Circulation最新文献

{"title":"SIRT5 Ameliorates Cardiac Fibrosis via PCK2 Desuccinylation-Mediated Metabolic Reprogramming in Cardiac Fibroblasts.","authors":"Maoxiong Wu,Jing Tan,Weibin Zhou,Zenghui Zhang,Qingyuan Gao,Yangwei Cai,Guanghong Liao,Zhengyu Cao,Chuanrui Zeng,Yi Zhang,Zhiteng Chen,Qiong Qiu,Zhaoyu Liu,Jingfeng Wang,Haifeng Zhang,Yangxin Chen","doi":"10.1161/circulationaha.125.077756","DOIUrl":"https://doi.org/10.1161/circulationaha.125.077756","url":null,"abstract":"BACKGROUNDSIRT5 (sirtuin 5) is a member of the sirtuin family known to regulate cardiac metabolism, aging, and function. However, its role in cardiac fibroblast (CFB) metabolism, activation, and fibrosis remains elusive.METHODSExpression changes of SIRT5 in CFBs from cardiac tissue of human and mouse with heart failure were determined. The functional role of SIRT5 in cardiac fibrosis was evaluated through CFB-specific knockout and overexpression of Sirt5 in mice. The involvement of succinylation of lysine 489 (Lys489) on PCK2 (phosphoenolpyruvate carboxykinase 2) in SIRT5-mediated regulation of cardiac fibrosis was assessed by introducing the Lys489-to-arginine mutation of PCK2 in Sirt5-deficient CFBs and in CFB-specific Sirt5 knockout mice.RESULTSSIRT5 expression was markedly reduced in CFBs from humans and mice with heart failure and showed a negative correlation with cardiac fibrosis severity. Loss of Sirt5 in CFBs exacerbated left ventricular dysfunction, cardiac hypertrophy, and cardiac fibrosis in mice subjected to transverse aortic constriction, whereas overexpression of Sirt5 in CFBs significantly attenuated these pathological changes. Sirt5 deficiency promoted CFB activation by driving a metabolic shift from oxidative phosphorylation to glycolysis. Mechanistically, Sirt5 deficiency increased the succinylation of PCK2 at Lys489, a key enzyme linking glycolysis and the tricarboxylic acid cycle, which consequently inhibited this enzyme activity in CFBs. Importantly, this specific modification at the Lys489 mutation that prevents succinylation effectively reversed both the metabolic reprogramming and the hyperactivation of CFBs induced by Sirt5 knockout. In vivo, introducing the Pck2 K489R mutation fully rescued the exacerbated cardiac fibrosis and dysfunction observed in Sirt5-deficient mice after transverse aortic constriction.CONCLUSIONSBy desuccinylating PCK2 at Lys489, SIRT5 prevents the metabolic reprogramming and subsequent activation of CFBs, protecting against cardiac fibrosis.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"7 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147733965","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":"TRPM7 Deficiency Protects Against Myocardial Ischemia-Reperfusion Injury by Regulating Intracellular Zn²⁺ Homeostasis.","authors":"Xin Li, Xiaohan Li, Cindy Xintong Li, Jianlin Feng, Zhichao Yue, Jiajie Yan, Masayuki Matsushita, Yibing Qyang, Loren W Runnels, Xun Ai, Lixia Yue","doi":"10.1161/CIRCULATIONAHA.125.074791","DOIUrl":"10.1161/CIRCULATIONAHA.125.074791","url":null,"abstract":"<p><strong>Background: </strong>Ischemic heart disease is one of the leading causes of death worldwide. Timely reperfusion is necessary for myocardium salvage but triggers paradoxical cardiomyocyte death and contributes to up to 50% of the final infarct size, known as lethal ischemia/reperfusion (I/R) injury. TRPM7 (transient receptor potential melastatin 7) is a divalent cation-permeable, nonselective channel kinase that can sense oxidative stress and release Zn<sup>2+</sup> from unique intracellular TRPM7 vesicles. However, the pathophysiological role of intracellular TRPM7 remains poorly understood.</p><p><strong>Methods: </strong>TRPM7 expression was determined in hearts from patients with ischemic heart failure and I/R-injured mice. Global (<i>gTrpm7<sup>-/-</sup></i>), cardiomyocyte-specific (<i>cmTrpm7</i><sup><i>-/-</i></sup>), and fibroblast-specific (<i>fibTrpm7</i><sup><i>-/-</i></sup>) <i>Trpm7</i> knockout mice were used to determine the role of TRPM7 in I/R injury. Mechanistic investigations were conducted in neonatal and adult mouse cardiomyocytes and human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) with patch-clamp, Zn<sup>2</sup><sup>+</sup> imaging, and molecular biology techniques. An inducible TRPM7 channel-dead (TRPM7-E1047K) knock-in mouse model was generated to elucidate the functional domains of TRPM7 for therapeutic strategies.