Circulation: Heart Failure最新文献

{"title":"Systemic Circulation in Advanced Heart Failure and Cardiogenic Shock: State-of-the-Art Review.","authors":"Sara L Hungerford, Kay D Everett, Gaurav Gulati, Kenji Sunagawa, Daniel Burkhoff, Navin K Kapur","doi":"10.1161/CIRCHEARTFAILURE.124.012016","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012016","url":null,"abstract":"<p><p>The integrative physiology of the left ventricle and systemic circulation is fundamental to our understanding of advanced heart failure and cardiogenic shock. In simplest terms, any increase in aortic stiffness increases the vascular afterload presented to the failing left ventricle. The net effect is increased myocardial oxygen demand and reduced coronary perfusion pressure, thereby further deteriorating contractile function. Although mechanical circulatory support devices should theoretically work in concert with guideline-directed medical therapy, cardiac resynchronization and inotropic and vasopressor agents designed to support myocardial performance and enhance left ventricle recovery, this does not always occur. Each therapy and intervention may result in vastly different and sometimes deleterious effects on vascular afterload. Although best described by a combination of both steady-state and pulsatile components, the latter is frequently overlooked when mean arterial pressure or systemic vascular resistance alone is used to quantify vascular afterload in advanced heart failure and cardiogenic shock. In this state-of-the-art review, we examine what is known about vascular afterload in advanced heart failure and cardiogenic shock, including the use of temporary and permanent mechanical circulatory support systems. Importantly, we outline 4 key components for a more complete assessment of vascular afterload. Unlike previous discussions on this topic, we set aside considerations of venous return and ventricular preload, as important as they are, to focus exclusively on the hydraulic load within the systemic circulation against which the impaired left ventricle must contract.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012016"},"PeriodicalIF":7.8,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001091","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":"Pulseless Paradoxus: Pulsus Paradoxus of the 21st Century.","authors":"Hadi Beaini, Anas Jawaid, Maryjane A Farr, Faris G Araj","doi":"10.1161/CIRCHEARTFAILURE.124.012657","DOIUrl":"https://doi.org/10.1161/CIRCHEARTFAILURE.124.012657","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012657"},"PeriodicalIF":7.8,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001137","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":"Sympathetic Response to 1-Leg Cycling Exercise Predicts Exercise Capacity in Patients With Heart Failure With Preserved Ejection Fraction.","authors":"Mark B Badrov, Tomoyuki Tobushi, Catherine F Notarius, Evan Keys, Massimo Nardone, David Z Cherney, Susanna Mak, John S Floras","doi":"10.1161/CIRCHEARTFAILURE.124.011962","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.011962","url":null,"abstract":"<p><strong>Background: </strong>In heart failure, sympathetic excess and exercise intolerance impair quality of life. In heart failure with reduced ejection fraction, exercise stimulates a reflex increase in muscle sympathetic nerve activity (MSNA) that relates inversely to peak oxygen uptake (V̇O_2peak). Whether similar sympathoexcitatory responses are present in heart failure with preserved EF (HFpEF) and relate to V̇O_2peak are unknown.</p><p><strong>Methods: </strong>In 13 patients with HFpEF (70±6 years), 17 comorbidity-matched controls (CMC; 67±8 years), and 18 healthy controls (65±8 years), we measured heart rate, blood pressure, and MSNA (microneurography) during (1) 7-minute baseline; (2) 2-minute isometric handgrip (40% maximal voluntary contraction) or rhythmic handgrip (50% and 30% maximal voluntary contraction) exercise, followed by 2-minute postexercise circulatory occlusion; and (3) 4-minute 1-leg cycling (2 minutes each at mild and moderate intensity). V̇O_2peak was obtained by open-circuit spirometry.</p><p><strong>Results: </strong>Resting MSNA was higher and V̇O_2peak was lower in HFpEF versus CMCs and healthy controls (all <i>P</i><0.05). During handgrip, MSNA increased in all groups (all <i>P</i><0.05); in HFpEF, MSNA was greater than CMCs and healthy controls during HG and postexercise circulatory occlusion at 40% isometric handgrip (all <i>P</i><0.05) and HG only at 50% and 30% rhythmic handgrip (all <i>P</i><0.05). During cycling, MSNA (bursts·min^-1) decreased during mild (-4±4; <i>P</i>=0.01) and moderate (-8±6; <i>P</i><0.001) cycling in healthy controls, was unchanged during mild (+1±7; <i>P</i>=0.42) and moderate (+2±8; <i>P</i>=0.28) cycling in CMCs, yet increased in HFpEF during mild (+8±8; <i>P</i><0.001) and moderate (+9±10; <i>P</i><0.001) cycling. In HFpEF, the change in MSNA during moderate cycling related inversely to relative (<i>r</i>=-0.72; <i>R</i> ²=0.51; <i>P</i><0.01) and percent-predicted (<i>r</i>=-0.63; <i>R</i> ²=0.39; <i>P</i>=0.03) V̇O_2peak. No statistically significant relationships were detected in controls (<i>P</i>>0.05).