JAMA cardiologyPub Date : 2024-09-01DOI: 10.1001/jamacardio.2024.2464
{"title":"Change to Open Access Status.","authors":"","doi":"10.1001/jamacardio.2024.2464","DOIUrl":"10.1001/jamacardio.2024.2464","url":null,"abstract":"","PeriodicalId":14657,"journal":{"name":"JAMA cardiology","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11292569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141855516","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}
JAMA cardiologyPub Date : 2024-09-01DOI: 10.1001/jamacardio.2024.1724
Sarah K Gualano, James Henderson, Stacy Menees, Ashwini Kerkar, Erika Parisi, Eve A Kerr
{"title":"Women's Representation in Interventional Cardiology.","authors":"Sarah K Gualano, James Henderson, Stacy Menees, Ashwini Kerkar, Erika Parisi, Eve A Kerr","doi":"10.1001/jamacardio.2024.1724","DOIUrl":"10.1001/jamacardio.2024.1724","url":null,"abstract":"","PeriodicalId":14657,"journal":{"name":"JAMA cardiology","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11238065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141563354","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}
JAMA cardiologyPub Date : 2024-08-30DOI: 10.1001/jamacardio.2024.2298
Jasmine Melissa Madsen, Thomas Engstrøm, Laust Emil Roelsgaard Obling, Yan Zhou, Lars Nepper-Christensen, Rasmus Paulin Beske, Niels Grove Vejlstrup, Lia Evi Bang, Christian Hassager, Fredrik Folke, Kasper Kyhl, Lars Bredevang Andersen, Helle Collatz Christensen, Laura Rytoft, Ketina Arslani, Lene Holmvang, Frants Pedersen, Ole Ahlehoff, Reza Jabbari, Charlotte Barfod, Mikkel Hougaard, Mikko Minkkinen, Hans-Henrik Tilsted, Rikke Sørensen, Jacob Thomsen Lønborg
{"title":"Prehospital Pulse-Dose Glucocorticoid in ST-Segment Elevation Myocardial Infarction","authors":"Jasmine Melissa Madsen, Thomas Engstrøm, Laust Emil Roelsgaard Obling, Yan Zhou, Lars Nepper-Christensen, Rasmus Paulin Beske, Niels Grove Vejlstrup, Lia Evi Bang, Christian Hassager, Fredrik Folke, Kasper Kyhl, Lars Bredevang Andersen, Helle Collatz Christensen, Laura Rytoft, Ketina Arslani, Lene Holmvang, Frants Pedersen, Ole Ahlehoff, Reza Jabbari, Charlotte Barfod, Mikkel Hougaard, Mikko Minkkinen, Hans-Henrik Tilsted, Rikke Sørensen, Jacob Thomsen Lønborg","doi":"10.1001/jamacardio.2024.2298","DOIUrl":"https://doi.org/10.1001/jamacardio.2024.2298","url":null,"abstract":"ImportanceIn patients with ST-segment elevation myocardial infarction (STEMI), acute inflammation is related to the extent of myocardial damage and may increase infarct size. Thus, administration of pulse-dose glucocorticoid in the very early phase of infarction may reduce infarct size.ObjectiveTo determine the cardioprotective effect of prehospital pulse-dose glucocorticoid in patients with STEMI.Design, Setting, and ParticipantsThis was a 1:1 investigator-initiated, blinded, placebo-controlled, randomized clinical trial conducted between November 14, 2022, and October 17, 2023, with last follow-up on January 17, 2024. Patients 18 years and older with less than 12 hours of acute chest pain and STEMI were included in the prehospital setting throughout the Region Zealand and Capital Region of Denmark and transferred to Rigshospitalet, Denmark.InterventionPatients were randomly allocated to intravenous glucocorticoid (methylprednisolone, 250 mg) or placebo in the prehospital setting.Main Outcomes and MeasuresThe primary outcome was final infarct size on cardiac magnetic resonance (CMR) at 3 months. The power calculation was based on an anticipated final infarct size of 13%. Secondary outcomes included CMR outcomes on acute scan and at 3 months, peak of cardiac biomarkers, clinical end points at 3 months, and adverse events.ResultsOf 530 included patients (median [IQR] age, 65 [56-75] years; 418 male [78.9%]) with STEMI, 401 (76%) were assessed for the primary outcome, with 198 patients treated with glucocorticoid and 203 with placebo. Median final infarct size was similar in the treatment groups (glucocorticoid, 5%; IQR, 2%-11% vs placebo, 6%; IQR, 2%-13%; <jats:italic>P</jats:italic> = .24). Compared with placebo, the glucocorticoid group had smaller acute infarct size (odds ratio, 0.78; 95% CI, 0.61-1.00), less microvascular obstruction (relative risk ratio, 0.83; 95% CI, 0.71-0.99), and greater acute left ventricular ejection fraction (mean difference, 4.44%; 95% CI, 2.01%-6.87%). Other secondary outcomes were similar in both groups.Conclusions and RelevanceIn patients with STEMI, treatment with prehospital pulse-dose glucocorticoid did not reduce final infarct size after 3 months. However, the trial was likely underpowered as the final infarct size was smaller than anticipated. The glucocorticoid group had improved acute parameters compared with placebo.Trial RegistrationClinicalTrials.gov Identifier: <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" ext-link-type=\"uri\" xlink:href=\"https://clinicaltrials.gov/study/NCT05462730\">NCT05462730</jats:ext-link>","PeriodicalId":14657,"journal":{"name":"JAMA cardiology","volume":null,"pages":null},"PeriodicalIF":24.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100612","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}
JAMA cardiologyPub Date : 2024-08-30DOI: 10.1001/jamacardio.2024.2566
Henri Lu, Brian L. Claggett, Milton Packer, Carolyn S. P. Lam, Karl Swedberg, Jean Rouleau, Michael R. Zile, Martin Lefkowitz, Akshay S. Desai, Pardeep Jhund, John J. V. McMurray, Scott D. Solomon, Muthiah Vaduganathan
{"title":"Effects of Sacubitril/Valsartan on All-Cause Hospitalizations in Heart Failure","authors":"Henri Lu, Brian L. Claggett, Milton Packer, Carolyn S. P. Lam, Karl Swedberg, Jean Rouleau, Michael R. Zile, Martin Lefkowitz, Akshay S. Desai, Pardeep Jhund, John J. V. McMurray, Scott D. Solomon, Muthiah Vaduganathan","doi":"10.1001/jamacardio.2024.2566","DOIUrl":"https://doi.org/10.1001/jamacardio.2024.2566","url":null,"abstract":"ImportanceSacubitril/valsartan is indicated to reduce the risk of cardiovascular death and heart failure (HF) hospitalizations in patients with chronic HF. However, many of these patients are older and have multiple comorbidities that increase the risk of hospitalization for causes other than HF.ObjectiveTo assess the effects of sacubitril/valsartan on hospitalizations of any cause across the spectrum of left ventricular ejection fraction (LVEF).Design, Setting, and ParticipantsThis post hoc, participant-level, pooled analysis of the PARADIGM-HF (in patients with an LVEF ≤40%) and PARAGON-HF (in patients with an LVEF ≥45%) randomized clinical trials was conducted from February 5, 2024, to April 5, 2024. Participants with chronic HF, New York Heart Association classes II through IV symptoms, and elevated natriuretic peptides were randomized to treatment with either sacubitril/valsartan or a renin-angiotensin system inhibitor (RASi)—enalapril in the PARADIGM-HF trial or valsartan in the PARAGON-HF trial.InterventionSacubitril/valsartan vs RASi (enalapril or valsartan).Main Outcomes and MeasuresThe effects of sacubitril/valsartan on time to first investigator-reported all-cause and cause-specific hospitalizations were examined using Cox proportional hazards models, stratified by geographic region and trial. Effect modification by LVEF as a continuous function was examined.ResultsAmong 13 194 participants in the PARADIGM-HF and PARAGON-HF trials, mean (SD) patient age was 67 (11) years, 8883 patients (67.3%) were male, and mean (SD) LVEF was 40% (15%). Sacubitril/valsartan significantly reduced the risk of all-cause