Circulation: Heart Failure最新文献

{"title":"Letter by Araj and Mammen Regarding Article, \"Disseminated Intracardiac Thrombosis Due to Long-Standing, Asymptomatic Ventricular Fibrillation Under LVAD Support\".","authors":"Faris G Araj, Pradeep P A Mammen","doi":"10.1161/CIRCHEARTFAILURE.125.013221","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.125.013221","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013221"},"PeriodicalIF":7.8,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590580","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":"Mid-Term Reassessment of Waitlist and Posttransplant Outcomes Under the 2018 Heart Allocation System: Improved All-Cause Survival.","authors":"Yeahwa Hong, Nidhi Iyanna, Ander Dorken-Gallastegi, Umar Nasim, Edward T Horn, Michael A Mathier, Dennis M McNamara, Gavin W Hickey, Mary E Keebler, David J Kaczorowski","doi":"10.1161/CIRCHEARTFAILURE.124.012663","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.012663","url":null,"abstract":"<p><strong>Background: </strong>This study evaluates clinical trends and mid-term waitlist and posttransplant outcomes following the 2018 heart allocation policy change.</p><p><strong>Methods: </strong>The United Network for Organ Sharing registry was queried to analyze adult waitlisted and transplanted patients undergoing isolated heart transplantation. Two analyses were conducted: (1) waitlist and (2) posttransplant outcomes. For the waitlist analysis, candidates were stratified into seasonally matched prepolicy (October 18, 2012-June 30, 2017) and postpolicy (October 18, 2018-June 30, 2023) groups, with a 1-year follow-up period. Waitlist outcomes included 1-year cumulative incidences of transplantation, delisting due to death/clinical deterioration, and all-cause survival from the initial waitlisting. For the posttransplant analysis, recipients were stratified into seasonally matched prepolicy (October 18, 2014-June 30, 2018) and postpolicy (October 18, 2018-June 30, 2020) groups, with a 4-year follow-up period. Posttransplant outcomes included 4-year survival. Propensity score-matching and multivariable Cox regression were used for risk adjustment.</p><p><strong>Results: </strong>Under the 2018 allocation system, there was a continued shift toward the use of older donors, longer graft ischemic times, and shorter waitlist durations. In the waitlist analysis, 30 620 waitlisted candidates were analyzed, with 14 908 (48.7%) listed after the policy change. The postpolicy candidates had a higher 1-year cumulative incidence of transplantation (subhazard ratio, 2.06 [95% CI, 2.00-2.12]; <i>P</i><0.001) and a lower 1-year cumulative incidence of delisting (subhazard ratio, 0.58 [95% CI, 0.53-0.63]; <i>P</i><0.001) compared with the prepolicy candidates. In addition, the postpolicy candidates had significantly improved 1-year survival from initial waitlisting compared with the prepolicy candidates (90.0% versus 86.8%; <i>P</i><0.001). In the posttransplant analysis, 13 712 recipients were analyzed, with 4597 (33.5%) transplanted following the policy change. The 4-year post-transplant survival was similar between the groups (83.3% versus 82.8%; <i>P</i>=0.593). Furthermore, the comparable 4-year post-transplant survival persisted in the propensity score-matched comparison and multivariable Cox regression.</p><p><strong>Conclusions: </strong>Despite the changes in donor and recipient profiles following the 2018 allocation system change, this mid-term reassessment demonstrates its success in significantly improving waitlist survival, while maintaining comparable posttransplant survival.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012663"},"PeriodicalIF":7.8,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552483","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":"Mucopolysaccharidosis Type IIIA Presenting as Hypertrophic Cardiomyopathy.","authors":"Filippo Pinto E Vairo, Jeffrey B Geske, Ravinder J Singh, Roy B Dyer, Konstantinos C Siontis, Maria O'Connell, Christopher Schmitz, Laura Lambert, Karl J Clark, Kimiyo M Raymond, Joseph J Maleszewski, Tim Wood, Pavel N Pichurin, Eric W Klee, Naveen L Pereira","doi":"10.1161/CIRCHEARTFAILURE.124.012632","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012632","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012632"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751247","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":"Left Atrial Reverse Remodeling in Patients Supported With Durable Left Ventricular Assist Devices and Clinical Implications.","authors":"Christos P Kyriakopoulos, Konstantinos Sideris, Iosif Taleb, Eleni Maneta, Eleni Tseliou, Jake Aadland, Andrew S Baird, Michael J Bonios, Marisca Nelson, Elizabeth Dranow, Matthew L Goodwin, Thomas C Hanff, Spencer Carter, Craig H Selzman, Josef Stehlik, Omar Wever-Pinzon, Satvik Ramakrishna, Ethan Tumarkin, Stavros G Drakos","doi":"10.1161/CIRCHEARTFAILURE.125.012807","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.012807","url":null,"abstract":"<p><strong>Background: </strong>The left atrium (LA) maintains a dynamic interaction with the left ventricle (LV). LA forward and reverse remodeling affect prognosis in patients with chronic heart failure. We examined LA reverse remodeling in patients supported with LV assist devices (LVADs) and investigated a potential impact on clinical outcomes.