Cardio-oncology最新文献

{"title":"Cancer and myocardial injury in patients with suspected acute coronary syndrome.","authors":"Marta Sabaté-Tormos, Alfredo Bardají, Oscar M Peiró, Anna Carrasquer, German Cediel, Jose Luis Ferreiro","doi":"10.1186/s40959-025-00320-x","DOIUrl":"10.1186/s40959-025-00320-x","url":null,"abstract":"<p><strong>Background: </strong>Cancer and cardiovascular diseases are the leading causes of mortality worldwide, as they share common risk factors and exacerbate cardiovascular outcomes when they coexist. This study aimed to assess the clinical characteristics and cardiovascular outcomes of patients with a history of cancer and myocardial injury (MI) presenting with suspected acute coronary syndrome (ACS) in an emergency setting.</p><p><strong>Methods: </strong>This retrospective cohort study included 3,626 patients admitted to the emergency department with suspected ACS between 2012 and 2013. Patients were categorized on the basis of their cancer history and the presence of MI. Clinical variables and the associations between cancer history and MI with all-cause mortality were analyzed over a four-year follow-up period via univariate and multivariate Cox regression models.</p><p><strong>Results: </strong>Of the cohort, 10.6% (n = 384) had a history of cancer. Compared with other groups, cancer patients with MI were older, had more comorbidities, and presented a higher incidence of type 2 myocardial infarction (T2MI). At the four-year follow-up, all-cause mortality was significantly greater among cancer patients with MI (68.8%) than among cancer patients without MI (32.4%) and noncancer patients with or without MI (42.5% vs. 11.3%, respectively). Multivariate analysis identified cancer patients, particularly those with MI, as independent predictors of mortality.</p><p><strong>Conclusions: </strong>Patients who present to emergency departments with suspected ACS, a history of cancer, or the presence of MI face greater cardiovascular risk and mortality than other patients do. The higher prevalence of T2MI in this population underscores the need for tailored management strategies.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"21"},"PeriodicalIF":3.2,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11846249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Percutaneous coronary intervention-lobectomy for Lung Cancer hybrid surgery: an initial case series.","authors":"Jing Zeng, Junyi Yu, Qiao Mei, Ye Yuan, Taiming Zhang, Longyong Mei, Lingling Huang, Yijie Hu, Bo Deng, Gengze Wu, Chunyu Zeng","doi":"10.1186/s40959-025-00317-6","DOIUrl":"10.1186/s40959-025-00317-6","url":null,"abstract":"<p><strong>Background: </strong>For patients diagnosed with both lung cancer and severe coronary heart disease (CHD), the conflict between revascularization and lung cancer surgery remains to be settled to balance how to attenuate the cardiovascular risk for lung surgery and shorten the waiting time of anti-platelet therapy after revascularization. This study presents the percutaneous coronary intervention (PCI)-lobectomy for lung cancer hybrid surgery (PLHS), and its antithrombotic therapeutic strategy.</p><p><strong>Methods: </strong>From October 2020 to June 2023, 14 patients, with unstable angina and resectable lung cancer received PLHS. All procedures were performed in a hybrid operating room. Drug-eluting stents (DES) were implanted during PCI. Lobectomy was carried out within one hour after PCI.</p><p><strong>Results: </strong>Procedural success was 100%. All the patients subjected to PLHS were alive after 12 months of follow-up; 2 patients (14.29%) died due to distant metastasis within 12-24 months post-PLHS. There were no intraoperative complications, or 30-day- and 3-month-mortality. Except for one patient who suffered pneumothorax, no other postoperative complications, including severe bleeding, or in-stent restenosis, occurred in the 31.7 ± 10.9 months follow-up.</p><p><strong>Conclusions: </strong>PLHS is a feasible and potentially safe option for patients with both lung cancer and severe CHD.