461. A Novel Hidden Protein p-414aa Encoded by circSETD2(14,15) Inhibits Vascular Remodeling.
作者: 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.
来源: Circulation. 2025年151卷22期1568-1582页
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.
463. Cost-Effectiveness of Aortic Valve Replacement in Low- and Intermediate-Risk Chinese Patients With Severe Aortic Stenosis.
作者: Jin Peng.;Xinglong Zheng.;Minghuan Jiang.;Xuelin Yao.;Yue Ma.;Mao Fu.;Tao Ma.;Xiaolong Shang.;Yang Yan.;Vinod H Thourani.;Yu Fang.
来源: Circ Cardiovasc Qual Outcomes. 2025年18卷4期e010858页
Transcatheter aortic valve replacement (TAVR) remains debated as an alternative to surgical aortic valve replacement (SAVR). We aimed to evaluate the cost-effectiveness of aortic valve replacement strategies in low- and intermediate-risk patients with severe aortic stenosis in China.
465. Correction to: Tadalafil for Treatment of Combined Postcapillary and Precapillary Pulmonary Hypertension in Patients With Heart Failure and Preserved Ejection Fraction: A Randomized Controlled Phase 3 Study.
作者: Marius M Hoeper.;Britta Oerke.;Max Wissmüller.;Hanno Leuchte.;Christian Opitz.;Michael Halank.;Hans-Juergen Seyfarth.;Stephan Baldus.;Johann Bauersachs.;Michael Böhm.;Hossein-Ardeschir Ghofrani.;Stavros Konstantinides.;Karen M Olsson.;Rolf Wachter.;Carolyn S P Lam.;Behnaz Aminossadati.;Stephan Rosenkranz.
来源: Circulation. 2025年151卷11期e763页 466. Correction to: Low Penetrance Sarcomere Variants Contribute to Additive Risk in Hypertrophic Cardiomyopathy.
作者: Joshua K Meisner.;Aaron Renberg.;Eric D Smith.;Yao-Chang Tsan.;Brynn Elder.;Abbey Bullard.;Owen L Merritt.;Sean L Zheng.;Neal K Lakdawala.;Anjali T Owens.;Thomas D Ryan.;Erin M Miller.;Joseph W Rossano.;Kimberly Y Lin.;Brian L Claggett.;Euan A Ashley.;Michelle Michels.;Rachel Lampert.;John C Stendahl.;Dominic Abrams.;Christopher Semsarian.;Victoria N Parikh.;Matthew T Wheeler.;Jodie Ingles.;Iacopo Olivotto.;Sharlene M Day.;Sara Saberi.;Mark W Russell.;Michael Previs.;Carolyn Y Ho.;James S Ware.;Adam S Helms.
来源: Circulation. 2025年151卷11期e762页 472. Risk of Cancer in Newborns With Congenital Heart Disease and Their Mothers: A Nationwide Cohort Study.
作者: Danbee Kang.;Gwang-Jun Choi.;Jihye Heo.;Seung Woo Park.;Juyoung Sung.;Insung Kim.;Taegyun Park.;Juhee Cho.;June Huh.
来源: Circulation. 2025年151卷11期807-809页 474. Withdrawal of Guideline-Directed Medical Therapy in Patients With Heart Failure and Improved Ejection Fraction.
作者: Christian Basile.;Felix Lindberg.;Lina Benson.;Federica Guidetti.;Ulf Dahlström.;Massimo Francesco Piepoli.;Peter Mol.;Raffaele Scorza.;Aldo Pietro Maggioni.;Lars H Lund.;Gianluigi Savarese.
来源: Circulation. 2025年151卷13期931-945页
Limited evidence exists on the prognostic role of continuing medical therapy in patients with heart failure (HF) and an ejection fraction (EF) that has improved over time. This study assessed rates of, patient profiles, and associations with morbidity/mortality of renin-angiotensin inhibitors (RASi), angiotensin receptor-neprilysin inhibitors (ARNi), beta-blockers (BBL), and mineralocorticoid receptor antagonists (MRA) withdrawal in patients with HF with improved EF.
476. Hereditary Transthyretin Cardiac Amyloidosis With the p.V142I Variant: Mechanistic Insights and Diagnostic Challenges.
作者: Simon Vanhentenrijk.;Justin L Grodin.;Silvio Nunes Augusto.;W H Wilson Tang.
来源: Circ Heart Fail. 2025年18卷6期e012469页
The most common form of hereditary transthyretin cardiac amyloidosis (hATTR-CA) in the United States and the United Kingdom is the p.V142I variant. About 3% to 4% of patients with African ancestry carry this genetic predisposition to develop signs and symptoms of hATTR-CA. Nevertheless, clinical manifestations of hATTR-CA appear only late in the fifth and sixth decades of life, despite its clear genetic background. Imbalances in native protein-stabilizing and elementary breakdown cellular mechanisms are postulated as potential causes for affecting transthyretin structural integrity and myocardial fibril deposition. Noncoding variants, epigenetic and environmental factors, as well as gut microbiome derangements may serve as disease-modifying factors that feature detrimental amyloidogenic organ involvement and impact disease severity. Organ amyloid deposition varies widely among different carriers of a genetic transthyretin variant. The genotype-phenotype interdependence causes unpredictable phenotypic penetrance that results in a variety of signs and symptoms and patient outcomes. Cardiovascular biomarkers and multimodality imaging may identify initial amyloidogenic organ involvement. These early clinical clues through the course of hATTR-CA offer a window of opportunity for early treatment onset to cease disease progression and alter prognosis. Identifying at-risk patients requires information on the genetic background of probands and their relatives. Initiatives to reveal asymptomatic gene carriers early in the disease should be encouraged, as it necessitates stringent patient follow-up and immediate treatment onset to reduce the burden of heart failure hospitalization and mortality in hATTR-CA.
