Circulation最新文献

{"title":"The Amyloid Atrium: A Distinct Phenotype Demanding a Distinct Paradigm.","authors":"Ashwin A Pillai, Keyur B Shah, Ajay Pillai","doi":"10.1161/CIRCULATIONAHA.126.079713","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.079713","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 15","pages":"1421-1423"},"PeriodicalIF":41.3,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164376","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":"Clarifying the Clinical Relevance of V Waves.","authors":"Eric A Secemsky, Ryan J Tedford","doi":"10.1161/CIRCULATIONAHA.126.083625","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.083625","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164996","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":"Prominent V Waves Augment Right Ventricular Afterload Independent of the Lung Vessels in Heart Failure: Implications for Clinical Assessment of Pulmonary Vascular Disease.","authors":"Thanat Chaikijurajai, Yogesh N V Reddy, Tomonari Harada, Jwan A Naser, Sho Kazui, Naoyuki Akashi, Takahiro Okuno, Fahime Ghanbari, Barry A Borlaug","doi":"10.1161/CIRCULATIONAHA.126.081799","DOIUrl":"10.1161/CIRCULATIONAHA.126.081799","url":null,"abstract":"<p><strong>Background: </strong>Left atrial (LA) stiffening augments the LA V wave, pressurizing the pulmonary artery (PA) out of proportion to left ventricular end-diastolic pressure. We characterized the pathophysiologic, diagnostic, and clinical implications of LA stiffening, as defined by prominent V waves, in heart failure with preserved ejection fraction.</p><p><strong>Methods: </strong>In this retrospective cohort study, patients with heart failure with preserved ejection fraction and less than moderate mitral regurgitation at rest underwent invasive hemodynamic exercise testing. Patients with heightened operant LA stiffening were defined by the PA wedge pressure (PAWP) V wave exceeding mean PAWP by ≥10 mm Hg. A previously used formula for V wave-corrected PAWP was validated against the PAWP waveform pressure-time-area to explore impact of the V wave on transpulmonary pressure gradients. Clinical, echocardiographic, hemodynamic, and outcome data were compared for patients with and without prominent V waves.</p><p><strong>Results: </strong>Compared with patients without prominent V waves (n=844, 79%), those with prominent V waves (n=225, 21%) were older and more likely to be women, with more severe LA myopathy, evidenced by greater LA volume index (42.2±15.0 versus 32.5±13.0 mL/m<sup>2</sup>, <i>P</i><0.001), lower LA reservoir strain (16.4±7.5% versus 23.2±8.3%, <i>P</i><0.001), more atrial fibrillation (61.3% versus 22.9%, <i>P</i><0.001), and increased operant LA reservoir stiffness (0.59±0.25 versus 0.23±0.24 mm Hg/mL, <i>P</i><0.001). Patients with prominent V waves had markedly higher PA systolic pressure than those without (54±16 versus 38±12 mm Hg, <i>P</i><0.001) despite no difference in end-diastolic PAWP-PA pressure gradient (3±5 versus 3±4 mm Hg, <i>P</i>=0.950). Incorporating the V wave into PAWP improved correlation between directly measured PAWP pressure-time integral compared with mid-A wave PAWP (R<sup>2</sup>=0.96 versus R<sup>2</sup>=0.86, <i>P</i><0.001 for comparison). In patients with prominent V waves, the prevalence of combined pre- and postcapillary pulmonary hypertension decreased from 60.2% to 29.3% after V wave correction for the transpulmonary pressure gradients. Despite similar corrected pulmonary vascular resistances in patients with and without prominent V waves, apparent PA compliance was much lower in patients with prominent V waves (3.03±1.56 versus 4.90±2.27 mL/mm Hg, <i>P</i><0.001), augmenting right ventricular afterload, and these changes were coupled with more severe right ventricular dysfunction, tricuspid regurgitation, blunted cardiopulmonary exercise reserve, and increased risk of hospitalization for heart failure or death in patients with versus without prominent V waves (adjusted hazard ratio, 2.09 [95% CI, 1.53-2.86]; <i>P</i><0.001).