{"title":"Rethinking atrial pacing support in cardiac resynchronization therapy: insights from the CRT-NEXT trial.","authors":"Arman Soltani Moghadam, Saman Soltani Moghadam, Mandana Ebrahimzade, Yasaman Daryabari, Aida Zeinali, Toshiki Kuno, Kaveh Hosseini","doi":"10.1007/s10741-026-10664-w","DOIUrl":"10.1007/s10741-026-10664-w","url":null,"abstract":"<p><p>Cardiac resynchronization therapy defibrillators traditionally require a dedicated right atrial lead to provide atrial sensing and pacing in addition to biventricular pacing. However, the clinical value of routine atrial pacing in CRT recipients without sinus node dysfunction remains uncertain, while additional transvenous leads increase procedural complexity and lead-related complications. The CRT-NEXT trial evaluated whether a simplified two-lead CRT-DX system, capable of atrial sensing through a floating atrial dipole but without atrial pacing, was non-inferior to conventional three-lead CRT-D. In this randomized non-inferiority trial, CRT-DX met the prespecified non-inferiority criterion for the composite endpoint of all-cause mortality, cardiovascular hospitalization, and lead-related complications at 12 months. Mortality, cardiovascular hospitalization, arrhythmic outcomes, reverse remodeling, and functional capacity were comparable between groups, while CRT-DX was associated with shorter procedure time and fewer atrial lead-related complications. Importantly, atrial sensing remained reliable during follow-up, CRT delivery was preserved, and only one patient required late atrial lead implantation. These findings challenge the routine need for atrial pacing support in carefully selected CRT-D candidates and suggest that reliable atrial sensing may be sufficient for most patients without sinus node dysfunction. Future integration of DX-based atrial sensing with conduction system pacing may further advance device simplification toward single-lead CRT-D platforms.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758894","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":"The role of IL-6 in hypertrophic and dilated cardiomyopathy: clinical and therapeutic implications.","authors":"Lydia Krexi, Dimitra Krexi, Timothy Rider Betts","doi":"10.1007/s10741-026-10665-9","DOIUrl":"10.1007/s10741-026-10665-9","url":null,"abstract":"<p><p>Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are genetically heterogeneous myocardial disorders in which disease progression is influenced by secondary modifiers beyond structural gene mutations. Increasing evidence suggests that inflammatory signalling plays a role in modulating disease phenotype and progression. Among inflammatory mediators, interleukin-6 (IL-6) has emerged as a potential contributor to myocardial remodelling and dysfunction.A structured literature review was performed using Ovid MEDLINE and the Cochrane Library for studies published up to 10 October 2025. Findings were synthesised narratively because of substantial heterogeneity in study design, populations, and outcomes.This review synthesises clinical, genetic, and experimental evidence on the role of IL-6 in HCM and DCM, with a focus on its potential therapeutic relevance. Across studies, elevated IL-6 levels are consistently associated with greater disease severity. Mechanistic data indicate that IL-6 signalling via the gp130/STAT3 pathway may promote cardiomyocyte hypertrophy, fibrosis, and apoptosis, with genetic polymorphisms likely influencing disease susceptibility and phenotypic expression. Pharmacological interventions with anti-inflammatory properties, including statins, pentoxifylline, and growth hormone, have been associated with reductions in IL-6 levels and improvements in cardiac function, although these effects are not specific to IL-6 signalling.In summary, current evidence supports IL-6 as an important component of the inflammatory milieu associated with HCM and DCM and suggests potential utility as a biomarker of disease activity. However, evidence supporting a causal pathogenic role remains limited, and IL-6-directed therapies have not been systematically evaluated in cardiomyopathy populations.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148701179","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}
Georgios Papingiotis, Marina Mantzourani, Helen Gogas, Gerasimos Filippatos, Dimitrios Farmakis
{"title":"Iron overload cardiomyopathy.","authors":"Georgios Papingiotis, Marina Mantzourani, Helen Gogas, Gerasimos Filippatos, Dimitrios Farmakis","doi":"10.1007/s10741-026-10663-x","DOIUrl":"10.1007/s10741-026-10663-x","url":null,"abstract":"<p><p>Iron overload cardiomyopathy (IOC) remains an important cause of morbidity and mortality in patients with hereditary haemochromatosis and transfusion-dependent conditions such as haemoglobinopathies. The condition arises when excess iron, due to increased intestinal iron absorption or repetitive transfusions, saturates transferrin-binding capacity, generating non-transferrin-bound iron. This form of iron enters cardiomyocytes through L-type and T-type calcium channels, divalent metal transporter 1, and ZIP14 and triggers oxidative stress