</p><p><strong>Results: </strong>We found that TRPM7 was significantly upregulated in myocardium from both patients with ischemic heart failure and I/R-injured mice. Global TRPM7 deficiency markedly reduced infarct size and improved cardiac function after I/R injury. Using <i>cmTrpm7</i><sup><i>-/-</i></sup> and <i>fibTrpm7</i><sup><i>-/-</i></sup> mice, we demonstrated that TRPM7 deficiency in myocytes, rather than in fibroblasts, confers protection against I/R injury by inhibiting pyroptosis as evaluated. Furthermore, using mouse cardiomyocytes and hiPSC-CMs, we revealed that Zn<sup>2+</sup> release from intracellular TRPM7 vesicles during I/R injury triggers cardiomyocyte death by activating gasdermin-D to release its N-terminal and form the membrane pore. The critical role of intracellular TRPM7 was further supported by the inability of membrane TRPM7 inhibition to protect mice against I/R injury. To elucidate whether the channel or kinase activity of TRPM7 mediates pyroptosis in I/R injury, we generated an inducible channel-dead TRPM7-E1047K knock-in mouse model. By comparing with kinase-inactive TRPM7 knock-in mice, we uncovered that the channel but not the kinase function of TRPM7 mediates I/R injury.</p><p><strong>Conclusions: </strong>TRPM7-mediated intracellular Zn<sup>2</sup><sup>+</sup> release contributes to myocardial I/R injury by triggering apoptotic and pyroptotic cardiomyocyte death. Given that TRPM7 is highly upregulated in patients with ischemic heart failure, our findings suggest that targeting TRPM7 may represent a novel therapeutic strategy for ischemic h","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1210-1229"},"PeriodicalIF":38.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13019533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124105","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":"The Fontan Outcomes Network: Findings After 2 Years and 1121 Participants.","authors":"Thomas M Glenn, Nadine A Kasparian, Shahnawaz Amdani, David Renaud, Michael V DiMaria, Jennifer Teh, David M Leone, Arjun K Mahendran, Nancy A Pike, Stephen J Dolgner, Andrew L Cheng, Rahul H Rathod, Sumeet S Vaikunth, Surendranath R Veeram Reddy, Rohith Vanam, Jeff Theobald, Kurt R Schumacher, Sarah A Hummel, Jennifer Conway, David J Goldberg, Dala Zakaria, Sarah B Clauss, Divya Suthar, Roni M Jacobsen, Evonne M Morell, John C Dykes, Angela J Weingarten, Deepti P Bhat, Benjamin E Reinking, Tarek Alsaied, Carole Lannon, Kiona Y Allen, Jeff B Anderson, Lacie B Patterson, David W Brown, Richard James, Jack Rychik, Alexander R Opotowsky","doi":"10.1161/CIRCULATIONAHA.125.078152","DOIUrl":"10.1161/CIRCULATIONAHA.125.078152","url":null,"abstract":"<p><strong>Background: </strong>Survival after Fontan palliation for single ventricle heart disease has improved substantially, yet the long-term trajectory remains poorly defined. The Fontan Outcomes Network, a learning health network of 38 congenital heart centers in the United States and Canada, was established to address this gap. We report baseline characteristics and early findings from the first 1121 participants enrolled in this prospective clinical registry.</p><p><strong>Methods: </strong>We performed a cross-sectional analysis of individuals who had undergone Fontan palliation enrolled in the Fontan Outcomes Network from August 2022 through August 2024. Demographic, clinical, imaging, procedural, and medication data were analyzed descriptively, overall and by age group (<12, 12 to <18, and ≥18 years).</p><p><strong>Results: </strong>A total of 1121 participants were enrolled (mean age, 16.3±10.2 years; 471 [42%] female). Hypoplastic left heart syndrome (n=431 [38.5%]) and right ventricular-dominant anatomy (n=615 [54.9%]) were the most common primary cardiac diagnoses, especially in younger age groups. Extracardiac conduit was the most frequent Fontan type (n=749 [66.8%]). Typical Fontan-related adverse events were noted in 59% of cases (n=662), including chylous pleural effusions (n=108 [9.6%]), Fontan thrombosis (n=79 [7.1%]), and nonperioperative stroke (n=73 [6.5%]). A history of arrhythmia was present in 41.3% of patients (n=463) overall, increasing with age. Acquired comorbidities were present in 57.5% of patients (n=645), including asthma (n=132 [12%]) and sleep apnea (n=103 [9%]), with burden increasing by age. Antithrombotic medication use was nearly universal. Use of other medications varied widely by age, and included β-blockers, angiotensin-converting enzyme inhibitors, and pulmonary vasodilators. A clinical diagnosis of an anxiety disorder was present in 34.1% of patients (n=382), including 48.1% of adults (n=194 of 403), and antidepressants were prescribed in 11.8% of patients (n=132), including 23.6% of adults (n=95 of 403), highlighting the mental health needs of this population.