Heart Failure Reviews最新文献

{"title":"Subcutaneous furosemide in an ambulatory heart failure clinic: a single center reflection on implementation.","authors":"Todd McVeigh, Rebecca S Steinberg, Allison Fox, Veraprapas Kittipibul, Marat Fudim","doi":"10.1007/s10741-026-10686-4","DOIUrl":"https://doi.org/10.1007/s10741-026-10686-4","url":null,"abstract":"<p><p>Subcutaneous (SC) furosemide offers an outpatient option for decongestion in chronic heart failure (HF) patients who remain symptomatic on oral diuretics or who would otherwise require recurrent intravenous (IV) therapy. Furoscix, the only FDA-approved SC furosemide, delivers 80 mg over 5 hours via an on-body infusor with pharmacokinetics and diuretic effects comparable to IV dosing. In this primer, we summarize the evidence supporting SC furosemide and share our institutional experience implementing it in a multidisciplinary ambulatory HF clinic, where it has now been prescribed to more than 75 patients. We argue that successful adoption depends less on the drug itself than on the workflows-patient selection, prescribing logistics, education, and post-administration monitoring-built around it, and we outline emerging opportunities to extend SC furosemide to advanced HF, hospital discharge, and emergency department transitions.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Worsening heart failure is not a single endpoint: a severity-gradient perspective from digoxin in rheumatic heart disease.","authors":"Koichiro Yuji, Wakako Yuji","doi":"10.1007/s10741-026-10684-6","DOIUrl":"https://doi.org/10.1007/s10741-026-10684-6","url":null,"abstract":"<p><p>The composite of cardiovascular or all-cause death and worsening heart failure (WHF) has become the principal efficacy endpoint of heart failure trials. Yet WHF is not one event: it spans outpatient oral-diuretic escalation, urgent intravenous-diuretic visits, hospitalisation, and HF-related death-tiers that differ markedly in frequency, ascertainment, and prognostic weight. A composite WHF benefit therefore cannot be properly interpreted without knowing which tier carries the signal, and we argue that this tier is both phenotype- and setting-dependent. Two trials published on the same day in 2026 make the point with unusual clarity. In the Dig-RHD trial of digoxin in rheumatic heart disease, the benefit concentrated in outpatient diuretic events, with neutral results at hospitalisation and death; in a contemporaneous meta-analysis of digitalis glycosides in reduced or mildly reduced ejection fraction, the same drug class reduced worsening heart failure mainly through hospitalisation, again without a mortality benefit. We use this contrast to propose a severity-gradient framework for reporting and interpreting worsening heart failure, and discuss its implications for trial design, for the translation of guideline-based evidence across health systems, and for the use of inexpensive therapies such as digoxin in low- and middle-income settings.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149170034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ventriculo-arterial coupling in acute heart failure: prognostic and therapeutic insights - a systematic review and meta-analysis of multivariable-adjusted data.","authors":"Dragos Guz, Daniela Filipescu, Beth Davison, Elena-Laura Antohi, Andrew P Ambrosy, Serban Mihaileanu, Oliviana Geavlete, Sean P Collins, Razvan Radu, Marianna Adamo, Nicolas Girerd, Radu Filipescu, Luca Monzo, Jan Biegus, Gad Cotter, Ovidiu Chioncel","doi":"10.1007/s10741-026-10680-w","DOIUrl":"10.1007/s10741-026-10680-w","url":null,"abstract":"<p><p>In acute heart failure (AHF), non-invasive ventricular-arterial coupling (VAC) surrogates, including right ventricular-pulmonary arterial (RV-PA) and left ventricular-arterial (LV-Ao) coupling, have emerged as practical bedside indices, but their prognostic significance remains largely unknown systematically. We performed a systematic review and meta-analysis to evaluate the prognostic significance of non-invasive VAC assessment, in patients hospitalized with AHF. Outcomes included all-cause mortality, HF hospitalization, length of hospital stay, use of therapies, the composite of all-cause mortality and HF hospitalization, and in-hospital adverse cardiovascular events. Adjusted hazard ratios (aHRs) and odds ratios (aORs) were pooled using random-effects. Subgroup-analyses were performed according to follow-up duration and left ventricular ejection fraction. Thirty-six studies comprising 36,989 patients were analysed. Twenty-eight studies evaluated RV-PA coupling, predominantly the TAPSE/PASP ratio, and eight evaluated LV-Ao coupling, mainly using non-invasive Ea/Ees estimates. RV-PA uncoupling was independently associated with increased all-cause mortality (aHR 1.90; 95% CI 1.42-2.56; I²=49%), with consistent associations at 12 months (aHR 2.03; 95% CI 1.44-2.85) and long-term follow-up (aHR 1.67; 95% CI 1.06-2.64). Associations with HF hospitalization, hospital stay, and the composite endpoint were directionally consistent but not statistically significant. LV-Ao uncoupling was associated with increased in-hospital adverse cardiovascular events (aOR 1.70; 95% CI 1.29-2.24). Sensitivity analyses confirmed robustness of these findings. RV-PA uncoupling predicts mortality, whereas LV-Ao uncoupling identifies patients at increased risk of in-hospital adverse cardiovascular events, supporting VAC-risk-stratification in AHF and future evaluation of VAC-guided therapeutic strategies.