via the Fenton reaction, mitochondrial dysfunction, calcium dysregulation, and ferroptosis. The resulting clinical spectrum ranges from diastolic dysfunction to overt heart failure and fatal arrhythmias. Cardiac magnetic resonance T2* has revolutionized diagnosis and risk stratification, enabling MRI-guided chelation strategies that have dramatically reduced cardiac mortality over the past decades. Phlebotomy remains the cornerstone of treatment in primary haemochromatosis, while iron chelators, including deferoxamine, deferiprone and deferasirox, is the standard for transfusion-dependent patients. Adjunctive amlodipine has also emerged as a strategy to reduce myocardial iron accumulation. Novel disease-modifying or curative treatments for thalassaemia, such as luspatercept, mitapivat and gene therapy offer the prospect of addressing the root cause of iron loading. This review provides an updated comprehensive, evidence-based overview of the pathophysiology, diagnosis, and management of IOC.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148684432","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":"Contemporary medical therapy for heart failure with mildly reduced or preserved ejection fraction.","authors":"Craig J Beavers, Stephen J Greene","doi":"10.1007/s10741-026-10656-w","DOIUrl":"10.1007/s10741-026-10656-w","url":null,"abstract":"<p><p>Treatment for heart failure with mildly reduced ejection fraction (HFmrEF) and preserved ejection fraction (HFpEF) has evolved significantly in recent years. This period of therapeutic progress follows a span of over two decades during which randomized controlled trials (RCTs) of neurohormonal blockade and other therapies failed to definitively demonstrate clinical benefits. As such, traditionally, management guidelines for HFmrEF and HFpEF were limited to recommendations focused on optimization of volume status with diuretics, management of comorbidities, and consideration of certain medications such as angiotensin receptor-neprilysin inhibitor (ARNi) or steroidal mineralocorticoid receptor antagonists (MRA) to subsets of patients. After definitive results from multiple RCTs, sodium-glucose cotransporter 2 inhibitors (SGLT2i) are currently a main pillar in treating HFmrEF and HFpEF in European and American guidelines. However, other therapies, including non-steroidal mineralocorticoid receptor antagonists (nsMRA) and glucagon-like peptide-1 receptor agonists (GLP-1 RA), are proving to be additional effective treatments for HFmrEF and HFpEF and preventing the progression of cardiovascular-kidney-metabolic (CKM) syndrome. There is now increasing justification for combining multiple proven treatments for HFmrEF and HFpEF to maximize potential benefits.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13451241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148684340","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}
Kate Haichin, Janie Leroux, Nadia Giannetti, Abhinav Sharma
{"title":"Innovative strategies to reduce heart failure hospitalizations: insights from the ESC heart failure congress 2026.","authors":"Kate Haichin, Janie Leroux, Nadia Giannetti, Abhinav Sharma","doi":"10.1007/s10741-026-10662-y","DOIUrl":"10.1007/s10741-026-10662-y","url":null,"abstract":"<p><p>Heart failure (HF) represents a major burden on healthcare systems globally, driven by high rates of hospitalizations and readmissions, as well as prolonged length of stay (LOS). To address this, a wide range of innovative strategies have emerged and evolved in recent years. These approaches span a broad spectrum, ranging from novel routes of medication administration to digital health technologies such as telemonitoring, wearable devices, as well as implantable devices. Given the rapid expansion of available innovations, it can be challenging for clinicians to remain fully up to date with emerging tools and evidence. At the 2026 ESC Heart Failure Congress in Barcelona, Spain, global experts in the field highlighted different technologies and the key clinical trials supporting them. This review aims to synthesize the most recent innovative strategies aimed at reducing HF hospitalizations (HFH), as presented during the congress.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669341","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}
Maximilian Autherith, Laurenz Hauptmann, Raghuram Palaparti, Philipp E Bartko, Christian Nitsche
