Pub Date : 2025-04-11DOI: 10.1093/eurheartj/ehaf219
Lawrence Lau, Larry Baddour, Núria Fernández Hidalgo, Thomas D Brothers, William K F Kong, Michael A Borger, Xavier Duval, Christophe Tribouilloy, Jean-Francois Obadia, Mehrdad Golian, Vicente F Corrales-Medina, Francois Auclair, Mikael Mazighi, Kwan Leung Chan, Bernard Prendergast, Gilbert Habib, Fraser D Rubens, David Messika-Zeitoun
Infective endocarditis (IE) is a relatively rare but life-threatening systemic infection, which remains associated with high morbidity and mortality. The epidemiology of IE has shifted to involve an increasing numbers of older patients with both cardiovascular and other types of prosthetic devices, multiple comorbid conditions often requiring invasive procedures, increasingly virulent pathogens, in particular Staphylococcus aureus, or that can harbour anti-microbial resistance, and an escalation of injection drug use in many areas of the world. In parallel, advancements in diagnostic and therapeutic options have led to complex strategies in patients’ management. Despite these epidemiologic shifts, clinical trials have been rare and most of the evidence guiding IE management derives from expert consensus or analysis of large registries. Because of this, a multi-disciplinary IE team-based approach has been recommended as the standard of care. The aim of this review is to explore the rationale for a multi-disciplinary team-based approach to the management of IE. This approach has proved to be potentially beneficial based on multiple investigations that have evaluated patient outcomes. In addition, implementation strategies, feasibility and options of the team approach have also been highlighted.
{"title":"Infective endocarditis: it takes a team","authors":"Lawrence Lau, Larry Baddour, Núria Fernández Hidalgo, Thomas D Brothers, William K F Kong, Michael A Borger, Xavier Duval, Christophe Tribouilloy, Jean-Francois Obadia, Mehrdad Golian, Vicente F Corrales-Medina, Francois Auclair, Mikael Mazighi, Kwan Leung Chan, Bernard Prendergast, Gilbert Habib, Fraser D Rubens, David Messika-Zeitoun","doi":"10.1093/eurheartj/ehaf219","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf219","url":null,"abstract":"Infective endocarditis (IE) is a relatively rare but life-threatening systemic infection, which remains associated with high morbidity and mortality. The epidemiology of IE has shifted to involve an increasing numbers of older patients with both cardiovascular and other types of prosthetic devices, multiple comorbid conditions often requiring invasive procedures, increasingly virulent pathogens, in particular Staphylococcus aureus, or that can harbour anti-microbial resistance, and an escalation of injection drug use in many areas of the world. In parallel, advancements in diagnostic and therapeutic options have led to complex strategies in patients’ management. Despite these epidemiologic shifts, clinical trials have been rare and most of the evidence guiding IE management derives from expert consensus or analysis of large registries. Because of this, a multi-disciplinary IE team-based approach has been recommended as the standard of care. The aim of this review is to explore the rationale for a multi-disciplinary team-based approach to the management of IE. This approach has proved to be potentially beneficial based on multiple investigations that have evaluated patient outcomes. In addition, implementation strategies, feasibility and options of the team approach have also been highlighted.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"39 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143822629","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}
Pub Date : 2025-04-11DOI: 10.1093/eurheartj/ehaf214
Jan Borén,Chris Packard,Børge G Nordestgaard,Alberico L Catapano
{"title":"Great debate: Plasma triglycerides are an important causal factor and therapeutic target for atherosclerotic cardiovascular disease.","authors":"Jan Borén,Chris Packard,Børge G Nordestgaard,Alberico L Catapano","doi":"10.1093/eurheartj/ehaf214","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf214","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"183 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143822580","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}
Pub Date : 2025-04-11DOI: 10.1093/eurheartj/ehaf250
Lijuan Qian,Jie Yu
{"title":"Rosai-Dorfman disease of the ascending aorta and pulmonary artery mimicking intramural hematoma and mass.","authors":"Lijuan Qian,Jie Yu","doi":"10.1093/eurheartj/ehaf250","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf250","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"37 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143822579","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}
Pub Date : 2025-04-11DOI: 10.1093/eurheartj/ehaf225
Masatake Kobayashi, Bertram Pitt, João Pedro Ferreira, Patrick Rossignol, Nicolas Girerd, Faiez Zannad
Treatment-resistant hypertension (TRH) often coexists with chronic kidney disease (CKD), and the presence of both conditions increases the risk of adverse cardiovascular outcomes. Patients with TRH and CKD exhibit enhanced aldosterone and mineralocorticoid receptor expression, which promote inflammation and fibrosis in cardiac and renal tissues, contributing to the development and progression of cardiorenal diseases. Both achieving optimal blood pressure (BP) control and mitigating the risk of aldosterone-related adverse events are cornerstones in the management of patients with TRH and CKD. Mineralocorticoid receptor antagonists (MRAs) are recommended for the treatment of TRH. To date, the efficacy has been investigated in populations with mostly normal renal function. However, the potential risk of hyperkalaemia limits the use of MRAs, particularly in patients with CKD. Non-steroidal MRAs and sodium glucose cotransporter-2 inhibitors have slowed renal function decline and shown cardiorenal benefits. Additionally, aldosterone synthase inhibitors may emerge as a therapeutic option for patients with TRH. Clinical trials for TRH primarily centred on assessing BP-lowering effects; however, merely lowering BP might not be a sufficient target to prevent a risk of cardiorenal disease progression. This paper presents evidence and potential benefits of aldosterone-targeted therapy in the treatment of TRH and CKD and re-consider the treatment strategies in clinical practice and trial design.
