Circulation最新文献

{"title":"Pulmonary Arterial Hypertension Risk With BCR-ABL Tyrosine Kinase Inhibitors: Refining Risk With Nationwide Data.","authors":"Jonah D Garry,Evan L Brittain","doi":"10.1161/circulationaha.126.079012","DOIUrl":"https://doi.org/10.1161/circulationaha.126.079012","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"7 1","pages":"980-982"},"PeriodicalIF":37.8,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147578069","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 Xu and Sun Regarding Article, \"Subclinical Primary Aldosteronism and Major Adverse Cardiovascular Events: A Longitudinal Population-Based Cohort Study\".","authors":"Jiaqian Xu,Yinghan Sun","doi":"10.1161/circulationaha.125.076781","DOIUrl":"https://doi.org/10.1161/circulationaha.125.076781","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"46 1","pages":"e1052"},"PeriodicalIF":37.8,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147578010","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":"Sotatercept for Combined Post- and Pre-capillary Pulmonary Hypertension Associated With Heart Failure: Results from the Phase 2, Randomized, Placebo-Controlled CADENCE Study.","authors":"Mardi Gomberg-Maitland,Ryan J Tedford,David Langleben,Stephan Rosenkranz,Barry Miller,Aaron D Jones,Alessia Urbinati,Ciaran J McMullan,Alexandra G Cornell,Jean-Luc Vachiery","doi":"10.1161/circulationaha.126.079918","DOIUrl":"https://doi.org/10.1161/circulationaha.126.079918","url":null,"abstract":"BACKGROUNDCombined post- and pre-capillary pulmonary hypertension in heart failure with preserved ejection fraction (CpcPH-HFpEF) involves remodeling in both the heart and pulmonary vasculature. Despite significant mortality, there are no proven therapies.METHODSIn this multicenter, randomized, placebo-controlled, phase 2 trial, adults received sotatercept (0.3 or 0.7 mg/kg) or placebo every 3 weeks. The primary end point was change in pulmonary vascular resistance at week 24. Hodges-Lehmann shift estimates described placebo-adjusted changes.RESULTS164 patients were randomized 54:55:55 to sotatercept 0.3 mg/kg, 0.7 mg/kg, and placebo, and baseline median pulmonary vascular resistance was 5.2 (interquartile range [IQR] 4.0-6.9) Wood units. The median change from baseline in pulmonary vascular resistance at week 24 was -0.67 Wood units in the sotatercept 0.3 mg/kg group, -0.33 Wood units in the sotatercept 0.7 mg/kg group, and 0.26 Wood units in the placebo group. The Hodges-Lehmann shift estimates in pulmonary vascular resistance were -1.02 Wood units (95% CI, -1.81 to -0.23; P=0.004) for 0.3 mg/kg and -0.75 Wood units (95% CI, -1.52 to 0.03; P=0.024) for 0.7 mg/kg sotatercept. Reductions were observed in mean pulmonary arterial pressure (0.3 and 0.7 mg/kg: -9.19 mm Hg [95% CI, -13.00 to -5.38] and -9.22 [95% CI, -12.97 to -5.46]) and pulmonary arterial wedge pressure (0.3 and 0.7 mg/kg: -3.04 mm Hg [95% CI, -5.77 to -0.32] and -2.53 [95% CI, -5.33 to 0.28]). Changes in 6-minute walk distance were 20.3 meters (95% CI, 1.5-39.1) for 0.3 mg/kg and 5.8 meters (95% CI, -17.3 to 28.9) for 0.7 mg/kg sotatercept. The most common adverse events with sotatercept (both groups) were increased hemoglobin and diarrhea.CONCLUSIONSThese findings provide proof of concept for improved pulmonary vascular and cardiac hemodynamics following activin signalling inhibition with sotatercept in patients with CpcPH-HFpEF.