Circulation最新文献

{"title":"Letter by Zhang and Zeng Regarding Article, \"Long-Term Outcomes After Septal Reduction Therapies in Obstructive Hypertrophic Cardiomyopathy: Insights From the SHARE Registry\".","authors":"Qing Zhang, Qingshi Zeng","doi":"10.1161/CIRCULATIONAHA.124.072924","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.124.072924","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 22","pages":"e1043-e1044"},"PeriodicalIF":35.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207833","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":"Population Screening With Natriuretic Peptides Is Ready for Prime Time.","authors":"Antoni Bayés-Genis","doi":"10.1161/CIRCULATIONAHA.125.074048","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.125.074048","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 22","pages":"1547-1549"},"PeriodicalIF":35.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207834","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 Maurizi et al to Letter Regarding Article, \"Long-Term Outcomes After Septal Reduction Therapies in Obstructive Hypertrophic Cardiomyopathy: Insights From the SHARE Registry\".","authors":"Niccolò Maurizi, Panagiotis Antiochos, Sharlene M Day, Iacopo Olivotto","doi":"10.1161/CIRCULATIONAHA.125.073968","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.125.073968","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 22","pages":"e1045-e1046"},"PeriodicalIF":35.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207835","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":"Cardiac Biomarkers in Patients With Asymptomatic Severe Aortic Stenosis: Analysis From the EARLY TAVR Trial.","authors":"Brian R Lindman, Philippe Pibarot, Allan Schwartz, J Bradley Oldemeyer, Yan Ru Su, Kashish Goel, David J Cohen, William F Fearon, Vasilis Babaliaros, David Daniels, Adnan Chhatriwalla, Hussam S Suradi, Pinak Shah, Molly Szerlip, Michael J Mack, Thom Dahle, William W O'Neill, Charles J Davidson, Raj Makkar, Tej Sheth, Jeremiah Depta, James T DeVries, Jeffrey Southard, Andrei Pop, Paul Sorajja, Rebecca T Hahn, Yanglu Zhao, Martin B Leon, Philippe Généreux","doi":"10.1161/CIRCULATIONAHA.125.074425","DOIUrl":"10.1161/CIRCULATIONAHA.125.074425","url":null,"abstract":"<p><strong>Background: </strong>The EARLY TAVR trial (Evaluation of TAVR Compared to Surveillance for Patients With Asymptomatic Severe Aortic Stenosis) demonstrated that early transcatheter aortic valve replacement (TAVR) intervention was superior to clinical surveillance with delayed TAVR in patients with asymptomatic severe aortic stenosis. Cardiac biomarkers are associated with maladaptive remodeling, symptom onset, and worse outcomes after TAVR. Whether elevated biomarkers identify asymptomatic patients more likely to benefit from early intervention is unknown.</p><p><strong>Methods: </strong>A core laboratory measured NT-proBNP (N-terminal pro-B-type natriuretic peptide) and high-sensitivity cardiac troponin T (hs-cTnT) levels. Associations between biomarker levels and risk of the trial primary end point (death, stroke, or unplanned cardiovascular hospitalization) and other secondary end points were examined with Kaplan-Meier curves and Cox proportional hazard models. Interaction tests were performed to assess whether the treatment effect of early TAVR, compared with clinical surveillance, differed according to biomarker levels.</p><p><strong>Results: </strong>Among 901 patients randomized in EARLY TAVR, 798 (89%) had biospecimens measured (median NT-proBNP level, 287 [145, 601]; median hs-cTnT level, 14.6 [10.5, 21.0]). Higher levels of NT-proBNP and hs-cTnT were broadly associated with higher event rates for multiple end points. In general, there was no significant interaction between baseline biomarkers and treatment group with respect to any composite or individual end point examined, although trends broadly demonstrated a greater relative benefit of early TAVR at lower biomarker levels. There was a significant interaction between hs-cTnT level and treatment group with respect to death or heart failure hospitalization (<i>P</i> _interaction=0.04) and heart failure hospitalization alone (<i>P</i> _interaction=0.03) such that the relative benefit of early TAVR was greater for patients with normal, rather than elevated, levels of hs-cTnT at baseline. For some end points, higher baseline NT-proBNP level was associated with numerically greater absolute risk reduction with early TAVR than were lower NT-proBNP levels.