Circulation最新文献

{"title":"Response by Oldgren and Wallentin to Letter Regarding Article, \"Biomarker-Based ABC-AF Risk Scores for Personalized Treatment to Reduce Stroke or Death in Atrial Fibrillation: A Registry-Based, Multicenter, Randomized, Controlled Study\".","authors":"Jonas Oldgren, Lars Wallentin","doi":"10.1161/CIRCULATIONAHA.126.080165","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.080165","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 12","pages":"e404"},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016023","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":"The β-Blocker Breakup: Individualizing the AβYSS of Deprescription.","authors":"Sean van Diepen, Shaun G Goodman","doi":"10.1161/CIRCULATIONAHA.126.079321","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.079321","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 12","pages":"1066-1069"},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015994","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":"Association of Adherence to Various Dietary Patterns With Mortality Among Survivors of Myocardial Infarction: A Prospective Cohort Study.","authors":"Le Ma, Yang Hu, Gang Liu, Kathryn M Rexrode, JoAnn E Manson, Frank B Hu, Eric B Rimm, Qi Sun","doi":"10.1161/CIRCULATIONAHA.126.079972","DOIUrl":"10.1161/CIRCULATIONAHA.126.079972","url":null,"abstract":"<p><strong>Background: </strong>Current dietary guidelines are largely based on evidence from the general population, and data on dietary patterns and survival after myocardial infarction (MI) remain limited. We evaluated post-MI adherence to multiple healthy dietary patterns, as well as changes in adherence from before to after MI diagnosis, in relation to mortality among MI survivors.</p><p><strong>Methods: </strong>We included 3277 women from the Nurses' Health Study and 2618 men from the Health Professionals Follow-Up Study who survived a nonfatal MI. The mean age at MI diagnosis was 68.2 (SD, 10.2) years. Diet was assessed using validated food frequency questionnaires and updated every 2 to 4 years. We calculated post-MI adherence scores for 8 healthy patterns: the Alternate Healthy Eating Index, the Healthy Eating Index-2015, the Alternate Mediterranean Diet Score, the Dietary Approaches to Stop Hypertension, the Healthful Plant-Based Diet Index, the reversed empirical dietary inflammatory pattern, the reversed empirical dietary index for hyperinsulinemia, and the reversed empirical dietary index for insulin resistance. The main outcome was total mortality, with cardiovascular disease mortality and recurrent nonfatal MI as secondary outcomes.</p><p><strong>Results: </strong>During 15.7 years of follow-up after MI, 3858 deaths (65.4%) were documented, including 1639 cardiovascular disease deaths (42.5% of deaths). Comparing the highest with the lowest quintile, higher post-MI dietary scores were consistently associated with lower total mortality, with the hazard ratio of 0.67 (95% CI, 0.60-0.74) for Alternate Healthy Eating Index, 0.73 (95% CI, 0.65-0.81) for Healthy Eating Index-2015, 0.66 (95% CI, 0.59-0.75) for Alternate Mediterranean Diet Score, 0.77 (95% CI, 0.69-0.86) for Dietary Approaches to Stop Hypertension, 0.74 (95% CI, 0.66-0.83) for Healthful Plant-Based Diet Index, 0.77 (95% CI, 0.68-0.86) for reversed empirical dietary inflammatory pattern, 0.73 (95% CI, 0.65-0.83) for reversed empirical dietary index for insulin resistance, and 0.71 (95% CI, 0.64-0.80) for reversed empirical dietary index for hyperinsulinemia. Similar inverse associations were observed for cardiovascular disease mortality and recurrent nonfatal MI. Improved Alternate Healthy Eating Index adherence from before to after MI was associated with lower mortality (hazard ratio, 0.86 [95% CI, 0.76-0.97]), whereas decreased adherence to most patterns was associated with higher mortality.</p><p><strong>Conclusions: </strong>Among individuals who survived MI, adherence to post-MI dietary patterns emphasizing higher diet quality was associated with better long-term survival. These findings support dietary guidance focusing on overall diet quality for the secondary prevention of deaths among MI survivors.