effects of MRAs on clinical outcomes between Black and non-Black patients with HF, regardless of HF phenotype.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014355"},"PeriodicalIF":8.3,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683440","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":"Fetal Cardiomyopathy in the Contemporary Era: A Multicenter Fetal Heart Society Research Collaborative Study.","authors":"Angela McBrien, Astha Burande, Oana Caluseriu, Jennifer Conway, Shabnam Peyvandi, Elijah Bolin, Tiscar Cavallé-Garrido, Sue Chandra, James Cnota, Sara Creighton, Bettina F Cuneo, Marlayna Despres, Tam T Doan, J Scott Doucet, Lindsay R Freud, Michelle Grenier, Whitnee Hogan, Michelle Kaplinski, Ann Kavanaugh-McHugh, Sam Keller, Elena N Kwon, Mrinal Lad, Meredith Leslie, Amara Majeed, Gitanjali Mansukhani, Amanda M McIntosh, Deani McVadon, Erik Michelfelder, Michelle Miller, Caitlin Milligan, Adriana Montes Gil, Anita J Moon-Grady, Neda Mulla, Sheetal R Patel, Cathleen Pruitt, Amna Qasim, Hari G Rajagopal, Sanghee Ro, David Schidlow, Kristin Scheider, Ranjini Srinivasan, Jennifer Sutton, Carolyn Taylor, Mahima K Trivedi, Seema Mital, Steven E Lipshultz, Lisa K Hornberger","doi":"10.1161/CIRCHEARTFAILURE.126.014394","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.126.014394","url":null,"abstract":"<p><strong>Background: </strong>Fetal cardiomyopathy is a rare condition, often with an unknown cause and associated with high perinatal mortality. Recent years have seen improvement in fetal cardiac screening, genetic testing, and management. We sought to investigate genetic associations and clinical outcomes of fetal cardiomyopathy in the contemporary era.</p><p><strong>Methods: </strong>A single-arm (descriptive) retrospective cohort study of fetal cardiomyopathy cases diagnosed from January 2017 to December 2021 at 26 North American centers in the Fetal Heart Society Research Collaborative was undertaken. Cases attributable to maternal diabetes, extra-cardiac conditions, structural heart disease, or arrhythmias were excluded. Genetic testing results, extra-cardiac structural anomalies, and outcomes were collected. Logistic regression was performed to determine prenatal risk factors for death or cardiac transplantation by 1-year of age. Descriptive competing-risk analyses (cumulative incidence functions) and Kaplan-Meier survival estimates were used to describe outcomes. Multivariable logistic regression with 5 prespecified covariates was performed to identify prenatal factors associated with death or cardiac transplantation by 1-year of age.</p><p><strong>Results: </strong>In 148 cases of fetal cardiomyopathy, 6.7% (10/148) opted for pregnancy termination, 8.6% (12/138) of continuing pregnancies experienced fetal death, and 1.4% (2/138) were lost to follow-up. Among continuing pregnancies, overall 1-year survival was 61.5% (85/138) with 1-year transplant-free survival of 50.0% (69/138). Of live births, 8.8% (11/124) received palliative care from the outset, and 21.2% (24/113) of those with intention to treat were listed for cardiac transplant, of whom 75.0% (18/24) received transplantation by age 1-year. Genetic etiologies were found in 34.0% (50/147) of the cohort, with variants of uncertain significance detected in an additional 27.2% (40/147). Fetal hydrops at the time of prenatal diagnosis (<i>P</i>=0.001) and a prenatal diagnosis of extracardiac structural anomalies (<i>P</i>≤0.001) were significantly associated with death or transplant by 1-year of age.</p><p><strong>Conclusions: </strong>Fetal cardiomyopathy outcomes have improved in the current era, although only half achieve 1-year cardiac transplant-free survival. Genetic testing identifies a cause in one-third of cases. Hydrops at the time of fetal cardiomyopathy diagnosis and a prenatal diagnosis of extra-cardiac structural anomalies remain important risk factors for mortality.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014394"},"PeriodicalIF":8.3,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683486","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":"Hemodynamic Effects of Veno-Arterial Extracorporeal Life Support on Right Ventricular Systolic Function.","authors":"Sebastian Rosch, Karl-Philipp Rommel, Philipp Lurz, Karl-Patrik Kresoja","doi":"10.1161/CIRCHEARTFAILURE.126.014771","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.126.014771","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014771"},"PeriodicalIF":8.3,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676880","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":"V₀ -- the Loneliest Number That I Ever Knew.","authors":"Hannah Kempton, Michael I Brener, Jörg Hausleiter, Daniel Burkhoff","doi":"10.1161/CIRCHEARTFAILURE.126.014720","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.126.014720","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014720"},"PeriodicalIF":8.3,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673184","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 McMurray to Letter Regarding Article, \"Finerenone, Liver Biomarkers, and Heart Failure With Mildly Reduced/Preserved Ejection Fraction: An Analysis of FINEARTS-HF\".","authors":"Jawad H Butt, John J V McMurray","doi":"10.1161/CIRCHEARTFAILURE.126.014385","DOIUrl":"10.1161/CIRCHEARTFAILURE.126.014385","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014385"},"PeriodicalIF":8.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148307305","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":"Letter by Nie and Xiong Regarding Article, \"Finerenone, Liver Biomarkers, and Heart Failure With Mildly Reduced/Preserved Ejection Fraction: An Analysis of FINEARTS-HF\".","authors":"Zhenyun Nie, Qianfeng Xiong","doi":"10.1161/CIRCHEARTFAILURE.126.014373","DOIUrl":"10.1161/CIRCHEARTFAILURE.126.014373","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014373"},"PeriodicalIF":8.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148307229","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}