</p><p><strong>Conclusions: </strong>In patients with asymptomatic severe high-gradient aortic stenosis, higher NT-proBNP and hs-cTnT levels were broadly associated with higher event rates, as expected. However, the relative benefit of an early TAVR strategy was consistent regardless of baseline biomarker levels and, contrary to our hypothesis, tended to be more pronounced in patients with the lowest biomarker levels. These findings suggest limited value for single measurements of these biomarkers to guide the timing of TAVR in asymptomatic patients.</p><p><strong>Registration: </strong>URL: https://www.clinicaltrials.gov; Unique identifier: NCT03042104.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1550-1564"},"PeriodicalIF":35.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12124205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751425","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":"XBP1s-EDEM2 Prevents the Onset and Development of HFpEF by Ameliorating Cardiac Lipotoxicity.","authors":"Oveena Fonseka, Rida Raja, Claire Ross, Sanskruti R Gare, Jiayan Zhang, Susanne S Hille, Katharine King, Andrea Ruiz-Velasco, Namrita Kaur, Xinyi Chen, Jessica M Miller, Riham R E Abouleisa, Qinghui Ou, Zhiyong Zou, Xiangjun Zhao, Cristian Sotomayor-Flores, Derk Frank, Eileithyia Swanton, Martin R Pool, Sara Missaglia, Daniela Tavian, Gabriele G Schiattarella, Tao Wang, Luigi Venetucci, Christian Pinali, Martin K Rutter, Bernard D Keavney, Elizabeth J Cartwright, Tamer M A Mohamed, Oliver J Müller, Wei Liu","doi":"10.1161/CIRCULATIONAHA.124.072194","DOIUrl":"10.1161/CIRCULATIONAHA.124.072194","url":null,"abstract":"<p><strong>Background: </strong>Morbidity and mortality of heart failure with preserved ejection fraction (HFpEF) is increased in metabolic disorders. However, options for preventing and treating these prevalent outcomes are limited. Intramyocardial lipotoxicity contributes to cardiac dysfunction. Here, we investigate the mechanisms underlying EDEM2 (endoplasmic reticulum degradation-enhancing alpha-mannosidase-like protein 2) regulation of cardiac lipid homeostasis and assess strategies that inhibit the incidence and progression of HFpEF.</p><p><strong>Methods: </strong>Metabolic stress was induced in C57BL/6 male mice using a high-fat diet and <i>N</i>ω-nitro-L-arginine methyl ester. The recombinant adeno-associated virus 9 delivery system was used for loss- and gain-of-function studies. Palmitic acid and oleic acid stimulation of rat cardiomyocytes and human induced pluripotent stem cell-derived cardiomyocytes imitated a condition of high lipids in vitro. Molecular mechanisms were investigated via RNA sequencing, mass spectrometry proteomics, lipidomic analyses, transmission electron microscopy, histology, and luciferase reporter assays.</p><p><strong>Results: </strong>In the human heart, we first detected lipid overload accompanied by a reduction of <i>XBP1</i> (X-box binding protein 1) under metabolic stress. Thereafter, a decrease in EDEM2 was confirmed in human and mouse HFpEF hearts. Given that XBP1s (spliced X-box binding protein 1) is a transcription factor, EDEM2 was identified as its new target in cardiomyocytes. EDEM2 knockdown mice manifested lipid droplet accumulation and higher levels of triglycerides and diglycerides in the myocardium, aggravating oxidative stress, hypertrophy, and the onset and progression of HFpEF under metabolic stress. XBP1s ablation mice displayed a similar myocardial lipid disturbance and cardiac phenotypes, which were reversed by EDEM2 overexpression. Mechanistically, the findings obtained from rat cardiomyocytes and human induced pluripotent stem cell-derived cardiomyocytes demonstrated that, in the presence of EDEM2, SEC23A mediated intracellular translocation of ATGL (adipose triglyceride lipase) under fatty acid stimulation, inhibiting ATGL degradation and excessive intracellular lipid droplets. Furthermore, the functional studies supported that EDEM2 prevention of lipid overload occurred in an ATGL-dependent manner. Therapeutically, cardiac XBP1s or EDEM2 restoration mitigated lipid deposition and preserved lipid profiles in the myocardium, thus preventing the development of HFpEF.