Ohad Oren MD, MPH , Aeron M. Small MD, MTR , Amy E. Lin MD, PhD , Peter Libby MD
{"title":"Managing Cardiovascular Risk in Clonal Hematopoiesis of Indeterminate Potential","authors":"Ohad Oren MD, MPH , Aeron M. Small MD, MTR , Amy E. Lin MD, PhD , 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}
Orly Leiva MD , Olivia Liu BA , Anthony Kanelidis MD , Stanley Swat MD , Leo Gozdecki MD , Mark Belkin MD , Jonathan Grinstein MD , Sara Kalantari MD , Gene Kim MD , Jeanne DeCara MD , Ben Chung MD , Anand Patel MD , Olatoyosi Odenike MD , Eric H. Yang MD , Michelle Bloom MD , Jose Alvarez-Cardona MD , Joan How MD , Gabriela Hobbs MD
{"title":"Beyond Thrombosis: Pulmonary Hypertension and Heart Failure in Patients With Myeloproliferative Neoplasms","authors":"Orly Leiva MD , Olivia Liu BA , Anthony Kanelidis MD , Stanley Swat MD , Leo Gozdecki MD , Mark Belkin MD , Jonathan Grinstein MD , Sara Kalantari MD , Gene Kim MD , Jeanne DeCara MD , Ben Chung MD , Anand Patel MD , Olatoyosi Odenike MD , Eric H. Yang MD , Michelle Bloom MD , Jose Alvarez-Cardona MD , Joan How MD , 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}
Zhengyi Deng MBBS, PhD , Minji Jung PharmD, PhD , Mingyi Li MHS , Jinhui Li MD, PhD , Marvin E. Langston PhD , Benjamin I. Chung MD
{"title":"Longitudinal Patterns of Cardiovascular Disease and Cancer Mortality in Renal Cell Carcinoma Patients by Tumor Stage","authors":"Zhengyi Deng MBBS, PhD , Minji Jung PharmD, PhD , Mingyi Li MHS , Jinhui Li MD, PhD , Marvin E. Langston PhD , 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, 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}
{"title":"Mind the Translational Gap","authors":"Caitlin Bell MD","doi":"10.1016/j.jaccao.2025.04.005","DOIUrl":"10.1016/j.jaccao.2025.04.005","url":null,"abstract":"","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 590-592"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144162949","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}
Seug Yun Yoon MD , Mina Kim MS , Hoseob Kim MPH , Duk Won Bang MD, PhD , Byoung-Won Park MD, PhD , Sun Young Jeong MD , Min-Young Lee MD, PhD , Kyoung Ha Kim MD, PhD , Namsu Lee MD, PhD , Jong-Ho Won MD, PhD , Inki Moon MD, PhD , Jon Suh MD, PhD , Seong Soon Kwon MD, PhD
{"title":"Risk of Hematologic Malignancies in Patients With Acute Myocardial Infarction","authors":"Seug Yun Yoon MD , Mina Kim MS , Hoseob Kim MPH , Duk Won Bang MD, PhD , Byoung-Won Park MD, PhD , Sun Young Jeong MD , Min-Young Lee MD, PhD , Kyoung Ha Kim MD, PhD , Namsu Lee MD, PhD , Jong-Ho Won MD, PhD , Inki Moon MD, PhD , Jon Suh MD, PhD , Seong Soon Kwon MD, PhD","doi":"10.1016/j.jaccao.2025.04.003","DOIUrl":"10.1016/j.jaccao.2025.04.003","url":null,"abstract":"<div><h3>Background</h3><div>Acute myocardial infarction (AMI) and cancer are leading causes of death worldwide. However, the relationship between AMI and hematologic malignancies remains unclear.</div></div><div><h3>Objectives</h3><div>The authors aimed to investigate the association between AMI and the subsequent risk of incident hematologic malignancies.</div></div><div><h3>Methods</h3><div>This retrospective cohort study included 103,686 patients with AMI and no history of hematologic malignancies, and 103,686 age- and sex-matched individuals with no history of AMI or hematologic malignancies, diagnosed between January 1, 2003, and December 31, 2021. Data were obtained from the Korean National Health Insurance claims database. We compared the cumulative incidence of hematologic malignancies between groups using Gray’s method. HRs and 95% CIs were calculated using Gray’s competing risk regression model, with death treated as a competing risk.</div></div><div><h3>Results</h3><div>During follow-up (AMI, 7.9 years [Q1-Q3: 5.2-11.4 years]; control group, 17.8 years [Q1-Q3: 14.8–17.9 years]), 1,043 and 1,479 individuals in the AMI and control groups, respectively, were newly diagnosed with hematologic malignancies (incidence rate per 1,000 person-years: 1.21 vs 0.93). Competing risk analysis revealed that the AMI group had a higher risk of hematologic malignancy than the control group (HR: 1.49; 95% CI: 1.31-1.69). Findings were consistent in sensitivity and standardized incidence ratio analyses.</div></div><div><h3>Conclusions</h3><div>Patients with AMI had a higher risk of hematologic malignancies than those without AMI. These findings suggest an association between AMI and hematologic malignancies, and underscore the importance of considering hematologic malignancy development in patients with AMI.