</p><p><strong>Conclusions: </strong>More than 1 in 5 patients with heart failure with preserved ejection fraction display prominent V waves in excess of end-diast","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13660403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165814","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":"When VT Storm, PET Positivity, and a Negative Endomyocardial Biopsy Collide","authors":"Mary K. Nielson,Ike Okwuosa,Lisa D. Wilsbacher,Nishant Verma,Paul Cremer,Peter H.S. Sporn,Arjun Seth,Jane E. Wilcox","doi":"10.1161/circulationaha.126.081290","DOIUrl":"https://doi.org/10.1161/circulationaha.126.081290","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"11 1","pages":"1404-1411"},"PeriodicalIF":37.8,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149088005","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":"Cardiovascular Disease Risk Assessment in United States Military Service Members.","authors":"John-Henry L Dean, Caroline E Murphy, M Alaric Franzos, Bradley J Petek","doi":"10.1161/CIRCULATIONAHA.126.081464","DOIUrl":"10.1161/CIRCULATIONAHA.126.081464","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1417-1419"},"PeriodicalIF":41.3,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886571","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 Wang et al Regarding Article, “Association of Statin Discontinuation in Pregnancy With Maternal Cardiovascular Health and Birth Outcomes: A Nationwide Cohort Study”","authors":"Yaomin Wang,Yaling Li,Gang Xing","doi":"10.1161/circulationaha.126.080633","DOIUrl":"https://doi.org/10.1161/circulationaha.126.080633","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"36 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149088007","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":"Metrnl Reduces Thrombosis and Acute Myocardial Injury Through Inhibition of Platelet Activation via CD36 Receptor Degradation.","authors":"Zhu-Wei Miao, Can-Xin Chen, Pin Wang, Si-Li Zheng, Jie-Bing Jiang, Wen-Jun Hu, Xiao-Yan Zhu, Bin Lu, Li-Ming Chen, Liang Hu, Chao-Yu Miao","doi":"10.1161/CIRCULATIONAHA.126.077134","DOIUrl":"10.1161/CIRCULATIONAHA.126.077134","url":null,"abstract":"<p><strong>Background: </strong>Metrnl (Meteorin-like) is a secreted protein that plays a pivotal role in regulating insulin sensitivity, angiogenesis, and atherosclerosis. The circulating Metrnl levels are mainly derived from the endothelium and associated with atherosclerosis and arterial thrombotic disease in patients. However, Metrnl effects on platelets and thrombosis are not yet fully understood.</p><p><strong>Methods: </strong>By using global Metrnl knockout mice, platelet-specific Metrnl knockout mice, recombinant Metrnl protein, and Metrnl-neutralizing antibody, combined with visualization techniques, we investigated the effects of Metrnl on human and rodent platelet activation in vitro, and thrombosis in vivo as well as its action mode. To screen and verify receptor-mediated mechanisms for Metrnl, we used immunoprecipitation-based mass spectrometry, protein-protein interaction tests, and functional assays under antagonist and knockout conditions. Receptor binding domains, functional sites, and downstream mechanisms were further explored using various protein mutations, specific interventions, and signaling examinations. A myocardial ischemia/reperfusion model was used to better understand the effects of Metrnl on microvascular thrombosis obstruction and acute myocardial injury.</p><p><strong>Results: </strong>Metrnl deficiency potentiated thrombosis via platelet activation rather than coagulation or the fibrinolysis system. Exogenous Metrnl administration could directly inhibit platelet activation and thrombosis without causing bleeding risk when using Metrnl alone or in combination with clopidogrel. Metrnl in platelets also inhibited platelet activation and thrombosis in a secretory manner. In a molecular mechanism, CD36 was identified as a receptor for Metrnl on platelets. Metrnl induced CD36 degradation via interaction with a previously uncharacterized domain (amino acids 280-439) and acetylation at lysine 403 of CD36, thereby decreasing the downstream signaling pathway (SRC-extracellular signal-related kinase 5 [ERK5]) in platelets. Further, mouse model experiments demonstrated Metrnl protein's antiplatelet function in mitigating microvascular thrombosis and acute myocardial ischemia/reperfusion injury.