</p><p><strong>Methods: </strong>Consecutive patients with advanced heart failure receiving durable, continuous-flow LVADs were prospectively evaluated (n=263). After excluding patients with unavailable echocardiographic data, 241 patients were studied. Echocardiographic assessment was performed pre- and serially post-LVAD implantation. We assessed LA and LV structure and function and their association, and the impact of LA reverse remodeling on all-cause mortality, LVAD-related adverse events, and atrial fibrillation (AF).</p><p><strong>Results: </strong>Most patients were male, White, with a mean age of 56±15 years. Forty-four percent had underlying ischemic cardiomyopathy, and 65% were profile 1 to 3 as per the Interagency Registry for Mechanically Assisted Circulatory Support, with a mean LV ejection fraction of 19±7%, and end-diastolic diameter of 6.7±1.1 cm pre-LVAD. LA structure and function improved by 1 month on LVAD support and remained improved by 12 months, as evidenced by LA volumes, emptying volumes, emptying fractions, and strain parameters. LA changes were shown to be associated with LV structural and functional changes. The magnitude of LA reverse remodeling was associated with all-cause mortality, but not cerebrovascular accident/transient ischemic attack, LVAD thrombosis, or late right heart failure rates by 12 months on LVAD support. Of 46 patients with AF pre-LVAD, 28 (61%) converted to sinus rhythm, and 18 (39%) remained in AF during serial echocardiographic assessment.</p><p><strong>Conclusions: </strong>LA structure and function improved early post-LVAD support, showed stability of improvement during follow-up, and were associated with simultaneous LV changes. Implications on all-cause mortality and AF might inform the care of heart failure patients being considered for advanced therapies, as well as the broader population of patients with heart failure and concomitant AF undergoing pharmacological unloading.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012807"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12263335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983210","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":"Impact of Neighborhood Factors on Exercise Capacity in Children With Hypertrophic Cardiomyopathy.","authors":"Imran R Masood, Lei Wang, Helen M Stanley, Jonathan J Edwards, Humera Ahmed, Kimberly Y Lin, Carol A Wittlieb-Weber, Matthew J O'Connor, Joseph W Rossano, Shannon O'Malley, Stephen M Paridon, Vicky W Tam, Jonathan B Edelson","doi":"10.1161/CIRCHEARTFAILURE.124.012501","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012501","url":null,"abstract":"<p><strong>Background: </strong>Restricting certain patients with hypertrophic cardiomyopathy (HCM) from exercise likely has negative cardiovascular effects and has not been shown to reduce the risk of sudden cardiac death. Promoting exercise in children with HCM is complex and requires knowledge of the environmental factors that impact exercise capacity in children with HCM.</p><p><strong>Methods: </strong>This retrospective, cross-sectional analysis includes children with HCM who underwent exercise stress testing at a single, children's tertiary-care center between 2000 and 2023. Addresses from contemporaneous exercise stress testing were accessed and geocoded to census tracts. The child opportunity index was the primary exposure of interest. Granular neighborhood measures including the walkability index, rural-urban commuting area codes, index of concentration at the extremes, and uniform crime reporting rates were measured. The primary outcome measure was peak oxygen consumption. Linear regression and multivariable analyses were performed.</p><p><strong>Results: </strong>A total of 155 patients were identified who met inclusion criteria, 23% (n=35) of whom were female. The mean age at the time of exercise stress testing was 15.8±3.1 years. More than half of the included patients were from a high or very high child opportunity index (30%, n=46, and 35%, n=54, respectively). Most patients lived in urban environments (rural-urban commuting area codes score, 1 or 2, 96.7%, n=150). The mean peak oxygen consumption was 2159±906 mm/min, and the adjusted peak oxygen consumption was 35.5±9.3 mL/kg per min. A multivariate model adjusting for disease severity, age at diagnosis of HCM, race, and accounting for collinearity showed that low child opportunity index, higher levels of urbanization, and lower concentration of neighborhood wealth were independently associated with lower peak oxygen consumption.