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"20"},"PeriodicalIF":3.2,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TAVR in cancer patients: outcomes in survivors with radiation and active cancer.","authors":"Umesh C Sharma, Saraswati Pokharel","doi":"10.1186/s40959-025-00301-0","DOIUrl":"10.1186/s40959-025-00301-0","url":null,"abstract":"","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"19"},"PeriodicalIF":3.2,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrotroponin interference and association with cardiotoxicity in patients receiving cardiotoxic breast cancer therapy: a pilot study.","authors":"Andrea Soosaipillai, Inbar Nardi-Agmon, Davor Brinc, Anselmo Fabros, Peter A Kavsak, Paaladinesh Thavendiranathan, Ashley Di Meo","doi":"10.1186/s40959-025-00314-9","DOIUrl":"10.1186/s40959-025-00314-9","url":null,"abstract":"<p><strong>Background: </strong>Cancer therapy-related cardiac dysfunction (CTRCD) is an important adverse effect in patients receiving potential cardiotoxic cancer therapies. Interpretation of cardiac troponin results can be affected by presence of macrotroponin, which can complicate CTRCD assessment. We aimed to assess whether macrotroponin is detectable in women with ERBB2 + breast cancer receiving sequential therapy with anthracyclines and trastuzumab.</p><p><strong>Methods: </strong>A total of 20 serum samples from 12 ERBB2 + breast cancer patients (median age: 55 years, range: 30-69 years) who exhibited a significant increase in high-sensitivity cardiac troponin I (hs-cTnI) from baseline to post-anthracycline (~ 2 months after therapy initiation) and/or 3-months into trastuzumab therapy (~ 5 months after therapy initiation) and/or who had at least one hs-cTnI value above the female-specific 99th percentile (hs-cTnI > 16 ng/L) and had available banked blood for analysis were included in this pilot study. Samples were analyzed using the Abbott STAT High-Sensitive Troponin-I and Roche Elecsys Troponin T hs STAT assays. Macrotroponin was detected by treating the sample with protein G and re-measuring hs-cTn. Macrotroponin presence was defined as a hs-cTnI or hs-cTnT recovery of < 40% or 85%, respectively.</p><p><strong>Results: </strong>Macrotroponin was not identified after anthracycline treatment but was present in four patients 3-months into trastuzumab therapy, two of which had hs-cTnI concentrations above the 99th percentile. None of these patients exhibited a significant reduction in LVEF and/or GLS despite having significant elevations in hs-cTnI.</p><p><strong>Conclusions: </strong>Clinicians should be cautious of benign hs-cTn elevations resulting from macrotroponin presence, as it can complicate CTRCD assessment.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"18"},"PeriodicalIF":3.2,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11827144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Discovery of plasma proteins and metabolites associated with left ventricular cardiac dysfunction in pan-cancer patients.","authors":"Jessica C Lal, Michelle Z Fang, Muzna Hussain, Abel Abraham, Reina Tonegawa-Kuji, Yuan Hou, Mina K Chung, Patrick Collier, Feixiong Cheng","doi":"10.1186/s40959-025-00309-6","DOIUrl":"10.1186/s40959-025-00309-6","url":null,"abstract":"<p><strong>Background: </strong>Cancer-therapy related cardiac dysfunction (CTRCD) remains a significant cause of morbidity and mortality in cancer survivors. In this study, we aimed to identify differential plasma proteins and metabolites associated with left ventricular dysfunction (LVD) in cancer patients.</p><p><strong>Methods: </strong>We analyzed data from 50 patients referred to the Cleveland Clinic Cardio-Oncology Center for echocardiograph assessment, integrating electronic health records, proteomic, and metabolomic profiles. LVD was defined as an ejection fraction ≤ 55% based on echocardiographic evaluation. Classification-based machine learning models were used to predict LVD using plasma metabolites and proteins as input features.</p><p><strong>Results: </strong>We identified 13 plasma proteins (P < 0.05) and 14 plasma metabolites (P < 0.05) associated with LVD. Key proteins included markers of inflammation (ST2, TNFRSF14, OPN, and AXL) and chemotaxis (RARRES2, MMP-2, MEPE, and OPN). Notably, sex-specific associations were observed, such as uridine (P = 0.003) in males. Furthermore, metabolomic features significantly associated with LVD included 1-Methyl-4-imidazoleacetic acid (P = 0.015), COL1A1 (P = 0.009), and MMP-2 (P = 0.016), and pointing to metabolic shifts and heightened inflammation in patients with LVD.</p><p><strong>Conclusion: </strong>Our findings suggest that circulating metabolites may non-invasively detect clinical and molecular differences in patients with LVD, providing insights into underlying disease pathways and potential therapeutic targets.