{"title":"Aldosterone-targeted therapies: early implementation in resistant hypertension and chronic kidney disease","authors":"Masatake Kobayashi, Bertram Pitt, João Pedro Ferreira, Patrick Rossignol, Nicolas Girerd, Faiez Zannad","doi":"10.1093/eurheartj/ehaf225","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf225","url":null,"abstract":"Treatment-resistant hypertension (TRH) often coexists with chronic kidney disease (CKD), and the presence of both conditions increases the risk of adverse cardiovascular outcomes. Patients with TRH and CKD exhibit enhanced aldosterone and mineralocorticoid receptor expression, which promote inflammation and fibrosis in cardiac and renal tissues, contributing to the development and progression of cardiorenal diseases. Both achieving optimal blood pressure (BP) control and mitigating the risk of aldosterone-related adverse events are cornerstones in the management of patients with TRH and CKD. Mineralocorticoid receptor antagonists (MRAs) are recommended for the treatment of TRH. To date, the efficacy has been investigated in populations with mostly normal renal function. However, the potential risk of hyperkalaemia limits the use of MRAs, particularly in patients with CKD. Non-steroidal MRAs and sodium glucose cotransporter-2 inhibitors have slowed renal function decline and shown cardiorenal benefits. Additionally, aldosterone synthase inhibitors may emerge as a therapeutic option for patients with TRH. Clinical trials for TRH primarily centred on assessing BP-lowering effects; however, merely lowering BP might not be a sufficient target to prevent a risk of cardiorenal disease progression. This paper presents evidence and potential benefits of aldosterone-targeted therapy in the treatment of TRH and CKD and re-consider the treatment strategies in clinical practice and trial design.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"25 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143822578","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}
Pub Date : 2025-04-10DOI: 10.1093/eurheartj/ehaf213
Alex Hørby Christensen,Gang Pan,Rasmus L Marvig,Francisco German Rodriguez Gonzalez,Christoffer Rasmus Vissing,Elvira Silajdzija,Rasmus Frosted,Etsehiwot Girum Girma,Migle Gabrielaite,Henrik Kjærulf Jensen,Kasper Rossing,Finn Lund Henriksen,Niels Christian Foldager Sandgaard,Gustav Ahlberg,Jonas Ghouse,Pia Rengtved Lundegaard,Joachim Weischenfeldt,Claes Wadelius,Henning Bundgaard
BACKGROUND AND AIMSFamilial ST-depression syndrome (FSTD) is a recently identified inherited cardiac disease associated with arrhythmias and systolic dysfunction. The underlying genetic aetiology has remained elusive. This study aimed at finding the causative variant.METHODSA total of 67 FSTD patients (20 families) were studied. Linkage analysis and whole-genome sequencing (WGS) were initially performed. An identified non-coding variant was functionally characterized in AC16 human cardiomyocytes, muscle tissue, and human myocardium. In silico analyses, luciferase and dCas9-activator/repressor assays, protein-DNA experiments, chromosome conformation capture (4C), and RNA sequencing were also performed.RESULTSThe electrocardiographic (ECG) phenotype was inherited in an autosomal dominant manner in all families. Linkage analysis revealed a single peak on chromosome 20, and WGS identified a single, rare, non-coding variant located 18 kb downstream of KCNB1 on chromosome 20 in all affected individuals. Perfect co-segregation with the ECG phenotype was observed together with full penetrance in all families. The variant creates a MEF2-binding site and presence of the variant allele or MEF2 co-expression enhanced transcriptional activity. dCas9-activator/repressor assays showed that KCNB1 was the only gene consistently regulated by the locus and 4C experiments in AC16 cells and human muscle tissue confirmed the locus-KCNB1 promoter interaction. Expression analysis in human endocardial tissue did not document any change in gene expression likely explained by expressional heterogeneity.CONCLUSIONSA gain-of-function enhancer variant creates a hyperactive regulatory locus that interacts with the KCNB1 promoter and causes FSTD. This is the first time that KCNB1 has been implicated in human cardiac electrophysiology and arrhythmogenesis.