{"title":"Myocardial remodeling in valvular heart disease: pathophysiology, multimodality imaging and treatment implications.","authors":"Maximilian Autherith, Laurenz Hauptmann, Raghuram Palaparti, Philipp E Bartko, Christian Nitsche","doi":"10.1007/s10741-026-10660-0","DOIUrl":"10.1007/s10741-026-10660-0","url":null,"abstract":"<p><p>Valvular cardiomyopathy has emerged as a key concept linking valvular heart disease (VHD) with myocardial remodeling and the development of heart failure (HF). This state-of-the-art review provides a comprehensive overview of pathophysiological mechanisms, multimodality imaging, and implication for valve interventions across the spectrum of VHD. We systematically address HF in the context of aortic valve disease, including aortic stenosis and aortic regurgitation, mitral valve disease with a particular focus on mitral regurgitation, and tricuspid valve regurgitation. For each valvular lesion, we integrate evidence on pathophysiological mechanisms on myocardial (mal)adaptation leading to myocardial fibrosis and ultimately HF and death. Additionally, we highlight the role of multimodality imaging for early detection of myocardial remodeling and discuss implications for patient selection and timing of valve interventions. Beyond single-valve disease, we further explore the complex interplay of multiple and mixed valvular heart disease and review emerging data on the interaction between VHD and cardiac amyloidosis, an increasingly recognized and clinically relevant overlap. Overall, this state-of-the-art review underscores that outcomes in VHD are not solely determined by severity of valvular lesions but critically depend on the extent of associated myocardial damage. A deeper understanding of valvular cardiomyopathy may improve risk stratification, refine patient selection, and support the implementation of tailored therapeutic strategies.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13421278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148619298","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}
Anne-Sophie Roy, E Marc Jolicoeur, Lyne Bérubé, Jessica Forcillo, Christine Pacheco, Brian J Potter, Matthieu Pelletier-Galarneau, Nadia Bouabdallaoui
{"title":"A sex-specific perspective on coronary microvascular dysfunction in HFpEF: from vascular to myocardial disease.","authors":"Anne-Sophie Roy, E Marc Jolicoeur, Lyne Bérubé, Jessica Forcillo, Christine Pacheco, Brian J Potter, Matthieu Pelletier-Galarneau, Nadia Bouabdallaoui","doi":"10.1007/s10741-026-10661-z","DOIUrl":"10.1007/s10741-026-10661-z","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) is the most prevalent form of heart failure and is characterized by high morbidity, limited therapeutic options, and marked biological heterogeneity. Coronary microvascular dysfunction (CMD) has emerged as a central pathophysiological mechanism linking cardiometabolic comorbidities to myocardial remodeling and clinical HFpEF phenotypes. Impaired coronary flow reserve, endothelial dysfunction, reduced nitric oxide bioavailability, and microvascular rarefaction contribute to myocardial stiffening, energetic inefficiency, and ultimately diastolic dysfunction, often preceding overt structural heart disease in the setting of HFpEF. Notably, HFpEF disproportionately affects females, yet the biological mechanisms underlying this sex difference remain incompletely understood. Accumulating evidence suggests that sex-specific differences in vascular biology, immune-metabolic signaling, hormonal regulation, and myocardial-vascular coupling modulate susceptibility to CMD and influence the progression from vascular dysfunction to myocardial disease. Females exhibit a higher prevalence of CMD in the absence of obstructive coronary artery disease, distinct inflammatory and metabolic profiles, and accelerated vascular and ventricular stiffening, particularly after menopause. In contrast, males more frequently display eccentric remodeling and obstructive epicardial coronary disease. This narrative review synthesizes current evidence on the mechanistic role of CMD in HFpEF, with a specific focus on sex-specific biological pathways that shape disease trajectory. Understanding how sex modifies CMD may inform improved diagnostic strategies, risk stratification, and the development of precision-based therapeutic approaches in HFpEF.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578351","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}
Mateusz Garus, Mateusz Guzik, Rafał Tymków, Piotr Gajewski, Robert Zymliński, Jan Biegus
{"title":"Dyspnea in heart failure: pathophysiology, clinical assessment, and evidence from clinical trials.","authors":"Mateusz Garus, Mateusz Guzik, Rafał Tymków, Piotr Gajewski, Robert Zymliński, Jan Biegus","doi":"10.1007/s10741-026-10659-7","DOIUrl":"10.1007/s10741-026-10659-7","url":null,"abstract":"<p><p>Dyspnea is a key symptom of heart failure (HF), particularly in its acute form, where it represents the most common cause of hospitalization. Although traditionally attributed to pulmonary congestion, dyspnea in HF is a multidimensional phenomenon resulting from complex interactions among elevated cardiac filling pressures, hemodynamic alterations, fluid redistribution, impaired gas exchange, activation of mechano- and chemoreceptors, and maladaptive neurohormonal activation. Comorbidities, including chronic lung disease, obesity, cachexia, renal dysfunction, anemia, and chronic inflammation, further modulate symptom perception and lower the threshold for its occurrence. In this review, we synthesize current knowledge on the pathophysiological mechanisms underlying dyspnea in HF, emphasizing its heterogeneity and the complex interplay between hemodynamics, ventilatory regulation, and peripheral factors. We discuss available dyspnea assessment tools, highlighting their strengths and methodological limitations in clinical practice and randomized trials. Despite the use of standardized scales, dyspnea remains a subjective and dynamically evolving symptom. Data from large clinical trials in acute HF indicate that early improvement in dyspnea is common but does not translate into reduced mortality or rehospitalization, whereas residual dyspnea identifies patients at higher risk of adverse events. A better understanding of its multidimensional pathophysiology, measurement limitations, and prognostic significance has important implications for the interpretation of clinical trial results and for optimizing the assessment and management of this fundamental symptom.