</div></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 580-589"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144162953","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 Mechanisms in Cancer and Cardiovascular Disease: S100A8/9 and the NLRP3 Inflammasome","authors":"Sophie Van Linthout PhD","doi":"10.1016/j.jaccao.2024.10.010","DOIUrl":"10.1016/j.jaccao.2024.10.010","url":null,"abstract":"<div><div>Inflammation and a dysregulated immune system are common denominators in cancer and cardiovascular disease (CVD). The Canakinumab Anti-Inflammatory Thrombosis Outcome Study (CANTOS) highlighted the convergence of interleukin (IL)-1β biology in cancer and CVD, and the potential of anti–IL-1β drugs for the treatment of both disease entities. Accumulating evidence further supports the role of the innate immunity members and IL-1β activators, S100A8/9 and the NLRP3 inflammasome, in both cancer and CVD. This review outlines the common involvement of S100A8/9 and the NLRP3 inflammasome, in cancer and CVD. Specifically, their time-, cell-, and context-dependent actions and hereto-related dichotomous role in different cancers and CVD are addressed, highlighting the need for further insights to allow tailored therapies.</div></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 501-513"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143992664","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}
Milad Nazarzadeh DPhil , Emma Copland MSc , Karl Smith Byrne DPhil , Dexter Canoy MD , Zeinab Bidel MSc , Mark Woodward PhD , Qianqian Yang MSc , James McKay PhD , Anders Mälarstig PhD , Åsa K. Hedman PhD , John Chalmers MD , Koon K. Teo MD , Carl J. Pepine MD , Barry R. Davis MD , Sverre E. Kjeldsen MD , Johan Sundström MD , Kazem Rahimi DM , Blood Pressure Lowering Treatment Trialists’ Collaboration
{"title":"Blood Pressure Lowering and Risk of Cancer","authors":"Milad Nazarzadeh DPhil , Emma Copland MSc , Karl Smith Byrne DPhil , Dexter Canoy MD , Zeinab Bidel MSc , Mark Woodward PhD , Qianqian Yang MSc , James McKay PhD , Anders Mälarstig PhD , Åsa K. Hedman PhD , John Chalmers MD , Koon K. Teo MD , Carl J. Pepine MD , Barry R. Davis MD , Sverre E. Kjeldsen MD , Johan Sundström MD , Kazem Rahimi DM , Blood Pressure Lowering Treatment Trialists’ Collaboration","doi":"10.1016/j.jaccao.2025.03.005","DOIUrl":"10.1016/j.jaccao.2025.03.005","url":null,"abstract":"<div><h3>Background</h3><div>Pharmacologic blood pressure (BP) lowering is typically a lifelong treatment, and both clinicians and patients may have concerns about the long-term use of antihypertensive agents and the risk for cancer. However, evidence from randomized controlled trials (RCTs) regarding the effect of long-term pharmacologic BP lowering on the risk for new-onset cancer is limited, with most knowledge derived from observational studies.</div></div><div><h3>Objectives</h3><div>The aim of this study was to assess whether long-term BP lowering affects the risk for new-onset cancer, cause-specific cancer death, and selected site-specific cancers.</div></div><div><h3>Methods</h3><div>Individual-level data from 42 RCTs were pooled using a one-stage individual participant data meta-analysis. The primary outcome was incident cancer of all types, and secondary outcomes were cause-specific cancer death and selected site-specific cancers. Prespecified subgroup analyses were conducted to assess the heterogeneity of the BP-lowering effect by baseline variables and over follow-up time. Cox proportional hazards regression, stratified by trial, was used for the statistical analysis. For site-specific cancers, analyses were complemented with Mendelian randomization, using naturally randomized genetic variants associated with BP lowering to mimic the design of a long-term RCT.</div></div><div><h3>Results</h3><div>Data from 314,016 randomly allocated participants without known cancer at baseline were analyzed. Over a median follow-up of 4 years (Q1-Q3: 3-5 years), 17,954 participants (5.7%) developed cancer, and 4,878 (1.5%) died of cancer. In the individual participant data meta-analysis, no associations were found between reductions in systolic or diastolic BP and cancer risk (HR per 5 mm Hg reduction in systolic BP: 1.03 [95% CI: 0.99-1.06]; HR per 3 mm Hg reduction in diastolic BP: 1.03 [95% CI: 0.98-1.07]). No changes in relative risk for incident cancer were observed over follow-up time, nor was there evidence of heterogeneity in treatment effects across baseline subgroups. No effect on cause-specific cancer death was found. For site-specific cancers, no evidence of an effect was observed, except a possible link with lung cancer risk (HR for systolic BP reduction: 1.17; 99.5% CI: 1.02-1.32). Mendelian randomization studies showed no association between systolic or diastolic BP reduction and site-specific cancers, including overall lung cancer and its subtypes.</div></div><div><h3>Conclusions</h3><div>Randomized data analysis provided no evidence to indicate that pharmacologic BP lowering has a substantial impact, either increasing or decreasing, on the risk for incident cancer, cause-specific cancer death, or selected site-specific cancers.</div></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":"7 5","pages":"Pages 609-623"},"PeriodicalIF":12.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057388","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}