Circulation: Heart Failure最新文献

{"title":"<i>Lactobacillus</i> Restructures the Micro/Mycobiome to Combat Inflammation-Mediated Right Ventricular Dysfunction in Pulmonary Arterial Hypertension.","authors":"Sasha Z Prisco, Madelyn Blake, Felipe Kazmirczak, Ryan Moon, Benjamin P Kremer, Lynn M Hartweck, Minwoo Kim, Neal Vogel, Jenna B Mendelson, Daphne Moutsoglou, Thenappan Thenappan, Kurt W Prins","doi":"10.1161/CIRCHEARTFAILURE.124.012524","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012524","url":null,"abstract":"<p><strong>Background: </strong>Inflammation suppresses right ventricular (RV) function in pulmonary arterial hypertension (PAH). In particular, we showed GP130 (glycoprotein-130) signaling promotes pathological microtubule remodeling and RV dysfunction in rodent PAH. Emerging data demonstrate the intestinal microbiome regulates systemic inflammation, but the impact of modulating the gut microbiome on the GP130-microtubule axis in RV failure is unknown.</p><p><strong>Methods: </strong>Two weeks following monocrotaline injection, rats were administered daily <i>Lactobacillus rhamnosus</i> (4×10⁷ colony-forming units) via oral gavage for 10 days. Next-generation metagenomics and internal transcribed spacer 2 sequencing delineated fecal bacterial and fungal compositions. SomaScan proteomics measured levels of 7596 serum proteins. RV immunoblots quantified protein abundances. Light or super resolution confocal microscopy assessed RV, lung, and jejunal morphology. Echocardiography and invasive closed-chest pressure-volume loops evaluated PAH severity and RV function. The relationship between <i>Lactobacillus</i> abundance and RV function was assessed in 65 patients with PAH.</p><p><strong>Results: </strong><i>Lactobacillus</i> administration restructured both the intestinal micro- and mycobiome. The alteration in the gut ecosystem improved intestinal health as demonstrated by increased jejunal villus length and glycocalyx thickness and diminished intestinal permeability biomarkers. Serum proteomics revealed <i>Lactobacillus</i> modulated systemic inflammation and decreased circulating GP130 ligands. <i>Lactobacillus</i>-mediated suppression of GP130 signaling blunted pathological microtubule remodeling in RV cardiomyocytes. Microtubule-associated phenotypes, including RV cardiomyocyte and nuclear hypertrophy, transverse tubule integrity, and connexin-43 localization, were all corrected with <i>Lactobacillus</i>. These cellular changes manifested as improved RV function despite no significant alteration in PAH severity. Finally, patients with PAH and detectable fecal <i>Lactobacillus</i> had superior RV function despite similar mean pulmonary arterial pressure and pulmonary vascular resistance as compared with those without detectable <i>Lactobacillus</i>.</p><p><strong>Conclusions: </strong><i>Lactobacillus</i> supplementation restructures the gut micro/mycobiome, restores intestinal health, dampens systemic inflammation, and reduces GP130 ligands and associated RV cardiomyocyte microtubule remodeling. These data identify a novel microbiome-inflammation-microtubule axis that has therapeutic relevance for RV dysfunction.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012524"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12263318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076388","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":"Review of the Global Activity of Heart Transplant.","authors":"Abdelghani El Rafei, Rebecca Cogswell, Fernando A Atik, Andreas Zuckermann, Larry A Allen","doi":"10.1161/CIRCHEARTFAILURE.124.012272","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012272","url":null,"abstract":"<p><p>Heart failure is a global disease with significant morbidity. Heart transplant (HT) can be a lifesaving therapy for select patients with end-stage heart failure. In 2020, over 7000 HTs were performed globally; 90% of HTs were performed in the United States and Western Europe, with only 10% throughout the rest of the world. In this article, we offer an overview of the global landscape of HT, exploring challenges and prospects worldwide. We review HT practices, rates and post-HT outcomes, underscoring the differences between countries within each region. We review limitations hindering HT expansion, such as sociocultural factors, as seen in Japan and Israel; health care funding, in countries like India and South Africa; socioeconomic disparities in access, like the United States; and shortage in organ supply, as seen in China and Saudi Arabia. This review underscores the need to address limitations and highlights opportunities to enhance global HT accessibility, especially in lower- and middle-income countries.