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13642461/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149108629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Engineering the geriatric heart to model HFpEF.","authors":"Sebastian Bass-Stringer, Jarmon G Lees, Shiang Y Lim","doi":"10.1007/s10741-026-10683-7","DOIUrl":"10.1007/s10741-026-10683-7","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) clinical trials suffer from high rates of attrition due to a biological mismatch between preclinical models and patients. While clinical HFpEF is fundamentally driven by advanced age, female sex, systemic inflammation, and progressive myocardial stiffness, preclinical screening still relies predominantly on young male rodents or foetal-like pluripotent stem cell derivatives. In this perspective, we propose a modular and testable geriatric engineering framework for reconstructing the myocardial features of this disease in vitro. The framework integrates four pathogenic drivers: inducible nuclear senescence to mimic ageing-like phenotypes, post-menopausal estrogen withdrawal, programmable biomaterial-driven stiffness, and macrophage-mediated immune activation. De-risking HFpEF drug development requires deliberately engineering this target pathophysiology, ensuring candidate compounds are evaluated against the biology of the ageing myocardium. Because such platforms isolate myocardial phenotypes from the broader multisystem clinical syndrome, we outline the strict model inputs, functional outputs, and clinical benchmarking criteria required to establish their translational validity.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149108713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complication management in hypertrophic cardiomyopathy.","authors":"Viktoria Höller, Peter-Paul Zwetsloot, Viktoria Santner, Nora Schwegel, Sophie Luise Pötsch, Nicolas Verheyen, Michelle Michels","doi":"10.1007/s10741-026-10682-8","DOIUrl":"https://doi.org/10.1007/s10741-026-10682-8","url":null,"abstract":"<p><p>Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disorder, yet remains substantially underdiagnosed in clinical practice. Although current guidelines define HCM primarily based on left ventricular wall thickness, this approach alone does not capture the full spectrum of disease expression. Comprehensive phenotyping using multimodality imaging, combined with genetic testing and systematic family screening, allows for more accurate diagnosis and earlier detection, although its integration into routine clinical algorithms remains incomplete. Clinical outcomes and therapeutic strategies in HCM are largely driven by disease-related complications. These include heart failure, atrial fibrillation, ventricular arrhythmias, and sudden cardiac death, where risk stratification and prevention are central. While left ventricular outflow tract obstruction represents a major therapeutic target with rapidly evolving treatment options, alternative obstruction phenotypes and non-obstructive disease have received comparatively less attention. In these patients, symptoms are often determined by microvascular dysfunction, diastolic impairment, and myocardial fibrosis, contributing to myocardial ischemia and heart failure. Recent advances in targeted therapies, particularly cardiac myosin inhibitors, highlight the increasing importance of precise phenotypic characterization for treatment selection. However, their long-term impact on disease progression and clinical outcomes remains to be established. Overall, HCM should be considered a dynamic and heterogeneous disease continuum requiring individualized, phenotype-driven diagnostic and therapeutic strategies.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13627219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149108449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioimpedance utility in heart failure.","authors":"Archana Ganapathy, Jason N Dungu, Anthony D Dimarco, Andrew Chisom Madu, Samantha Langley, Peter Watters, Henry Oluwasefunmi Savage","doi":"10.1007/s10741-026-10681-9","DOIUrl":"10.1007/s10741-026-10681-9","url":null,"abstract":"<p><p>Congestion is a central pathophysiological feature of heart failure (HF) and a major contributor to symptoms and prognosis. Despite the substantial mortality benefit of disease-modifying therapies [1], assessing and managing congestion remains challenging. Existing tools such as clinical examination, blood and urinary biomarkers, and cardiac and lung ultrasound are limited by observer variability, logistical constraints and the need for technical expertise [2]. Comorbidities such as chronic kidney disease (CKD), which co-exist in up to 60% of patients with heart failure and may contribute to congestion, further complicate assessments, which can lead to worse outcomes [3, 4]. Consequently, there is growing interest in objective, reproducible and accessible tools that complement conventional approaches to congestion assessment by providing additional information on fluid distribution within body compartments. Bioimpedance analysis (BIA) is a non-invasive technique that