Cardio-oncology最新文献

{"title":"Real-world prevalence and outcome of elevated right ventricular systolic pressure in myelofibrosis.","authors":"Alexis Behne Sharma, Elicia Wang, Sruthi Selvakumar, Himara Koelmeyer, Sanath Shetty, Kinley Buckley, Qianxing Mo, Teagen Smith, Austin Chao, Carson Balen, Gowtam Mannam, Jacob Yudiono, Kyle Lien, Sami Khatib, Varshith Paduchuri, Najla Al Ali, Jinming Song, Taiga Nishihori, Jeffrey E Lancet, Mohammed Alomar, John L Cleveland, Andrew Kuykendall, Rami S Komrokji, Seongseok Yun, Dae Hyun Lee","doi":"10.1186/s40959-026-00474-2","DOIUrl":"https://doi.org/10.1186/s40959-026-00474-2","url":null,"abstract":"<p><strong>Background: </strong>Myelofibrosis (MF) is a subgroup of Philadelphia chromosome-negative myeloproliferative neoplasms that are associated with an increased risk of cardiovascular disease, including pulmonary hypertension. Here we report the real-world prevalence, risk factors, and clinical outcomes of eRVSP in MF patients.</p><p><strong>Methods: </strong>A retrospective, single-center cohort study was conducted on 208 patients with MF that were diagnosed between 2013 and 2023. Elevated right ventricular systolic pressure (eRVSP) was defined as RVSP > 35 mmHg. Major adverse cardiac events (MACE) were defined as new-onset congestive heart failure, coronary artery disease requiring intervention, cerebrovascular events, or cardiovascular death after MF diagnosis. Univariate and multivariable Cox proportional hazard ratio regression model with eRVSP status as time-dependent covariate was used to estimate overall survival.</p><p><strong>Results: </strong>Echocardiograms were performed in 208 MF patients, with RVSP estimates available in 156 patients (75%). eRVSP was present in 61 patients (39.1%). Patients with eRVSP were older (65 vs. 62 years, p = 0.053) and had higher rates of baseline hypertension (65.6% vs. 43.2%, p = 0.01), atrial fibrillation (16.4% vs. 4.2%, p = 0.02). MACE after diagnosis of MF occurred in 43 (20.7%) patients and was more frequent in eRVSP patients (36.1% vs. 15.8% p = 0.007), and this was predominantly driven by increased rates of new-onset congestive heart failure (27.9% vs. 8.4%, p = 0.003). In multivariable analysis, the presence of time-dependent eRVSP was associated with reduced survival (aHR: 4.41; 95%CI:2.84-6.85) after adjustment for clinically relevant covariates.</p><p><strong>Conclusions: </strong>eRVSP was prevalent among MF patients undergoing echocardiogram and this was associated with increased cardiovascular morbidity, particularly HF. Furthermore, eRVSP was associated with inferior survival and underscores the need for targeted screening and management in MF patients with cardiovascular risk factors and diseases. Prospective studies with baseline cardiovascular assessment and echocardiograms in all MF patients will establish true prevalence and may further elucidate the morbidity and mortality implication of eRVSP in MF patients.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of ivabradine for anthracycline-induced cardiotoxicity: a meta-analysis.","authors":"Muhammad Umar, Aizaz Ali, Avirup Guha, Mirza Mohammad Ali Baig, Fazia Khattak, Daniel Addison","doi":"10.1186/s40959-026-00491-1","DOIUrl":"https://doi.org/10.1186/s40959-026-00491-1","url":null,"abstract":"<p><strong>Purpose: </strong>Anthracyclines are widely used anticancer agents but are limited by dose-dependent cardiotoxicity. Ivabradine selectively reduces heart rate without negative inotropy and may offer cardio protection in cancer patients, though its efficacy in anthracycline-induced cardiotoxicity (AIC) remains unclear.</p><p><strong>Methods: </strong>We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) comparing ivabradine versus placebo in adult patients receiving anthracycline therapy. PubMed, Cochrane Central, Embase, Web of Science, Google Scholar, Scopus and ClinicalTrials.gov, and reference lists were searched through August 2025. Outcomes included left ventricular ejection fraction (LVEF), heart rate, blood pressure, NT-proBNP, and strain-based parameters. Risk of bias was assessed with the Cochrane RoB 2 tool.