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012272"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779325","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":"Atrioventricular Dyssynchrony and Dyspnea in Heart Failure With Preserved Ejection Fraction.","authors":"Teodora Donisan, Sara Inglis, Samuel J Asirvatham, Barry A Borlaug","doi":"10.1161/CIRCHEARTFAILURE.125.013183","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.013183","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013183"},"PeriodicalIF":8.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12352622/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092870","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":"Detection of Hypertrophic Cardiomyopathy on Electrocardiogram Using Artificial Intelligence.","authors":"James M Hillis, Bernardo C Bizzo, Sarah F Mercaldo, Ankita Ghatak, Ashley L MacDonald, Madeleine A Halle, Alexander S Schultz, Eric L'Italien, Victor Tam, Nicole K Bart, Filipe A Moura, Amine Awad, David Bargiela, Sarajune Dagen, Danielle Toland, Alexander J Blood, David A Gross, Karola S Jering, Mathew S Lopes, Nicholas A Marston, Victor D Nauffal, Keith J Dreyer, Benjamin M Scirica, Carolyn Y Ho","doi":"10.1161/CIRCHEARTFAILURE.124.012667","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012667","url":null,"abstract":"<p><strong>Background: </strong>Hypertrophic cardiomyopathy (HCM) is associated with significant morbidity and mortality, including sudden cardiac death in the young. Its prevalence is estimated to be 1 in 500, although many people are undiagnosed. The ability to screen electrocardiograms for its presence could improve detection and enable earlier diagnosis. This study evaluated the accuracy of an artificial intelligence device (Viz HCM) in detecting HCM based on a 12-lead electrocardiogram.</p><p><strong>Methods: </strong>The device was previously trained using deep learning and provides a binary outcome (HCM suspected or not suspected). This study included 293 HCM-positive and 2912 HCM-negative cases, which were selected from 3 hospitals based on chart review incorporating billing diagnostic codes, cardiac imaging, and electrocardiogram features. The device produced an output for 291 (99.3%) HCM-positive and 2905 (99.8%) HCM-negative cases.</p><p><strong>Results: </strong>The device identified HCM with sensitivity of 68.4% (95% CI, 62.8-73.5%), specificity of 99.1% (95% CI, 98.7-99.4%), and area under the curve of 0.975 (95% CI, 0.965-0.982). With assumed population prevalence of 0.002 (1 in 500), the positive predictive value was 13.7% (95% CI, 10.1-19.9%) and the negative predictive value was 99.9% (95% CI, 99.9-99.9%). The device demonstrated broadly consistent performance across demographic and technical subgroups.</p><p><strong>Conclusions: </strong>The device identified HCM based on a 12-lead electrocardiogram with good performance. Coupled with clinical expertise, it has the potential to augment HCM detection and diagnosis.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012667"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968317","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":"Diastolic Perfusion Pressure Predicts Response to Inotropes and Vasopressors and Benefit From Mechanical Circulatory Support in Cardiogenic Shock.","authors":"Hoong Sern Lim, Dagmar Vondrakova, Jan Belohlavek, Richard Rokyta, Petr Ostadal","doi":"10.1161/CIRCHEARTFAILURE.125.012847","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.012847","url":null,"abstract":"<p><strong>Background: </strong>Hemodynamic response to escalation of vasoactive drugs has not been well-characterized in patients with cardiogenic shock (CS). We tested the hypothesis that lower diastolic perfusion pressure (DPP=diastolic blood pressure-right atrial pressure) was associated with more limited hemodynamic response to uptitration of vasoactive drugs and with possible benefit from early mechanical circulatory support in patients with CS.</p><p><strong>Methods: </strong>This study consisted of 2 parts: (1) we evaluated the relationship between baseline DPP and changes in cardiac power output index (CPOI) in response to increase in vasoactive drugs in a cohort of patients with CS (n=93) and (2) we compared all-cause mortality based on baseline DPP in a post hoc analysis of the ECMO-CS trial (Extracorporeal Membrane Oxygenation in the Therapy of Cardiogenic Shock). CPOI responders were defined as postescalation CPOI ≥0.28 W/m².</p><p><strong>Results: </strong>Vasoactive inotrope score escalated from 11.2±3.9 to 24.5±4.7. Escalation of vasoactive drugs was associated with increases in CPOI to 0.23±0.06 W/m² (all <i>P</i><0.001). Postescalation CPOI was directly related to baseline cardiac index and DPP. Baseline DPP discriminated cardiac power output responders from nonresponders with an optimal cutoff of 37 mm Hg. Patients with baseline DPP ≥37 mm Hg had greater CPOI increase and lactate clearance. In the ECMO-CS trial, patients with DPP <37 mm Hg had lower mortality (hazard ratio, 0.37 [95% CI, 0.14-0.97]; <i>P</i>=0.044) with immediate venoarterial extracorporeal membrane oxygenation compared with early conservative management but no significant difference in the subgroup with DPP ≥37 mm Hg.