Circulation: Heart Failure最新文献

{"title":"Letter by Wang and Sheu Regarding Article, \"Impact of Pregnancy on Mortality in Dilated Cardiomyopathy: Immediate and 12-Month Postpartum Outcomes: Data From the InCor Pregnancy and Heart Disease Registry\".","authors":"Po-Hui Wang, Kai-Lun Sheu","doi":"10.1161/CIRCHEARTFAILURE.126.014203","DOIUrl":"10.1161/CIRCHEARTFAILURE.126.014203","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014203"},"PeriodicalIF":8.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764167","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":"DIGIT-HF: Results From the Win Ratio Analyses.","authors":"Xiaofei Liu, Nele Henrike Thomas, Dominik Berliner, Johannes Schwab, Andreas Rieth, Christina Strack, Sven Schallhorn, Samira Soltani, Lea Haebel, Welf Geller, Marija Zdravkovic, Martin Hülsmann, Heiko von der Leyen, Christian Veltmann, Stefan Störk, Michael Böhm, Johann Bauersachs, Armin Koch, Udo Bavendiek, Anika Großhennig","doi":"10.1161/CIRCHEARTFAILURE.126.014396","DOIUrl":"10.1161/CIRCHEARTFAILURE.126.014396","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014396"},"PeriodicalIF":8.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148041462","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":"Letter by Robert et al Regarding Article, \"Arterial Versus Mixed Venous Lactate Levels in 1526 Cardiac Intensive Care Patients\".","authors":"Charleen Robert, Antoine Villa, Adrien Picod","doi":"10.1161/CIRCHEARTFAILURE.126.014444","DOIUrl":"10.1161/CIRCHEARTFAILURE.126.014444","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014444"},"PeriodicalIF":8.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148210425","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":"Donor-Derived Cell-Free DNA at Diagnosis of Cardiac Allograft Rejection Stratifies Risk of Mortality and Graft Dysfunction.","authors":"Zaid N Safiullah, Han Su, Hyesik Kong, Moon Kyoo Jang, Keyur Shah, Gerald J Berry, Palak Shah, Hannah A Valantine, Xin Tian, Sean Agbor-Enoh","doi":"10.1161/CIRCHEARTFAILURE.125.013718","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.013718","url":null,"abstract":"<p><strong>Background: </strong>Cardiac acute rejection (AR) is a risk factor for poor outcomes; however, there are limited risk prediction models to stratify these patients for death or prolonged left ventricular (LV) dysfunction. We assessed the prognostic utility of percent donor-derived cell-free DNA (%dd-cfDNA) measured at AR diagnosis for predicting adverse outcomes.</p><p><strong>Methods: </strong>The prospective multicenter GRAfT study (Genomic Research Alliance for Transplantation) enrolled heart transplant recipients and collected serial plasma samples to quantitate %dd-cfDNA. AR was defined as acute cellular rejection, antibody-mediated rejection, as well as biopsy-negative antibody-mediated rejection (donor-specific antibody positivity with LV dysfunction). In the primary analyses, AR was stratified by %dd-cfDNA at diagnosis using a data-driven threshold of 0.15%. Cox regression models assessed the associations between the time-dependent covariates of AR and %dd-cfDNA levels at the AR diagnosis and the outcome of prolonged LV ejection fraction decline (≤50% for ≥90 days) and death.</p><p><strong>Results: </strong>The study included 277 patients and 3218 %dd-cfDNA measurements. Over a median follow-up of 4.9 years (interquartile range, 2.5-5.0), 53 patients experienced the composite outcome of death or prolonged LV dysfunction, and 75 (27%) patients developed AR, including 43 (15%) patients with acute cellular rejection, 18 (7%) with pathological antibody-mediated rejection, and 14 (5%) with donor-specific antibody+/LV dysfunction. AR was associated with an increased risk of the primary composite outcome (hazard ratio, 4.47 [95% CI, 2.42-8.26]; <i>P</i><0.001). When AR was stratified by %dd-cfDNA at diagnosis, patients with %dd-cfDNA ≥0.15% had higher risks of prolonged LV dysfunction, death, and the composite outcome compared with patients who had not developed AR at the same follow-up time (hazard ratio, 6.28 [95% CI, 3.04-13.0]; <i>P</i><0.001 for the composite outcome). In contrast, the risks of death and prolonged LV ejection fraction reduction were not statistically significantly increased among patients who developed AR with %dd-cfDNA <0.15% at diagnosis.</p><p><strong>Conclusions: </strong>AR with elevated %dd-cfDNA levels at diagnosis is associated with an increased risk of adverse outcomes after heart transplant, offering novel prognostic utility.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013718"},"PeriodicalIF":8.