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"17"},"PeriodicalIF":3.2,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11823021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Troponin i-induced cardiac inflammation and dysfunction in mice: a comparative study with the AT-3 tumor-bearing model.","authors":"Shirley Xu, Swati D Sonkawade, Badri Karthikeyan, Victoire-Grace Karambizi, Prachi S Kulkarni, Sarmila Nepali, Saraswati Pokharel, Umesh C Sharma","doi":"10.1186/s40959-025-00315-8","DOIUrl":"10.1186/s40959-025-00315-8","url":null,"abstract":"<p><strong>Background: </strong>Myocarditis is a potentially fatal condition, with a mortality rate of up to 50% in severe cases. Studies, including those by Nobel Laureate Honjo, have implicated autoantibodies against cardiac troponin I (cTnI) in driving cardiac inflammation in mice. Research has also identified autoantibodies under baseline conditions in some cancer models. However, data on the effects of recombinant cTnI on autoantibody production, myocardial inflammation, and contractile function remain limited. This study investigated cTnI-associated myocardial inflammation and autoantibody formation in both tumor-free and tumor-bearing mouse models.</p><p><strong>Methods: </strong>Female BALB/c mice were immunized with recombinant cTnI combined with adjuvants and compared to adjuvant-only controls. Cardiac function was assessed using gated cardiac MRI, including myocardial velocities, acceleration, deceleration, and standard volumetric parameters including ejection fraction (EF). Anti-cTnI autoantibodies were quantified using a custom-designed ELISA, while myocardial inflammation was assessed by analyzing T-cell subsets (CD4 + and CD8 +) in myocardial tissue samples. Baseline autoantibody reactivity was evaluated in tumor-bearing mice and tumor-free controls for comparison.</p><p><strong>Results: </strong>The left ventricular ejection fraction trended lower in the cTnI + adjuvant group (57.80 ± 1.7%) compared to controls (61.67 ± 4.1%), but the difference was not statistically significant (p = 0.073). Myocardial velocity, reflecting contraction speed, was significantly reduced in cTnI-treated mice (control:-1.2 ± 0.8 cm/s; cTnI:-1.05 ± 0.07 cm/s; p = 0.015). Anti-cTnI autoantibody levels increased significantly in cTnI-treated mice at 8 weeks (control:0.1 ± 0.02; cTnI:0.77 ± 0.28; p = 0.007). Additionally, the density of CD8 + T-cells in myocardial tissue was significantly higher in the cTnI group (control:2.2 ± 1.2 cells/mm²; cTnI:4.4 ± 2 cells/mm²; p = 0.013), indicating an enhanced cytotoxic T-cell response. The CD4/CD8 ratio was significantly lower in cTnI-treated mice (control: 8.2 ± 6.8; cTnI:3.1 ± 0.9; p = 0.029), further suggesting a shift toward a cytotoxic immune profile. Baseline autoantibody reactivity in tumor-bearing mice was not significantly different from controls (tumor-bearing: absorbance 0.049 ± 0.029; control: absorbance 0.068 ± 0.05 at 450 nm), indicating no inherent autoimmune reactivity in the tumor-bearing model.</p><p><strong>Conclusions: </strong>Recombinant cTnI induces myocardial contractile dysfunction and promotes a cytotoxic immune response, supporting its role as an autoantigen in myocarditis. Advanced cardiac MRI revealed subtle functional impairments that EF alone could not detect. These findings highlight the potential for therapies targeting cTnI-induced autoimmunity, particularly in patients with ICI-associated myocarditis.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"16"},"PeriodicalIF":3.2,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11816743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143406009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SGLT2 inhibitors for prevention and management of cancer treatment-related cardiovascular toxicity: a review of potential mechanisms and clinical insights.","authors":"Carl Simela, J Malcolm Walker, Arjun K Ghosh, Daniel H Chen","doi":"10.1186/s40959-024-00284-4","DOIUrl":"10.1186/s40959-024-00284-4","url":null,"abstract":"<p><p>More evidence-based strategies are needed for preventing and managing cancer treatment-related cardiovascular toxicity (CTR-CVT). Owing to the growing body of evidence supporting their cardioprotective role in several cardiac injury scenarios, sodium-glucose cotransporter 2 inhibitors (SGLT2i) may be beneficial for preventing and treating CTR-CVT. In October 2024, a search was conducted of the PubMed database to review full studies investigating the cardioprotective role of SGLT2i against CTR-CVT. We identified 44 full published/pre-print studies and 3 ongoing randomised controlled trial across eight types of cancer treatment (anthracyclines, platinum-containing therapy, immune checkpoint inhibitors, HER2-targeted therapies, kinase inhibitors, androgen deprivation therapies, multiple myeloma therapies and 5-fluorouracil). Most studies used animal models and focussed on primary prevention. 