</p><p><strong>Conclusions: </strong>In contrast to CMCs, patients with HFpEF exhibit augmented MSNA at rest and during exercise. The magnitude of such paradoxical sympathoexcitation during dynamic cycling relates inversely to V̇O_2peak, consistent with a neurogenic, vasoconstrictor limit on exercise capacity in HFpEF.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e011962"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784305","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":"Medical Expert System for Intelligent Telemonitoring of Patients With Chronic Heart Failure: Preliminary Validation and Perspectives.","authors":"Annamaria Vianello, Martina Olivelli, Massimiliano Donati, Luca Fanucci, Alessio Bechini, Ilaria Petrucci, Stefano Masi","doi":"10.1161/CIRCHEARTFAILURE.124.012478","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012478","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012478"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615673","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":"Pathways to Precision Medicine in Hypertrophic Cardiomyopathy: Opportunities and Challenges in Plasma Proteomics.","authors":"Usman A Tahir","doi":"10.1161/CIRCHEARTFAILURE.124.012593","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012593","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012593"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11891881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853074","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":"NETosis Is an Important Component of Chronic Myocardial Inflammation in Patients With Heart Failure.","authors":"Sawa Kostin, Manfred Richter, Florian Krizanic, Benjamin Sasko, Theodoros Kelesidis, Nikolaos Pagonas","doi":"10.1161/CIRCHEARTFAILURE.124.012231","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012231","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012231"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603430","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":"Mavacamten: Real-World Experience From 22 Months of the Risk Evaluation and Mitigation Strategy (REMS) Program.","authors":"Milind Y Desai, Dewey Seto, Michael Cheung, Sonia Afsari, Niki Patel, Arnaud Bastien, Jeffrey Lockman, Michele Coiro, Matthew W Martinez","doi":"10.1161/CIRCHEARTFAILURE.124.012441","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012441","url":null,"abstract":"<p><strong>Background: </strong>Mavacamten is the only cardiac myosin inhibitor approved by the U.S. Food and Drug Administration for the treatment of patients with symptomatic New York Heart Association class II-III obstructive hypertrophic cardiomyopathy. Under the Risk Evaluation and Mitigation Strategy program for mavacamten, patients are required to be monitored for the development of systolic heart failure and reduction of left ventricular ejection fraction (LVEF) to <50%. We report results from the mavacamten Risk Evaluation and Mitigation Strategy database (April 28, 2022 to February 27, 2024).</p><p><strong>Methods: </strong>Data on health care providers and pharmacy certification, patient monitoring (from Patient Status Forms, based partly on echocardiograms), and screening for drug interactions before each dispense were collected.</p><p><strong>Results: </strong>Of the 6299 patients who received ≥1 dose of mavacamten, 60.0% were women; 64.6% were aged >60 years. Of the 5573 patients with submitted Patient Status Forms, 256 (4.6%) developed LVEF <50%, and 71 (1.3%) experienced heart failure requiring hospitalization. On the 29 111 status forms in these patients, each representing an assessment of an echocardiogram, LVEF <50% was reported on 276 (0.9%), and heart failure requiring hospitalization was reported on 86 (0.3%). Of the 1929 patients with ≥1 year of treatment, 78 (4.0%) had an LVEF reduction to <50%, and 4 (0.2%) experienced LVEF <50% and heart failure requiring hospitalization but later resumed treatment. Of the 3228 patients initiated on 5 mg/d mavacamten and were treated for at least 6 months, 2391 (74.1%) remained at 5 or 10 mg/d. At 3 and 6 months following mavacamten treatment initiation, 57.2% and 70.3%, respectively, demonstrated post-Valsalva left ventricular outflow tract gradient <30 mm Hg.