measures the electrical properties of biological tissues to estimate body composition and fluid distribution. Since the pioneering work of Nyboer in 1959 and Hoffer et al. in 1969 [5], BIA has evolved from a research tool for body composition into a broader clinical technology used across multiple specialties [6]. Advances in multifrequency, segmental, and spectroscopy-based systems have further expanded its potential for assessing fluid compartments in conditions such as HF and Chronic Kidney Disease (CKD). However, BIA encompasses heterogeneous technologies, parameters and prediction models, and its clinical role remains incompletely defined, with recommendations for further research [7]. This narrative review outlines the physiological principles of bioimpedance, evaluates its applications in HF diagnosis, prognostication, therapeutic guidance and remote monitoring, and explores the methodological and clinical barriers that have restricted its widespread adoption. We discuss its potential as an adjunctive tool for assessing congestion and highlight the key evidence gaps that must be addressed before bioimpedance can be more widely integrated into routine HF care.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149030373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heart failure with a preserved ejection fraction: synergy between cardiac and extracardiac mechanisms and effects of novel therapies.","authors":"Soufiane Nassiri, M Louis Handoko, Arno A van de Bovenkamp, Vanessa P M van Empel, Daniël H van Raalte, Etto C Eringa","doi":"10.1007/s10741-026-10671-x","DOIUrl":"10.1007/s10741-026-10671-x","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) is a systemic disease in which metabolic comorbidities obesity, type 2 diabetes (T2D), and chronic kidney disease (CKD) converge to drive systemic inflammation, endothelial dysfunction, and myocardial fibrosis. Microvascular dysfunction represents an important link between these comorbidities and abnormalities within and beyond the heart, although its causal contribution to HFpEF remains incompletely established. In addition to promoting myocardial stiffness and diastolic dysfunction, impaired microvascular function across the pulmonary and peripheral circulations may contribute to reduced tissue perfusion, exercise intolerance, and dyspnoea. CKD may further aggravate this process through volume and neurohormonal pathways as well as circulating uraemic and inflammatory factors that impair endothelial function, through a kidney-microvascular axis. Despite its high prevalence and poor prognosis, therapeutic options for HFpEF have historically been limited. Recent advances, including sodium-glucose cotransporter 2 inhibitors (SGLT2i), glucagon-like peptide-1 (GLP-1) receptor agonists and dual incretin therapies (GLP-1/GIP RAs), and (non-steroidal) mineralocorticoid receptor antagonists, have reshaped the therapeutic landscape by improving cardiovascular and renal outcomes in patients with HFpEF. These agents exert complementary effects on hemodynamic stress, metabolic dysregulation, inflammation, and fibrosis, and may also improve microvascular function across multiple vascular beds. In this narrative review, we provide an organ-by-organ synthesis of the pathophysiological interactions among the heart, kidney, systemic microvasculature, pulmonary circulation, and skeletal muscle in CKMS-related HFpEF. We further map the clinical and mechanistic effects of aforementioned therapies across these interconnected organ systems and highlight areas in which mechanistic and clinical evidence gaps remain.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13590455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149011977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repaired tetralogy of Fallot across adulthood: from right ventricular remodelling to targeted intervention.","authors":"Krzysztof Cienkowski, Maciej Moll, Alicja Cienkowska, Karolina Kupczynska, Maciej Banach, Agata Bielecka-Dabrowa","doi":"10.1007/s10741-026-10678-4","DOIUrl":"10.1007/s10741-026-10678-4","url":null,"abstract":"<p><p>Adults with repaired tetralogy of Fallot (rTOF) constitute a rapidly growing adult congenital heart disease population with excellent early survival but substantial late morbidity. Chronic pulmonary regurgitation and/or residual right ventricular outflow tract obstruction drive progressive right ventricular dilatation, dysfunction, dyssynchrony, and myocardial fibrosis, predisposing to heart failure and ventricular arrhythmias. This review summarizes contemporary concepts in the surveillance and management of adults with rTOF, focusing on multimodality imaging, pulmonary valve replacement (PVR), arrhythmia risk stratification, aortopathy, and emerging pharmacological strategies. Echocardiography remains the first-line modality for assessing residual lesions and aortic dimensions, while cardiac magnetic resonance is central for quantifying right ventricular volumes, regurgitant fraction, and fibrosis; computed tomography complements anatomical evaluation when magnetic resonance imaging is not feasible. PVR, increasingly performed using transcatheter techniques, is a cornerstone intervention, with guideline-based decisions integrating symptoms, right ventricular volumes, functional testing, and ventricular