Cardio-oncology最新文献

{"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}

{"title":"Socioeconomic status and left ventricular ejection fraction decline in breast cancer survivors following receipt of doxorubicin (PREVENT WF-98213).","authors":"Arnethea L Sutton, Nathaniel S O'Connell, Alexander R Lucas, Kristine C Olson, Kerryn W Reding, Vanessa B Sheppard, Bonnie Ky, Kathryn J Ruddy, Kathryn E Weaver, W Gregory Hundley","doi":"10.1186/s40959-025-00311-y","DOIUrl":"10.1186/s40959-025-00311-y","url":null,"abstract":"<p><p>Cancer survivors receiving doxorubicin may experience left ventricular ejection fraction (LVEF) decline during and following treatment; however, explanations for variations in decline beyond dosage differences, such as those related to socioeconomic status (SES), have not been fully examined. We conducted a retrospective analysis of a cohort of 215 breast cancer survivors receiving doxorubicin. SES factors (e.g., household income, education) were collected via a survey at a baseline and EF was assessed using magnetic resonance imaging. Linear regression models showed that prior to treatment, no SES factors were associated with LVEF. However, six months following treatment, survivors who were unemployed for reasons other than retirement and disability experienced greater LVEF declines compared to survivors who were employed ((b = 2.79 [95% confidence interval (CI): 0.37-5.20; p = 0.026). Our study demonstrated that non-clinical factors associated with social drivers of health, such as socioeconomic status, contribute to subclinical cardiovascular dysfunction and therefore supports further investigation of mechanisms behind these associations. Trial registration NCT01988571 (WF-98213).</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"11"},"PeriodicalIF":3.2,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11796113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254771","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":"Screening for coronary artery disease among cancer survivors: rationale and design of the REDEEM-CAD study.","authors":"Cheng Hwee Soh, Joel Smith, Shristy Shrestha, Mark Nolan, Joshua Wong, Nitesh Nerlekar, Thomas H Marwick","doi":"10.1186/s40959-025-00308-7","DOIUrl":"10.1186/s40959-025-00308-7","url":null,"abstract":"<p><strong>Background: </strong>Cancer survivors are reported to be at a heightened risk of coronary artery disease (CAD) due to shared risk factors, potentially cardiotoxic cancer treatments and premature aging in survivors. Early identification of those who are at greater risk, followed by protective treatment, can prevent CAD progression. However, to date there was a relative paucity of prospective data to optimally guide management of atherosclerotic coronary risk among cancer survivors.</p><p><strong>Methods: </strong>The REDEEM-CAD (Risk-guidEd DisEasE Management plan to prevent CAD in patients with previous cancer) study is a prospective cohort study conducted in Victoria and Tasmania, Australia aiming to evaluate the efficacy of a comprehensive CAD screening strategy. Cancer survivors aged ≥ 40 years with cancer treatment ≥ 5 years prior are eligible for the study. Consented participants will be stratified into low, intermediate or high risk of major atherosclerotic adverse events based on clinical assessment and biochemistry tests. Subsequently, those within the intermediate risk will be referred for coronary artery calcium (CAC) scoring, with computed tomography coronary angiography (CTCA) completed where CAC > 0 and < 400. Participants with high risk or CAC > 400 will be informed about strategies (including lipid-lowering therapy) to manage asymptomatic CAD. Those with low clinical risk or CAC = 0 will conclude their participation while those with CTCA imaged at baseline will be referred for a follow-up CTCA 2-year post-baseline. The primary endpoint is to identify the prevalence of CAD, identified via CAC scoring, among cancer survivors classified as intermediate risk. Secondary endpoint includes the absolute change in total coronary plaque volume over 24 months among those imaged at baseline and follow-up. The REDEEM-CAD study will be the first study to systematically evaluate risk of CAD in cancer survivors, and subsequent responsiveness to coronary risk reduction. This will offer valuable insights into the efficacy of the CAD screening strategies among cancer survivors and the impact of treatment on managing plaque progression.</p><p><strong>Trial registration: </strong>NCT05366153.