</p><p><strong>Conclusions: </strong>Lower DPP was associated with more limited hemodynamic response to escalation of vasoactive drugs and potentially greater benefit from early venoarterial extracorporeal membrane oxygenation in CS.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012847"},"PeriodicalIF":8.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993244","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":"Right Ventricular Function, Inflammation, and the Gut Microbiome in Pulmonary Hypertension: A Translational Frontier.","authors":"Franz P Rischard, Anna R Hemnes","doi":"10.1161/CIRCHEARTFAILURE.125.013198","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.013198","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013198"},"PeriodicalIF":7.8,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309567","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":"Musclin and HFpEF: Unlocking Skeletal Muscle Potential to Improve Exercise Tolerance.","authors":"Stephen J Foulkes, Michael D Nelson, Mark J Haykowsky","doi":"10.1161/CIRCHEARTFAILURE.125.013130","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.013130","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e013130"},"PeriodicalIF":7.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980749","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":"Proteomic Analysis of Valsartan for Attenuating Disease Evolution in Early Sarcomeric Hypertrophic Cardiomyopathy (VANISH) Clinical Trial.","authors":"Constantin-Cristian Topriceanu, Christoffer Rasmus Vissing, Anna Axelsson Raja, Sharlene M Day, Mark W Russell, Kenneth Zahka, Alexandre C Pereira, Steven D Colan, Anne M Murphy, Charles Canter, Richard G Bach, Matthew T Wheeler, Joseph W Rossano, Anjali T Owens, Luisa Mestroni, Matthew R G Taylor, James C Moon, Gabriella Captur, Amit R Patel, Ivan Wilmot, Jonathan H Soslow, Jason R Becker, Christine E Seidman, Neal K Lakdawala, Henning Bundgaard, Usman A Tahir, Carolyn Y Ho","doi":"10.1161/CIRCHEARTFAILURE.124.012393","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012393","url":null,"abstract":"<p><strong>Background: </strong>In hypertrophic cardiomyopathy (HCM), the mechanisms through which pathogenic sarcomere variants (G+) lead to left ventricular hypertrophy (LVH) are not understood.</p><p><strong>Methods: </strong>VANISH (Valsartan for Attenuating Disease Evolution in Early Sarcomeric Hypertrophic Cardiomyopathy) was a multicenter, double-blind, placebo-controlled, randomized trial testing valsartan's ability to attenuate phenotypic progression in early sarcomeric (G+LVH+) and subclinical HCM (G+LVH‒). The outcome was a composite z-score reflecting change in cardiac remodeling from baseline to year 2 (end of study). Baseline and year 2 blood samples were used to quantify 276 proteins using a proximity extension assay (Olink, Sweden). We explored relative differences in protein abundance between early and subclinical HCM at baseline. In addition, we compared proteomic changes between baseline and year 2 in subclinical HCM participants who experienced phenotypic conversion to early HCM (convertors) versus nonconvertors; early HCM participants receiving valsartan versus placebo; and in association with changes in the phenotypic progression z-score. Comparisons were made using the <i>t</i>-test, Mann-Whitney <i>U</i> test, linear mixed models, and generalized linear models, correcting for multiple testing using a 5% false discovery rate.</p><p><strong>Results: </strong>Circulating proteins were analyzed in 192 participants (32 subclinical and 160 early HCM [81 allocated to valsartan]). NT-proBNP (N-terminal pro-B-type natriuretic peptide) differentiated early from subclinical HCM and tracked with phenotypic progression in early HCM (1-unit worsening in z-score associated with a 27% increase in NT-proBNP [95% CI, 17-37%]). Some extracellular matrix remodeling proteins showed a higher abundance (eg, tissue-type plasminogen activator) in early compared with subclinical HCM or tracked with disease progression (decorin) in early HCM. Some growth factors had a higher relative abundance in early HCM (eg, fibroblast growth factor-21). While no individual protein was able to distinguish phenotypic convertors from nonconvertors, multiprotein panels including lipocalin 2, lectin-like oxidized low-density lipoprotein receptor 1, and either NT-proBNP or interleukin-17 receptor A, could distinguish these groups.