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"46 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147536283","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":"Stepping into a New Era - Sotatercept for the Treatment of Cpc-PH from HFpEF.","authors":"Satyam Sarma,Kelly M Chin","doi":"10.1161/circulationaha.126.080191","DOIUrl":"https://doi.org/10.1161/circulationaha.126.080191","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"106 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147536284","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":"Multi-modality Imaging to Determine Underlying Causes of MINOCA in Women and Men.","authors":"Harmony R Reynolds,Akiko Maehara,Bobby Heydari,Nathaniel R Smilowitz,Tara Sedlak,Yader Sandoval,Hayder D Hashim,Kevin R Bainey,Akl C Fahed,Natalia Pinilla Echeverri,Mitsuaki Matsumura,Mobeen Ahmed,Jacqueline Saw,Aun-Yeong Chong,Atul Sharma,Anais Hausvater,Yuhe Xia,Jennifer A Tremmel,Shuangbo Liu,Puja K Mehta,Bryan Har,Sripal Bangalore,Michael Attubato,Lori Vales Lay,Alair Holden,Chang Yu,Judith S Hochman, ","doi":"10.1161/circulationaha.126.080234","DOIUrl":"https://doi.org/10.1161/circulationaha.126.080234","url":null,"abstract":"BACKGROUNDMyocardial infarction with non-obstructive coronary arteries (MINOCA) has several underlying causes, including mimicking conditions in some cases. Imaging is recommended to identify MINOCA etiologies, but it remains unclear which patients are most likely to have abnormal findings. We characterized MINOCA mechanisms, analyzed predictors of imaging abnormalities and explored sex differences.METHODSWe enrolled patients with clinical diagnosis of MI in an international, prospective, diagnostic study at 28 sites in US, Canada and UK. After a women-only phase, we included both sexes. Individuals with ≥50% diameter stenosis or coronary dissection on angiography, or alternate causes for the clinical presentation, were excluded. Participants had multi-vessel coronary optical coherence tomography (OCT) during index coronary angiography and cardiac magnetic resonance imaging (CMR) within one week. Independent core laboratories interpreted imaging, blinded to other results.RESULTSAmong 754 patients enrolled, 389 had MINOCA and 336 with MINOCA underwent OCT (270 women and 66 men); CMR was completed in 284 (85%). An OCT-defined culprit lesion was identified in 45% (116/270 women [43% ] and 35/66 men [53%], p=0.18). CMR demonstrated an ischemic pattern in 114/284 (40%), similar by sex (96/225 women [43%] vs. 18/59 men [31%], p=0.12). A non-ischemic pattern was observed in 23% (23% of women, 25% of men, p=0.78). We identified a cause of the clinical presentation in 79% of patients with both tests completed: 59% had an ischemic cause of MINOCA and 20% had a non-ischemic mimicking condition. OCT alone found a MINOCA etiology in 151/336 (45%) and CMR alone in 180/284 (63%). Predictors of an OCT culprit lesion included age, abnormal angiogram, and number of vessels imaged, but 27% of normal angiograms harbored a culprit lesion. Predictors of abnormal CMR were peak troponin, shorter time to CMR, and non-Asian race, but CMR was abnormal in 40% when troponin was <4-fold above the upper reference limit.CONCLUSIONSThe combination of multi-vessel coronary OCT and CMR in patients with a clinical diagnosis of MINOCA confirmed MI in 59% and identified an alternate cause (MINOCA mimic) in 20%. Clinical factors had limited utility to predict imaging abnormalities. No sex differences in imaging results were detected.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"16 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147535691","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":"Automated Echocardiographic Detection of Congenital Heart Disease Using Artificial Intelligence.","authors":"Platon Lukyanenko,Sunil Ghelani,Yuting Yang,Bohan Jiang,Timothy Miller,David Harrild,Nao Sasaki,Francesca Sperotto,Danielle Sganga,John Triedman,Andrew Powell,Tal Geva,William G La Cava,Joshua Mayourian","doi":"10.1161/circulationaha.126.079781","DOIUrl":"https://doi.org/10.1161/circulationaha.126.079781","url":null,"abstract":"BACKGROUNDDelayed or missed diagnosis of congenital heart disease (CHD) contributes to excess pediatric mortality worldwide. Echocardiography (echo) is central to diagnosing and triaging CHD, yet expert interpretation remains a scarce and maldistributed global resource. Artificial