</p><p><strong>Conclusions: </strong>We identify Metrnl in both endogenous secretion and exogenous administration as a novel inhibitor of platelet activation and thrombus formation without causing bleeding risk. Metrnl is a novel ligand for the CD36 receptor, which has a specific Metrnl binding domain. Metrnl inhibits platelet activation by promoting CD36 degradation via acetylation at lysine 403 of CD36. Metrnl holds promise to be a novel therapeutic target for thrombotic disease, such as in the treatment of acute myocardial infarction.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1360-1377"},"PeriodicalIF":41.3,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13641263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788517","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":"Lipid Burden and Efficacy of Preventive PCI of Vulnerable Atherosclerotic Coronary Plaques: Post Hoc Analysis From the PREVENT Trial","authors":"Seong-Bong Wee,Jung-Min Ahn,Do-Yoon Kang,Ju Hyeon Kim,Jung-Bok Lee,Han Su Park,Soo Yeon An,Kyeong-Won Seo,Seung Han Lee,Young-Keun Ahn,Won-Jang Kim,Chang-Wook Nam,Jin-Ok Jeong,In-Ho Chae,Hiroki Shiomi,Hsien-Li Kao,Joo-Yong Hahn,Sung-Ho Her,Bong-Ki Lee,Tae Hoon Ahn,Ki-Yuk Chang,David Smyth,Gary S. Mintz,Gregg W. Stone,Duk-Woo Park,Seung-Jung Park,for the PREVENT Investigators","doi":"10.1161/circulationaha.126.080384","DOIUrl":"https://doi.org/10.1161/circulationaha.126.080384","url":null,"abstract":"BACKGROUND: Preventive percutaneous coronary intervention (PCI) of non–flow-limiting lesions (fractional flow reserve &gt;0.80) that are high-risk plaques has emerged as a potential strategy to reduce cardiac events. However, identifying which lesions derive the greatest benefit from preventive PCI compared with optimal medical therapy alone remains challenging. This post hoc analysis evaluates the role of the near-infrared spectroscopy–derived lipid core burden index in identifying high-risk plaques that may benefit from preventive PCI. METHODS: Among the 1606 patients enrolled in the PREVENT trial (Preventive Coronary Intervention on Stenosis with Functionally Insignificant Vulnerable Plaque) from September 2015 to September 2021, an investigator-initiated, multicenter, open-label, randomized controlled trial, this post hoc analysis included 598 patients (mean age, 64.1±8.8 years; 27.9% women) comprising 632 lesions with a plaque burden &gt;70% and a minimal lumen area &lt;4 mm 2 by intravascular ultrasound in whom near-infrared spectroscopy evaluation was also performed. Lipid-rich plaque (LRP) was prespecified as having a maximum lipid core burden index over a 4-mm segment &gt;315. The primary outcome was a composite of death from cardiac causes, target-vessel myocardial infarction, ischemia-driven target-vessel revascularization, or hospitalization for unstable or progressive angina. RESULTS: LRPs were present in 223 patients (37.3%) with 234 lesions. During median follow-up of 5.6 years, primary outcome events occurred more frequently in patients with LRPs than in those with non-LRPs (12.5% versus 4.7%; unadjusted hazard ratio, 2.08; 95% CI, 1.03–4.19; P =0.039) in the overall population. Within the LRP group, preventive PCI was associated with a lower risk of the primary outcome compared with optimal medical therapy alone (7.3% vs. 17.6%; adjusted hazard ratio, 0.23; 95% CI, 0.13–0.41; P &lt;0.001). Conversely, no benefit of preventive PCI was observed in the non-LRP group (5.5% versus 4.2%; adjusted hazard ratio, 1.00; 95% CI, 0.54–1.86; P =0.97). A significant interaction was found between treatment strategy and the presence of LRP ( P interaction &lt;0.001). CONCLUSIONS: In this post hoc analysis of the PREVENT trial, preventive PCI was associated with a lower risk of the primary composite outcome in patients with near-infrared spectroscopy–defined LRPs, whereas no significant association was observed in those with non-LRPs despite their large plaque burden and small minimal lumen area. These findings suggest the importance of plaque composition, beyond morphological severity alone, in guiding preventive PCI. