Circulation最新文献

{"title":"Response by Bortolin and Pu to Letter Regarding Article, \"Antisense Oligonucleotide Therapy for Calmodulinopathy\".","authors":"Raul H Bortolin,William T Pu","doi":"10.1161/circulationaha.125.073965","DOIUrl":"https://doi.org/10.1161/circulationaha.125.073965","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"115 1","pages":"e970-e971"},"PeriodicalIF":37.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914808","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":"CD206⁺IL-4Rα⁺ Macrophages Are Drivers of Adverse Cardiac Remodeling in Ischemic Cardiomyopathy.","authors":"Qiongxin Wang, Mohamed Ameen Ismahil, Yujie Zhu, Gregg Rokosh, Tariq Hamid, Guihua Zhou, Steven M Pogwizd, Sumanth D Prabhu","doi":"10.1161/CIRCULATIONAHA.124.072411","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.124.072411","url":null,"abstract":"<p><strong>Background: </strong>The role of cardiac CD (cluster of differentiation) 206<sup>+</sup> macrophages in chronic heart failure (HF) is unknown. We examined whether CD206<sup>+</sup> macrophages expressing IL (interleukin)-4Rα are key drivers of adverse left ventricular (LV) remodeling in HF.</p><p><strong>Methods: </strong>Adult C57BL/6 mice underwent nonreperfused myocardial infarction to induce HF. Macrophages in murine and human hearts were profiled using flow cytometry and immunostaining. In vivo myeloid-specific IL-4Rα deletion and intramyocardial macrophage adoptive transfer defined the functional effects of M[IL-4] macrophages. Antisense oligonucleotides were used for in vivo IL-4Rα gene silencing in mice.</p><p><strong>Results: </strong>CD206<sup>+</sup> macrophages steadily expanded in hearts after myocardial infarction, such that at 8 weeks after myocardial infarction, they comprised ≈85% of all macrophages. These macrophages were proliferative, predominantly CCR2<sup>-</sup> (C-C motif chemokine receptor) and MHC (major histocompatibility complex) II<sup>hi</sup>, and correlated with LV dysfunction and fibrosis. Nearly half of CD206<sup>+</sup> macrophages expressed IL-4Rα, and the majority of CD206<sup>+</sup>IL-4Rα<sup>+</sup> macrophages coexpressed profibrotic FIZZ (found in inflammatory zone) 1. IL-4-polarized bone marrow-derived CD206<sup>+</sup> macrophages also exhibited marked upregulation of FIZZ1 and induced FIZZ1-dependent myofibroblast differentiation of both cardiac mesenchymal stem cells and cardiac fibroblasts, in part related to DLL-4/Jagged1-Notch1 signaling in cardiac mesenchymal stem cells. Intramyocardial adoptive transfer of M[IL-4], but not M[IL-10], CD206<sup>+</sup> macrophages to naïve mice induced progressive LV remodeling over 4 weeks, increasing fibrosis, cardiomyocyte hypertrophy, and apoptosis. Myeloid-specific IL-4Rα gene deletion in HF (initiated 4 weeks after myocardial infarction) in IL-4Rα<sup>f/f</sup>LysM-Cre<sup>ERT2</sup> mice significantly reduced CD206<sup>+</sup> macrophage proliferation and effectively depleted CD206<sup>+</sup>IL-4Rα<sup>+</sup> cardiac macrophages. This was associated with abrogation of LV remodeling progression, reduction of cardiac fibrosis, and improved neovascularization. In vivo IL-4Rα gene silencing in mice with established HF effectively depleted cardiac CD206<sup>+</sup>IL-4Rα<sup>+</sup> macrophages and reversed LV remodeling, improving fibrosis, neovascularization, and dysfunction, and suppressed both local and systemic inflammation. Last, alternatively activated CD206<sup>+</sup> and CD163<sup>+</sup> macrophages were significantly expanded in human failing hearts and correlated with fibrosis. The majority of CD163<sup>+</sup> macrophages expressed IL-4Rα and FIZZ3, the human homolog of FIZZ1.</p><p><strong>Conclusions: </strong>Cardiac CD206<sup>+</sup>IL-4Rα<sup>+</sup> macrophages proliferate and expand in HF and are key mediators of pathological rem","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":""},"PeriodicalIF":35.