</p><p><strong>Results: </strong>Three RCTs (n = 210) met inclusion criteria. Ivabradine showed no significant effect on LVEF (MD 0.32%, 95% CI - 0.90 to 1.54; p = 0.61) or NT-proBNP. Heart rate reduction was directionally favorable but not statistically significant (MD - 4.11 bpm, 95% CI - 8.69 to 0.46; p = 0.08). Systolic and diastolic blood pressure were unchanged. Strain-based outcomes were inconsistently reported, precluding pooled analysis.</p><p><strong>Conclusions: </strong>Given the limited sample size, heterogeneity, and variability in endpoint definitions, current evidence is insufficient to establish a definitive cardioprotective role for ivabradine in AIC. Larger, rigorously designed trials with standardized imaging and biomarker endpoints are needed to determine its role.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical utility of the HFA-ICOS risk tool in real-world HER2-positive breast cancer patients receiving therapy.","authors":"Lama Alfehaid, Nada Alsuhebany, Khalid Alamer, Ahmed S Alanazi, Hadi Skouri","doi":"10.1186/s40959-026-00500-3","DOIUrl":"https://doi.org/10.1186/s40959-026-00500-3","url":null,"abstract":"<p><strong>Background: </strong>The HFA-ICOS baseline cardiovascular risk stratification framework is widely recommended to guide surveillance in patients receiving potentially cardiotoxic cancer therapies, yet real-world evidence supporting its clinical risk separation remains limited.</p><p><strong>Methods: </strong>We conducted a multicenter retrospective study of adults with HER2-positive breast cancer treated at tertiary centers from 2016 to 2023. Baseline cardiovascular risk was classified by the HFA-ICOS framework (low to very high). The primary outcome was composite cardiotoxicity, defined by a decline in left ventricular ejection fraction (LVEF), deterioration in global longitudinal strain (GLS), ECG/arrhythmia events, or elevated cardiac biomarkers. Cardiovascular risk rates and patterns were compared across categories. Discrimination and calibration were explored, with logistic regression and Kaplan-Meier analyses performed.</p><p><strong>Results: </strong>Among 687 patients, 273 (39.7%) developed composite cardiotoxicity during follow-up. Cardiotoxicity occurred across all HFA-ICOS risk categories, with overlap in event rates and timing. Discrimination analyses showed modest performance for LVEF, GLS, ECG, and composite outcomes, with AUCs of 0.51-0.55. Sensitivity was low (0.28-0.37), while specificity was moderate (0.73-0.74). Calibration analyses indicated acceptable risk prediction. Multivariable models adjusted for age, comorbidities, baseline LVEF, prior anthracycline, and radiation therapy showed that baseline HFA-ICOS category was not independently associated with cardiotoxicity (aOR: 0.88; 95% CI: 0.56-1.37). Kaplan-Meier curves showed overlapping event-free survival across risk groups.</p><p><strong>Conclusions: </strong>In this real-world cohort of HER2-positive breast cancer patients, baseline HFA-ICOS stratification showed limited ability to clearly distinguish cardiotoxicity risk across categories. These findings suggest that baseline risk assessment alone may be insufficient for individualized prediction and should be complemented by dynamic, on-treatment surveillance strategies.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Echocardiographically occult nonbacterial thrombotic endocarditis with tumor cell-containing valvular vegetations in metastatic breast cancer.","authors":"Kristina Charaya, Irina Sokolova, Elnara Abdullaeva, Aleksei Volovchenko, Tamerlan Erdniev, Nurudin Nurutdinov, Nana Gogiberidze, Dmitry Shchekochikhin, Petr Chomakhidze, Alexandra Bogdanova, Irina Ingisonis, Yulia Lerner, Alexander Zanozin, Yulia Andreeva, Denis Andreev, Maria Poltavskaya","doi":"10.1186/s40959-026-00498-8","DOIUrl":"https://doi.org/10.1186/s40959-026-00498-8","url":null,"abstract":"<p><strong>Background: </strong>Nonbacterial thrombotic endocarditis (NBTE) is an uncommon but important cause of systemic arterial embolism, most often occurring in advanced malignancy. Diagnosis is frequently difficult because vegetations may be small, transient, or not visualized on echocardiography, which may delay recognition.