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1070-1084"},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13508043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812431","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":"Real-World Experience With the Extravascular Implantable Cardioverter Defibrillator Through 1 Year: The Enlighten Post Approval Registry Study.","authors":"Lucas V A Boersma, Anish Amin, Francis Murgatroyd, Maciej Sterliński, Jens Brock Johansen, Karim Saleh, Pamela K Mason, Jaime Casares, Gregory Engel, David Duncker, Alexander Breitenstein, Theodore Takata, Laurence M Epstein, Jurren M van Opstal, Nicolas Clémenty, Paul Friedman, Oliver Monfredi, Marianne Gwechenberger, Nobuhiro Nishii, Christopher Wiggenhorn, Jeff D Lande, Jennifer Lee, Amy E Thompson, Thomas R Holmes, Ian Crozier","doi":"10.1161/CIRCULATIONAHA.126.080942","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.080942","url":null,"abstract":"<p><strong>Background: </strong>The extravascular implantable cardioverter defibrillator (EV-ICD) was developed to provide defibrillation and antitachycardia pacing therapy without the need for intravascular lead placement. Premarket clinical trials reported EV-ICD safety and efficacy through 3 years, but a real-world assessment of the Aurora EV-ICD system, which includes a novel sensing discriminator, is needed. The objective of this analysis was to assess real-world therapy efficacy and safety of the EV-ICD through 1 year.</p><p><strong>Methods: </strong>Enlighten: The EV-ICD Post Approval Registry is a prospective, global, real-world registry that included patients who underwent an EV-ICD implantation attempt. The main safety analysis was freedom from all system- or procedure-related major complications through 1 year. Event rates at 1 year were calculated using the Kaplan-Meier method.</p><p><strong>Results: </strong>EV-ICD system implantation was attempted by 168 implanters in 787 patients (49.1±15.2 years old; 28.7% women; 34.1% secondary prevention). Tunneling and lead placement in the substernal space were achieved in 781 of 787 patients (99.2%), with 758 patients (96.3%) remaining implanted following defibrillation and electrical testing. One-year freedom from major system- or procedure-related complications was 89.1% (95% CI, 86.3%-91.3%). The 1-year rate of first appropriate therapy (shock, antitachycardia pacing, or both) was 7.3% (95% CI, 5.5-9.6). Shock success for discrete spontaneous episodes was 100% (61 of 61), and the generalized estimating equations antitachycardia pacing success rate, to account for multiple episodes per patient, was 74.2% for monomorphic ventricular tachycardia. The 1-year rate of first inappropriate shock was 7.1% (95% CI, 5.4-9.4), with noncardiac oversensing as the main cause (40.5% of inappropriately shocked episodes).</p><p><strong>Conclusions: </strong>In the largest prospective worldwide cohort of patients with an EV-ICD to date, both antitachycardia pacing and shock therapy were effective, while the rate of major complications agreed with the premarket experience through 1 year. These data demonstrate that positive outcomes of the EV-ICD are retained in everyday clinical practice in a large, global cohort with an expanded number of implanters.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT06048731.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015845","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":"Response by Maurer and Fontana to Letter Regarding Article, \"Coramitug, a Humanized Monoclonal Antibody for the Treatment of Transthyretin Amyloid Cardiomyopathy: A Phase 2, Randomized, Multicenter, Double-Blind, Placebo-Controlled Trial\".","authors":"Mathew S Maurer, Marianna Fontana","doi":"10.1161/CIRCULATIONAHA.126.080972","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.080972","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 12","pages":"e407-e408"},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015972","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":"Asb2-KIF11 Axis Protects Against Heart Failure by Restoring Lysosomal Distribution and Mitochondrial Homeostasis.","authors":"Yicheng Lv, Zhao Sha, Shi Peng, Zhenzhen Duan, Qingye Zeng, Shengli Li, Hao Wu, Xiaoyu Zhang, Xiaoxun Huang, Jincheng Zhang, Shengkai Zuo, Deping Kong","doi":"10.1161/CIRCULATIONAHA.126.080625","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.080625","url":null,"abstract":"<p><strong>Background: </strong>Heart failure remains a leading cause of mortality globally, driven by persistent mitochondrial dysfunction and maladaptive cardiac hypertrophy. Although impaired autophagic flux contributes to cardiac deterioration, the precise molecular mechanisms are still unclear. The ubiquitin-proteasome system serves as a critical regulator linking protein ubiquitination to autophagic flux and mitochondrial homeostasis. Asb2 (ankyrin repeat-containing protein with suppressor of cytokine signaling box 2), a muscle-specific E3 ubiquitin ligase essential for embryonic cardiogenesis, is uncharacterized in adult cardiac homeostasis and disease pathogenesis.</p><p><strong>Methods: </strong>Male mice with inducible cardiomyocyte-specific Asb2 knockout were generated to investigate Asb2's role in cardiac remodeling. Adeno-associated virus 9-mediated cardiomyocyte-specific Asb2 overexpression and KIF11 (kinesin family member 11) downregulation were used in transverse aortic constriction-induced hypertrophy and aging models. RNA sequencing, metabolite profiling, and mass spectrometry were used to assess the molecular mechanism by which Asb2 regulates cardiac metabolism and hypertrophy.