Jacc: Cardiooncology最新文献

{"title":"Cardiovascular Risk, Health Metrics, and Cancer Prediction","authors":"Gretell Henriquez-Santos MD ,&nbsp;Ji-Eun Kim PhD ,&nbsp;Sant J. Kumar MD ,&nbsp;Alicia A. Livinski MPH, MA ,&nbsp;Jacqueline B. Vo PhD, RN, MPH ,&nbsp;Fang Zhu PhD, MPH ,&nbsp;Jungnam Joo PhD ,&nbsp;Joseph J. Shearer PhD, MPH ,&nbsp;Maryam Hashemian MD, PhD ,&nbsp;Véronique L. Roger MD, MPH","doi":"10.1016/j.jaccao.2025.05.011","DOIUrl":"10.1016/j.jaccao.2025.05.011","url":null,"abstract":"<div><h3>Background</h3><div>Cardiovascular disease (CVD) and cancer are leading global causes of morbidity and mortality. Given the shared risk factors, it is plausible that CVD risk scores and cardiovascular health (CVH) metrics could predict cancer risk.</div></div><div><h3>Objectives</h3><div>The authors sought to identify and summarize studies examining the association between CVD risk scores, CVH metrics, and incident cancer.</div></div><div><h3>Methods</h3><div>A systematic search of 4 databases (Embase, PubMed, Scopus, Web of Science: Core) was conducted in April 2024 without language or date restrictions. Five reviewers (G.H., J.K., S.J.K., M.H., V.L.R.) independently screened records using Covidence software and extracted data from eligible prospective studies (adults aged ≥18 years; cancer incidence as outcome; CVD risk scores or CVH metrics as exposure).</div></div><div><h3>Results</h3><div>Of 4,165 records screened, 13 studies (14 CVD or CVH metrics) were included. Heterogeneity between scales precluded a meta-analysis. Four studies evaluated CVD risk scores (eg, atherosclerotic CVD) and 10 reported CVH metrics (eg, the American Heart Association’s Life’s Simple 7). Sample sizes ranged from 1,880 to 342,226, with median follow-up from 8.1 to 29.6 years. The majority included all types of cancer (71.4%), including breast, lung, colorectal, and prostate cancer types, with cancer events ranging from 387 to 11,643. Higher CVD risk scores were consistently associated with increased cancer risk incidence (HRs: 1.16-3.71). Ideal CVH metrics were associated with reduced risk (HRs: 0.49-0.95).</div></div><div><h3>Conclusions</h3><div>Despite heterogeneity in CVD risk metrics and cancer types, most studies suggested that worse CVD risk scores or CVH metrics predict greater cancer risk. Future studies should focus on specific CVD risk metrics and cancer types to produce evidence suitable for a meta-analysis.</div></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 593-606"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144643905","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":"Current Insights in Bidirectional Cardio-Oncology: Heart Failure Driving Cancer","authors":"Rudolf A. de Boer MD, PhD ,&nbsp;Laura I. Yousif MSc ,&nbsp;Joseph Pierre Aboumsallem PhD,&nbsp;Wouter C. Meijers MD, PhD","doi":"10.1016/j.jaccao.2025.05.014","DOIUrl":"10.1016/j.jaccao.2025.05.014","url":null,"abstract":"","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 518-522"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865125","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":"Ischemic Injury Drives Nascent Tumor Growth Via Accelerated Hematopoietic Aging","authors":"Alexandra A.C. Newman PhD ,&nbsp;José Gabriel Barcia Durán PhD ,&nbsp;Richard Von Itter MPhil ,&nbsp;Jessie M. Dalman BA ,&nbsp;Brian Lim MD ,&nbsp;Morgane Gourvest PhD ,&nbsp;Tarik Zahr PhD ,&nbsp;Kristin M. Wang MPhil ,&nbsp;Tracy Zhang MS ,&nbsp;Noah Albarracin BS ,&nbsp;Whitney G. Rubin BS ,&nbsp;Fazli K. Bozal PhD ,&nbsp;Kory J. Lavine MD, PhD ,&nbsp;Chiara Giannarelli MD, PhD ,&nbsp;Michael Gildea PhD ,&nbsp;Coen van Solingen PhD ,&nbsp;Kathryn J. Moore PhD","doi":"10.1016/j.jaccao.2025.06.005","DOIUrl":"10.1016/j.jaccao.2025.06.005","url":null,"abstract":"<div><h3>Background</h3><div>Patients with peripheral artery disease have an increased risk of cancer development. Aging-associated changes in hematopoietic stem and progenitor cells (HSPCs), including inflammation and increased myelopoiesis, are implicated in both cardiovascular disease and cancer, but their contributions to cardiovascular disease–driven tumor progression are unclear.</div></div><div><h3>Objectives</h3><div>This study sought to study tumor growth after peripheral ischemia and consequent changes within the HSPC bone marrow compartment to uncover mechanisms through which altered hematopoiesis promotes cancer.