hospitalization (ACH) compared with RASi over a median (IQR) follow-up period of 2.5 (1.8-3.1) years (hazard ratio [HR], 0.92; 95% CI, 0.88-0.97; <jats:italic>P</jats:italic> = .002). The incidence rate of first ACH was 25 (95% CI, 24-26) per 100 patient-years in the sacubitril/valsartan arm and 27 (95% CI, 26-28) per 100 patient-years in the RASi arm. The absolute risk reduction (ARR) was 2.1 per 100 patient-years, corresponding to a number needed to treat (NNT) of 48 patient-years of treatment exposure to prevent 1 ACH. Reductions in overall hospitalizations seemed primarily driven by lower rates of cardiac and pulmonary hospitalizations with sacubitril/valsartan. Patients in the 2 treatment arms had similar rates of composite noncardiac hospitalizations. Treatment heterogeneity on ACH by LVEF was observed (<jats:italic>P</jats:italic> for interaction = .03), with benefits most apparent in patients with an LVEF less than 60% (HR, 0.91; 95% CI, 0.86-0.96), but not in patients with an LVEF of 60% or more (HR, 0.97; 95% CI, 0.86-1.09).Conclusions and RelevanceIn this post hoc pooled analysis of 13 194 patients with chronic HF in the PARADIGM-HF and PARAGON-HF randomized clinical trials, sacubitril/valsartan significantly reduced hospitalization for any reason, with benefits most apparent in patients with an LVEF below normal. This reductio","PeriodicalId":14657,"journal":{"name":"JAMA cardiology","volume":null,"pages":null},"PeriodicalIF":24.0,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100611","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}
JAMA cardiologyPub Date : 2024-08-28DOI: 10.1001/jamacardio.2024.2574
Stefano Savonitto, Patrizio Sarto
{"title":"Comment on Risk of Cardiac Arrhythmias Among Climbers on Mount Everest.","authors":"Stefano Savonitto, Patrizio Sarto","doi":"10.1001/jamacardio.2024.2574","DOIUrl":"https://doi.org/10.1001/jamacardio.2024.2574","url":null,"abstract":"","PeriodicalId":14657,"journal":{"name":"JAMA cardiology","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080282","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}
JAMA cardiologyPub Date : 2024-08-28DOI: 10.1001/jamacardio.2024.2577
Thomas Pilgrim, Martina Rothenbühler, Kunjang Sherpa
{"title":"Comment on Risk of Cardiac Arrhythmias Among Climbers on Mount Everest-Reply.","authors":"Thomas Pilgrim, Martina Rothenbühler, Kunjang Sherpa","doi":"10.1001/jamacardio.2024.2577","DOIUrl":"https://doi.org/10.1001/jamacardio.2024.2577","url":null,"abstract":"","PeriodicalId":14657,"journal":{"name":"JAMA cardiology","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080283","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}
JAMA cardiologyPub Date : 2024-08-28DOI: 10.1001/jamacardio.2024.2190
Nay Aung, Hannah L Nicholls, C Anwar A Chahal, Mohammed Y Khanji, Elisa Rauseo, Sucharitha Chadalavada, Steffen E Petersen, Patricia B Munroe, Perry M Elliott, Luis R Lopes
{"title":"Prevalence, Cardiac Phenotype, and Outcomes of Transthyretin Variants in the UK Biobank Population.","authors":"Nay Aung, Hannah L Nicholls, C Anwar A Chahal, Mohammed Y Khanji, Elisa Rauseo, Sucharitha Chadalavada, Steffen E Petersen, Patricia B Munroe, Perry M Elliott, Luis R Lopes","doi":"10.1001/jamacardio.2024.2190","DOIUrl":"10.1001/jamacardio.2024.2190","url":null,"abstract":"<p><strong>Importance: </strong>The population prevalence of cardiac transthyretin amyloidosis (ATTR) caused by pathogenic variation in the TTR gene (vATTR) is unknown.</p><p><strong>Objective: </strong>To estimate the population prevalence of disease-causing TTR variants and evaluate associated phenotypes and outcomes.