intelligence (AI) offers the potential to democratize diagnostics and extend expert-level interpretation beyond large academic centers, but its application in CHD remains underexplored.METHODSWe developed EchoFocus-CHD, an AI-enabled model for automated detection of 12 critical and 8 non-critical CHD lesions, individually and as composites. The composite critical CHD outcome was the primary endpoint. The model expands on a multi-task, view-agnostic architecture (PanEcho) with a transformer encoder to improve focus on relevant echo views. The model was internally trained (80%) and tested (20%) on the first echo per patient from Boston Children's Hospital (BCH), with further evaluation on a referral cohort of echo studies performed at external US and international centers.RESULTSThe internal and referral cohorts included 3.4 million videos from 54,727 echos (median age at echo 7.1 [IQR, 0.2-15.0] years; 5.8% critical CHD; 23.6% non-critical CHD) and 167,484 videos from 3,356 echos (median age at echo 2.5 [IQR, 0.3-9.4] years; 29.4% critical CHD; 45.6% non-critical CHD), respectively. EchoFocus-CHD showed excellent internal ability to detect the composite critical CHD outcome (AUROC 0.94, LR+ 7.50, LR- 0.14) and individual critical lesions (AUROC 0.83-1.00), as well as composite non-critical CHD (AUROC 0.90, LR+ 5.00, LR- 0.23) and individual non-critical lesions (AUROC 0.70-0.96). Performance declined during evaluation on the referral cohort to detect critical CHD (AUROC 0.77), coinciding with greater expert disagreement on referral cases (k=0.72 versus 0.82 for internal cases). Explainability analyses demonstrated that the model prioritized the same clinically relevant views (parasternal long-axis, parasternal short-axis, subxiphoid long-axis, apical) across internal and referral cohorts, while UMAP analysis revealed a domain shift between cohorts. Retraining on all available US patients attenuated domain shift effects, improving international critical CHD detection (AUROC 0.87) and calibration.CONCLUSIONSEchoFocus-CHD shows promise for automated CHD detection to advance equitable global cardiovascular care, and highlights the need to address domain shift and establish external validation prior to real-world deployment.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"30 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147535692","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":"Recovery From Heart Failure: Microvascular Mechanisms.","authors":"Shuang Li, Krishan Gupta, Rajul K Ranka, Alexander J Lu, Felix Naegele, Michael Graber, Kaylee N Carter, Lili Zhang, Arvind Bhimaraj, Li Lai, Anahita Mojiri, Keith A Youker, Kaifu Chen, John P Cooke","doi":"10.1161/CIRCULATIONAHA.125.078996","DOIUrl":"10.1161/CIRCULATIONAHA.125.078996","url":null,"abstract":"<p><strong>Background: </strong>Heart failure (HF) is a significant global health problem. Left ventricular assist device (LVAD) implantation serves as a bridge for patients awaiting heart transplantation. Intriguingly, LVAD support often improves cardiac histology and function, sometimes enough to avoid transplantation after LVAD removal. However, the cellular programs underlying this recovery remain unclear.</p><p><strong>Methods: </strong>Myocardial tissues were obtained from patients with HF at the time of LVAD implantation (pre LVAD) and explantation (post LVAD) for histological analysis and single-nucleus RNA sequencing. A murine model of HF recovery, combined with lineage tracing studies, was employed to define cellular sources of vascular repair. Cardiac function, fibrosis, and vascular density were assessed using echocardiography, histology, and fluorescent microsphere perfusion. A patient-derived cardiac nonmyocyte culture system was established to interrogate mechanisms of cell fate regulation.