</p><p><strong>Conclusions: </strong>The Fontan Outcomes Network includes one of the largest prospective, multi-institutional data sets of patients with Fontan circulation. These initial findings demonstrate the potential for a collaborative learning health network to advance research and quality improvement for this rare disease population.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1182-1195"},"PeriodicalIF":38.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509692","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":"Nonoptimal Temperature and Cardiovascular Health: A Scientific Statement From the American Heart Association.","authors":"Kate Hanneman, Barrak Alahmad, Arnab Ghosh, Sameed Ahmed M Khatana, Mu Huang, Jingwen Liu, Azar Abadi, Haitham Khraishah, Theresa Beckie, Sanjay Rajagopalan, Sonia Angell","doi":"10.1161/CIR.0000000000001419","DOIUrl":"10.1161/CIR.0000000000001419","url":null,"abstract":"<p><p>Ambient temperature is a key environmental driver of cardiovascular health. With rising global temperatures and increasing frequency, intensity, and duration of extreme temperature events, understanding the cardiovascular impacts of nonoptimal temperature is more urgent than ever. Short-term exposures to both heat and cold increase the risk of cardiovascular events, including myocardial infarction, stroke, heart failure decompensation, arrhythmias, and sudden cardiac death. Climate, built environment, socioeconomic variables, physiological vulnerability, and systemic inequities exacerbate these risks. There is also a growing appreciation of the importance of contextual factors such as geographic location, housing, occupation, and individual-level exposure. A range of biological mechanisms, including autonomic and neurohormonal activation, endothelial dysfunction, inflammation, hemoconcentration, and impaired thermoregulation, mediate temperature-related cardiovascular risk. Nonoptimal temperatures affect not only the incidence of cardiovascular disease but also health care access and delivery. They can increase demand for emergency care, disrupt operations, and pose challenges to the resilience and sustainability of health systems. Meanwhile, cardiovascular care contributes significantly to health care-related greenhouse gas emissions, highlighting a paradox in which efforts to protect cardiovascular health can indirectly contribute to climate-driven risks. This scientific statement synthesizes current knowledge of the relationship between nonoptimal temperature and cardiovascular health, highlights inequalities in exposure and outcomes, and identifies actionable strategies at the individual, community, health system, and public policy levels. Last, this scientific statement outlines significant research gaps and future priorities, including the need for improved exposure assessment, better understanding and measurement of the impact of long-term exposures, interactions with medications and coexposures, and identification of risk modifiers. Coordinated action is needed in research, clinical practice, and policy to mitigate the rising risks of nonoptimal temperatures on cardiovascular health in a changing climate.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"e1130-e1150"},"PeriodicalIF":38.