Circulation最新文献

{"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":"https://doi.org/10.1161/CIRCULATIONAHA.126.081464","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-09-03","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":"Clinical Considerations for the Care of the Tactical Athlete With Cardiovascular Abnormalities: A Scientific Statement From the American College of Cardiology and the American Heart Association.","authors":"Elizabeth H Dineen, Mark C Haigney, Benjamin D Levine, Michael J Ackerman, Aaron L Baggish, Travis C Batts, Alan C Braverman, Eugene H Chung, Geoffrey J Cole, William K Cornwell, Eddie Davenport, Peter N Dean, Harry C Dietz, Alexander Eastman, Marc Alaric Franzos, J Sawalla Guseh, Travis E Harrell, Edward A Hulten, Cynthia A James, Jonathan H Kim, Rachel J Lampert, Matthew W Martinez, Joseph W May, Francis G O'Connor, Bradley J Petek, Ankit B Shah, Denise L Smith, Paul D Thompson, Meagan M Wasfy, James A Watts","doi":"10.1161/CIR.0000000000001476","DOIUrl":"https://doi.org/10.1161/CIR.0000000000001476","url":null,"abstract":"<p><strong>Aim: </strong>The American College of Cardiology/American Heart Association Scientific Statement, \"Clinical Considerations for the Care of the Tactical Athlete With Cardiovascular Abnormalities,\" was written to provide guidance and education for clinicians caring for the tactical athlete (ie, firefighters, law enforcement officers, military) with cardiovascular disease or risk for cardiovascular disease, and for the organizations overseeing the care and wellness of these athletes. The considerations are shaped by the interaction between occupational demands and fit for full duty assessments, including risk discussions about how a cardiovascular event in a tactical athlete could impact teammates' well-being, community safety, and overall mission success.</p><p><strong>Methods: </strong>This scientific statement is organized into 11 sections focused on cardiovascular disease processes and other topics that are relevant when considering the potential risks and benefits of performing tasks specific to the tactical athlete. Task forces, comprised of experts in tactical athlete domains, sports cardiology, and the respective topics covered, were assigned to each section, and specific \"Clinical Considerations Tables\" for clinicians to reference were prepared. Comprehensive literature reviews and an emphasis on tactical athlete-focused data, as available, were integral in the writing of all clinical considerations presented. The framework mirrors that of the recently published, \"Clinical Considerations for Competitive Sports Participation for Athletes With Cardiovascular Abnormalities: A Scientific Statement From the American Heart Association and American College of Cardiology.\"</p><p><strong>Structure: </strong>The specific sections in this document include: Section 1: Tactical Tasks Classification; Section 2: The Tactical Athlete Preparticipation Cardiac Evaluation; Section 3: Ethical and Legal Aspects of Tactical Clinical Management; Section 4: Genetic Cardiomyopathies; Section 5: Myocarditis and Other Acquired Cardiac Conditions; Section 6: Congenital Heart Disease; Section 7: Aortopathy, Bicuspid Aortic Valve, and Spontaneous Coronary Artery Dissection; Section 8: Syncope, SCA, Arrhythmias, and Devices; Section 9: Cardiac Channelopathies; Section 10: Older Tactical Athlete; Section 11: Environmental Exposures, PED/S, and Additional Cardiac Conditions and Considerations. Each section provides a summary detailing the rationale for key clinical considerations and the respective Clinical Considerations Table(s).