</p><p><strong>Conclusions: </strong>Our study identified previously unrecognized environmental determinants of exercise capacity in children with HCM, with lower child opportunity index, increased urbanization, and lower neighborhood wealth independently associated with lower exercise performance. Programs designed to increase physical activity levels and exercise performance in children with HCM should account for neighborhood and economic factors.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012501"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324604","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":"Hierarchical Analysis of Composite Time-to-Event End Points in Heart Failure Clinical Trials Using Time in Clinical State.","authors":"Eric S Leifer, James F Troendle, Mitchell A Psotka, Vandana Sachdev","doi":"10.1161/CIRCHEARTFAILURE.124.011783","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.011783","url":null,"abstract":"<p><p>Much work has been done on developing hierarchical composite end point analysis methods, which meaningfully measure the effect of a treatment for patients with heart failure. Two motivations for this work have been as follows: (1) trying to ensure that more severe outcomes are weighted more heavily in the analysis; (2) combining different types of end points such as death, number of recurrent hospitalizations, and continuous functional or biologic end points. Such methods include the win ratio, the win odds, and the proportion in favor of treatment. In this article, our focus is when all components are clinical end points such as death or hospitalizations and do not include continuous end points. We review these methods using HF-ACTION (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training). We also describe recent methods for combining different clinical end points, which take into account the time a subject is in a particular clinical state. These include the pairwise win time, the restricted mean time in favor of treatment, the expected win time, and the expected win time against reference. We discuss the US Food and Drug Administration guidances and make general recommendations.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e011783"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076390","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":"Skeletal Muscle Quantity Versus Quality in Heart Failure: Exercise Intolerance and Outcomes in Older Patients With HFpEF Are Related to Abnormal Skeletal Muscle Metabolism Rather Than Age-Related Skeletal Muscle Loss.","authors":"Sabra C Lewsey, T Jake Samuel, Michael Schär, Joevin Sourdon, Joseph R Goldenberg, Lisa R Yanek, Shenghan Lai, Angela M Steinberg, Paul A Bottomley, Gary Gerstenblith, Robert G Weiss","doi":"10.1161/CIRCHEARTFAILURE.124.012512","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012512","url":null,"abstract":"<p><strong>Background: </strong>Heart failure with preserved ejection fraction (HFpEF) is a systemic process with contributions from peripheral factors, including skeletal muscle (SM). Age-associated SM loss and impaired energy metabolism occur without heart failure, but the relative importance of changes in SM quantity versus metabolic quality in patients with HFpEF for exercise intolerance (EI) or outcomes has not been studied. We hypothesized that EI and subsequent clinical outcomes across the adult lifespan in patients with HFpEF are related to impaired SM energy metabolism rather than age-associated SM loss.</p><p><strong>Methods: </strong>Patients with HFpEF (n=64; aged 34-86 years) with left ventricular ejection fraction ≥50% were stratified by age in a prospective study. They underwent 3T magnetic resonance imaging to measure calf muscle quantity and ³¹P magnetic resonance spectroscopy to measure muscle high-energy phosphate metabolism during plantar flexion exercise.</p><p><strong>Results: </strong>Older patients with HFpEF exhibited more severe EI, less calf muscle, faster exercise-induced high-energy phosphate decline, and worse SM energetics at fatigue than younger patients. EI correlated closely with muscle metabolic quality, not quantity. Neither magnetic resonance imaging exercise time, 6-minute walk distance, nor peak oxygen uptake at cardiopulmonary exercise testing on cardiopulmonary bicycle exercise testing correlated with calf SM area. In contrast, the 6-minute walk distance or peak oxygen uptake at cardiopulmonary exercise testing were inversely related to rapid exercise-induced high-energy phosphate decline and worse SM energetic profile at fatigue. Rapid exercise-induced high-energy phosphate decline and lower ATP at fatigue were associated with increased cardiovascular death or heart failure hospitalizations in univariate analysis over a median of 39.3 months.