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"10"},"PeriodicalIF":3.2,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143188257","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":"Impact of advanced lung cancer inflammation index on all-cause mortality among patients with heart failure: a systematic review and meta-analysis with reconstructed time-to-event data.","authors":"Ahmed Mazen Amin, Ramy Ghaly, Hossam Elbenawi, Abdelrahman Ewis, Ubaid Khan, Khaled S M Elshaer, Mohamed Abuelazm, Basel Abdelazeem, Brijesh Patel, Farris K Timimi, Islam Y Elgendy","doi":"10.1186/s40959-024-00295-1","DOIUrl":"10.1186/s40959-024-00295-1","url":null,"abstract":"<p><strong>Background: </strong>Heart failure (HF) is associated with systemic inflammation and hypercatabolic syndrome, impacting body metabolism. The advanced lung cancer inflammation index (ALI) is a novel inflammatory and nutritional biomarker. We aimed to investigate the prognostic role of ALI in patients with HF.</p><p><strong>Methods: </strong>We comprehensively searched PubMed, WOS, SCOPUS, EMBASE, and CENTRAL through October 2024. We conducted a pair-wise and prognostic systematic review and meta-analysis with a reconstructed time-to-event data meta-analysis. All analyses were performed using R V. 4.3.1. This meta-analysis was registered at PROSPERO (CRD42024535227).</p><p><strong>Results: </strong>We included five studies with 2,795 patients. In the pair-wise meta-analysis, ALI ≤ 25 was significantly associated with an increased incidence of all-cause mortality compared with ALI > 25 (risk ratio [RR] 1.73, 95% confidence interval [CI] 1.36-2.21, P < 0.01). On the adjusted prognostic meta-analysis, higher ALI was significantly associated with a reduction in the risk of all-cause mortality (hazards ratio [HR] 0.45, 95% CI 0.35-0.58-, P < 0.01). The reconstructed Kaplan Meier showed that ALI > 25 was significantly associated with a 56% reduction in the risk of all-cause mortality compared with ALI ≤ 25 (HR 0.44, 95% CI 0.38-0.50, P < 0.000001).</p><p><strong>Conclusion: </strong>Among patients with HF, a low ALI was associated with a higher incidence of all-cause mortality rate than those with a high ALI. These findings suggest that ALI can be used for prognostic stratification and aid clinical decision-making in HF management.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"9"},"PeriodicalIF":3.2,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11780879/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064165","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":"Rationale and design of the HOVON 170 DLBCL-ANTICIPATE trial: preventing anthracycline-induced cardiac dysfunction with dexrazoxane.","authors":"Marijke Linschoten, Jesse Geels, Erik van Werkhoven, Heleen Visser-Wisselaar, Martine E D Chamuleau, Arco J Teske, Lourens Robbers, Simone Oerlemans, Heleen Crommelin, Marleen Breems-de Ridder, Astrid Schut, Folkert W Asselbergs, Anna van Rhenen","doi":"10.1186/s40959-025-00303-y","DOIUrl":"10.1186/s40959-025-00303-y","url":null,"abstract":"<p><strong>Background: </strong>Dexrazoxane has been studied for its ability to prevent anthracycline-induced cardiac dysfunction (AICD) in several trials but its use in clinical practice remains limited. This is related to the low to moderate quality of the generated evidence, safety concerns and restricted prescribing indications. Additional randomized trials are needed before this drug can be routinely integrated into cardio-oncology clinical practice.</p><p><strong>Objectives: </strong>To describe the rationale and design of the HOVON 170 DLBCL - ANTICIPATE trial. This trial aims to establish the efficacy and safety of dexrazoxane for the primary prevention of AICD in patients diagnosed with Diffuse Large B-Cell Lymphoma (DLBCL) treated with six cycles R-CHOP₂₁ chemo-immunotherapy.</p><p><strong>Methods: </strong>This is a multicenter, parallel-group, open-label, phase III trial, randomizing 324 patients between either no cardioprotective treatment or dexrazoxane from the first R-CHOP cycle. The primary and co-primary endpoints are the incidence of AICD within 12 months of registration and the percentage of patients with complete metabolic remission at the end-of-treatment PET-CT respectively. The trial is registered at the EU Clinical Trials Register (EU-CT number 2023-505377-32) and ClinicalTrials.gov (NCT06220032).</p><p><strong>Results: </strong>The medical research ethics committee approved the trial in May 2024. Recruitment has started in September 2024 and is expected to last for three years.</p><p><strong>Conclusions: </strong>This trial is poised to contribute crucial evidence concerning the efficacy and safety on the use of dexrazoxane in the primary prevention of AICD. The trial is anticipated to address critical knowledge gaps and offer important insights into the value of dexrazoxane in cardio-oncology practice.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":"11 1","pages":"8"},"PeriodicalIF":3.2,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058165","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}