</p><p><strong>Results: </strong>Asb2β expression was significantly reduced in multiple forms of human cardiomyopathy and in hypertrophic murine hearts. Inducible Asb2 deletion in adult male mice led to the spontaneous development of cardiac hypertrophy and heart failure, accompanied by progressive accumulation of dysfunctional mitochondria and metabolic dysregulation. Mechanistically, Asb2 deficiency impaired ubiquitin-mediated degradation of KIF11, causing aberrant peripheral lysosomal redistribution and disrupting autophagosome-lysosome fusion, which resulted in impaired late-stage autophagic flux and metabolic disturbances. Notably, therapeutic restoration of Asb2 expression via adeno-associated virus 9-mediated delivery attenuated pressure overload-induced and age-related cardiac hypertrophy and heart failure. Moreover, both genetic and pharmacological inhibition of KIF11 effectively restored autophagic flux and mitochondrial homeostasis, thereby reversing pathological cardiac remodeling in Asb2-deficient hearts and transverse aortic constriction-induced cardiac dysfunction.</p><p><strong>Conclusions: </strong>Asb2 is a novel regulator of mitochondrial quality control in cardiomyocytes via KIF11-mediated lysosomal redistribution. Targeting the Asb2-KIF11 axis may be a promising strategy for improving mitochondrial homeostasis and cardiomyocyte function in chronic heart failure.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015885","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":"Artificial Intelligence in Cardiovascular Science and Publishing.","authors":"Thomas M Maddox","doi":"10.1161/CIRCULATIONAHA.126.080230","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.080230","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 12","pages":"1053-1055"},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015927","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":"Postpartum Monitoring for Hypertensive Disorders of Pregnancy Through Community-Clinical Linkages.","authors":"Faith E Metlock, Modele O Ogunniyi, Kathryn Lindley, Garima Sharma","doi":"10.1161/CIRCULATIONAHA.126.080499","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.080499","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 12","pages":"1155-1161"},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015982","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":"ABHD11-Mediated mtDNA Transcription Restored Mitochondrial Function to Attenuate Cardiomyocyte Ferroptosis After Myocardial Infarction.","authors":"Yu Liu, Yijin Chen, Hao Zheng, Yingxuan Li, Chuling Li, Wenlong Xu, Wei Chen, Zhiwen Xiao, Guojun Chen, Senlin Huang, Xinzhong Li, Jia-Guo Zhou, Ying Wu, Wangjun Liao, Yulin Liao, Jianping Bin, Yanmei Chen","doi":"10.1161/CIRCULATIONAHA.125.078593","DOIUrl":"10.1161/CIRCULATIONAHA.125.078593","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Cardiomyocytes exhibit marked susceptibility to ferroptosis after myocardial infarction (MI), rendering ferroptosis inhibition a promising therapeutic strategy to mitigate ischemic myocardial injury. Although mitochondrial dysfunction is recognized as a core driver of ferroptosis, the potential role of mitochondrial DNA transcription in regulating cardiomyocyte ferroptosis remains unexplored.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;To clarify the temporal role of the various modes of cell death in MI progression, we performed time-course echocardiography in MI models treated with various cell death inhibitors. To characterize the crucial process and molecular regulator in cardiomyocyte ferroptosis, we integrated RNA sequencing and single-nucleus RNA sequencing data from murine post-MI hearts and performed functional rescue experiments using mitochondrial protective agents. To determine the role of ABHD11 (αβ-hydrolase domain-containing protein 11) in cardiomyocyte ferroptosis and cardiac repair after MI, we used loss- and gain-of-function approaches. To elucidate the underlying mechanisms, we conducted transcriptomics, nontargeted lipidomics, site-specific mutagenesis, molecular docking, coimmunoprecipitation, native gel electrophoresis, proximity ligation assay, methylation-specific polymerase chain reaction, and chromatin immunoprecipitation assay.