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964319","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":"Palpitations After Leadless Pacemaker Implantation.","authors":"Khush M Kharidia, Mason D Marcus, Nimesh S Patel","doi":"10.1161/CIRCULATIONAHA.125.074657","DOIUrl":"https://doi.org/10.1161/CIRCULATIONAHA.125.074657","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 17","pages":"1291-1293"},"PeriodicalIF":35.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953596","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":"Genetic and Lifestyle Risks for Coronary Artery Disease and Long-Term Risk of Incident Dementia Subtypes.","authors":"Arisa Sittichokkananon, Victoria Garfield, Scott T Chiesa","doi":"10.1161/CIRCULATIONAHA.124.070632","DOIUrl":"10.1161/CIRCULATIONAHA.124.070632","url":null,"abstract":"<p><strong>Background: </strong>Shared genetic and lifestyle risk factors may underlie the development of both coronary artery disease (CAD) and dementia. We examined whether an increased genetic risk for CAD is associated with long-term risk of developing all-cause, Alzheimer's, or vascular dementia, and investigated whether differences in potentially modifiable lifestyle factors in the mid- to late-life period may attenuate this risk.</p><p><strong>Methods: </strong>A prospective cohort study of 365 782 participants free from dementia for at least 5 years after baseline assessment was conducted within the UK Biobank cohort. Genetic risk was assessed using a genomewide polygenic risk score (PRS) for CAD and lifestyle risk using a modified version of the American Heart Association's Life's Essential 8 Lifestyle Risk Score (LRS). Higher values for both scores were deemed to represent increased risk. Primary outcomes were incident all-cause, Alzheimer's, and vascular dementia diagnoses obtained from self-report and electronic health records. Secondary outcomes were neuroimaging phenotypes measured in 32 028 participants recalled for magnetic resonance imaging. Sensitivity analyses were conducted to test the extent by which biological and behavioral risk factors contributed to observed associations.</p><p><strong>Results: </strong>A total of 8870 cases of all-cause dementia were observed over a median 13.9-year follow-up. Both genetic (PRS) and lifestyle (LRS) risk scores for CAD were associated with a modestly elevated risk of all-cause dementia (subhazard ratio per SD increase, 1.10 [1.08, 1.12], <i>P</i><0.001, for PRS and 1.04 [1.02, 1.06], <i>P</i>=0.006, for LRS). This risk appeared largely attributable to underlying vascular dementia diagnoses (subhazard ratio, 1.16 [1.11, 1.21], <i>P</i><0.001 for PRS and 1.15 [1.09, 1.22], <i>P</i><0.001, for LRS), because Alzheimer's disease was found to demonstrate moderate associations with PRS alone (subhazard ratio, 1.09 [1.06, 1.13]; <i>P</i><0.001). LRS was found to have an additive rather than interactive effect with PRS, with individuals in the highest tertiles for both genetic and lifestyle risk for CAD ≈70% more likely to develop vascular dementia during follow-up compared with those in the lowest tertiles for both (subhazard ratio, 1.71 [1.39, 2.11]; <i>P</i><0.001). This was substantially attenuated in those with a low LRS at baseline, however, regardless of underlying genetic risk (30% reduction for low versus high LRS tertile regardless of PRS tertile; <i>P</i><0.001 for all). In a subset of individuals recalled for neuroimaging assessments, those in the highest tertiles for genetic and lifestyle risk for CAD demonstrated a ≈25% greater volume of white matter hyperintensities than those in the lowest risk tertiles, but showed little difference in gray matter or hippocampal volumes. Sensitivity analyses identified associations between both biological and behavioral risk scores with white matte","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1235-1247"},"PeriodicalIF":35.