</p><p><strong>Results: </strong>Post-LVAD myocardial tissues exhibited reduced fibrosis and increased capillary density compared with pre-LVAD samples. Across samples, fibroblast abundance was inversely correlated with endothelial cell abundance, consistent with enhanced angiogenesis during recovery. Single-nucleus RNA sequencing identified a fibroblast subset predisposed to undergo mesenchymal-to-endothelial transition, acquiring an endothelial cell identity. Additionally, nonmyocytes from pre-LVAD hearts proliferated poorly and failed to form vascular structures, whereas nonmyocytes from post-LVAD hearts displayed greater proliferation and angiogenesis capacity, forming vessel-like structures, reinforcing the association of HF recovery with angiogenic reprogramming. Mechanistically, knockdown of c-Myc by siRNA shifted post-LVAD nonmyocytes to a pre-LVAD-like state, while c-Myc overexpression by mRNA in pre-LVAD cells induced a post-LVAD-like phenotype, implicating c-Myc as 1 contributor to this fate switch. A model of HF recovery in mice mimicked the histological and functional changes in patients, with physiological evidence of increased microvascular perfusion, associated with a fibroblast-to-endothelial transition, documented by lineage tracing.</p><p><strong>Conclusions: </strong>HF recovery involves reduced fibrosis and enhanced microvascularization, partly driven by fibroblast-to-endothelial cell fate transition. c-Myc functions as 1 regulator of this transition, offering a mechanistic entry point to develop regenerative therapies in HF.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":38.6,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509193","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":"PAM-VT 2 Study: Long-Term Scar Evolution and Ablation Lesion Assessment by Late Gadolinium Enhancement Cardiac Magnetic Resonance After Ventricular Tachycardia Ablation.","authors":"Ivo Roca-Luque, Paz Garre, Sara Vázquez-Calvo, José Tomás Ortiz-Pérez, Susana Prat-González, Rosario Jesús Perea, Pasquale Valerio Falzone, Jean-Baptiste Guichard, Mariona Regany-Closa, Till F Althoff, Eduard Guasch, Jose María Tolosana, Elena Arbelo, Paula Sánchez-Somonte, Levio Quinto, Roger Borràs, Rebeca Domingo, Mireia Niebla, Ana García-Alvarez, Marta Sitges, Josep Brugada, Lluís Mont, Andreu Porta-Sánchez","doi":"10.1161/CIRCULATIONAHA.125.074748","DOIUrl":"10.1161/CIRCULATIONAHA.125.074748","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) is useful for identifying ventricular tachycardia (VT) substrate in patients with structural heart disease. While preprocedural LGE-CMR is widely used for planning, the role of postprocedural LGE-CMR in evaluating VT ablation success and long-term scar evolution has been less explored. This study aimed to prospectively and systematically assess the long-term evolution of scar and ablation lesions using serial postablation LGE-CMR with long-term follow-up.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;This prospective study included 51 patients (mean age, 65.2±9.8 years; men, 95.8%; ischemic heart disease, 83%; left ventricular ejection fraction, 34.5±10.4%) undergoing their first substrate-based VT ablation between March 2019 and July 2020. Preprocedural LGE-CMR and 2 postprocedural scans at 3 to 6 months (CMR-1) and 18 to 24 months (CMR-2) were performed. Scar characteristics, including core scar, border zone, and conducting channels, were analyzed. VT recurrence was monitored, and factors associated with recurrence were evaluated using a Cox proportional hazards model. A Kaplan-Meier curve was used to represent the VT-free survival function.