Pub Date : 2024-02-01DOI: 10.1016/j.jaccao.2023.12.004
Richard Von Itter BA , Kathryn J. Moore PhD
{"title":"Cross-Disease Communication in Cardiovascular Disease and Cancer∗","authors":"Richard Von Itter BA , Kathryn J. Moore PhD","doi":"10.1016/j.jaccao.2023.12.004","DOIUrl":"https://doi.org/10.1016/j.jaccao.2023.12.004","url":null,"abstract":"","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":null,"pages":null},"PeriodicalIF":11.1,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666087324000024/pdfft?md5=9e4aac0ee7ae024776dec474fe852e9d&pid=1-s2.0-S2666087324000024-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139915509","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}
Pub Date : 2024-02-01DOI: 10.1016/j.jaccao.2023.12.001
Tzu-Fei Wang MD, MPH , Jean M. Connors MD
{"title":"The Pursuit of “Best” Anticoagulant for Cancer-Associated Thrombosis","authors":"Tzu-Fei Wang MD, MPH , Jean M. Connors MD","doi":"10.1016/j.jaccao.2023.12.001","DOIUrl":"10.1016/j.jaccao.2023.12.001","url":null,"abstract":"","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":null,"pages":null},"PeriodicalIF":11.1,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666087323003551/pdfft?md5=0f3024ead28f3d16baf38f52469ec6e5&pid=1-s2.0-S2666087323003551-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139456779","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}
Pub Date : 2024-02-01DOI: 10.1016/j.jaccao.2023.12.008
Rawan A. Hammoud MD , Daniel A. Mulrooney MD, MS , Isaac B. Rhea MD , Christine Yu MD , Jason N. Johnson MD, MHSc , Eric J. Chow MD, MPH , Matthew J. Ehrhardt MD, MS , Melissa M. Hudson MD , Kirsten K. Ness PhD , Gregory T. Armstrong MD, MSCE , Stephanie B. Dixon MD, MPH
The growing community of childhood cancer survivors faces a heavy burden of late onset morbidities and mortality, with cardiovascular diseases being the leading noncancer cause. In addition to demographics and cancer treatment exposures, which cannot be altered, cardiometabolic risk factors (obesity, hypertension, diabetes, and dyslipidemia) and frailty potentiate the risk of morbidity and mortality associated with chronic health conditions. Important opportunities exist to target these risk factors and improve late health outcomes for survivors. Unfortunately, limited evidence exists on the optimal methods to prevent, screen, and treat cardiometabolic risk factors among survivors, resulting in significant underdiagnosis and undertreatment. In this review, we discuss the prevalence of, risk factors for, current survivor-specific recommendations, and gaps in knowledge to mitigate potentially modifiable cardiometabolic risk factors and frailty among survivors of childhood cancer.
{"title":"Modifiable Cardiometabolic Risk Factors in Survivors of Childhood Cancer","authors":"Rawan A. Hammoud MD , Daniel A. Mulrooney MD, MS , Isaac B. Rhea MD , Christine Yu MD , Jason N. Johnson MD, MHSc , Eric J. Chow MD, MPH , Matthew J. Ehrhardt MD, MS , Melissa M. Hudson MD , Kirsten K. Ness PhD , Gregory T. Armstrong MD, MSCE , Stephanie B. Dixon MD, MPH","doi":"10.1016/j.jaccao.2023.12.008","DOIUrl":"https://doi.org/10.1016/j.jaccao.2023.12.008","url":null,"abstract":"<div><p>The growing community of childhood cancer survivors faces a heavy burden of late onset morbidities and mortality, with cardiovascular diseases being the leading noncancer cause. In addition to demographics and cancer treatment exposures, which cannot be altered, cardiometabolic risk factors (obesity, hypertension, diabetes, and dyslipidemia) and frailty potentiate the risk of morbidity and mortality associated with chronic health conditions. Important opportunities exist to target these risk factors and improve late health outcomes for survivors. Unfortunately, limited evidence exists on the optimal methods to prevent, screen, and treat cardiometabolic risk factors among survivors, resulting in significant underdiagnosis and undertreatment. In this review, we discuss the prevalence of, risk factors for, current survivor-specific recommendations, and gaps in knowledge to mitigate potentially modifiable cardiometabolic risk factors and frailty among survivors of childhood cancer.</p></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":null,"pages":null},"PeriodicalIF":11.1,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666087324000085/pdfft?md5=76782cd2929183fd9403582f5787a94d&pid=1-s2.0-S2666087324000085-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139915507","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}
Pub Date : 2024-02-01DOI: 10.1016/j.jaccao.2023.12.003
M. Andres, Theodore Murphy, Nana Poku, M. S. Nazir, S. Ramalingam, John Baksi, Julian W.E. Jarman, R. Khattar, Rakesh Sharma, Stuart D. Rosen, Alexander R. Lyon
{"title":"The United Kingdom’s First Cardio-Oncology Service","authors":"M. Andres, Theodore Murphy, Nana Poku, M. S. Nazir, S. Ramalingam, John Baksi, Julian W.E. Jarman, R. Khattar, Rakesh Sharma, Stuart D. Rosen, Alexander R. Lyon","doi":"10.1016/j.jaccao.2023.12.003","DOIUrl":"https://doi.org/10.1016/j.jaccao.2023.12.003","url":null,"abstract":"","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":null,"pages":null},"PeriodicalIF":11.1,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139828679","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}
Epidemiological investigations suggest that patients with heart failure have a higher incidence of cancer; however, the causal role of cardiac disease on cancer progression remains unclear.