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12036788/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779268","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":"Causal Relevance of Lp(a) for Coronary Heart Disease and Stroke Types in East Asian and European Ancestry Populations: A Mendelian Randomization Study.","authors":"Robert Clarke,Neil Wright,Kuang Lin,Canqing Yu,Robin G Walters,Jun Lv,Michael Hill,Christiana Kartsonaki,Iona Y Millwood,Derrick A Bennett,Daniel Avery,Ling Yang,Yiping Chen,Huaidong Du,Paul Sherliker,Xiaoming Yang,Dianjianyi Sun,Liming Li,Chan Qu,Santica Marcovina,Rory Collins,Zhengming Chen,Sarah Parish,","doi":"10.1161/circulationaha.124.072086","DOIUrl":"https://doi.org/10.1161/circulationaha.124.072086","url":null,"abstract":"BACKGROUNDElevated plasma levels of Lp(a) [lipoprotein(a)] are a causal risk factor for coronary heart disease and stroke in European individuals, but the causal relevance of Lp(a) for different stroke types and in East Asian individuals with different Lp(a) genetic architecture is uncertain.METHODSWe measured plasma levels of Lp(a) in a nested case-control study of 18 174 adults (mean [SD] age, 57 [10] years; 49% female) in the China Kadoorie Biobank (CKB) and performed a genome-wide association analysis to identify genetic variants affecting Lp(a) levels, with replication in ancestry-specific subsets in UK Biobank. We further performed 2-sample Mendelian randomization analyses, associating ancestry-specific Lp(a)-associated instrumental variants derived from CKB or from published data in European individuals with risk of myocardial infarction (n=17 091), ischemic stroke (IS [n=29 233]) and its subtypes, or intracerebral hemorrhage (n=5845) in East Asian and European individuals using available data from CKB and genome-wide association analysis consortia.RESULTSIn CKB observational analyses, plasma levels of Lp(a) were log-linearly and positively associated with higher risks of myocardial infarction and IS, but not with ICH. In genome-wide association analysis, we identified 29 single nucleotide polymorphisms independently associated with Lp(a) that together explained 33% of variance in Lp(a) in Chinese individuals. In UK Biobank, the lead Chinese variants identified in CKB were replicated in 1260 Chinese individuals, but explained only 10% of variance in Lp(a) in European individuals. In Mendelian randomization analyses, however, there were highly concordant effects of Lp(a) across both ancestries for all cardiovascular disease outcomes examined. In combined analyses of both ancestries, the proportional reductions in risk per 100 nmol/L lower genetically predicted Lp(a) levels for myocardial infarction were 3-fold greater than for total IS (rate ratio, 0.78 [95% CI, 0.76-0.81] versus 0.94 [0.92-0.96]), but were similar to those for large-artery IS (0.80 [0.73-0.87]; n=8134). There were weaker associations with cardioembolic IS (0.92 [95% CI, 0.86-0.98]; n=11 730), and no association with small-vessel IS (0.99 [0.91-1.07]; n=12 343) or with intracerebral hemorrhage (1.08 [0.96-1.21]; n=5845).CONCLUSIONSThe effects of Lp(a) on risk of myocardial infarction and large-artery IS were comparable in East Asian and European individuals, suggesting that people with either ancestry could expect comparable proportional benefits for equivalent reductions in Lp(a), but there was little effect on other stroke types.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"71 1","pages":""},"PeriodicalIF":37.8,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143889325","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":"Correction to: BOLA (BolA Family Member 3) Deficiency Controls Endothelial Metabolism and Glycine Homeostasis in Pulmonary Hypertension.","authors":"Qiujun Yu, Yi-Yin Tai, Ying Tang, Jingsi Zhao, Vinny Negi, Miranda K Culley, Jyotsna Pilli, Wei Sun, Karin Brugger, Johannes Mayr, Rajeev Saggar, Rajan Saggar, W Dean Wallace, David J Ross, Aaron B Waxman, Stacy G Wen-Dell, Steven J Mullett, John Sembrat, Mauricio Rojas, Omar F Khan, James E Dahlman, Masataka Sugahara, Nobuyuki Kagiyama, Taijyu Satoh, Manling Zhang, Ning Feng, John Gorcsan, Sara O Vargas, Kathleen J Haley, Rahul Kumar, Brian B Graham, Robert Langer, Daniel G Anderson, Bing Wang, Sruti Shiva, Thomas Bertero, Stephen Y Chan","doi":"10.1161/CIR.0000000000001337","DOIUrl":"https://doi.org/10.1161/CIR.0000000000001337","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 17","pages":"e967"},"PeriodicalIF":35.