</div></div><div><h3>Methods</h3><div>Mammary cancer (E0771) growth was monitored in C57BL/6J mice after hind limb ischemia (HLI) or sham surgery. The tumor immune microenvironment, circulatory immune cells, and HSPC compartment were assessed by flow cytometry. Next-generation single-cell RNA and assay for transposase-accessible chromatin sequencing of bone marrow progenitors was performed to assess the distinct and synergistic transcriptomic and epigenetic changes of cancer and peripheral ischemia. The functional impact on tumor progression and persistence of ischemia-induced epigenetic reprogramming of HSPCs and their myeloid progeny was examined by bone marrow transplantation.</div></div><div><h3>Results</h3><div>Peripheral ischemia increased monocyte and neutrophil output at the expense of lymphocytes, driven by a shift toward CD150^hi myeloid-biased hematopoietic stem cells. This was associated with accelerated cancer growth and enrichment of tumors with myeloid cells (monocytes, macrophages, neutrophils) and regulatory T cells. Increased myelopoiesis was also supported by sequencing analyses showing HLI and tumor-induced transcriptional and epigenetic enrichment for inflammatory (NLRP3 inflammasome) and aging-associated neogenin-1, thrombospondin-1) signatures in subsets of monocyte/dendritic progenitors. HLI-accelerated tumor growth and myeloid-skewing was transmissible via bone marrow transplantation, indicating long-term reprogramming of innate immune responses.</div></div><div><h3>Conclusions</h3><div>Peripheral ischemia enhances inflammaging of hematopoietic stem cells and long-lasting alterations to antitumoral immunity, accelerating breast tumor growth.</div></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 559-577"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144867403","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":"Shared Pathways, Shared Predictions","authors":"Ziwen Long MD, PhD ,&nbsp;Wenying Gao MD, MSc ,&nbsp;Xiang Gao MD, PhD","doi":"10.1016/j.jaccao.2025.06.002","DOIUrl":"10.1016/j.jaccao.2025.06.002","url":null,"abstract":"","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 607-608"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865102","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":"Managing Cardiovascular Risk in Clonal Hematopoiesis of Indeterminate Potential","authors":"Ohad Oren MD, MPH ,&nbsp;Aeron M. Small MD, MTR ,&nbsp;Amy E. Lin MD, PhD ,&nbsp;Peter Libby MD","doi":"10.1016/j.jaccao.2025.05.013","DOIUrl":"10.1016/j.jaccao.2025.05.013","url":null,"abstract":"","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 496-500"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865123","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":"Beyond Thrombosis: Pulmonary Hypertension and Heart Failure in Patients With Myeloproliferative Neoplasms","authors":"Orly Leiva MD ,&nbsp;Olivia Liu BA ,&nbsp;Anthony Kanelidis MD ,&nbsp;Stanley Swat MD ,&nbsp;Leo Gozdecki MD ,&nbsp;Mark Belkin MD ,&nbsp;Jonathan Grinstein MD ,&nbsp;Sara Kalantari MD ,&nbsp;Gene Kim MD ,&nbsp;Jeanne DeCara MD ,&nbsp;Ben Chung MD ,&nbsp;Anand Patel MD ,&nbsp;Olatoyosi Odenike MD ,&nbsp;Eric H. Yang MD ,&nbsp;Michelle Bloom MD ,&nbsp;Jose Alvarez-Cardona MD ,&nbsp;Joan How MD ,&nbsp;Gabriela Hobbs MD","doi":"10.1016/j.jaccao.2025.05.010","DOIUrl":"10.1016/j.jaccao.2025.05.010","url":null,"abstract":"<div><div>Patients with myeloproliferative neoplasms (MPNs) are at increased risk for cardiovascular disease. Although thrombosis is a well-recognized complication, emerging evidence indicates that nonthrombotic conditions, including heart failure (HF) and pulmonary hypertension (PH), are also prevalent and associated with adverse cardiovascular and hematologic outcomes. Clinical and preclinical data suggest a shared pathophysiology linking MPNs to the development and progression of cardiomyopathy, HF, and both precapillary and postcapillary PH. Recent studies further support a bidirectional relationship, in which HF and PH are associated with hematologic progression and vice versa. Elucidating the mechanisms underlying these interactions may uncover novel therapeutic targets and inform clinical management. Here, the authors review the pathophysiology and impact of HF and PH in patients with MPNs.