</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886558","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":"Vacuolar H⁺-ATPase Preserves Cardiolipin Homeostasis Through the Lysosomal-Mitochondrial Axis to Restrain Cardiac Aging.","authors":"Hongtao Tie, Mengqian Hou, Yumeng Li, Min Pan, Dietbert Neumann, Ruimin Liu, Jun Zhang, Martijn F Hoes, Miranda Nabben, Jan F C Glatz, Xi Li, Xin Wu, Joost J F P Luiken, Shujin Wang","doi":"10.1161/CIRCULATIONAHA.125.078376","DOIUrl":"10.1161/CIRCULATIONAHA.125.078376","url":null,"abstract":"<p><strong>Background: </strong>Cardiac aging involves progressive mitochondrial dysfunction, contributing to heart failure. Cardiolipin (CL), essential for mitochondrial function, is increasingly depleted in aging cardiomyocytes, promoting mitochondrial decline. Lysosomal degradation relies on v-ATPase (vacuolar-type H+-ATPase)-mediated acidification, and although lysosomes regulate phospholipid metabolism, their roles in CL homeostasis during aging remains unclear. This study examines whether v-ATPase dysfunction drives age-related cardiac changes by disrupting CL metabolism and mitochondrial function.</p><p><strong>Methods: </strong>To investigate underlying mechanisms and causality, we use RNA sequencing, targeted lipidomics, immunofluorescence microscopy, co-immunoprecipitation, proximity ligation assays, subcellular fractionation, mitochondrial respiration analysis and echocardiography, a cardiolipin synthase-1 (<i>Crsl1</i>) knockout mouse model, and 2 v-ATPase knockout models. In addition, we assess whether a nutraceutical intervention targeting v-ATPase dysfunction can mitigate heart failure in aging mouse models and elderly people.</p><p><strong>Results: </strong>Our present findings reveal a sequence of events driving age-related cardiomyopathy: declining cardiac nicotinamide adenine dinucleotide levels impair v-ATPase-mediated lysosomal acidification by weakening the interaction between nicotinamide adenine dinucleotide-dependent glycolytic enzyme aldolase and v-ATPase. This disruption increases lysosomal membrane permeability by reducing lysosomal acidification, allowing cathepsin B to leak into mitochondria. There, cathepsin B disrupts mitochondrial CRLS1 (cardiolipin synthase I), impairing CL synthesis and remodeling. The resulting CL deficiency causes mitochondrial oxidative stress and programmed cell death, leading to mitochondrial and cardiac dysfunction. Genetic or chemical inhibition of v-ATPase and of CRLS1 in mouse models reproduce these age-related defects, highlighting their central roles in cardiac aging. Restoring nicotinamide adenine dinucleotide levels rescues lysosomal acidification and CL metabolism, protecting against age-related cardiomyopathy in rodents and humans.</p><p><strong>Conclusions: </strong>Augmenting v-ATPase-mediated lysosomal acidification offers novel therapeutic strategies to combat age-related cardiomyopathy by rewiring CL homeostasis.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"835-858"},"PeriodicalIF":41.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148263691","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 Multitask Deep Learning Model for Pediatric Echocardiography Analysis: Promises and Limitations.","authors":"John Simpson, Franz Gerald Greil","doi":"10.1161/CIRCULATIONAHA.126.081606","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.081606","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 9","pages":"801-804"},"PeriodicalIF":41.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863800","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":"Inhibition of Programmed Cell Death-1 in Cytotoxic CD8⁺ T Cells Exacerbates Pressure Overload-Induced Cardiac Injury.","authors":"Ming-Ming Wu, Yu Sun, Yue Zhang, Yan-Chao Yang, Zhi-Xi He, Shuang Zhou, Xia Wang, Han Xiao, Miao Yu, Chang Miao, Bo-Wen Zhang, Xiao-Long Liu, Jie-Yu Chang, Di Zhu, Zi Hong, Mei Zhang, Hao-Tian Xu, Xin Bi, Song-Qi Han, Jian-Jun Mao, Jing Shi, Chen Liang, Qiu-Shi Wang, Qun Shao, Jun Zhang, Chang-Jiang Yu, Jian-Yu Liu, Xin-Hao Han, Tong Liu, Hai-Xia Liu, Lu-Yang Yu, Hai-Bo Jia, Yong Ji, Zhen-Wei Pan, Yue Li, Zhi-Ren Zhang","doi":"10.1161/CIRCULATIONAHA.125.074024","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.125.074024","url":null,"abstract":"<p><strong>Background: </strong>The use of anti-programmed cell death-1 (PD-1) antibody increases heart failure (HF) risk in patients with cancer with preexisting cardiovascular conditions. However, the underlying mechanism remains incompletely understood.