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509993","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":"Macrophage PRMT9 Ameliorates Acute Myocardial Infarction by Promoting Symmetric Dimethylation and Degradation of STAT1.","authors":"Xuemei Bai, Ruiqing Ren, Jiahua Yuan, Liwen Yu, Na Dong, Nan Cao, Min Zhou, JiaJia Zhang, Xiaoxiao Li, Ziye He, Bingyu Liu, Meng Zhang, Chengjiang Gao","doi":"10.1161/CIRCULATIONAHA.125.076101","DOIUrl":"10.1161/CIRCULATIONAHA.125.076101","url":null,"abstract":"<p><strong>Background: </strong>During myocardial infarction (MI), M1-like macrophages exacerbate myocardial injury by excessively secreting inflammatory cytokines. Therefore, modulating the activity of M1-like macrophages may represent a novel therapeutic strategy for MI. PRMTs (protein arginine methyltransferases) primarily regulate protein function via asymmetric dimethylation, but PRMT9 does so through symmetric dimethylation. However, its role in cardiovascular diseases has yet to be established. In this study, we investigated the role of PRMT9 in macrophage polarization in the context of MI and explored its therapeutic effect for MI.</p><p><strong>Methods: </strong>The correlation between PRMT9 in monocytes/macrophages and MI was investigated using the MI dataset GSE166780. Peripheral blood mononuclear cells were obtained from healthy individuals and patients with MI and analyzed to assess PRMT9 expression. We elucidated the functional role of PRMT9 in MI using macrophage-specific <i>Prmt9</i> knockout mice and macrophage-specific overexpression adeno-associated virus vectors. We explored the underlying mechanisms through flow cytometry, transcriptome analysis, immunoprecipitation/mass spectrometry analysis, and functional experiments.</p><p><strong>Results: </strong>We discovered that PRMT9 was highly expressed in murine and human peripheral blood mononuclear cells in the early stages of MI. PRMT9 deficiency enhanced M1-like polarization and exacerbated cardiac damage in murine models of MI. Conversely, PRMT9 overexpression in macrophages reduced infarct size, accelerated inflammation resolution, and improved cardiac function after MI. Our findings established that PRMT9-catalyzed methylation played an important role in STAT1 (signal transducer and activator of transcription 1)-mediated macrophage polarization. Mechanistically, PRMT9 directly binds to STAT1 and facilitates its symmetric dimethylation at R588 and R736. Further analysis revealed that PRMT9-mediated symmetric dimethylation facilitated STAT1 ubiquitination, which promoted STAT1 recognition by SQSTM1/p62 (sequestosome-1) and NDP52/CALCOCO2 (nuclear dot protein 52), facilitating STAT1-selective autophagic degradation and suppressing excessive M1-like macrophage responses. Moreover, we demonstrated that the STAT1 inhibitor fludarabine, a clinically used chemotherapeutic agent, mitigated the exacerbation of post-MI myocardial injury induced by PRMT9 deletion in macrophages.</p><p><strong>Conclusions: </strong>This study discovered a novel PRMT9-driven symmetric dimethylation of STAT1, resulting in its ubiquitination and lysosomal degradation, which suppresses the proinflammatory polarization of macrophages and mitigates myocardial damage following MI.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1233-1254"},"PeriodicalIF":38.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13105769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146156400","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":"JNK2 Is a Stress Integrator Driving Atrial Fibrillation Pathogenesis in Aging via Gut-Heart Crosstalk.","authors":"Jiajie Yan,Elena Carrillo,Aaryan Kohli,Saugat Khanal,Nikola Ricchiuti,Jaime DeSantiago,Xiaoping Wan,Mei Han,Abigail Richardson,Mei Yang,Jesus Rondon,Le Shen,Jun Sun,Qiangrong Liang,Thomas J Hund,Jarek Meller,Isabelle Deschenes,Dan J Bare,Xun Ai","doi":"10.1161/circulationaha.125.076147","DOIUrl":"https://doi.org/10.1161/circulationaha.125.076147","url":null,"abstract":"BACKGROUNDAtrial fibrillation (AF) is the most common arrhythmia and is associated with high morbidity and mortality, particularly in the aging population. Current treatment and prevention strategies remain suboptimal, highlighting the urgent need to better understand the mechanisms underlying aging-associated AF. We recently reported a causal role of the stress-activated kinase JNK2 (c-Jun N-terminal kinase 2) in aging-associated AF pathogenesis, mediated by JNK2-driven sarcoplasmic reticulum Ca2+ dysfunction. However, the mechanisms by which cardiac JNK2 is activated during aging to promote AF remain unclear. Emerging evidence suggests that interorgan crosstalk contributes critically to the development of cardiovascular