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975320","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":"Role of Cardiovascular Disease Journals in Reporting Sex and Gender in Research.","authors":"C Noel Bairey Merz, Robert O Bonow, Mercedes Carnethon, Filippo Crea, Joseph A Hill, Harlan M Krumholz, Roxana Mehran, Erica S Spatz","doi":"10.1161/CIRCULATIONAHA.125.074517","DOIUrl":"10.1161/CIRCULATIONAHA.125.074517","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1211-1212"},"PeriodicalIF":35.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729039","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":"Fast Degradation of MecciRNAs by SUPV3L1/ELAC2 Provides a Novel Opportunity to Tackle Heart Failure With Exogenous MecciRNA.","authors":"Xu Liu, Qinwei Wang, Xinya Li, Yan Yang, Yuqi Deng, Xiaolin Wang, Peipei Wang, Liang Chen, Likun Ma, Ge Shan","doi":"10.1161/CIRCULATIONAHA.124.070840","DOIUrl":"10.1161/CIRCULATIONAHA.124.070840","url":null,"abstract":"<p><strong>Background: </strong>Circular RNAs derived from both nuclear and mitochondrial genomes are identified in animal cells. Mitochondria-encoded circular RNAs (mecciRNAs) are attracting more attention, and several members of mecciRNAs have already been recognized in regulating mitochondrial functions. Mitochondria dysfunctions are well-known to participate in heart failure (HF). This study was designed to investigate the RNA metabolism of mecciRNAs and the relevant roles and potential application of mecciRNAs in HF.</p><p><strong>Methods: </strong>Compared with highly stable nuclear genome-encoded circular RNAs, the fast degradation feature of mecciRNAs is identified by RNA sequencing and a series of molecular, biochemical, and cellular experiments. The substantial protective effects of in vitro synthesized mecciRNAs were tested in both doxorubicin- and pressure overload-induced mouse models of HF.</p><p><strong>Results: </strong>We discover that mecciRNAs are promptly degraded by an animal-conserved complex of helicase SUPV3L1 (suppressor of var1, 3-like protein 1) and endoribonuclease ELAC2 (elaC ribonuclease Z 2). MecciRNA degradation complex and mecciRNAs interact with mitochondrial permeability transition pore and its regulators including TRAP1 (TNF receptor-associated protein 1) and CypD (cyclophilin D). MecciRNAs regulate mitochondrial levels of TRAP1 and CypD to modulate the opening of mitochondrial permeability transition pore and the release of mitochondrial reactive oxygen species. Exogenously applied mecciRNAs interact with cytosolic TRAP1 and increase mitochondrial levels of TRAP1, and lead to a more closed state of mitochondrial permeability transition pore to constrain deleterious reactive oxygen species release. HF conditions lead to stimulated mecciRNA degradation, and administration of in vitro synthesized mecciRNAs exhibits substantial protective effects in both doxorubicin- and pressure overload-induced mouse models of HF.</p><p><strong>Conclusions: </strong>This study demonstrates the fast degradation of mecciRNAs and the associated regulations of mitochondrial reactive oxygen species release of mitochondrial permeability transition pore by mecciRNAs. HF conditions lead to dysregulated mecciRNA degradation, and exogenous mecciRNAs demonstrate treatment potential in mouse models of HF.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1272-1290"},"PeriodicalIF":35.