</p><p><strong>Conclusions: </strong>NT-proBNP was the most informative protein, showing a higher abundance in early compared with subclinical HCM and tracking with the phenotypic progression z-score in early-stage HCM. Studying pathways involving growth factors and extracellular matrix remodeling may yield additional insights into the mechanisms behind disease progression in sarcomevere variant carriers and early HCM.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT01912534.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012393"},"PeriodicalIF":7.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12173761/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983587","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":"Relationship Between Remote, Ambulatory Pulmonary Artery Pressures, and All-Cause Mortality in Patients With Chronic Heart Failure.","authors":"Michael R Zile, William T Abraham, Lynne W Stevenson, Maria Rosa Costanzo, Christiane E Angermann, Mandeep R Mehra, Akshay S Desai, Anique Ducharme, Nessa Johnson, John Henderson, JoAnn Lindenfeld","doi":"10.1161/CIRCHEARTFAILURE.124.012754","DOIUrl":"10.1161/CIRCHEARTFAILURE.124.012754","url":null,"abstract":"<p><strong>Background: </strong>Hemodynamically guided management of patients with chronic heart failure (HF), using a remote, ambulatory pulmonary artery (PA) pressure monitor, has been shown to reduce mortality and morbidity. These improved outcomes were associated with a reduction in PA pressure. However, several pivotal questions remain unanswered: do systolic, diastolic, or mean PA pressures each predict all-cause mortality? Do PA pressures predict mortality across the ejection fraction (EF) spectrum? Do increases or decreases in PA pressure over time predict increases or decreases in mortality?</p><p><strong>Methods: </strong>Retrospective analyses of data from CHAMPION (CardioMEMS Heart Sensor Allows Monitoring of Pressure to Improve Outcomes in NYHA Class III Heart Failure Patients; n=550), GUIDE-HF (Hemodynamic-GUIDEed management of Heart Failure; n=2358), US PAS (CardioMEMS HF System Post Approval Study; n=1200), and MEMS-HF (CardioMEMS Monitoring Study for Heart Failure; n=234) were performed, including all enrolled patients regardless of treatment assignments (Total N=4342). PA systolic, PA diastolic, and PA mean pressures were examined in patients with HF and reduced EF (<50%, n=2562) and preserved EF (≥50%, n=1454). Baseline pressure (averaged over 14 days after implantation) and change in pressure (increase/decrease/no change) from baseline to 6 months (averaged over 14 days just before the 6-month time point) were related to all-cause mortality over a 2-year follow-up period.</p><p><strong>Results: </strong>Baseline PA diastolic, independent of other covariates, was a significant predictor of mortality (hazard ratio, 1.04 [95% CI, 1.03-1.05]; <i>P</i><0.0001). Change in PA diastolic from baseline to 6 months (assessed as a continuous variable) was an independent predictor of mortality after 6 months (landmark analysis; hazard ratio, 1.03 [95% CI, 1.01-1.05]; <i>P</i>=0.0042). Change in PA diastolic from baseline to 6 months(assessed as a categorical variable) decrease or increase of >2 mm Hg compared with no change predicted a 14.7% decrease and 26.7% increase in mortality, respectively (<i>P</i>=0.0237). PA systolic and PA mean pressures in both HF with reduced EF and HF with preserved EF patients, for both baseline and change from baseline to 6 months, were also predictive of all-cause mortality.</p><p><strong>Conclusions: </strong>Baseline PAP (systolic, diastolic, and mean) and change in PAP (systolic, diastolic, and mean) from baseline to 6 months were independent predictors of 2-year mortality in patients with chronic HF in both preserved and reduced EF.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifiers: CHAMPION, NCT00531661; GUIDE-HF, NCT03387813; USPAS, NCT02279888; MEMS-HF, NCT02693691.</p>","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012754"},"PeriodicalIF":7.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12165488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143977236","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":"Racial and Social Vulnerability Hotspots in Premature Heart Failure Mortality Across US Counties.","authors":"Akshaya Srikanth Bhagavathula, Edwin Akomaning, Samuel Prince Osei, Miranda Ashley Griechen","doi":"10.1161/CIRCHEARTFAILURE.125.012889","DOIUrl":"10.1161/CIRCHEARTFAILURE.125.012889","url":null,"abstract":"","PeriodicalId":10196,"journal":{"name":"Circulation: Heart Failure","volume":" ","pages":"e012889"},"PeriodicalIF":7.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763064","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}