diseases. A hyperpermeable gastrointestinal epithelial barrier (\"leaky gut\"), commonly observed in aged individuals, is associated with elevated levels of proinflammatory cytokines and an increased risk of AF. Although proinflammatory cytokines have been proposed as predisposing factors for AF, clinical and experimental studies have yielded inconsistent results, underscoring the complexity of inflammation-associated AF pathogenesis. Here, we investigated whether cardiac JNK2 integrates diverse stress stimuli, including proinflammatory cytokines and lipopolysaccharide, to drive AF pathogenesis.METHODSWe used aged mice, intestinal epithelium-specific tight junction OD (occludin) knockdown (OD+/-) mice, and a well-established dextran sulfate sodium-induced leaky gut mouse model characterized by reduced gastrointestinal epithelial occludin expression. A series of physiological and molecular approaches was applied to assess cardiac and gastrointestinal responses.RESULTSWe found that leaky gut significantly activates atrial JNK2, which, in turn, drives Ca2+-triggered arrhythmic activity and increases AF inducibility in aged, dextran sulfate sodium-treated, and OD+/- mouse models. Restoration of gut barrier function in dextran sulfate sodium mice, a clinically relevant model, reduced AF susceptibility. Similarly, either JNK2 inhibition or TNF-α (tumor necrosis factor α) blockade abolished the increased AF risk associated with leaky gut. Furthermore, we demonstrate, for the first time, that leaky gut-associated proinflammatory cytokines, including TNF-α and IL-17A (interleukin-17A), together with lipopolysaccharide, activate cardiac JNK2. This activation promotes AF pathogenesis through JNK2-mediated arrhythmogenic mechanisms, including diastolic sarcoplasmic reticulum Ca2+ leak, Ca2+ waves, and delayed afterdepolarizations.CONCLUSIONActivated JNK2 functions as a pathological nodal integrator of leaky gut-associated stress signals, mediating gut-to-heart crosstalk and driving inflammation-induced AF pathogenesis. Targeting JNK2 may represent a novel therapeutic strategy for AF.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"5 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147719505","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":"Letter by Chen et al Regarding Article, \"Prognostic Role of Myocarditis-Like Episodes and Their Treatment in Patients With Pathogenic Desmoplakin Variants\".","authors":"Xiu-Xiu Chen,Yi-Qi Chen,Zheng-Qi Song","doi":"10.1161/circulationaha.125.077100","DOIUrl":"https://doi.org/10.1161/circulationaha.125.077100","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"9 1","pages":"e1122-e1123"},"PeriodicalIF":37.8,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147726021","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":"Intracellular TRPM7-Mediated Zn2+ Release: A Novel Pyroptotic Axis in Myocardial Ischemia-Reperfusion Injury.","authors":"Beijian Zhang,Aijun Sun,Junbo Ge","doi":"10.1161/circulationaha.126.079461","DOIUrl":"https://doi.org/10.1161/circulationaha.126.079461","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"11 1","pages":"1230-1232"},"PeriodicalIF":37.8,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147726025","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":"When the Heart Cannot Fill: An Unusual Cause of Congestive Heart Failure.","authors":"Jaya Batra,Andrew J Einstein,Gabriel Sayer,Koji Takeda,Nir Uriel","doi":"10.1161/circulationaha.125.079086","DOIUrl":"https://doi.org/10.1161/circulationaha.125.079086","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"65 1","pages":"1255-1260"},"PeriodicalIF":37.8,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147725991","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 Mori et al to Letter Regarding Article, \"Screening-Detected Atrial Fibrillation and Cardiovascular Outcomes in Working-Age Adults\".","authors":"Yuichiro Mori,Mitsuaki Sawano,Shun Kohsaka,Yusuke Tsugawa,Motoko Yanagita,Shingo Fukuma","doi":"10.1161/circulationaha.126.079913","DOIUrl":"https://doi.org/10.1161/circulationaha.126.079913","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"12 1","pages":"e1128-e1129"},"PeriodicalIF":37.8,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147726228","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}