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148249468","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":"Epicardial Contributions to Fibro-Inflammatory Signaling in a Pkp2-Deficient Arrhythmogenic Cardiomyopathy Model.","authors":"Daniel D Han, Alan C Brooks, Cameron D Baker, Ronald A Dirkx, Deanne M Mickelsen, Benjamin Fisler, Kavya Phadke, John M Ashton, Mario Delmar, Eric M Small","doi":"10.1161/CIRCHEARTFAILURE.125.013966","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.013966","url":null,"abstract":"<p><strong>Background: </strong>Arrhythmogenic cardiomyopathy (ACM) is an inherited disease that is characterized by lethal ventricular arrhythmias stemming from myocyte dysfunction. ACM is associated with considerable subepicardial fibrosis and inflammation with right ventricle predominance. Most cases of gene-positive ACM are caused by a desmosome protein mutation, with plakophilin-2 (<i>Pkp2</i>) mutations being the most common. We hypothesized that <i>Pkp2</i>-deficiency in epicardium-derived cells (EPDCs) contributes to fibro-inflammatory signaling and ACM pathogenesis.</p><p><strong>Methods: </strong>We developed transgenic mice that lack <i>Pkp2</i> in cardiomyocytes (Pkp2-cKO), in EPDC (Pkp2-eKO), or in both cardiomyocyte and EPDC (Pkp2-ceKO) via the tissue-specific expression of tamoxifen-inducible Cre recombinase. Nonmyocyte populations were isolated 21 days posttamoxifen injection for single-cell RNA-sequencing. Immunohistochemistry, flow cytometry, quantitative reverse transcription polymerase chain reaction, and echocardiography were used to interrogate cardiac physiology and cellular composition.</p><p><strong>Results: </strong>We identified a population of epicardium-derived fibroblasts characterized by the expression of <i>Ccl2</i>, <i>Ccl7</i>, <i>Thbs1</i>, and <i>Ptx3</i> that accumulated on <i>Pkp2</i> deletion in both cardiomyocytes and EPDC. <i>Pkp2</i> deletion in cardiomyocytes induced a moderate fibro-inflammatory EPDC phenotype, while deletion in EPDC did not elicit a pathological phenotype, suggesting cardiomyocyte involvement is necessary for ACM pathogenesis. Proinflammatory fibroblasts acquired the senescence-associated secretory phenotype, correlating with elevated senescence associated-βgal staining in the right ventricle. Gene expression, flow cytometry, and histological data also revealed an exaggerated inflammatory response in Pkp2-ceKO mice, which progresses from right to left ventricular predominance. Importantly, macrophages and B cells accumulate in both Pkp2-cKO and Pkp2-ceKO mice compared with controls. Although B cell depletion delays the early inflammatory and fibrosis response, it did not alter end-stage cardiac physiology.</p><p><strong>Conclusions: </strong><i>Pkp2</i> deletion in EPDC facilitates the emergence of a fibro-inflammatory phenotype that may contribute to ACM pathogenesis.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013966"},"PeriodicalIF":8.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13245365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148162215","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":"Phenotypic Characterization of Unclassified Pulmonary Hypertension.","authors":"Yogesh N V Reddy, Robert P Frantz, Alexander C Egbe, William R Miranda, Aneesh K Asokan, Paul M Hassoun, Anna R Hemnes, Evelyn Horn, Jane A Leopold, Franz Rischard, Erika B Rosenzweig, Nicholas S Hill, Serpil C Erzurum, J Emanuel Finet, Monica Mukherjee, W H Wilson Tang, K Sreekumaran Nair, Barry A Borlaug","doi":"10.1161/CIRCHEARTFAILURE.125.014480","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.014480","url":null,"abstract":"<p><strong>Background: </strong>Some symptomatic patients manifest pulmonary hypertension (PH), despite normal pulmonary vascular resistance and pulmonary artery wedge pressure-a condition termed unclassified PH. Although hypothesized to reflect increased flow as seen in congenital heart disease, broader clinical implications remain unknown.</p><p><strong>Methods: </strong>The current analysis included pulmonary vascular disease phenomics participants with either no PH or unclassified PH who underwent dynamic right heart catheterization and transpulmonary metabolomics. In a validation cohort, patients with no PH or unclassified PH underwent exercise right heart catheterization. In exploratory cohorts to understand the impact of increased flow, the prevalence of unclassified PH was assessed in (1) adult congenital heart disease and (2) high output heart failure.