Pub Date : 2025-08-01DOI: 10.1016/j.jaccao.2025.05.013
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}
Pub Date : 2025-08-01DOI: 10.1016/j.jaccao.2025.05.010
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
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.
{"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}
Pub Date : 2025-08-01DOI: 10.1016/j.jaccao.2025.06.006
Megan A. Evans PhD, Kenneth Walsh PhD
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.
{"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}
Pub Date : 2025-08-01DOI: 10.1016/j.jaccao.2025.06.004
Zhengyi Deng MBBS, PhD , Minji Jung PharmD, PhD , Mingyi Li MHS , Jinhui Li MD, PhD , Marvin E. Langston PhD , Benjamin I. Chung MD
Background
Cardiovascular disease (CVD) is the leading cause of non-cancer deaths among patients with renal cell carcinoma (RCC).
Objectives
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.
Methods
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.
Results
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.
Conclusions
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.
{"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}
Pub Date : 2025-08-01DOI: 10.1016/j.jaccao.2024.10.010
Sophie Van Linthout PhD
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.
{"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}
Pub Date : 2025-08-01DOI: 10.1016/j.jaccao.2025.04.005
Caitlin Bell MD
{"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}
Pub Date : 2025-08-01DOI: 10.1016/j.jaccao.2025.04.003
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
Background
Acute myocardial infarction (AMI) and cancer are leading causes of death worldwide. However, the relationship between AMI and hematologic malignancies remains unclear.
Objectives
The authors aimed to investigate the association between AMI and the subsequent risk of incident hematologic malignancies.
Methods
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.
Results
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.
Conclusions
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.
背景:急性心肌梗死(AMI)和癌症是世界范围内死亡的主要原因。然而,AMI与血液系统恶性肿瘤之间的关系尚不清楚。目的:作者旨在调查AMI与随后发生血液恶性肿瘤的风险之间的关系。方法:本回顾性队列研究纳入2003年1月1日至2021年12月31日诊断的103,686例AMI且无血液恶性肿瘤病史的患者,以及103,686例年龄和性别匹配且无AMI或血液恶性肿瘤病史的个体。数据来自韩国国民健康保险索赔数据库。我们使用Gray的方法比较两组间血液恶性肿瘤的累积发病率。hr和95% ci采用Gray竞争风险回归模型计算,死亡被视为竞争风险。结果:随访(AMI) 7.9年[Q1-Q3: 5.2-11.4年];AMI组(17.8年[Q1-Q3: 14.8-17.9年])、AMI组(1043例)和对照组(1479例)新诊断为血液系统恶性肿瘤(每1000人年发病率:1.21 vs 0.93)。竞争风险分析显示,AMI组发生血液系统恶性肿瘤的风险高于对照组(HR: 1.49;95% ci: 1.31-1.69)。敏感性和标准化发病率分析的结果是一致的。结论:AMI患者发生血液系统恶性肿瘤的风险高于非AMI患者。这些发现提示AMI与血液恶性肿瘤之间存在关联,并强调了AMI患者考虑血液恶性肿瘤发展的重要性。
{"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}