</p><p><strong>Methods: </strong>To evaluate the effects of anti-PD-1 antibody on transverse aortic constriction (TAC)-induced cardiac remodeling and HF, anti-PD-1 antibody-treated mice; T cell-, myeloid-, and CD8⁺ T cell-specific <i>Pdcd1</i> knockout; C-X-C motif chemokine receptor 3 (<i>Cxcr3</i>) knockout; and granzyme B (<i>Gzmb</i>) knockout mice combined with flow cytometry, Western blotting, immunofluorescence staining, pharmacological approaches, and bulk RNA-sequencing analyses were used.</p><p><strong>Results: </strong>Administration of anti-PD-1 antibody, T cell-, or CD8⁺ T cell-specific <i>Pdcd1</i> deletion, but not myeloid-specific <i>Pdcd1</i> knockout, aggravated TAC-induced cardiomyopathy and HF in mice. Mechanistically, PD-1 blockade or deletion increased myocardial infiltration of CXCR3⁺ CD8⁺ T cells, leading to granzyme B/perforin-mediated impairment of cardiomyocyte mitochondrial complex I to exacerbate TAC-induced cardiac injury and HF. TAC-enhanced chemotaxis, between cardiac fibroblast-derived CXCL9/CXCL10 and CXCR3⁺ CD8⁺ T cells, was a driving force for recruiting CXCR3⁺ CD8⁺ T cells under the conditions of PD-1 blockade or deletion. The worsened TAC-induced cardiomyopathy caused by anti-PD-1 antibody or T cell-specific <i>Pdcd1</i> deletion was rescued by genetic deletion or pharmacological blockade of granzyme B and CXCR3.</p><p><strong>Conclusions: </strong>Anti-PD-1 antibody enhances myocardial infiltration of CXCR3⁺ CD8⁺ T cells under TAC condition through CXCL9/CXCL10-mediated chemotaxis. The increased granzyme B and perforin likely derived from CD8⁺ T cells impair function of mitochondrial respiratory chain complexes to cause cardiomyocyte apoptosis, thereby exacerbating TAC-induced cardiomyopathy and HF. CXCL9/CXCL10-CXCR3⁺ CD8⁺ T cell axis may represent a promising target for combating anti-PD-1 antibody-associated cardiotoxicity.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863770","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 Pediatric Pulmonary Hypertension International Risk Score: A Prediction Model for Outcomes Using Machine Learning.","authors":"Megan Griffiths, Bhargava K Chinni, Chantal Lokhorst, Johannes M Douwes, Lynn A Sleeper, Jennifer Tingo, Steven H Abman, Erika B Rosenzweig, Jennifer E Schramm, Eric D Austin, Mary P Mullen, Alba Torrent-Vernetta, Carlos Labrandero, Raymond Benza, Maria Jesus Del Cerro, Rolf M F Berger, Cedric Manlhiot, Allen D Everett","doi":"10.1161/CIRCULATIONAHA.125.077391","DOIUrl":"10.1161/CIRCULATIONAHA.125.077391","url":null,"abstract":"<p><strong>Background: </strong>Risk prediction is fundamental to pulmonary hypertension (PH) guideline-based care, yet pediatric-specific risk prediction models remain limited, relying primarily on single predictors, expert opinion, or application of adult models to children. The authors developed and externally validated a data-driven 1-year risk prediction model for pediatric PH.</p><p><strong>Methods: </strong>Pediatric patients with PH (n=345; World Symposium on Pulmonary Hypertension groups 1 and 3) enrolled in the Pediatric Pulmonary Hypertension Network Registry (2014-2020; 50.4% male; median age, 4.9 years [interquartile range, 1.9-10.3]) were split into training (80%) and test cohorts (20%). The Dutch National Registry for Pulmonary Hypertension in Childhood (n=155 [1993-2020]) and the Spanish Registry of Pediatric Pulmonary Hypertension (n=327 [2009-2023]) were used for external validation. From 176 variables, BorutaSHAP feature selection with random forest identified 16 predictors for a 1-year outcome of time to death, transplant, Potts shunt, or atrial septostomy, modeled using extreme gradient boosting. Performance was assessed with the area under the receiver operating characteristic curve, confusion matrices, calibration, and Kaplan-Meier event-free survival.</p><p><strong>Results: </strong>The final model achieved an area under the receiver operating characteristic curve of 0.90 (0.79-0.97) and 99% (96%-99%) negative predictive value in testing, dividing participants into 3 groups with strong outcome discrimination. External validation showed an area under the receiver operating characteristic curve of 0.76 (Dutch National Registry for Pulmonary Hypertension in Childhood, 0.70-0.81) and 0.77 (Spanish Registry of Pediatric Pulmonary Hypertension, 0.73-0.82) with negative predictive values of 93% (93%-97%) and 96% (93%-97%), respectively. Kaplan-Meier analysis significantly differentiated outcomes by risk group.