</p><p><strong>Conclusions: </strong>We demonstrate a cardioprotective mechanism regulating myocardial lipid homeostasis. The findings provide a promising therapeutic target to prevent and treat HFpEF, a condition with limited treatment options.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1583-1605"},"PeriodicalIF":35.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12124211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699786","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":"TET2-Mutant Clonal Hematopoiesis Promotes Heart Failure With Preserved Ejection Fraction.","authors":"Ambarish Pandey, Toby Thomas, Yuanyuan Ji, Benjamin Kroger, Peter Carlsgaard, Camila I Irion, Fatma Kalkan, Matthew Segar, Vinayak Subramanian, Antoni Bayés-Genís, Albert Son, Kira A Young, Jennifer J Trowbridge, Naveen Premnath, Nan Jiang, Daniel Daou, Wenhuo Hu, Sarah A Ware, Dan Tong, Stephen S Chung","doi":"10.1161/CIRCULATIONAHA.124.072909","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.124.072909","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 22","pages":"1622-1625"},"PeriodicalIF":35.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207836","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":"A Novel Hidden Protein p-414aa Encoded by <i>circSETD2(14,15</i>) Inhibits Vascular Remodeling.","authors":"Si-Fan Wang, Li-Yun Yang, An-Qi Zhao, Zhao-Yi Wang, Sen Wang, Miao Gong, Ming-Qi Zheng, Gang Liu, Shu-Yan Yang, Jia-Jie Lin, Shao-Guang Sun","doi":"10.1161/CIRCULATIONAHA.124.070243","DOIUrl":"10.1161/CIRCULATIONAHA.124.070243","url":null,"abstract":"<p><strong>Background: </strong>Phenotypic switching of vascular smooth muscle cells (VSMCs), leading to neointimal hyperplasia, is a fundamental cause of vascular remodeling diseases such as atherosclerosis and hypertension. Novel hidden proteins encoded by circular RNAs play crucial roles in disease progression, yet their involvement in vascular remodeling diseases has not been comprehensively studied. This study identifies a novel protein derived from a circular RNA in VSMCs and demonstrates its potential role in regulating vascular remodeling.</p><p><strong>Methods: </strong>Cell proliferation assays were performed to investigate the effects of <i>circSETD2(14,15</i>) on VSMC proliferation. Techniques such as vector construction, immunoprecipitation-mass spectrometry, and dual-luciferase reporter gene were used to confirm that <i>circSETD2(14,15</i>) encoded a novel protein, p-414aa. The interaction between p-414aa and HuR (human antigen R) was validated with techniques such as co-immunoprecipitation, mass spectrometry, and proximity ligation assay. Through experiments including RNA sequencing and RNA immunoprecipitation, the interaction between HuR and <i>C-FOS</i> (C-Fos proto-oncogene) mRNA was revealed. The role of p-414aa in neointimal hyperplasia was assessed with a carotid artery ligation model in male mice.</p><p><strong>Results: </strong>Overexpression of <i>circSETD2(14,15</i>) inhibits VSMC phenotypic switching. The novel protein p-414aa, encoded by <i>circSETD2(14,15</i>), interacts with HuR to reduce <i>C-FOS</i> mRNA stability, thereby suppressing VSMC proliferation and ultimately inhibiting neointimal hyperplasia in male mice.</p><p><strong>Conclusions: </strong>We uncover a novel hidden protein derived from <i>circSETD2(14,15</i>), called p-414aa, that inhibits vascular remodeling. <i>CircSETD2(14,15</i>) and p-414aa may serve as potential therapeutic targets for vascular remodeling diseases.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1568-1582"},"PeriodicalIF":35.