function. Arrhythmia management combines risk stratification, catheter ablation, implantable cardioverter-defibrillators in selected patients, and individualized medical and pacing therapies. Aortic root dilatation is common, but dissection is rare; surveillance and surgery are guided by diameter thresholds and growth rate. Evidence for routine renin-angiotensin-aldosterone inhibition to improve right ventricular function remains limited, although selected agents and exercise-based interventions are under investigation. Infective endocarditis risk differs by pulmonary valve replacement modality and valve type, being generally higher after transcatheter than surgical replacement, and warrants individualized antiplatelet therapy and vigilant surveillance after implantation. Lifelong multidisciplinary follow-up in specialized adult congenital heart disease centers is essential to optimize reintervention timing and reduce arrhythmic and aortic complications in adults with rTOF. Graphical abstract summarises the overall pathophysiology and long-term management of repaired tetralogy of Fallot.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13574911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148967996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atrial fibrillation in transthyretin amyloid cardiomyopathy: marker of disease severity and implications for multidomain reassessment.","authors":"Carlos M Peñate, Orlando Henriquez Italin, Andrew S Dzebu, Kevin M Alexander","doi":"10.1007/s10741-026-10679-3","DOIUrl":"10.1007/s10741-026-10679-3","url":null,"abstract":"<p><p>Atrial fibrillation or flutter (AF/AFL) affects approximately 56% to 71% of patients with transthyretin amyloid cardiomyopathy (ATTR-CM), with prevalence rising in more advanced disease. AF usually arises on a background of amyloid atrial cardiomyopathy: atrial infiltration, increased stiffness, impaired reservoir and contractile mechanics, and a prothrombotic milieu present even in sinus rhythm. Whether AF contributes independently to mortality remains unsettled. Unadjusted analyses show higher mortality or event rates with AF, inconsistently significant; the association attenuates once amyloid severity is accounted for in single-center and trial datasets. The largest dataset, reported only as a conference abstract, is the exception: an association with a composite including cardiovascular hospitalization persisted after adjustment for stage. Its clinical relevance may lie less in mortality prediction than in symptoms, heart failure events, and thromboembolism. Conventional risk stratification performs poorly: CHA₂DS₂-VASc does not discriminate left atrial appendage thrombus, thrombus occurs during therapeutic anticoagulation, and in a large propensity-matched cohort stroke rates were comparable with and without AF, suggesting thromboembolic risk reflects the underlying atrial myopathy rather than rhythm status alone. Rate control is constrained by restrictive physiology; catheter ablation has been associated with favorable outcomes in observational cohorts, in selected patients and with clinically meaningful periprocedural decompensation. No disease-modifying therapy has prevented AF or reduced AF burden in a prospectively adjudicated trial. Throughout, we separate published evidence from expert practice. The data support a cross-sectional association between AF and greater ATTR-CM severity but do not establish that incident AF identifies biological progression in an individual patient.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148968005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tolvaptan in heart failure: Contemporary evidence and a framework for precision decongestion.","authors":"Teruhiko Imamura","doi":"10.1007/s10741-026-10677-5","DOIUrl":"10.1007/s10741-026-10677-5","url":null,"abstract":"<p><p>Congestion remains a major therapeutic target in heart failure (HF), despite advances in guideline-directed medical therapy. Tolvaptan, a selective vasopressin V2 receptor antagonist, promotes electrolyte-sparing free-water excretion and therefore offers a mechanistically distinct approach to decongestion. Randomized trials have generally shown short-term increases in urine output and reductions in body weight, whereas effects on dyspnea and other congestion-related symptoms have been variable; importantly, no reduction in mortality or HF hospitalization has been established. This evidence has led to divergent clinical positioning: tolvaptan is approved in Japan for fluid retention inadequately controlled by other diuretics, whereas the United States and Europe do not approve it for HF congestion. This review critically summarizes the pharmacology, clinical evidence, and regional regulatory context of tolvaptan in HF. It then presents a conceptual two-stage framework incorporating potential pretreatment and early-response markers to inform patient selection, with particular attention to urine osmolality and emerging pathway-based biomarkers. The complementary roles of oral and intravenous formulations and evidence in selected clinical settings are also discussed. Current data support tolvaptan as a monitored adjunct for selected patients, not as routine therapy or a treatment with established prognostic benefit.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}