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13395967/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578363","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}
Giacomo Mugnai, Davide Genovese, Laura De Michieli, Giacomo Marchi, Nicola Vitturi, Federico Migliore, Anna Piccoli, Gianni Carraro, Yuri Battaglia, Flavio Ribichini, Domenico Girelli
{"title":"Fabry disease cardiomyopathy: Time for a closer heart rhythm monitoring?","authors":"Giacomo Mugnai, Davide Genovese, Laura De Michieli, Giacomo Marchi, Nicola Vitturi, Federico Migliore, Anna Piccoli, Gianni Carraro, Yuri Battaglia, Flavio Ribichini, Domenico Girelli","doi":"10.1007/s10741-026-10657-9","DOIUrl":"10.1007/s10741-026-10657-9","url":null,"abstract":"<p><p>Cardiovascular disease represents the leading cause of death in patients with Anderson-Fabry disease (FD), with sudden cardiac death (SCD) being one of the most frequently reported causes of mortality. However, a significant diagnostic gap persists in identifying patients at risk, as current stratification tools are inadequate for predicting lethal arrhythmic events. This narrative review resumes the existing peer-reviewed literature regarding the pathophysiology of FD arrhythmias and evaluates the diagnostic limitations of the current standard intermittent monitoring tools, such as the 24-hour Holter. Standard monitoring tools, such as the 24-hour Holter often miss paroxysmal, asymptomatic arrhythmias. Recent studies using implantable loop recorders (ILRs) show a significantly higher burden of arrhythmias than previously recognized. Myocardial fibrosis, identified as late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR), is strongly associated with malignant arrhythmias, together with the degree of left ventricular hypertrophy (LVH). Current consensus statements may underestimate the need for continuous monitoring in FD. By providing a comprehensive narrative synthesis of available observational and registry data, this paper proposes an updated, exploratory risk-stratification clinical guide for the extension of countinuous rhythm monitoring in high-risk subgroups of FD.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148455326","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}
Shanshan Gustafson, Soham R Patel, Marat Fudim, Robert J Mentz, Andrew J Sauer, Anuradha Lala, Josephine A Harrington, Ambarish Pandey, Jana Svetlichnaya, Jesse K Fitzpatrick, Ankeet S Bhatt, Zara Fatima, Andrew P Ambrosy
{"title":"Ironing Out the Details: Advancing Diagnosis and Treatment of Iron Deficiency in Patients with Heart Failure with Preserved Ejection Fraction - A Narrative Review.","authors":"Shanshan Gustafson, Soham R Patel, Marat Fudim, Robert J Mentz, Andrew J Sauer, Anuradha Lala, Josephine A Harrington, Ambarish Pandey, Jana Svetlichnaya, Jesse K Fitzpatrick, Ankeet S Bhatt, Zara Fatima, Andrew P Ambrosy","doi":"10.1007/s10741-026-10653-z","DOIUrl":"10.1007/s10741-026-10653-z","url":null,"abstract":"<p><p>Iron deficiency (ID) is a highly prevalent and clinically significant comorbidity in heart failure with preserved ejection fraction (HFpEF), affecting 40-60% of patients. Independent of anemia, ID is associated with reduced exercise capacity, diminished quality of life (QoL), and increased healthcare utilization. Although intravenous (IV) iron therapy has demonstrated consistent benefits in HF with reduced ejection fraction (HFrEF), including improvements in symptoms, QoL, functional status, and reductions in hospitalizations, its role in HFpEF remains incompletely defined. This review synthesizes the epidemiology, pathophysiologic mechanisms, and diagnostic challenges of ID in HFpEF, with particular attention to emerging data for IV iron supplementation in this clinical setting. It summarizes recent and ongoing clinical trials, highlights limitations of current diagnostic criteria, and outlines innovative strategies, including pragmatic trial designs, patient-reported outcomes, and wearable technologies, to evaluate therapeutic response in this heterogeneous population. Together, these insights provide a roadmap for improving the diagnosis and management of ID in HFpEF and addressing a significant unmet clinical need in this growing patient population.</p>","PeriodicalId":12950,"journal":{"name":"Heart Failure Reviews","volume":"31 1","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148445925","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}