</p><p><strong>Results: </strong>The overall prevalence of unclassified PH in pulmonary vascular disease phenomics (n=1046) and the validation cohort (n=1202) was 7.8% (175/2248), which was comparable to the 6.6% (66/1005) prevalence in adult congenital heart disease (n=1005), and lower than high output heart failure (n=159, prevalence 14.5% [23/159]; <i>P</i>=0.006). Increased flow occurred in a minority of unclassified PH from both pulmonary vascular disease phenomics (28%; 15/53) and the validation cohort (11%; 13/122). Unclassified PH (n=53) was associated with greater adiposity, higher heart failure with preserved ejection fraction (HFpEF)-age, body mass index, atrial fibrillation score probability, and more left heart remodeling compared with those with no PH (n=216). Metabolomics revealed lower glycine metabolites in unclassified PH indicative of metabolic dysfunction. Left heart remodeling, quality of life, exercise capacity, and glycine levels were all abnormal in unclassified PH relative to healthy controls (n=96). In the validation cohort, pulmonary artery wedge pressure, pulmonary vascular resistance, and pulmonary artery compliance were subtly abnormal at rest in unclassified PH (n=122) compared with no PH (n=312). With exercise testing, 59% (72/122) with unclassified PH had exertional pulmonary artery wedge pressure elevation consistent with undiagnosed HFpEF.</p><p><strong>Conclusions: </strong>The presence of PH without obvious cause most often reflects subclinical left heart and metabolic dysfunction consistent with unrecognized early-stage HFpEF. Dynamic provocation during right heart catheterization can unmask unrecognized HFpEF in over half of unclassified PH, which may help guide appropriate initiation of proven HFpEF therapies to improve symptoms and functional status.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT02980887.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014480"},"PeriodicalIF":8.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13286243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148276262","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":"Potential Impact of the OPTN Status Escalation Policy for Adult Heart Transplant Candidates With Durable LVADs.","authors":"Daniel J Ahn, Antony Attia, Toshihiro Nakayama, Nikhil Narang, Kiran K Khush, William F Parker, Kazunari Sasaki","doi":"10.1161/CIRCHEARTFAILURE.125.013854","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.013854","url":null,"abstract":"<p><strong>Background: </strong>The 2018 heart allocation policy change substantially lowered the priority of candidates supported with durable left ventricular assist devices (LVADs) for heart transplantation. To provide stable candidates supported by durable LVADs with a quicker path to transplantation before they suffer complications, the Organ Procurement and Transplantation Network (OPTN) approved a policy stipulating that stable patients supported by durable LVADs for 6 and 8 years will obtain statuses 3 and 2, respectively.</p><p><strong>Methods: </strong>Using OPTN data, we identified all adult heart transplant candidates with a durable LVAD implanted between October 18, 2018 and May 31, 2025. We estimated the cumulative incidence of LVAD-related complications, treating transplantation and waitlist removal before experiencing complications as competing events. Furthermore, we assessed how the OPTN policy change would impact the status distribution of the waitlist.</p><p><strong>Results: </strong>In our study cohort, 4967 adult patients who were listed for heart transplant received a durable LVAD. Transplant centers submitted 2879 justifications for status upgrades due to LVAD-related complications for 1812 (36.5%) patients. At 6 years after durable LVAD implantation, the cumulative incidence of complications and status upgrades was 42.1% (95% CI, 40.5%-43.8%), and that of transplantation was 36.0% (95% CI, 34.6%-37.6%). Of the 3779 patients who were not censored administratively, only 47 (1.2%) remained on the waitlist by 6 years after durable LVAD implantation. Had the 6- to 8-year OPTN policy change been implemented on June 1, 2025, only 4.7% of the waitlist would have changed statuses instantaneously.</p><p><strong>Conclusions: </strong>Almost all listed candidates with durable LVADs either experience a complication, status upgrade or are removed from the waitlist within 6 years of obtaining a durable LVAD. The upcoming OPTN policy is unlikely to prevent device complications before granting status upgrades and will likely impact a small percentage of candidates with durable LVADs.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013854"},"PeriodicalIF":8.