Objectives
This study aimed to investigate the impact and underlying mechanisms of myocardial infarction (MI)–induced heart failure on tumor cell growth.
Methods
We generated a syngeneic mouse model by implanting mammary tumor–derived 4T1 cells into BALB/c mice with MI resulting from ligation of the left anterior descending artery.
Results
Mice with MI exhibited increased tumor volume, tumor weight, and Ki67-positive proliferative cells in the tumor tissue compared with the sham-operated mice. Furthermore, RNA sequencing analysis in the tumor tissue revealed significant enrichment of pathways related to tumor progression, particularly the PI3K-AKT pathway in the MI mice. Upregulation of tropomyosin receptor kinase A (TRKA) phosphorylation, an upstream regulator of PI3K-AKT signaling, was observed in the tumor tissue of the MI mice. We also observed elevated levels of circulating nerve growth factor (NGF), a ligand of TRKA, and increased NGF expressions in the myocardium after MI. In in vitro experiments, NGF stimulation led to increased cell proliferation, as well as phosphorylation of TRKA and AKT. Notably, inhibition of TRKA by small interfering RNA or the chemical inhibitor GW441756 effectively blocked these effects. Administration of GW441756 resulted in the suppression of tumor volume and cell proliferation in the MI mice.
Conclusions
Our study demonstrates that MI promotes mammary tumor growth through the NGF-TRKA pathway. Consequently, inhibiting TRKA could represent a therapeutic strategy for breast cancer patients concurrently experiencing heart failure after MI.
{"title":"Heart Failure Post-Myocardial Infarction Promotes Mammary Tumor Growth Through the NGF-TRKA Pathway","authors":"Tetsuya Tani MD , Masayoshi Oikawa MD, PhD , Tomofumi Misaka MD, PhD , Takafumi Ishida MD, PhD , Yasuchika Takeishi MD, PhD","doi":"10.1016/j.jaccao.2023.10.002","DOIUrl":"10.1016/j.jaccao.2023.10.002","url":null,"abstract":"<div><h3>Background</h3><p>Epidemiological investigations suggest that patients with heart failure have a higher incidence of cancer; however, the causal role of cardiac disease on cancer progression remains unclear.</p></div><div><h3>Objectives</h3><p>This study aimed to investigate the impact and underlying mechanisms of myocardial infarction (MI)–induced heart failure on tumor cell growth.</p></div><div><h3>Methods</h3><p>We generated a syngeneic mouse model by implanting mammary tumor–derived 4T1 cells into BALB/c mice with MI resulting from ligation of the left anterior descending artery.</p></div><div><h3>Results</h3><p>Mice with MI exhibited increased tumor volume, tumor weight, and Ki67-positive proliferative cells in the tumor tissue compared with the sham-operated mice. Furthermore, RNA sequencing analysis in the tumor tissue revealed significant enrichment of pathways related to tumor progression, particularly the PI3K-AKT pathway in the MI mice. Upregulation of tropomyosin receptor kinase A (TRKA) phosphorylation, an upstream regulator of PI3K-AKT signaling, was observed in the tumor tissue of the MI mice. We also observed elevated levels of circulating nerve growth factor (NGF), a ligand of TRKA, and increased NGF expressions in the myocardium after MI. In in vitro experiments, NGF stimulation led to increased cell proliferation, as well as phosphorylation of TRKA and AKT. Notably, inhibition of TRKA by small interfering RNA or the chemical inhibitor GW441756 effectively blocked these effects. Administration of GW441756 resulted in the suppression of tumor volume and cell proliferation in the MI mice.</p></div><div><h3>Conclusions</h3><p>Our study demonstrates that MI promotes mammary tumor growth through the NGF-TRKA pathway. Consequently, inhibiting TRKA could represent a therapeutic strategy for breast cancer patients concurrently experiencing heart failure after MI.</p></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":null,"pages":null},"PeriodicalIF":11.1,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666087323002971/pdfft?md5=5ecebcda649c9478a89d03ee55c5ed45&pid=1-s2.0-S2666087323002971-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135456286","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}
Pub Date : 2024-02-01DOI: 10.1016/j.jaccao.2023.10.011
Mohamed Dafaalla MSc , Dmitry Abramov MD , Harriette G.C. Van Spall MD , Arjun K. Ghosh PhD , Chris P. Gale PhD , Sarah Zaman PhD , Muhammad Rashid PhD , Mamas A. Mamas DPhil
Background
Although numerous studies have examined readmission with heart failure (HF) after acute myocardial infarction (AMI), limited data are available on HF readmission in cancer patients post-AMI.