</p><p><strong>Conclusions: </strong>We describe the feasibility and experience of the first 22 months of the Risk Evaluation and Mitigation Strategy program for prescribing mavacamten in >6000 patients with symptomatic obstructive hypertrophic cardiomyopathy. The need for temporary interruption for LVEF <50% was low, including for patients on therapy ≥1 year, with even fewer LVEF reductions associated with heart failure requiring hospitalization.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012441"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11745710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615683","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":"Social Determinants of Health and Disparities in Guideline-Directed Medical Therapy Optimization for Heart Failure.","authors":"Joshua A Jacobs, Iyanuoluwa Ayodele, Adam P Bress, Madeline R Sterling, Ambarish Pandey, Catherine G Derington, Alexander R Zheutlin, Kevin S Shah, Stephen J Greene, Brooke Alhanti, Rosalia Blanco, Gregg C Fonarow","doi":"10.1161/CIRCHEARTFAILURE.124.012357","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012357","url":null,"abstract":"<p><strong>Background: </strong>Fewer than 20% of eligible patients with heart failure with reduced ejection fraction receive all 4 pillars of guideline-directed medical therapy. Understanding disparities by race, ethnicity, sex, and adverse social determinants of health is necessary to equitably optimize quadruple therapy.</p><p><strong>Methods: </strong>Utilizing the American Heart Association's Get With The Guidelines-Heart Failure registry, we examined associations between race and ethnicity, sex, and adverse social determinants of health (insurance type and documented social need [any barrier to accessing health care]) with quadruple therapy optimization (QTO) in patients with heart failure with reduced ejection fraction hospitalized between July 1, 2021, and September 30, 2023, with complete medication data at discharge. We calculated adjusted mean differences (AMDs) in the discharge QTO score (range, 0%-100%) reflecting the proportion of eligible use of renin-angiotensin system inhibitors, β-blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors and compared across demographic and adverse social determinants of health groups.</p><p><strong>Results: </strong>Among 82 637 patients (median age, 66 years; 32.5% female; 57.0% non-Hispanic White; 76.4% prior heart failure with reduced ejection fraction), the overall mean QTO score was 56.2% (SD, 25.5). After adjustment, compared with non-Hispanic White individuals, Black (AMD, 2.56 percentage points [95% CI, 2.16-2.96]) and Hispanic individuals (AMD, 0.71 percentage points [95% CI, 0.11-1.31]) had higher QTO scores. Females had higher QTO scores than males (AMD, 1.94 percentage points [95% CI, 1.58-2.31]). Patients with no insurance (AMD, -4.90 percentage points [-5.62 to -4.17]), Medicaid (AMD, -0.45 percentage points [-0.89 to -0.01]), and Medicare (AMD, -1.64 percentage points [-2.10 to -1.18]) had lower QTO scores versus private insurance. Those with an identified social need (n=24 651) had lower QTO scores than those without (AMD, -3.40 percentage points [95% CI, -4.10 to -2.71]).</p><p><strong>Conclusions: </strong>Disparities in QTO were most evident for patients with no insurance, Medicaid, Medicare, or potentially an identified social need. Future efforts should focus on reducing gaps to improve equitable guideline-directed medical therapy use.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012357"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615705","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":"Elevated Donor-Derived Cell-Free DNA Levels Are Associated With Reduced Myocardial Blood Flow but Not Angiographic Cardiac Allograft Vasculopathy: The EVIDENT Study.","authors":"Cathrine M Moeller, Daniel Oren, Andrea Fernandez Valledor, Gal Rubinstein, Ersilia M DeFilippis, Salwa Rahman, Yonatan Mehlman, Elena M Donald, Dor Lotan, Edward Lin, Kyung T Oh, Sun H Lee, Jayant K Raikhelkar, Justin A Fried, David Majure, Farhana Latif, Gabriel T Sayer, Nir Uriel, Kevin J Clerkin","doi":"10.1161/CIRCHEARTFAILURE.124.011756","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.011756","url":null,"abstract":"<p><strong>Background: </strong>Cardiac allograft vasculopathy (CAV) leads to impaired myocardial blood flow (MBF), increasing the risk of cardiovascular death or retransplant among heart transplantation (HT) recipients. Data on elevation in donor-derived cell-free DNA (dd-cfDNA) and CAV in the absence of rejection are mixed. We sought to test the hypothesis that CAV with reduced MBF (RMBF) is associated with elevated dd-cfDNA.