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;We found that cardiac ferroptosis peaked at day 7 after MI and was enriched in peri-infarct cardiomyocytes. Mitochondrial dysfunction was a key driver of cardiomyocyte ferroptosis after MI, and the lipid enzyme ABHD11 was identified as a potential regulator of both processes. ABHD11 expression was consistently reduced in mouse and human MI hearts, and its transcription was repressed by DNMT1 (DNA methyltransferase 1)-mediated promoter hypermethylation. Functionally, cardiac-specific overexpression of ABHD11 markedly alleviated cardiomyocyte ferroptosis and improved cardiac function after MI. Conversely, loss of ABHD11 in adult mice exacerbated pathological cardiac remodeling and heart failure. Mechanistically, independent of its canonical enzymatic activities, ABHD11 acted as a mitochondrial DNA transcription coactivator by enhancing the TEFM (mitochondrial transcription elongation factor)-POLRMT (mitochondrial RNA polymerase) interaction. This promoted mitochondrial DNA transcription, restored mitochondrial function, and reduced reactive oxygen species/PUFA-PLs (polyunsaturated fatty acid-containing glycerophospholipids)-driven lipid peroxidation and 4-hydroxynonenal generation. The reduction in 4-hydroxynonenal stabilized YY1 (Yin Yang 1), which subsequently regulated key ferroptosis-driving genes governing iron deposition, reactive oxygen species production, and polyunsaturated fatty acid lipids accumulation, further inhibiting lipid peroxidation and ferroptosis, and ultimately promoting cardiac recovery after MI.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1109-1130"},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592836/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705639","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":"Sotatercept Improves Right Heart Mechanics Despite Reduced Myocardial Contractility in Pulmonary Arterial Hypertension: A Prospective Exercise Hemodynamic Study.","authors":"Yogesh N V Reddy, Sho Kazui, William R Miranda, Tomonari Harada, Robert P Frantz, Daniel Burkhoff, Barry A Borlaug","doi":"10.1161/CIRCULATIONAHA.126.081334","DOIUrl":"10.1161/CIRCULATIONAHA.126.081334","url":null,"abstract":"<p><strong>Background: </strong>The right ventricular (RV) response to pressure overload is a crucial determinant of outcomes in pulmonary arterial (PA) hypertension. Sotatercept improves clinical outcomes, but its effects on the right ventricle have been inconsistent. We evaluated the effects of sotatercept on load-independent measures of RV contractility, RV-PA coupling, and right heart deformation at rest and exertion in patients with PA hypertension.</p><p><strong>Methods: </strong>In this prospective trial among participants with PA hypertension recruited between July 2024 and May 2025, we performed simultaneous echocardiography and invasive pressure measurements during rest and exercise to evaluate changes in RV contractility (end-systolic elastance [Ees]), afterload (PA elastance [Ea]), RV-PA coupling (ratio of arterial Ea to Ees), and right heart deformation, including RV and right atrial strain, before and after 24 weeks of sotatercept using mixed models.</p><p><strong>Results: </strong>Among 30 participants (n=21; 70% female; mean age, 49.3 years [SD 13.5]), sotatercept decreased PA Ea. These changes were associated with reduced RV contractility, PA pulsatility index, and the maximal rate of RV pressure increase over time (dP/dt_max; <i>P</i><0.001 for all). The decrease in Ees was associated with a decrease in PA Ea (r=+0.70 [95% CI, +0.44 to +0.85]; <i>P</i><0.0001) with preserved RV-PA coupling (mean difference, +0.08 [95% CI, -0.11 to +0.26]; <i>P</i>=0.42). Although systolic indices measured at the base of the right ventricle (tricuspid annular plane systolic excursion and systolic velocity of the lateral tricuspid annulus) decreased after sotatercept use, there was an increase in RV free wall-dependent systolic indices, including resting and exercise RV free wall strain (mean difference, +6.2% [95% CI, +4.5 to +7.8]; <i>P</i><0.0001) and fractional area change (<i>P</i>=0.0001). Beyond the right ventricle, there was also improved right atrial filling and contractile performance across rest and exercise (<i>P</i><0.0001 for all).</p><p><strong>Conclusions: </strong>Sotatercept decreases RV contractility in proportion to reduced afterload, while preserving the RV-PA coupling relationship. Despite decreased RV contractility, global measures of right heart performance, such as RV free wall strain and RA strain, improve, alongside redistribution of RV deformation from annular motion to free wall shortening. These data suggest that sotatercept causes an energetically favorable reduction in resting RV contractility to match the lower afterload, which does not appear physiologically detrimental when considering the concurrent improvement in RV free wall contractile mechanics and exertional right heart reserve.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT06409026.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13598951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149015854","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}