Objectives
This study aimed to assess the rates and factors associated with HF readmission in cancer patients presenting with ST-segment elevation myocardial infarction (STEMI).
Methods
A nationally linked cohort of STEMI patients between January 2005 and March 2019 were obtained from the UK Myocardial Infarction National Audit Project registry and the UK national Hospital Episode Statistics Admitted Patient Care registry. Multivariable Fine-Gray competing risk models were used to evaluate HF readmission at 30 days and 1 year.
Results
A total of 326,551 STEMI indexed admissions were included, with 7,090 (2.2%) patients having active cancer. The cancer group was less likely to be admitted under the care of a cardiologist (74.5% vs 81.9%) and had lower rates of invasive coronary angiography (62.2% vs 72.7%; P < 0.001) and percutaneous coronary intervention (58.4% vs. 69.5%). There was a significant prescription gap in the administration of post-AMI medications upon discharge such as an angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (49.5% vs 71.1%) and beta-blockers (58.4% vs 68.0%) in cancer patients. The cancer group had a higher rate of HF readmission at 30 days (3.2% vs 2.3%) and 1 year (9.4% vs 7.3%). However, after adjustment, cancer was not independently associated with HF readmission at 30 days (subdistribution HR: 1.05; 95% CI: 0.86-1.28) or 1 year (subdistribution HR: 1.03; 95% CI: 0.92-1.16). The opportunity-based quality indicator was associated with higher rates of HF readmission independent of cancer diagnosis.
Conclusions
Cancer patients receive care that differs in important ways from patients without cancer. Greater implementation of evidence-based care may reduce HF readmissions, including in cancer patients.
{"title":"Heart Failure Readmission in Patients With ST-Segment Elevation Myocardial Infarction and Active Cancer","authors":"Mohamed Dafaalla MSc , Dmitry Abramov MD , Harriette G.C. Van Spall MD , Arjun K. Ghosh PhD , Chris P. Gale PhD , Sarah Zaman PhD , Muhammad Rashid PhD , Mamas A. Mamas DPhil","doi":"10.1016/j.jaccao.2023.10.011","DOIUrl":"10.1016/j.jaccao.2023.10.011","url":null,"abstract":"<div><h3>Background</h3><p>Although numerous studies have examined readmission with heart failure (HF) after acute myocardial infarction (AMI), limited data are available on HF readmission in cancer patients post-AMI.</p></div><div><h3>Objectives</h3><p>This study aimed to assess the rates and factors associated with HF readmission in cancer patients presenting with ST-segment elevation myocardial infarction (STEMI).</p></div><div><h3>Methods</h3><p>A nationally linked cohort of STEMI patients between January 2005 and March 2019 were obtained from the UK Myocardial Infarction National Audit Project registry and the UK national Hospital Episode Statistics Admitted Patient Care registry. Multivariable Fine-Gray competing risk models were used to evaluate HF readmission at 30 days and 1 year.</p></div><div><h3>Results</h3><p>A total of 326,551 STEMI indexed admissions were included, with 7,090 (2.2%) patients having active cancer. The cancer group was less likely to be admitted under the care of a cardiologist (74.5% vs 81.9%) and had lower rates of invasive coronary angiography (62.2% vs 72.7%; <em>P</em> < 0.001) and percutaneous coronary intervention (58.4% vs. 69.5%). There was a significant prescription gap in the administration of post-AMI medications upon discharge such as an angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (49.5% vs 71.1%) and beta-blockers (58.4% vs 68.0%) in cancer patients. The cancer group had a higher rate of HF readmission at 30 days (3.2% vs 2.3%) and 1 year (9.4% vs 7.3%). However, after adjustment, cancer was not independently associated with HF readmission at 30 days (subdistribution HR: 1.05; 95% CI: 0.86-1.28) or 1 year (subdistribution HR: 1.03; 95% CI: 0.92-1.16). The opportunity-based quality indicator was associated with higher rates of HF readmission independent of cancer diagnosis.</p></div><div><h3>Conclusions</h3><p>Cancer patients receive care that differs in important ways from patients without cancer. Greater implementation of evidence-based care may reduce HF readmissions, including in cancer patients.</p></div>","PeriodicalId":48499,"journal":{"name":"Jacc: Cardiooncology","volume":null,"pages":null},"PeriodicalIF":11.1,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266608732300354X/pdfft?md5=a1df754389cdf8e3f9b6501308a58261&pid=1-s2.0-S266608732300354X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139454277","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}