</p><p><strong>Case presentation: </strong>A 37-year-old woman presented with multifocal ischemic strokes and visceral infarctions. Initial transesophageal echocardiography (TEE) showed a small isoechoic structure on the mitral valve, interpreted as a possible vegetation. Despite empiric broad-spectrum antibiotics and therapeutic anticoagulation, she developed progressive thrombocytopenia, hemolytic anemia, disseminated intravascular coagulation, and multiorgan failure. Repeated blood cultures were negative, and repeat TEE showed no valvular masses. The patient died despite plasma exchange, plasma infusion, corticosteroids, and transfusion support. Postmortem examination revealed previously undiagnosed bilateral metastatic invasive lobular breast carcinoma. Histopathology demonstrated tumor cell-containing fibrin-platelet vegetations on the mitral and tricuspid valves, with fibrin-rich microthrombi in renal arterioles consistent with secondary paraneoplastic thrombotic microangiopathy.</p><p><strong>Conclusion: </strong>This autopsy-confirmed case underscores that malignancy-associated NBTE may remain echocardiographically occult despite extensive arterial embolization. It also demonstrates that valvular thrombi may incorporate tumor cells, providing a direct substrate for embolic events.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiotoxicity of monoclonal antibody-based therapies in breast cancer: a contemporary narrative review.","authors":"Ana Cláudia Aparecida Santos Nussbaum, Marcelo Antonini, André Mattar, Fernando Bacal, Juliana Monte Real","doi":"10.1186/s40959-026-00490-2","DOIUrl":"https://doi.org/10.1186/s40959-026-00490-2","url":null,"abstract":"<p><p>Monoclonal antibody-based therapies have substantially improved outcomes in breast cancer, particularly through HER2-directed treatment strategies, but have also introduced important cardiovascular toxicities that require careful recognition and management. This narrative review summarizes current evidence on cardiotoxicity associated with monoclonal antibody therapies used in breast cancer, with emphasis on HER2-targeted antibodies, antibody-drug conjugates, and selected immune checkpoint inhibitors.Trastuzumab remains the best-characterized monoclonal antibody associated with cancer therapy-related cardiac dysfunction, most commonly presenting as left ventricular systolic dysfunction, particularly in patients previously exposed to anthracyclines or with baseline cardiovascular risk factors. Pertuzumab and currently available antibody-drug conjugates have not shown a major increase in cardiotoxic risk beyond that observed with established HER2-directed therapy, although long-term data remain limited for some newer agents. Immune checkpoint inhibitors are less commonly associated with cardiovascular toxicity, but may rarely cause severe immune-mediated complications, particularly myocarditis and also non-immune mediated toxicity such as cardiac dysfunction.Contemporary evaluation of cardiotoxicity increasingly relies on an integrated cardio-oncology framework incorporating left ventricular ejection fraction, global longitudinal strain, and cardiac biomarkers, with growing recognition of subclinical dysfunction and right ventricular involvement. Current management strategies emphasize baseline cardiovascular risk assessment, risk-adapted surveillance, early initiation of heart failure therapy when indicated, and individualized multidisciplinary decision-making regarding continuation of anticancer treatment, including permissive cardiotoxicity in selected patients.As the use of monoclonal antibody therapies continues to expand, optimizing the balance between oncologic efficacy and cardiovascular safety remains a central goal of modern breast cancer care.