Circulation最新文献

{"title":"Evidence Generation and Implementation of Transcatheter Interventions for Atrioventricular Valvular Heart Disease in Heart Failure: Current Status and Future Directions.","authors":"Marco Metra,Daniela Tomasoni,Marianna Adamo,Stefan D Anker,Antoni Bayes-Genis,Ralph Stephan von Bardeleben,Michael Böhm,Erwan Donal,Gerasimos S Filippatos,Francesco Maisano,Piotr Ponikowski,Gianluigi Savarese,Fabien Praz,Javed Butler","doi":"10.1161/circulationaha.124.070411","DOIUrl":"https://doi.org/10.1161/circulationaha.124.070411","url":null,"abstract":"Mitral regurgitation and tricuspid regurgitation are the most common valvular heart diseases in patients with heart failure and have independent prognostic value. Transcatheter interventions are now available for the treatment of valvular heart disease, and their efficacy and safety have been tested in randomized controlled trials. However, evidence is still limited and sometimes inconclusive because several aspects of these trials limit their interpretation or consistency. These include heterogeneity in the pathogenesis and clinical characteristics of patients, the dynamic nature of secondary atrioventricular valve disease severity, the role of heart failure medications and devices, dependency on procedural results and operators' skills, smaller number of patients enrolled and the power to detect differences in trials, and limitations to use patients' reported outcomes with unblinded study protocols. These specific aspects of trials in patients with atrioventricular valve disease are reviewed in this article with a focus on possible solutions to generate further evidence for the efficacy and safety for transcatheter treatments of atrioventricular valve disease in patients with heart failure.","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"68 1","pages":"1342-1363"},"PeriodicalIF":37.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914801","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 Gu et al Regarding Article, \"Antisense Oligonucleotide Therapy for Calmodulinopathy\".","authors":"Siyuan Gu,Ye Chen,Xiaojian Shi","doi":"10.1161/circulationaha.124.073198","DOIUrl":"https://doi.org/10.1161/circulationaha.124.073198","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"15 1","pages":"e968-e969"},"PeriodicalIF":37.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914803","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":"Does Coronary Calcium Mean the Same in Active and Sedentary Individuals?","authors":"Paul D Thompson","doi":"10.1161/circulationaha.125.074396","DOIUrl":"https://doi.org/10.1161/circulationaha.125.074396","url":null,"abstract":"","PeriodicalId":10331,"journal":{"name":"Circulation","volume":"38 1","pages":"1309-1311"},"PeriodicalIF":37.8,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143914802","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":"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}