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647519","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":"Joint Exposure to Ozone and Temperature and Acute Myocardial Infarction Among Adults Aged 18 to 64 Years in the United States.","authors":"Lingzhi Chu, Rong Wang, Cary P Gross, Jing Wei, Yuan Lu, Harlan M Krumholz, Xiaomei Ma, Kai Chen","doi":"10.1161/CIRCULATIONAHA.124.073614","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.124.073614","url":null,"abstract":"<p><strong>Background: </strong>Previous research suggests that exposures to air pollution and nonoptimal temperatures are associated with a higher risk of acute myocardial infarction (AMI), but few studies examined the exposures jointly. Furthermore, moderate exposures were often overlooked. We evaluated short-term exposure to ambient ozone pollution and ambient temperature jointly and over the entire range of exposures, with the occurrence of AMI among adults aged 18 to 64 years (an understudied population) in the contiguous United States.</p><p><strong>Methods: </strong>We identified eligible individuals with incident AMI insured by a nationwide private insurance company from 2016 to 2020. We designed a time-stratified case-crossover study in which each patient's ambient exposure to ozone and temperature on the day of their AMI was compared with their exposures on a nearby day. We used a 2-stage model to investigate the associations with joint exposures: (1) fitting climate- and region-specific models with statistical interaction terms between ozone and temperature, and (2) using a multivariate random-effects meta-analysis to pool the region-specific estimates.</p><p><strong>Results: </strong>We included 270 123 adults with incident AMI and observed a significant association between joint ozone-temperature exposures and increased AMI. Compared with the reference of ozone at 35 ppb and temperature at the first percentile, joint exposure to ozone at 60 ppb and temperature at the 95th percentile at lag 0 day was associated with a 33% (95% CI, 16%-51%) increase in incident AMI, and joint exposure to ozone at 50 ppb and temperature at the median was associated with a 15% (95% CI, 4%-28%) increase. There was heterogeneity by sex, with women showing increased odds when both ozone and temperature were high and men showing increased odds when either ozone or temperature was high.</p><p><strong>Conclusions: </strong>Joint exposure to ozone pollution and high temperature increased the probability of AMI among younger adults, even when 1 of the exposures was moderate. This study highlights the importance of addressing exposures to ozone and nonoptimal temperature simultaneously in AMI prevention strategies.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":35.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144207830","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":"Blood Pressure Lowering Effects of a Novel Long-Acting NPR1 Agonist, XXB750, in Healthy Participants: A Randomized, First-in-Human Clinical Study.","authors":"YanLing He, Xueping Wu, Andre Serra-Roma, Maggie Markiewicz, Emma Healy, Jing-He Yan, Kenneth Kulmatycki, Tong Zhang, John L Diener, Arvind G Kinhikar, Denise P Yates, David Nguyen, Markus Hinder, Cesare Russo, Christopher J O'Donnell","doi":"10.1161/CIRCULATIONAHA.124.072636","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.124.072636","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 21","pages":"1544-1546"},"PeriodicalIF":35.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157163","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":"Non-Randomized Database Analyses to Complement Randomized Clinical Trials: Promising Approaches for Cardiovascular Medicine.","authors":"Sebastian Schneeweiss, Nils Krüger","doi":"10.1161/CIRCULATIONAHA.125.073235","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.125.073235","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 21","pages":"1495-1497"},"PeriodicalIF":35.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144157224","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}