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Survival trends in the management of carcinoid heart disease among patients with neuroendocrine neoplasms.","authors":"Sarah Jung, Rebecca Steinberg, Angel Ji, Jeffrey M Switchenko, Anant Mandawat, Daniel M Halperin, Olatunji B Alese","doi":"10.1186/s40959-026-00475-1","DOIUrl":"https://doi.org/10.1186/s40959-026-00475-1","url":null,"abstract":"<p><strong>Background: </strong>Nearly 20% of patients with neuroendocrine tumors (NET) develop carcinoid syndrome (CS), and 20-25% of those with CS develop carcinoid heart disease (CHD). Contemporary risk factors for CHD and prognostic variables in NET management remain limited. This study aimed to characterize the clinical and imaging factors associated with the development, and prognostic impact of carcinoid heart disease in patients with neuroendocrine neoplasms.</p><p><strong>Methods: </strong>A single-institution, retrospective analysis of well-differentiated NET patients from January 2010 to December 2024 was conducted. Cox proportional hazards regression assessed associations between baseline covariates and CHD development (primary endpoint) and overall survival (OS; secondary endpoint). CHD was defined as moderate or severe tricuspid regurgitation on echocardiogram with echocardiographic features consistent with carcinoid valvulopathy. Survival curves were estimated using Kaplan-Meier methods. A p-value < 0.05 was considered significant.</p><p><strong>Results: </strong>We identified 270 patients with NET. Median age was 64.5 years; 52% were male; 5.6% developed CHD. CS was present in 10% (n = 27), and 41% of those with CS developed CHD. Fifteen patients (5.6%) developed carcinoid heart disease. Common primary sites were lung (26%), pancreas (17.4%), and small intestine (16.2%). CHD was associated with more hospitalizations and greater use of systemic or multimodal therapies. For OS, median OS for CHD patients was 90.8 months, while median OS was not reached for the full NET cohort. CHD independently predicted worse OS (HR 7.09; 95% CI: 1.84-27.40; p = 0.004). Systemic therapy use (HR 8.97; p = 0.0101) and high-grade tumors (HR 6.92; p < 0.001) were also associated with worse OS.</p><p><strong>Conclusion: </strong>In NET patients, CHD and high-grade tumors were associated with worse OS. Systemic therapy use was associated with worse overall survival, likely reflecting more advanced disease rather than a causal treatment effect. Although CHD incidence is low, early detection and close monitoring remain essential.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of angiotensin II in cardiovascular disease-induced cancer growth.","authors":"Benji van Berlo, Pierangela Esposito, Alessandra Greco, Charles X L van Assche, Tine Bruyns, Birgit Van Asbroeck, Celine Civati, Ronny Mohren, Berta Cillero-Pastor, Pieter-Jan Guns, Gilles W De Keulenaer, Vincent F M Segers","doi":"10.1186/s40959-026-00495-x","DOIUrl":"https://doi.org/10.1186/s40959-026-00495-x","url":null,"abstract":"<p><strong>Background: </strong>The higher incidence of cancer in patients with cardiovascular disease (CVD) has historically been explained by shared risk factors. Recent studies suggest, however, a causal relationship. Nevertheless, the mechanisms of CVD-induced cancer are incompletely understood. Here, we hypothesize that angiotensin II (ANGII) links CVD and increased cancer growth.</p><p><strong>Objective: </strong>We investigated the impact of ANGII-induced CVD on cancer growth in vivo, differentiating between a direct effect of ANGII on tumor cells or indirect effects secondary to CVD.</p><p><strong>Methods: </strong>The effect of ANGII on cancer growth was studied in C57BL/6J mice with cancer. Cancer was either induced by subcutaneous injection of Lewis lung carcinoma (LLC) cells, MC38 colon cancer cells, or by genetic susceptibility (APC_min mice). To differentiate between direct and indirect effects of ANGII on cancer growth three strategies were implemented: (i) Evaluating a protocol with and without overlap between ANGII treatment and the injection of tumor cells, (ii) comparing the effect of a high (2000 ng.kg^- 1.min^- 1) and low (400 ng.kg^- 1.min^- 1) dose of ANGII on intestinal polyp growth in APC_min mice and (iii) comparing the impact of ANGII on tumor growth in high (LLC) and low (MC38) angiotensin II receptor type I (AT1) expressing tumor cells.