</p><p><strong>Design, setting, and participants: </strong>This population-based cohort study analyzed UK Biobank (UKB) participants with whole-exome sequencing, electrocardiogram, and cardiovascular magnetic resonance data. Participants were enrolled from 2006 to 2010, with a median follow-up of 12 (IQR, 11-13) years (cutoff date for the analysis, March 12, 2024). Sixty-two candidate TTR variants were extracted based on rarity (minor allele frequency ≤0.0001) and/or previously described associations with amyloidosis if more frequent.</p><p><strong>Exposure: </strong>Carrier status for TTR variants.</p><p><strong>Main outcomes and measures: </strong>Associations of TTR carrier status with vATTR prevalence and cardiovascular imaging and electrocardiogram traits were explored using descriptive statistics. Associations between TTR carrier status and atrial fibrillation, conduction disease, heart failure, and all-cause mortality were evaluated using adjusted Cox proportional hazards models. Genotypic and diagnostic concordance was examined using International Statistical Classification of Diseases, Tenth Revision codes from the hospital record.</p><p><strong>Results: </strong>The overall cohort included 469 789 UKB participants (mean [SD] age, 56.5 [8.1] years; 54.2% female and 45.8% male). A likely pathogenic/pathogenic (LP/P) TTR variant was detected in 473 (0.1%) participants, with Val142Ile being the most prevalent (367 [77.6%]); 91 individuals (0.02%) were carriers of a variant of unknown significance . The overall prevalence of LP/P variants was 0.02% (105 of 444 243) in participants with European ancestry and 4.3% (321 of 7533) in participants with African ancestry. The LP/P variants were associated with higher left ventricular mass indexed to body surface area (β = 4.66; 95% CI, 1.87-7.44), and Val142Ile was associated with a longer PR interval (β = 18.34; 95% CI, 5.41-31.27). The LP/P carrier status was associated with a higher risk of heart failure (hazard ratio [HR], 2.68; 95% CI, 1.75-4.12) and conduction disease (HR, 1.88; 95% CI, 1.25-2.83). Higher all-cause mortality risk was observed for non-Val142Ile LP/P variants (HR, 1.98; 95% CI, 1.06-3.67). Thirteen participants (2.8%) with LP/P variants had diagnostic codes compatible with cardiac or neurologic amyloidosis. Variants of unknown significance were not associated with outcomes.</p><p><strong>Conclusions and relevance: </strong>This study found that approximately 1 in 1000 UKB participants were LP/P TTR variant carriers, exceeding previously reported prevalence. The findings emphasize the need for clinical vigilance in identifying individuals at risk of developing vATT","PeriodicalId":14657,"journal":{"name":"JAMA cardiology","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11359106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080285","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}
JAMA cardiologyPub Date : 2024-08-21DOI: 10.1001/jamacardio.2024.2555
Aldostefano Porcari, Ambra Masi, Ana Martinez-Naharro, Yousuf Razvi, Rishi Patel, Adam Ioannou, Muhammad U Rauf, Giulio Sinigiani, Brendan Wisniowski, Stefano Filisetti, Jasmine Currie-Cathey, Sophie O'Beara, Tushar Kotecha, Dan Knight, James C Moon, Gianfranco Sinagra, Ruta Virsinskaite, Janet Gilbertson, Lucia Venneri, Aviva Petrie, Helen Lachmann, Carol Whelan, Peter Kellman, Sriram Ravichandran, Oliver Cohen, Shameem Mahmood, Charlotte Manisty, Philip N Hawkins, Julian D Gillmore, Ashutosh D Wechalekar, Marianna Fontana