43 of the 44 studies found some cardioprotective effect of SGLT2i against CTR-CVT, which in some cases included preventing ejection fraction decline and aberrations in cardiac electrophysiological parameters. Some studies also observed beneficial effects on mortality. A central triad of anti-inflammatory, anti-oxidative and anti-apoptotic mechanisms likely underlie SGLT2i-mediated cardioprotection against CTR-CVT. Overall, this growing body of research suggests that SGLT2i may be a promising candidate for preventing CTR-CVT either as monotherapy or in combination with other cardioprotective drugs. However, the literature is limited in that no prospective randomised controlled trials investigating SGLT2i for the prevention and management of CTR-CVT exist and most existing human retrospective data is based on diabetic populations. Future work must focus on addressing these limitations of the current literature.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"15"},"PeriodicalIF":3.2,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11818010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute vascular and cardiac effects of lenvatinib in mice.","authors":"Dustin N Krüger, Patrizia Pannucci, Callan D Wesley, Cedric H G Neutel, Wim Martinet, Guido R Y De Meyer, Stephen J Hill, Jeanette Woolard, Constantijn Franssen, Pieter-Jan Guns","doi":"10.1186/s40959-025-00307-8","DOIUrl":"10.1186/s40959-025-00307-8","url":null,"abstract":"<p><strong>Background: </strong>Tyrosine kinase inhibitors (TKIs) targeting vascular endothelial growth factor (VEGF) receptor signalling are used in cancer therapy to inhibit angiogenesis. Unfortunately, VEGF inhibitors are known to induce severe hypertension in patients. This study aimed to elucidate the impact of the TKI lenvatinib on blood pressure, arterial stiffness, vascular reactivity, as well as cardiac function in a short-term murine model to shed light on potential contributors to cardiovascular (CV) toxicities associated with VEGF inhibition.</p><p><strong>Methods: </strong>Male C57BL/6J mice were randomly divided into 2 cohorts, either treated for 4 days with lenvatinib 4 mg/kg/day or 40% hydroxypropyl β-cyclodextrin as control. In an additional study, mice were subjected to a 4-day treatment followed by a 4-day wash-out, with echocardiography and blood pressure measurements performed on day 2 and 7. Subsequently, ex vivo vascular reactivity of thoracic aortic segments was determined.</p><p><strong>Results: </strong>Lenvatinib induced hypertension and arterial stiffness (i.e., increased pulse wave velocity), starting from day 2 of treatment. Further, left ventricular ejection fraction was reduced and the ventricle dilated upon treatment. Lenvatinib induced neither endothelial dysfunction nor impaired vascular smooth muscle cell reactivity to nitric oxide (NO). Interestingly, lenvatinib demonstrated a concentration-dependent increase in ATP-mediated relaxation. In addition, after the 4-day wash-out period, lenvatinib-treated mice did not show complete remission of hypertension. However, arterial stiffness, ATP-mediated relaxation and cardiac adaptation were recovered.</p><p><strong>Conclusion: </strong>This comprehensive investigation provides valuable insights into the interplay between VEGF inhibition, vascular function and cardiac outcomes, emphasising the need for nuanced understanding and further exploration of the differential effects of lenvatinib on the CV system. Additionally, the study proposes a synergistic formation between VEGF and ATP, indicating an enhanced response via P2Yx receptor signalling.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"14"},"PeriodicalIF":3.2,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11816767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term cardiac MRI follow up of MANTICORE (Multidisciplinary Approach to Novel Therapies in Cardio-Oncology REsearch).","authors":"Dina Labib, Mark Haykowsky, Emer Sonnex, John R Mackey, Richard B Thompson, D Ian Paterson, Edith Pituskin","doi":"10.1186/s40959-025-00313-w","DOIUrl":"10.1186/s40959-025-00313-w","url":null,"abstract":"<p><strong>Background: </strong>This study investigates the long-term cardiac effects of trastuzumab-based chemotherapy in early breast cancer (EBC) survivors. We extend the original MANTICORE trial which showed that angiotensin-converting enzyme inhibitors (ACEI) and beta-blockers (BB) could mitigate the decline in left ventricular (LV) ejection fraction (EF) during the first year of trastuzumab treatment.