</p><p><strong>Conclusions: </strong>This multicenter, validated model provides good 1-year risk prediction in pediatric PH across World Symposium on Pulmonary Hypertension groups 1 and 3, providing a robust tool for clinical risk stratification to guide therapy and addressing a gap in pediatric PH care.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"805-818"},"PeriodicalIF":41.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705244","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":"LDLR Variant Classification Through Activity-Normalized Prime Editing Screening.","authors":"Phillip J Zhou, Minja Velimirovic, Tian Yu, Vojislav Gligorovski, Nicolas Mathis, Jing Zhao, Quang Vinh Phan, Felicitas Vogd, Jayoung Ryu, Qisheng Pan, Atharva Tyagi, David B Ascher, Gerald Schwank, Luca Pinello, Christopher A Cassa, Richard I Sherwood","doi":"10.1161/CIRCULATIONAHA.125.078585","DOIUrl":"10.1161/CIRCULATIONAHA.125.078585","url":null,"abstract":"<p><strong>Background: </strong>Inherited variants in the LDL (low-density lipoprotein) receptor (<i>LDLR</i>) gene are the most common cause of familial hypercholesterolemia, significantly increasing coronary artery disease risk. Early identification of pathogenic <i>LDLR</i> variants enables prompt lipid-lowering therapy and cascade testing of at-risk relatives; however, most <i>LDLR</i> variants observed in the population have uncertain or absent clinical classifications, leaving many patients without actionable information.</p><p><strong>Methods: </strong>We developed the first activity-normalized prime editing screening pipeline to measure the impact of 5184 <i>LDLR</i> coding variants on LDL-cholesterol (LDL-C) uptake. Each prime editing guide RNA is paired with a genotypic outcome reporter to correct for variable editing efficiency, overcoming a key limitation of previous pooled genome editing screens. A statistical framework further improves variant effect estimates by jointly analyzing all missense variants at each amino acid position.</p><p><strong>Results: </strong>We show that prime editing of the reporter construct correlates with endogenous variant installation frequency, validating the activity normalization approach. The resulting scores capture a continuous spectrum of functional effects, robustly separate pathogenic versus benign ClinVar variants, and show concordance with LDL-C levels in UK Biobank participants. We calibrate functional evidence strengths to the ACMG/AMP variant interpretation framework, enabling integration into a clinical variant classification workflow. By combining functional, computational, population, and contextual evidence, 322 of 434 <i>LDLR</i> variants currently classified as variants of uncertain significance, conflicting, or absent from ClinVar appear to meet evidence thresholds for reclassification and can be prioritized for expert review, substantially expanding the pool of actionable variant classifications. The screen also reveals a cluster of gain-of-function variants in LDLR class A repeat 5, at least some of which enhance LDL-C uptake through increased apolipoprotein B interaction, with implications for therapeutic genome editing. Last, prime editing uniquely detects splice-altering coding variants missed by cDNA-based screens and pathogenicity predictors, revealing an advantage of endogenous variant installation.</p><p><strong>Conclusions: </strong>Altogether, activity-normalized prime editing provides a scalable framework for <i>LDLR</i> variant classification that substantially expands the proportion of variants with evidence for genetic diagnosis and reveals novel biology with therapeutic relevance.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":41.