</div></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 538-553"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144643903","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":"Lowering Blood Pressure, Raising Cancer Risk?","authors":"Fahmida Mannan MBBS, MRes ,&nbsp;Marie Pigeyre MD, PhD","doi":"10.1016/j.jaccao.2025.04.004","DOIUrl":"10.1016/j.jaccao.2025.04.004","url":null,"abstract":"","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 624-626"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865108","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":"FULL ISSUE PDF","authors":"","doi":"10.1016/S2666-0873(25)00279-0","DOIUrl":"10.1016/S2666-0873(25)00279-0","url":null,"abstract":"","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages I-CXCIX"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865119","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":"Longitudinal Patterns of Cardiovascular Disease and Cancer Mortality in Renal Cell Carcinoma Patients by Tumor Stage","authors":"Zhengyi Deng MBBS, PhD ,&nbsp;Minji Jung PharmD, PhD ,&nbsp;Mingyi Li MHS ,&nbsp;Jinhui Li MD, PhD ,&nbsp;Marvin E. Langston PhD ,&nbsp;Benjamin I. Chung MD","doi":"10.1016/j.jaccao.2025.06.004","DOIUrl":"10.1016/j.jaccao.2025.06.004","url":null,"abstract":"<div><h3>Background</h3><div>Cardiovascular disease (CVD) is the leading cause of non-cancer deaths among patients with renal cell carcinoma (RCC).</div></div><div><h3>Objectives</h3><div>The authors sought to investigate how CVD and RCC death rates change post-RCC diagnosis and time-dependent risk factors for death, across different tumor stages.</div></div><div><h3>Methods</h3><div>Adults diagnosed with a first RCC from the Surveillance, Epidemiology, and End Results database (2004-2020) were included in this study. Poisson regression was used to model RCC and CVD death rates over 16-year follow-up, identifying a crossover time when the curves intersected, overall and by tumor stage. Fine-Gray competing risk models were implemented to evaluate the time-varying associations of risk factors with CVD and RCC deaths.</div></div><div><h3>Results</h3><div>Among overall 116,836 RCC patients, the CVD death rate overtook RCC death rate at 13.7 (95% CI: 12.0-15.4) years during follow-up. For stage I RCC patients, the crossover time was sooner at 2.8 (95% CI: 2.0-3.7) years, with all subgroups either experiencing a crossover or having a consistently higher CVD death rate than RCC death rate. No crossover time was identified for stage II-IV overall. Patients aged ≥75 years and non-Hispanic Black patients experienced a crossover time across all tumor stages. Several sociodemographic and clinical characteristics showed consistent associations with short- and long-term mortality from RCC and CVD.</div></div><div><h3>Conclusions</h3><div>In RCC patients, stage I individuals showed a pronounced trend where CVD death became dominant over RCC death during survivorship, with consistent patterns by different sociodemographic and clinical characteristics. Management of both cancer and CVD during critical periods is essential for improving survival outcomes in RCC patients, with strategies tailored to tumor stage.</div></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 627-640"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865109","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":"Clonal Hematopoiesis in Cancer and Cardiovascular Disease","authors":"Megan A. Evans PhD,&nbsp;Kenneth Walsh PhD","doi":"10.1016/j.jaccao.2025.06.006","DOIUrl":"10.1016/j.jaccao.2025.06.006","url":null,"abstract":"<div><div>Emerging evidence suggests a dynamic relationship exists between cancer and cardiovascular disease (CVD). CVD is common among cancer survivors; however, it also may increase the risk of developing cancer. The underlying factors driving this connection remain poorly understood. Aging, chronic inflammation, and perturbed immune signaling are shared hallmarks of cancer and CVD. Clonal hematopoiesis (CH), the age-related accumulation of somatic mutations in hematopoietic cells leading to cells with a growth advantage, is associated with immune dysregulation in elderly people. Growing evidence suggests that CH is a risk factor for CVD. Although the link between CH and hematological cancer is well established, its relationship to solid organ cancers is far less understood. This review provides an in-depth analysis of the evidence linking CH with solid organ malignancies and explores its role as a shared risk factor for the development of both CVD and cancer. Furthermore, it discusses the potential mechanisms by which CH may contribute to CVD among cancer survivors.</div></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 470-495"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144865122","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}