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Core scar mass increased significantly from baseline to CMR-1 (12.2±1.5 to 19.8±1.6 g, &lt;i&gt;P&lt;/i&gt;&lt;0.01) and remained stable at CMR-2. In contrast, the border zone decreased significantly over time (pre, 25.3±1.8 g; CMR-1, 20.8±2.0 g; CMR-2, 16.7±2.1 g; &lt;i&gt;P&lt;/i&gt;&lt;0.01). A significant decrease in conducting channels was noted after ablation and persisted at CMR-2 (pre, mean 2.4±0.2/median 2 [interquartile range, 1-3]; CMR-1, mean 1.4±0.2/median 1 [interquartile range, 0-1]; CMR-2, mean 1.6±1.0/median 1 [interquartile range, 0-1]; &lt;i&gt;P&lt;/i&gt;&lt;0.001). VT recurrence occurred in 29.4% of patients during a median follow-up of 3.1 years. The number of conducting channels at CMR-1 and their relative reduction from baseline were related to VT recurrence. The persistence of 2 or more conducting channels at CMR-1 was associated with a higher recurrence rate: 75.6 versus 19.5% (hazard ratio [HR]; 4.1; 95% CI, 2.4-12.1; &lt;i&gt;P&lt;/i&gt;=0.012). Evidence of favorable left ventricular remodeling was observed, with a significant reduction in left ventricular volume at CMR-2 (131.8±8.6 mL; CMR-1, 156.7±8.1 mL and 160.8±7.6 mL at baseline &lt;0.01).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;Postablation LGE-CMR reveals durable changes in scar characteristics, with early scar evaluation at 3 to 6 months strongly associated with long-term VT recurrence. The reduction in scar heterogeneity and conducting channels is sustained over time, underscoring the usefulness of LGE-CMR for assessing ablation success. Additionally, VT ablation appeared to be associated with favorable reverse remodeling, highlighting potential benefits beyond arrhythmia control. These findings support the use of LGE-CMR for personalized management following VT ablatio","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"874-886"},"PeriodicalIF":38.6,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147324820","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":"CCR8 Expression on Regulatory T Cells Reveals Trajectories of Tissue Adaptation and Protects Against Myocardial Infarction-Induced Tissue Damage.","authors":"Nana Li, Zhiheng Hao, Haoyi Yang, Jie Cai, Meilin Liu, Junyi He, Rui Gao, Yuhan Shen, Zhehao Chen, Yuzhi Lu, Tingting Tang, Min Zhang, Jiao Jiao, Fen Yang, Jingyong Li, Muyang Gu, Desheng Hu, Weimin Wang, Qing Wang, Chen Chen, Zhilei Shan, Ni Xia, Xiang Cheng","doi":"10.1161/CIRCULATIONAHA.125.076426","DOIUrl":"10.1161/CIRCULATIONAHA.125.076426","url":null,"abstract":"<p><strong>Background: </strong>Tissue-specific regulatory T cells (Tregs) accumulate in the heart after myocardial infarction (MI) and play a vital role in limiting inflammation and promoting tissue repair. However, the developmental trajectory of heart Tregs and the molecular cues that guide their recruitment to the heart remain poorly understood, impeding therapeutic strategies that leverage Treg-mediated cardiac protection.</p><p><strong>Methods: </strong>We used single-cell and bulk RNA sequencing in a murine MI model to delineate the differentiation trajectory of Tregs from mediastinal lymph nodes to the heart. Functional validation was performed using Treg-specific <i>Ccr8</i> (CC motif chemokine receptor 8) knockout mice (<i>Ccr8</i>^flox/flox<i>Foxp3</i>^Cre), <i>Ccl1</i> (CC motif chemokine ligand 1) knockout mice (<i>Ccl1</i>^-/-), macrophage-targeted <i>Ccl1</i> knockdown mice, <i>Ccl1</i>-overexpressing mice, and DEREG mice. The CCL1-CCR8 axis was evaluated in cardiac tissues and circulating blood from patients with MI.</p><p><strong>Results: </strong>Single-cell RNA sequencing revealed a stepwise differentiation of mediastinal lymph node-derived naive Tregs into heart Tregs, marked by the progressive acquisition of CCR8 expression and reparative capacity. CCR8⁺ Tregs in the heart exhibited enhanced immunosuppressive and tissue-repair signatures. Treg-specific <i>Ccr8</i> deletion led to reduced Treg accumulation and worsened cardiac function after MI, along with increased proinflammatory macrophage features and number of CD8⁺ T cells and natural killer cells. In addition, Tregs promoted a shift of macrophages toward an anti-inflammatory phenotype by secreting IL-1R2 (interleukin 1 receptor, type 2). We identified cardiac macrophages as the main source of CCL1, which was essential for CCR8⁺ Treg recruitment. <i>Ccl1</i> deficiency or macrophage-specific <i>Ccl1</i> knockdown impaired Treg infiltration and aggravated ventricular remodeling; <i>Ccl1</i> overexpression promoted Treg recruitment and improved cardiac outcomes. Moreover, the cardioprotective effects of CCL1 were abolished in DEREG mice upon Treg depletion and <i>Ccr8</i>^flox/flox<i>Foxp3</i>^Cre mice, establishing a CCR8⁺ Treg-dependent mechanism. Furthermore, circulating CCR8⁺ Tregs and cardiac CCL1 were elevated in humans with MI, and the presence of CCR8⁺ Tregs and CCL1-expressing macrophages was confirmed in the hearts of patients with MI, suggesting important clinical relevance.</p><p><strong>Conclusions: </strong>Our findings reveal a 2-phase Treg specialization process and establish the CCL1-CCR8 axis as a crucial pathway for Treg recruitment and function in the infarcted heart. Therapeutic targeting of this axis may improve immune-regulated cardiac repair after MI.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"922-940"},"PeriodicalIF":38.6,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146178163","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":"2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.","authors":"Mark A Creager, Geoffrey D Barnes, Jay Giri, Debabrata Mukherjee, William Schuyler Jones, Allison E Burnett, Teresa Carman, Ana I Casanegra, Lana A Castellucci, Sherrell M Clark, Mary Cushman, Kerstin de Wit, Jennifer M Eaves, Margaret C Fang, Joshua B Goldberg, Stanislav Henkin, Hillary Johnston-Cox, Sabeeda Kadavath, Daniella Kadian-Dodov, William Brent Keeling, Andrew J P Klein, Jun Li, Michael C McDaniel, Lisa K Moores, Gregory Piazza, Karen S Prenger, Steven C Pugliese, Mona Ranade, Rachel P Rosovsky, Farla Russo, Eric A Secemsky, Akhilesh K Sista, Leben Tefera, Ido Weinberg, Lauren M Westafer, Michael N Young","doi":"10.1161/CIR.0000000000001415","DOIUrl":"10.1161/CIR.0000000000001415","url":null,"abstract":"<p><strong>Aim: </strong>The \"2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults\" is a de novo guideline that provides comprehensive recommendations for the evaluation, management, and follow-up of adult patients (≥18 years of age) with acute pulmonary embolism (PE). A key feature of this guideline is the introduction of the AHA/ACC Acute Pulmonary Embolism Clinical Categories, which enhance the precision of severity classification, prognosis assessment, and evidence-based therapeutic decision-making.</p><p><strong>Methods: </strong>A comprehensive literature search was conducted from February 2024 to October 2024 to identify clinical studies, reviews, and other evidence conducted on human subjects that were published in English from MEDLINE (through PubMed), EMBASE, the Cochrane Library, Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline. Select key studies published until April 2025 were added by the guideline writing committee as appropriate.</p><p><strong>Structure: </strong>The focus of this clinical practice guideline is an evidence-based and patient-centered approach for acute PE evaluation and management of the adult patient. This guideline encompasses the period from the onset of symptoms through clinical follow-up, focusing on risk outcomes assessment, clinical diagnosis of acute PE, appropriate use of adjunctive cardiovascular testing, and management in both the acute and early post-acute phases of PE. It addresses evidence-based diagnostic and management strategies (including pharmacological therapies, advanced interventional therapies, and in-hospital support) for acute PE and associated outcomes.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"e977-e1051"},"PeriodicalIF":38.6,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225720","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}