477. Differences in Pulmonary Artery Stiffness Measured by CMR in Preterm-Born Young Adults With and Without Bronchopulmonary Dysplasia.
作者: Wouter J van Genuchten.;Jarno J Steenhorst.;Gabrielle M J W van Tussenbroek.;Nikki van der Velde.;Lieke S Kamphuis.;Irwin K M Reiss.;Daphne Merkus.;Willem A Helbing.;Alexander Hirsch.
来源: Circ Cardiovasc Imaging. 2025年18卷4期e017791页
Very preterm-born infants are at risk for developing bronchopulmonary dysplasia (BPD), a chronic lung disease. Nowadays, the majority of these infants reach adulthood. Very preterm-born young adults are at risk for developing pulmonary arterial (PA) hypertension later in life. An early sign of PA hypertension is increased PA stiffness. This study aims to use cardiovascular magnetic resonance to compare PA stiffness using PA relative area change (RAC) and pulse wave velocity (PWV) to identify early signs for PA hypertension in young adults born very premature, with and without BPD.
478. Temporal Trends in Noninvasive and Invasive Cardiac Testing From 2010 to 2022 in the US Medicare Population.
作者: Yosef A Cohen.;Luca Bremner.;Mrinali Shetty.;Michelle Castillo.;Julia Susan Cappell.;Jay S Leb.;Lynne L Johnson.;Andrew J Einstein.
来源: Circ Cardiovasc Imaging. 2025年18卷4期e017567页
Cardiac diagnostic testing continues to evolve, and controversies remain regarding the optimal utilization of different procedures. We sought to evaluate changes in long-term utilization trends for a wide range of cardiac diagnostic tests in the context of advancing technologies and updated guidelines.
479. Direct-to-Consumer Genetic Testing for Cardiovascular Disease: A Scientific Statement From the American Heart Association.
作者: Leland E Hull.;Aaron W Aday.;Quan M Bui.;Jasmine A Luzum.;James M Muchira.;Hannah Wand.;C Anwar A Chahal.;Mina K Chung.;Anne E Kwitek.;Silvana Molossi.;Pradeep Natarajan.; .
来源: Circulation. 2025年151卷14期e905-e917页
Despite insufficient evidence to support direct-to-consumer genetic testing in routine clinical care, cardiovascular clinicians increasingly face questions about its utility and interpretation because individuals can purchase these tests directly from laboratories. A burgeoning marketplace offers an expanding array of testing options. In many cases, direct-to-consumer genetic testing advertises information that could inform one's risk of heritable disease, including insight into having a genetic predisposition to cardiovascular disease or data about gene-drug interactions that could affect response to cardiovascular medications. Navigating clinical questions about direct-to-consumer genetic testing involves understanding the evolution and oversight of the marketplace; the scope of direct-to-consumer genetic testing offerings; and the risks, benefits, and limitations of said testing. In this American Heart Association scientific statement, we summarize the state of the direct-to-consumer genetic testing industry, review types of cardiovascular genetic information that may be included in direct-to-consumer genetic testing, describe approaches to evaluate test quality, and provide resources for clinicians navigating questions about direct-to-consumer genetic testing. If direct-to-consumer genetic test information is used in clinical care, care should be taken to assess the limitations of the test, to contextualize the information specifically to the patient, and to corroborate potentially actionable monogenic findings.
480. PCSK9 Promotes LDLR Degradation by Preventing SNX17-Mediated LDLR Recycling.
作者: YangYang Guan.;Xiaomin Liu.;Zetian Yang.;Xinyu Zhu.;Min Liu.;Mingkun Du.;Xiaowei Pan.;Yan Wang.
来源: Circulation. 2025年151卷21期1512-1526页
Low-density lipoprotein (LDL) is internalized into cells mainly through LDLR (LDL receptor)-mediated endocytosis. In an acidic endosome, LDLR is released from LDL and recycles back to the cell surface, whereas LDL is left in the endosome and degraded in the lysosome. Circulating PCSK9 (proprotein convertase subtilisin/kexin 9) binds with LDLR and is internalized into the endosome, similar to LDL. In an acidic endosome, LDLR fails to disassociate from PCSK9, and both proteins are degraded in the lysosome. PCSK9 inhibitors are widely used for treating hypercholesterolemia. However, how PCSK9 diverts LDLR to the lysosome for degradation remains elusive. Some patients are resistant to PCSK9 inhibitors, for unknown reasons.
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