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13536972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863834","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":"Galectin-3 Regulates Smooth Muscle Contraction and Blood Pressure by Modulating Ca_V1.2 Channel Function.","authors":"Kelvin Wei Zhern Loh, Yanruo Zhou, Cong Liu, Jing Zhai, Chaitanya K Jaladanki, Cheryl Jia Yi Neo, Dejie Yu, Mui Cheng Liang, Mengxia Shen, Hao Fan, Ping Liao, Zhenyu Hu, Tuck Wah Soong","doi":"10.1161/CIRCULATIONAHA.126.080022","DOIUrl":"10.1161/CIRCULATIONAHA.126.080022","url":null,"abstract":"<p><strong>Background: </strong>Fine-tuning of Ca_V1.2 calcium channel activity by binding proteins represents a novel mechanism for regulating smooth muscle contraction and blood pressure (BP). This study aimed to elucidate the role of Gal-3 (galectin-3), a newly identified Ca_V1.2-binding protein, in the pathogenesis of hypertension.</p><p><strong>Methods: </strong>In vitro, ex vivo, and in vivo experiments involving molecular and biochemical assays, in silico prediction, patch-clamp electrophysiologic recordings, immunohistochemistry, pressure myography, and tail-cuff BP measurements were used to evaluate the molecular mechanisms by which Gal-3 binds to and elevates membrane insertion of Ca_V1.2 channels. The experiments were performed in transfected HEK 293 cells, isolated smooth muscle cells, and arteries from smooth muscle-specific Gal-3 knockout mice and their wild-type littermates; spontaneously hypertensive rats; or human patients. In vivo experiments involving delivery of the blocking iGal3BP (inhibitory galectin-3-binding peptide) into spontaneously hypertensive rats were performed to investigate its effect on BP.</p><p><strong>Results: </strong>We identified Gal-3 as a novel binding partner and unexpected positive modulator of the Ca_V1.2 channel through binding to the intracellular II-III loop. Gal-3 increased total and surface expression, current density, and open probability of Ca_V1.2 channels. Both Ca_V1.2 and Gal-3 were upregulated in hypertensive rat aortas and human pulmonary arteries. Conditional deletion of Gal-3 in smooth muscle markedly lowered Ca_V1.2 protein and BP in mice. With specific binding sites identified within both Gal-3 and the Ca_V1.2 II-III loop, the peptide iGal3BP, designed to block Ca_V1.2-Gal-3 interaction, significantly reduced BP in spontaneously hypertensive rats by decreasing Ca_V1.2 protein expression. Repeated iGal3BP administration resulted in cumulative peptide accumulation in mesenteric arteries and produced a sustained reduction in BP, which demonstrated greater long-lasting antihypertensive efficacy compared with amlodipine and losartan. Administration of iGal3BP in combination with a negative modulatory Gal-1 mimetic peptide that mimics Gal-1-Ca_V1.2 interaction returned systolic BP to normotensive levels within 4 hours and lowered BP in hypertensive rats in a sustained manner for 35 days.</p><p><strong>Conclusions: </strong>These results provide strong evidence that Gal-based Ca_V1.2 channel modulators are novel therapeutic pathways for normalizing BP.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"819-834"},"PeriodicalIF":41.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148249565","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":"Searching for the Uncommon: The Future of Population Science in Cardiovascular Disease.","authors":"Mercedes R Carnethon","doi":"10.1161/CIRCULATIONAHA.126.080228","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.080228","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 9","pages":"787-788"},"PeriodicalIF":41.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863863","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":"Left Circumflex Coronary-Pulmonary Arterial Collaterals in Chronic Thromboembolic Pulmonary Hypertension.","authors":"Patrick T Lynch, Shreya Makkapati, Jon C George, Anjali Vaidya","doi":"10.1161/CIRCULATIONAHA.126.081850","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.126.081850","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"154 9","pages":"872"},"PeriodicalIF":41.3,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863810","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}