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13293278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148307269","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":"Big Data and Trustworthy AI for Heart Failure: A Review.","authors":"Joan Perramon-Llussà, Grzegorz Skorupko, Shishir Rao, Esmeralda Ruiz Pujadas, Socayna Jouide El Kaderi, Ilia Stepin, Mohammad Mamouei, Machteld Boonstra, Andreas Triantafyllidis, Folkert W Asselbergs, Gholamreza Salimi-Khorshidi, Karim Lekadir, Polyxeni Gkontra","doi":"10.1161/CIRCHEARTFAILURE.125.013823","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.013823","url":null,"abstract":"<p><p>The rapid evolution of machine learning techniques, combined with the growing availability of large and diverse datasets, is poised to transform heart failure research and clinical care. This review first provides an overview of key machine learning and artificial intelligence concepts used in heart failure research and then examines how diverse data modalities-including electronic health records, patient registries, biobanks, imaging, telemonitoring, and synthetic data-are leveraged to develop machine learning applications for heart failure diagnosis, prognosis, risk stratification, and personalized treatment strategies. While the potential is considerable, we highlight key barriers to clinical translation, such as data heterogeneity, algorithmic bias, lack of interoperability, and privacy concerns. The review also examines the need for explainable and equitable artificial intelligence systems and evaluates emerging solutions, including Federated Learning and synthetic data generation to address fairness and data privacy challenges. Beyond technical innovations, we underscore the importance of human-centered design, stakeholder engagement, and regulatory readiness. We conclude by identifying future priorities and calling for interdisciplinary collaboration to ensure the scalable, ethical, and effective integration of AI in heart failure management.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013823"},"PeriodicalIF":8.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147866982","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":"Gene Therapy for Cardiomyopathy: Tools, Targets, and Trials.","authors":"Radhika Agarwal","doi":"10.1161/CIRCHEARTFAILURE.125.013361","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.013361","url":null,"abstract":"<p><p>Cardiomyopathy remains a leading cause of heart failure-related morbidity and mortality, driven by diverse genetic architectures that include monogenic variants, oligogenic interactions, and polygenic risk. Rapid advances in genomic medicine and vector engineering have positioned cardiac gene therapy as a transformative therapeutic approach. Adeno-associated virus-mediated gene replacement for hypertrophic, dilated, and arrhythmogenic cardiomyopathies has transitioned into early-phase clinical trials, with emerging data providing promising signals of myocardial transgene expression and improvements in circulating biomarkers such as NT-proBNP (N-terminal pro-B-type natriuretic peptide). Genome-editing platforms-including CRISPR-mediated base editing and prime editing-offer the potential for durable variant correction without introducing double-stranded breaks. Yet, major translational challenges remain, including strategies to bypass liver uptake to ensure high-efficiency transduction of cardiomyocytes, overcoming delivery constraints, including the cargo size of adeno-associated virus vectors, addressing toxicities, and establishing adequate immunosuppressive regimens. Novel strategies such as direct antegrade and retrograde coronary infusion, capsid engineering, split-intein dual-adeno-associated virus systems, miniaturization of CRISPR-related proteins, and nonviral nanoparticles are underway. As first-in-human cardiomyopathy gene therapy trials begin to define safety, dosing, and vector tropism in the failing human heart, the field is entering an inflection point where genomic diagnosis, molecular correction, and phenotype-guided delivery can converge into precision heart failure therapeutics. This review highlights current progress, emerging platforms, and scientific hurdles that must be overcome to realize a new era of potentially curative, mechanism-directed therapy for inherited and acquired cardiomyopathies.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013361"},"PeriodicalIF":8.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147866989","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 Zhang Regarding Article, \"Improving Heart Failure Quality of Care Over the First Twenty Years: The Get With The Guidelines-Heart Failure Program\".","authors":"Zhongyang Zhang","doi":"10.1161/CIRCHEARTFAILURE.126.014505","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.126.014505","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e014505"},"PeriodicalIF":8.3,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148344054","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}