{"title":"Gain-of-function enhancer variant near KCNB1 causes familial ST-depression syndrome.","authors":"Alex Hørby Christensen,Gang Pan,Rasmus L Marvig,Francisco German Rodriguez Gonzalez,Christoffer Rasmus Vissing,Elvira Silajdzija,Rasmus Frosted,Etsehiwot Girum Girma,Migle Gabrielaite,Henrik Kjærulf Jensen,Kasper Rossing,Finn Lund Henriksen,Niels Christian Foldager Sandgaard,Gustav Ahlberg,Jonas Ghouse,Pia Rengtved Lundegaard,Joachim Weischenfeldt,Claes Wadelius,Henning Bundgaard","doi":"10.1093/eurheartj/ehaf213","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf213","url":null,"abstract":"BACKGROUND AND AIMSFamilial ST-depression syndrome (FSTD) is a recently identified inherited cardiac disease associated with arrhythmias and systolic dysfunction. The underlying genetic aetiology has remained elusive. This study aimed at finding the causative variant.METHODSA total of 67 FSTD patients (20 families) were studied. Linkage analysis and whole-genome sequencing (WGS) were initially performed. An identified non-coding variant was functionally characterized in AC16 human cardiomyocytes, muscle tissue, and human myocardium. In silico analyses, luciferase and dCas9-activator/repressor assays, protein-DNA experiments, chromosome conformation capture (4C), and RNA sequencing were also performed.RESULTSThe electrocardiographic (ECG) phenotype was inherited in an autosomal dominant manner in all families. Linkage analysis revealed a single peak on chromosome 20, and WGS identified a single, rare, non-coding variant located 18 kb downstream of KCNB1 on chromosome 20 in all affected individuals. Perfect co-segregation with the ECG phenotype was observed together with full penetrance in all families. The variant creates a MEF2-binding site and presence of the variant allele or MEF2 co-expression enhanced transcriptional activity. dCas9-activator/repressor assays showed that KCNB1 was the only gene consistently regulated by the locus and 4C experiments in AC16 cells and human muscle tissue confirmed the locus-KCNB1 promoter interaction. Expression analysis in human endocardial tissue did not document any change in gene expression likely explained by expressional heterogeneity.CONCLUSIONSA gain-of-function enhancer variant creates a hyperactive regulatory locus that interacts with the KCNB1 promoter and causes FSTD. This is the first time that KCNB1 has been implicated in human cardiac electrophysiology and arrhythmogenesis.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"3 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819364","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}
Pub Date : 2025-04-10DOI: 10.1093/eurheartj/ehaf202
Rod S Taylor,Amy Blakemore
{"title":"Exercise-based cardiac rehabilitation: the importance of home-based approaches.","authors":"Rod S Taylor,Amy Blakemore","doi":"10.1093/eurheartj/ehaf202","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf202","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"110 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819247","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}
Pub Date : 2025-04-10DOI: 10.1093/eurheartj/ehaf196
Benjamin Bay,Richard Tanner,Michael Gao,Angelo Oliva,Samantha Sartori,Birgit Vogel,Mauro Gitto,Kenneth F Smith,Francesca Maria Di Muro,Amit Hooda,Joseph Sweeny,Parasuram Krishnamoorthy,Pedro Moreno,Prakash Krishnan,George Dangas,Annapoorna Kini,Samin K Sharma,Roxana Mehran
BACKGROUND AND AIMSElevated LDL-cholesterol levels and inflammation, as assessed by high-sensitivity C-reactive protein, correlate with cardiovascular risk. However, data on the relative impact of residual LDL-cholesterol and inflammatory risk among statin-treated patients undergoing percutaneous coronary intervention (PCI) is lacking. Hence, this study aimed to investigate the impact of residual cholesterol/inflammatory risk in patients on statin therapy undergoing PCI.METHODSFrom 2012 to 2022, patients at a tertiary centre undergoing PCI were analysed. Patients were stratified according to LDL-cholesterol (≥70 vs <70 mg/dL) and high-sensitivity C-reactive protein (≥2 vs <2 mg/L) levels: no residual cholesterol or inflammatory risk, residual cholesterol risk, residual inflammatory risk, and combined residual cholesterol and inflammatory risk. Patients presenting with acute myocardial infarction, cancer, no statin treatment at admission, or high-sensitivity C-reactive protein levels >10 mg/L were excluded. The primary endpoint was major adverse cardiovascular events (MACEs), defined as the composite of all-cause mortality, spontaneous myocardial infarction, and stroke 1 year after the index PCI.RESULTSA total of 15 494 patients were included. After 1-year follow-up, individuals with isolated residual inflammatory risk had the highest MACE rate (5.1%), followed by patients with combined cholesterol and inflammatory risk, no residual risk, and isolated residual cholesterol risk. After multivariable Cox regression analysis, patients with residual inflammatory risk had a 1.8-fold higher risk for MACE (adjusted hazard ratio: 1.78, 95% confidence interval 1.36-2.33, P < .001) compared with those with no residual cholesterol or inflammatory risk. This was similar in patients with combined residual cholesterol and inflammatory risk (adjusted hazard ratio: 1.56, 95% confidence interval 1.19-2.04, P = 0.001). Of note, no independent association of isolated residual cholesterol risk (adjusted hazard ratio: 1.01, 95% confidence interval .76-1.35, P-value = .920) with MACE was noted (P-trend across all groups <.001).CONCLUSIONSAmong statin-treated patients undergoing PCI, residual inflammation but not cholesterol risk was associated with an increased risk of MACE during follow-up.