{"title":"Redefining Cardiac Involvement and Targets of Treatment in Systemic Immunoglobulin AL Amyloidosis.","authors":"Aldostefano Porcari, Ambra Masi, Ana Martinez-Naharro, Yousuf Razvi, Rishi Patel, Adam Ioannou, Muhammad U Rauf, Giulio Sinigiani, Brendan Wisniowski, Stefano Filisetti, Jasmine Currie-Cathey, Sophie O'Beara, Tushar Kotecha, Dan Knight, James C Moon, Gianfranco Sinagra, Ruta Virsinskaite, Janet Gilbertson, Lucia Venneri, Aviva Petrie, Helen Lachmann, Carol Whelan, Peter Kellman, Sriram Ravichandran, Oliver Cohen, Shameem Mahmood, Charlotte Manisty, Philip N Hawkins, Julian D Gillmore, Ashutosh D Wechalekar, Marianna Fontana","doi":"10.1001/jamacardio.2024.2555","DOIUrl":"10.1001/jamacardio.2024.2555","url":null,"abstract":"<p><strong>Importance: </strong>Cardiac amyloid infiltration is the key determinant of survival in systemic light-chain (AL) amyloidosis. Current guidelines recommend early switching therapy in patients with a nonoptimal or suboptimal response regardless of the extent of cardiac amyloid infiltration.</p><p><strong>Objective: </strong>To assess the differences between serum biomarkers, echocardiography, and cardiovascular magnetic resonance (CMR) with extracellular volume (ECV) mapping in characterizing cardiac amyloid, the independent prognostic role of these approaches, and the role of ECV mapping to guide treatment strategies.</p><p><strong>Design, setting, and participants: </strong>Consecutive patients newly diagnosed with systemic AL amyloidosis (2015-2021) underwent echocardiography, cardiac biomarkers, and CMR with ECV mapping at diagnosis. Data were analyzed from January to June 2024.</p><p><strong>Main outcomes and measures: </strong>The primary outcomes of the study were all-cause mortality and hematological response as defined according to validated criteria: no response (NR), partial response (PR), very good partial response (VGPR), and complete response (CR). Secondary outcomes were the depth and speed of hematological response and overall survival according to ECV.</p><p><strong>Results: </strong>Of 560 patients with AL amyloidosis, the median (IQR) age was 68 years (59-74 years); 346 patients were male (61.8%) and 214 female (38.2%). Over a median (IQR) 40.5 months 9-58 months), ECV was independently associated with mortality. In the landmark analysis at 1 month, long-term survival was independent of the achieved hematological response in ECV less than 0.30% and ECV of 0.31% to 0.40%, while it was dependent on the depth of the hematological response in ECV greater than 0.40%. In the landmark analysis at 6 months, survival was independent of the achieved hematological response in ECV less than 0.30% and dependent on achieving at least PR in ECV of 0.31% to 0.40%. Survival was dependent on achieving CR in ECV of 0.41% to 0.50% and ECV greater than 0.50%. Achieving a deep hematological response at 1 month was associated with better survival compared with 6 months in patients with ECV greater than 0.40% but not with ECV less than 0.40%.</p><p><strong>Conclusions and relevance: </strong>This study found that ECV mapping, in systemic AL amyloidosis, is an independent predictor of prognosis, can help define the hematological response associated with better long-term outcomes for each patient and potentially inform treatment strategies.</p>","PeriodicalId":14657,"journal":{"name":"JAMA cardiology","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11339700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142017451","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}
JAMA cardiologyPub Date : 2024-08-07DOI: 10.1001/jamacardio.2024.2199
Karim Benali, Benjamin Seguy, Frederic Sacher
{"title":"Progressive Cardiogenic Shock After Catheter Ablation in a Man Aged 78 Years.","authors":"Karim Benali, Benjamin Seguy, Frederic Sacher","doi":"10.1001/jamacardio.2024.2199","DOIUrl":"https://doi.org/10.1001/jamacardio.2024.2199","url":null,"abstract":"","PeriodicalId":14657,"journal":{"name":"JAMA cardiology","volume":null,"pages":null},"PeriodicalIF":14.8,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897446","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}