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143457100","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":"Natural History and Clinical Outcomes of Patients With <i>DSG2/DSC2</i> Variant-Related Arrhythmogenic Right Ventricular Cardiomyopathy.","authors":"Liang Chen, Yuxiao Hu, Ardan M Saguner, Barbara Bauce, Yaxin Liu, Anteng Shi, Fu Guan, Zhongli Chen, Maria Bueno Marinas, Lingmin Wu, Deborah Foltran, Alexis Hermida, Veronique Fressart, Serena Pinci, Rudy Celeghin, Zixian Chen, Baowei Zhang, Yubi Lin, Xiaorui Liu, Marco Cason, Marika Martini, Ilaria Rigato, Corinna Brunckhorst, Ruth Biller, Cristina Basso, Bing Yang, Xiaoyan Zhao, Julia Cadrin-Tourigny, Alessio Gasperetti, Cynthia A James, Xianliang Zhou, Estelle Gandjbakhch, Kalliopi Pilichou, Firat Duru, Shengshou Hu","doi":"10.1161/CIRCULATIONAHA.124.072226","DOIUrl":"10.1161/CIRCULATIONAHA.124.072226","url":null,"abstract":"<p><strong>Background: </strong>Genetic variants in desmosomal cadherins, desmoglein 2 (<i>DSG2</i>) and desmocollin 2 (<i>DSC2</i>), cause a distinct form of arrhythmogenic right ventricular cardiomyopathy (ARVC), which remains poorly reported. In this study, we aimed to provide a comprehensive description of the phenotypic expression, natural history, and clinical outcomes of patients with this ARVC subset.</p><p><strong>Methods: </strong>Genetic and clinical data of <i>DSG2</i> and <i>DSC2</i> variant carriers were collected from 5 countries in Europe and Asia. We assessed the phenotypic profile of these patients and their clinical outcomes, focusing on heart failure and ventricular arrhythmia events.</p><p><strong>Results: </strong>Overall, 271 subjects, 254 with <i>DSG2</i> variants, were included in this study (median age, 38 years [interquartile range, 25-52]; 62.7% male). Of these, 165 were probands, and 200 were diagnosed with definite ARVC. A total of 181 (66.8%) individuals carried missense variants, mainly distributed in the extracellular domains. Notably, we included 78 (28.8%) individuals with multiple variants. Of the 200 cases with diagnosed ARVC, 41 (20.5%) experienced premature cardiac death before the age of 65. Among the 81 individuals for whom both left ventricular ejection fraction and right ventricular fractional area change data were available at presentation, 29 (35.8%) had isolated right ventricular dysfunction, and 16 (19.8%) had biventricular dysfunction. Single-variant carriers who engaged in intense physical exercise were younger at disease onset compared with those who did not (<i>P</i>=0.001). Compared with single-variant carriers, those with multiple variants were more likely to be diagnosed with ARVC (96.2% versus 64.8%; <i>P</i><0.001) and exhibited more severe left ventricular dysfunction (44.4% versus 22.1%; <i>P</i>=0.001) and right ventricular dilation (88.9% versus 55.8%, <i>P</i><0.001). Multiple-variant carriers were significantly younger at ARVC diagnosis compared with single-variant carriers (33 [18-49] years versus 42 [27-54] years; <i>P</i><0.001]. During follow-up, end-stage heart failure (<i>P</i><0.001) and malignant ventricular arrhythmias (<i>P</i>=0.004) were significantly more frequent in multiple-variant compared with single-variant carriers. Compared with <i>PKP2</i> patients, <i>DSG2/DSC2</i> patients exhibited a significantly higher risk of end-stage heart failure (<i>P</i><0.001).</p><p><strong>Conclusions: </strong>ARVC attributable to variants in desmosomal cadherins mostly present with right ventricular or biventricular disease. Multiple variants are common in these patients and are associated with more frequent clinical penetrance, earlier onset of disease, and adverse clinical outcomes.</p>","PeriodicalId":10331,"journal":{"name":"Circulation","volume":" ","pages":"1213-1230"},"PeriodicalIF":35.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691367","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":"Correction to: Core Components of Cardiac Rehabilitation Programs: 2024 Update: A Scientific Statement From the American Heart Association and the American Association of Cardiovascular and Pulmonary Rehabilitation.","authors":"Todd M Brown, Quinn R Pack, Ellen Aberegg, LaPrincess C Brewer, Yvonne R Ford, Daniel E Forman, Emily C Gathright, Sherrie Khadanga, Cemal Ozemek, Randal J Thomas","doi":"10.1161/CIR.0000000000001338","DOIUrl":"https://doi.org/10.1161/CIR.0000000000001338","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"151 17","pages":"e965-e966"},"PeriodicalIF":35.5,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953595","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}