{"title":"Residual cholesterol and inflammatory risk in statin-treated patients undergoing percutaneous coronary intervention†.","authors":"Benjamin Bay,Richard Tanner,Michael Gao,Angelo Oliva,Samantha Sartori,Birgit Vogel,Mauro Gitto,Kenneth F Smith,Francesca Maria Di Muro,Amit Hooda,Joseph Sweeny,Parasuram Krishnamoorthy,Pedro Moreno,Prakash Krishnan,George Dangas,Annapoorna Kini,Samin K Sharma,Roxana Mehran","doi":"10.1093/eurheartj/ehaf196","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf196","url":null,"abstract":"BACKGROUND AND AIMSElevated LDL-cholesterol levels and inflammation, as assessed by high-sensitivity C-reactive protein, correlate with cardiovascular risk. However, data on the relative impact of residual LDL-cholesterol and inflammatory risk among statin-treated patients undergoing percutaneous coronary intervention (PCI) is lacking. Hence, this study aimed to investigate the impact of residual cholesterol/inflammatory risk in patients on statin therapy undergoing PCI.METHODSFrom 2012 to 2022, patients at a tertiary centre undergoing PCI were analysed. Patients were stratified according to LDL-cholesterol (≥70 vs <70 mg/dL) and high-sensitivity C-reactive protein (≥2 vs <2 mg/L) levels: no residual cholesterol or inflammatory risk, residual cholesterol risk, residual inflammatory risk, and combined residual cholesterol and inflammatory risk. Patients presenting with acute myocardial infarction, cancer, no statin treatment at admission, or high-sensitivity C-reactive protein levels >10 mg/L were excluded. The primary endpoint was major adverse cardiovascular events (MACEs), defined as the composite of all-cause mortality, spontaneous myocardial infarction, and stroke 1 year after the index PCI.RESULTSA total of 15 494 patients were included. After 1-year follow-up, individuals with isolated residual inflammatory risk had the highest MACE rate (5.1%), followed by patients with combined cholesterol and inflammatory risk, no residual risk, and isolated residual cholesterol risk. After multivariable Cox regression analysis, patients with residual inflammatory risk had a 1.8-fold higher risk for MACE (adjusted hazard ratio: 1.78, 95% confidence interval 1.36-2.33, P < .001) compared with those with no residual cholesterol or inflammatory risk. This was similar in patients with combined residual cholesterol and inflammatory risk (adjusted hazard ratio: 1.56, 95% confidence interval 1.19-2.04, P = 0.001). Of note, no independent association of isolated residual cholesterol risk (adjusted hazard ratio: 1.01, 95% confidence interval .76-1.35, P-value = .920) with MACE was noted (P-trend across all groups <.001).CONCLUSIONSAmong statin-treated patients undergoing PCI, residual inflammation but not cholesterol risk was associated with an increased risk of MACE during follow-up.","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"65 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819333","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}
Pub Date : 2025-04-10DOI: 10.1093/eurheartj/ehaf200
Francesco Zito,Reda Rhellab,Adine R de Keijzer
{"title":"Patient-prosthesis mismatch after aortic valve replacement: one size does not fit all.","authors":"Francesco Zito,Reda Rhellab,Adine R de Keijzer","doi":"10.1093/eurheartj/ehaf200","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf200","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":"74 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819335","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}
Pub Date : 2025-04-09DOI: 10.1093/eurheartj/ehaf011
Dongze Zhang
{"title":"Cholinergic control of cardiac electrical conduction and ventricular arrhythmia: endogenous or exogenous?","authors":"Dongze Zhang","doi":"10.1093/eurheartj/ehaf011","DOIUrl":"https://doi.org/10.1093/eurheartj/ehaf011","url":null,"abstract":"","PeriodicalId":11976,"journal":{"name":"European Heart Journal","volume":" ","pages":""},"PeriodicalIF":37.6,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810821","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}
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