</p><p><strong>Conclusions: </strong>EI in older patients with HFpEF is closely linked to age-associated abnormalities in SM energy metabolism, namely, rapid exercise-induced energetic decline and worse energetic profile at fatigue, and not SM quantity. Abnormal SM energy metabolism is associated with worse outcomes in patients with HFpEF in unadjusted analysis. These findings support SM energy metabolism as a barometer of systemic HFpEF severity and the pursuit of new SM metabolic modulators to reduce disabling EI and possibly adverse outcomes in patients with HFpEF.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012512"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12286618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324605","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":"Late-Life Echocardiographic Effects of the Amyloidogenic p.V142I Transthyretin Variant.","authors":"Vishal N Rao, Brian L Claggett, Michel G Khouri, Amil M Shah, Scott D Solomon, Senthil Selvaraj","doi":"10.1161/CIRCHEARTFAILURE.125.013212","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.013212","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013212"},"PeriodicalIF":8.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12313242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092908","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":"Cardiac-Targeted AAV5-S100A1 Gene Therapy Protects Against Adverse Remodeling and Contractile Dysfunction in Postischemic Hearts.","authors":"Dorothea Kehr, Janek Salatzki, Birgit Seger, Karl Varadi, Jennifer Birkenstock, Philipp Schlegel, Erhe Gao, Walter J Koch, Hugo A Katus, Norbert Frey, Johannes Riffel, Florian André, Karsten Peppel, Andreas Jungmann, Martin Busch, Helga Pfannkuche, Julia Ritterhoff, Patrick Most","doi":"10.1161/CIRCHEARTFAILURE.124.012479","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012479","url":null,"abstract":"<p><strong>Background: </strong>Guided by long-term safety data for AAV5 (adeno-associated virus 5) in humans, our translational study investigated whether AAV5 effectively delivers genes to healthy and achieves therapeutic efficacy in dysfunctional human-sized hearts, using a clinically applicable mode of administration and vector dosages.</p><p><strong>Methods: </strong>AAV-mediated cardiac gene transfer in pigs was performed by percutaneous catheter-based retrograde intravenous vector delivery, and vector genome and transgene expression levels determined by reverse transcription-polymerase chain reaction and immunoblotting. Postmyocardial infarction (MI) cardiac dysfunction porcine and murine models were generated by coronary catheter-based occlusion and ligation, respectively. The study end points left ventricular ejection fraction and left ventricular MI size, were measured by cardiac magnetic resonance imaging and echocardiography. Bulk myocardial RNA-sequencing and weighted gene correlation network analysis were used to link study end points to molecular pathway mechanisms. Safety was assessed by clinical chemistry, blood count and ECG.</p><p><strong>Results: </strong>In a first biodistribution study, AAV5 (1×10¹³ vector genomes; vgs) with the reporter gene <i>luciferase</i> (<i>luc</i>) achieved broad and homogenous transduction of healthy pig hearts 30 days after catheter-based retrograde intravenous vector delivery without toxicity. Both its myocardial and extra-cardiac distribution patterns were advantageous compared with AAV9-<i>luc</i> and AAV6-<i>luc</i>. Using AAV5 with the cardioprotective human gene <i>S100A1</i> (<i>hS100A1</i>; 1×10¹³ vgcs) by catheter-based retrograde intravenous vector delivery in a subsequent therapy study in post-MI pigs prevented left ventricular MI extension and improved left ventricular ejection fraction after 3 months without clinical toxicity. Weighted gene correlation network analysis linked novel antiinflammatory actions and cardioprotective signaling mechanisms by hS100A1 to study end point improvements, which was confirmed in a post-MI mouse model.</p><p><strong>Conclusions: </strong>Providing the clinically relevant proof of concept for AAV5 to effectively transduce healthy and dysfunctional human-sized hearts, its clinical long-term safety, scalable producibility, and low preexisting immunity in humans may predestine AAV5 as an effective and safe gene carrier for a prevalent disease such as chronic heart failure, using therapeutic genetic effectors such as <i>hS100A1</i> or others.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012479"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12278446/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324602","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":"Two Years Transplant-Free Survival After LVAD Explantation in a Titin Truncating Variant Carrier With Peripartum Cardiomyopathy and Cardiogenic Shock.","authors":"Rita Godinho, Anna Nowacka, Zahurul Alam Bhuiyan, Zied Ltaief, Lucas Liaudet, Matthias Kirsch, Patrick Yerly","doi":"10.1161/CIRCHEARTFAILURE.124.012079","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012079","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012079"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980751","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}