</p><p><strong>Methods: </strong>A retrospective review was conducted on HT recipients at a high-volume center who underwent dd-cfDNA testing between September 2019 and November 2022. Inclusion criteria included undergoing CAV screening with cardiac positron emission tomography scans and coronary angiograms. Patients were grouped by the presence of angiographic CAV diagnosis and MBF reserve evaluated through cardiac positron emission tomography. The latter was subdivided into normal MBF or RMBF, with RMBF defined as an MBF reserve ≤2. Elevated dd-cfDNA was defined as ≥0.12%.</p><p><strong>Results: </strong>Two hundred fifty-six HT recipients were included (median age, 55 years; 27.6% female; median, 8 years [interquartile range (IQR), 5-14] post-HT). Ischemic etiology of heart failure was more prevalent in the RMBF group (36%) compared with the normal MBF group (20%; <i>P</i>=0.02). The prevalence and magnitude of a positive dd-cfDNA test with angiographic CAV (29%; median, 0.26% [IQR, 0.15%-0.62%]) were not significantly different from those without CAV (30%; <i>P</i>=0.94; median, 0.31% [IQR, 0.17%-0.71%]; <i>P</i>=0.38). However, RMBF patients exhibited significantly higher dd-cfDNA prevalence and levels (51%; median, 0.81% [IQR, 0.48%-1.11%]) compared with normal MBF patients (27%; <i>P</i><0.001; median, 0.25% [IQR, 0.15%-0.52%]; <i>P</i><0.001).</p><p><strong>Conclusions: </strong>HT recipients with angiographic CAV had similar dd-cfDNA levels and rates as those without. Notably, dd-cfDNA levels and rates were significantly elevated in patients with RMBF assessed by positron emission tomography compared with those with normal MBF.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e011756"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753942/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799647","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":"Comprehensive Proteomics Profiling Identifies Circulating Biomarkers to Distinguish Hypertrophic Cardiomyopathy From Other Cardiomyopathies With Left Ventricular Hypertrophy.","authors":"Keitaro Akita, Mathew S Maurer, Albree Tower-Rader, Michael A Fifer, Yuichi J Shimada","doi":"10.1161/CIRCHEARTFAILURE.124.012434","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012434","url":null,"abstract":"<p><strong>Background: </strong>Distinguishing hypertrophic cardiomyopathy (HCM) from other cardiomyopathies with left ventricular hypertrophy (LVH), such as hypertensive LVH, transthyretin amyloid cardiomyopathy, and aortic stenosis, is sometimes challenging. Using plasma proteomics profiling, we aimed to identify circulating biomarkers and dysregulated signaling pathways specific to HCM.</p><p><strong>Methods: </strong>In this multicenter case-control study, plasma proteomics profiling was performed in cases with HCM and controls with hypertensive LVH, transthyretin amyloid cardiomyopathy, and aortic stenosis. Two-thirds of patients enrolled earlier in each disease group were defined as the training set and the remaining one-third as the test set. Protein concentrations in HCM were compared with those in hypertensive LVH (comparison 1), transthyretin amyloid cardiomyopathy (comparison 2), and aortic stenosis (comparison 3). Candidate proteins that meet the following 2 criteria were selected: (1) higher abundance in HCM throughout all 3 comparisons or lower abundance in HCM throughout all 3 comparisons with univariable <i>P</i><0.05 and |log₂(fold change)| >0.5 in both the training and test sets and (2) independently associated with HCM with multivariable <i>P</i><0.05 after adjusting for clinical parameters significantly different between HCM and controls. Using the selected candidate proteins, a logistic regression model to distinguish HCM from controls was developed in the training set and applied to the test set. Finally, pathway analysis was performed in each comparison using proteins with different abundance.</p><p><strong>Results: </strong>Overall, 4979 proteins in 1415 patients (HCM, n=879; hypertensive LVH, n=331; transthyretin amyloid cardiomyopathy, n=169; aortic stenosis, n=36) were analyzed. Of those, 5 proteins were selected as candidate proteins. The logistic regression model with these 5 proteins had an area under the receiver operating characteristic curve of 0.86 (95% CI, 0.82-0.89) in the test set. The MAPK (mitogen-activated protein kinase) and HIF-1 (hypoxia-inducible factor 1) pathways were dysregulated in HCM throughout the 3 comparisons.</p><p><strong>Conclusions: </strong>This study identified circulating biomarkers that distinguish HCM from other cardiomyopathies with LVH independently from confounders and revealed signaling pathways associated with HCM.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012434"},"PeriodicalIF":7.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142615678","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}