</p><p><strong>Objectives: </strong>We hypothesized that, over time, cardiac function would decline further and adverse changes in cardiac geometry would occur due to the aging of the population and prior treatment.</p><p><strong>Methods: </strong>The study enrolled 52 participants from the original MANTICORE trial cohort, with cardiac magnetic resonance (CMR) imaging conducted at a median of 6.5 years post randomization to treatment.</p><p><strong>Results: </strong>We found that, contrary to the hypothesis, participants maintained LV EF over the follow-up period. Specifically, the placebo group exhibited a recovery in LV EF to levels comparable with the treatment groups, suggesting no long-term differential impact on cardiac function. However, a significant reduction in LV mass was observed across all groups, the clinical implications of which remain unclear.</p><p><strong>Conclusions: </strong>The findings suggest that in a selected population receiving trastuzumab-based chemotherapy, extended cardiac imaging surveillance beyond one-year post-treatment may be unnecessary. We posit that the presence of HER2 overexpressing breast cancer influenced hypertrophic changes to cardiac geometry observed at baseline and one year, which resolved after completing HER2-blocking treatment. The study also highlights the need for further research to understand the significance of changes in cardiac geometry during and after breast cancer treatment​.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"13"},"PeriodicalIF":3.2,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11806551/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143373789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Major adverse cardiovascular events among Black and White Veterans receiving androgen deprivation therapy for prostate cancer: a retrospective cohort study.","authors":"Alexander R Lucas, Dustin Bastiach, Bassam Dahman, Asit K Paul, Samina Hirani, Vanessa B Sheppard, W Gregory Hundley, Bhaumik B Patel, Rhonda L Bitting, Michael G Chang","doi":"10.1186/s40959-025-00312-x","DOIUrl":"10.1186/s40959-025-00312-x","url":null,"abstract":"<p><strong>Background: </strong>Androgen deprivation therapy (ADT) is the cornerstone treatment strategy for men diagnosed with high-risk prostate cancer (PC) but may increase risk for major adverse cardiovascular events (MACE). We examined whether men treated with ADT and radiation therapy (ADT + RT) developed MACE at a higher rate than men receiving RT alone. Secondly, we sought to determine if Black men receiving RT + ADT developed MACE at a higher rate than White men.</p><p><strong>Methods: </strong>This retrospective cohort study examined time to diagnosis of MACE among Veterans with PC. We used a 1:1 propensity score matching process to determine whether treatment type (ADT + RT vs. RT alone), race (Black vs. White men) or having a previous diagnosis of a cardiometabolic disease (CMD) were associated with differences in the rate at which men develop MACE.</p><p><strong>Results: </strong>Veterans with PC were White (68%) and Black (32%). At PC diagnosis, the mean age was 65.9 years. The majority had stage 2 disease (83.0%) classified as intermediate risk (43.1%). Treatment-matched models showed men receiving ADT + RT were less likely to develop MACE when they no pre-existing CMD. Men treated with ADT + RT or RT alone had significantly increased risks of MACE is they had pre-existing CMD. Black men had the same risk of MACE as non-Hispanic Whites.</p><p><strong>Conclusions: </strong>Preexisting CMD and multimorbidity are significant risks for MACE among men treated for PC within the VA healthcare system whether treated with ADT + RT or with RT alone, highlighting the importance pretreatment optimization of comorbidities.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"12"},"PeriodicalIF":3.2,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11800468/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143363980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}