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02316886.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"222 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149088009","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 Oxidized Phospholipid PGPC Impairs Angiogenesis by Inhibiting Endothelial Autophagosomal–Lysosomal Fusion Through NPC1-Induced Syntaxin 17 Acetylation and Ubiquitination","authors":"Le Li,Jian-Jun Gao,Yue-Ting Kang,Wan-Kai Pan,Yu-Peng Jian,Yu-Jia Liu,Meng-Jie Deng,Yang Cao,Chan-Yuan Lyu,Fang-Yuan Wu,Li Chen,Jia-Hui Liu,Gang Dai,Jia-Bao Liao,He-Jian Xie,Yong-Ping Bai,Jia-Guo Zhou,Yan Li,Zhi-Jun Ou,Jing-Song Ou","doi":"10.1161/circulationaha.126.079506","DOIUrl":"https://doi.org/10.1161/circulationaha.126.079506","url":null,"abstract":"BACKGROUND: Angiogenesis is essential for the recovery of ischemic hearts with coronary artery disease (CAD). PGPC (1-palmitoyl-2-glutamyl-sn-glycero-3-phosphocholine) is a major phospholipid oxidation product in atherosclerotic lesions. Autophagy participates in angiogenesis. However, whether PGPC affects angiogenesis in ischemic hearts by regulating autophagy remains unclear. METHODS: Plasma PGPC concentrations were quantified and the effects of PGPC on angiogenesis were evaluated in cultured endothelial cells and in vivo using a subcutaneous Matrigel plug assay, as well as in hindlimb ischemia and myocardial infarction models in C57BL/6J mice. Autophagic flux and the expression and modification of proteins associated with autophagy and angiogenesis were also assessed. RESULTS: Plasma PGPC levels were increased in patients with CAD, and they were positively correlated with the severity of CAD and negatively correlated with coronary collateral artery formation. PGPC inhibited endothelial cell migration and tube formation. PGPC suppressed neovascularization in Matrigel plugs and reduced blood flow recovery in hindlimb ischemia. In a mouse model of myocardial infarction, PGPC attenuated angiogenesis in the ischemic myocardium. These proangiogenic effects induced by VEGFA (vascular endothelial growth factor A) in ischemic hearts were significantly inhibited by PGPC. Mechanistically, PGPC inhibited the expression of STX17 (syntaxin 17), a crucial molecule that controls autophagosomal–lysosomal fusion by promoting the acetylation and subsequent ubiquitination and degradation of STX17. PGPC upregulated the expression of NPC1 (NPC intracellular cholesterol transporter 1) through CD36 (cluster of differentiation 36). NPC1 not only promoted the acetylation and subsequent ubiquitination and degradation of STX17 through the recruitment of ACAT1 (acetyl-CoA acetyltransferase 1), but also competed with STX17 to bind VAMP8 (vesicle-associated membrane protein 8), leading to inhibition of the expression of eNOS (endothelial nitric oxide synthase), ERK1/2 (extracellular signal-regulated kinase 1/2), and nitric oxide production. Oxidized phospholipid-neutralizing antibody E06, STX17 overexpression, or silencing of NPC1 reversed the inhibitory effect of PGPC on angiogenesis by restoring autophagic flux. CONCLUSIONS: PGPC promotes the acetylation and subsequent ubiquitin-mediated degradation of STX17 by increasing NPC1, leading to a reduction in the level of STX17 associated with VAMP8, which inhibits autophagosomal–lysosomal fusion and angiogenesis. Targeting PGPC, NPC1, or STX17 may represent novel therapeutic approaches to promote angiogenesis in patients with CAD.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"73 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087972","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":"An Elusive Cardiac Mass in a Patient With Previous Malignancy","authors":"Gary Peng,Anju Nohria","doi":"10.1161/circulationaha.126.079603","DOIUrl":"https://doi.org/10.1161/circulationaha.126.079603","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"13 1","pages":"1412-1416"},"PeriodicalIF":37.8,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087974","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}