</p><p><strong>Results: </strong>High dose ANGII-treatment induced left ventricle (LV) hypertrophy and cardiac fibrosis, and enhanced growth of injected tumor cells, but only when LCC tumor cells with high expression of AT1 were used, and when these cells were injected during ANGII treatment. ANGII did not increase cancer growth when LCC cells were injected after halting ANGII treatment, or when MC38 tumor cells with low AT1 levels were used. ANGII also increased the number of intestinal polyps in APC_min mice, even at a low dose that did not induce LV hypertrophy or cardiac fibrosis. Lastly, an analysis of publicly available cancer databases showed that AT1 gene copy number variation is increased in most human cancer lines and tumors.</p><p><strong>Conclusion: </strong>This study indicates that ANGII has direct effects on cancer growth, warranting further research into the role of an activated renin-angiotensin-aldosterone-system (RAAS) as a mechanistic link between CVD and cancer growth in AT1-positive tumors.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endoscopic ultrasound-guided transoesophageal pericardiocentesis: a case report on a therapeutic solution for pericardial tamponade with malignant posterior pericardial effusion.","authors":"Alfred Chung Pui So, John Conibear, Adam Januszweski, Charlotte Manisty, William Ricketts, David Waller, Patrick Wilson, Kelvin Lau","doi":"10.1186/s40959-026-00460-8","DOIUrl":"https://doi.org/10.1186/s40959-026-00460-8","url":null,"abstract":"<p><strong>Background: </strong>Treatment options for malignant loculated pericardial effusions are limited and effusions often reaccumulate following surgical management. For posterior effusions, access percutaneously is challenging, hence alternative approaches may be needed. Here, we report a rare case of transoesophageal endoscopic ultrasound (EUS)-guided pericardiocentesis for recurrent loculated posterior malignant pericardial effusion causing haemodynamic compromise.</p><p><strong>Case presentation: </strong>A 65-year-old male was diagnosed with metastatic lung adenocarcinoma following an emergency admission with malignant cardiac tamponade. He underwent percutaneous pericardiocentesis under transthoracic ultrasound guidance and was started on osimertinib for an EGFR-exon-19 sensitising mutation. 6 weeks later, he was readmitted with symptomatic pericardial effusion and underwent an urgent pericardial window. The procedure was complicated due to multiple loculations, densely adherent sac, and poor respiratory reserve. Re-staging CT scan at the time showed partial response to osimertinib. Two weeks post-discharge, repeat echocardiography showed a 4.0 cm loculated posterior pericardial effusion compressing the left atrium, with evidence of haemodynamic compromise. Further percutaneous drainage was not feasible due to the posterior location, and his anaesthetic risk for repeat thoracotomy was considered prohibitively high. Due to his good pre-morbid baseline, favourable genomic profile, and ongoing response to osimertinib, the multidisciplinary team trialled an unconventional approach using transoesophageal pericardiocentesis under endoscopic ultrasound (EUS) guidance under conscious sedation. The procedure was uncomplicated and 100mL of haemosanguinous fluid was drained with immediate symptomatic relief. Pericardial cytology was negative for malignant cells and extended pericardial culture grew Klebsiella, a contaminant from the gastrointestinal tract. The effusion reaccumulated four weeks later and restaging CT eight weeks post-drainage suggested early progressive disease. The patient further deteriorated and passed away, six months from his initial presentation with malignant pericardial tamponade.</p><p><strong>Conclusion: </strong>We present one of few reported cases of successful transoesophageal EUS-guided pericardiocentesis as a potential alternative for pericardial effusion drainage. Improved prognosis in patients with metastatic lung cancer, especially those with actionable genomic aberrations, should be considered for more aggressive therapeutic approaches when no other alternatives exist following clear discussion regarding risks and benefits.</p>","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular care in adult cancer survivorship post-therapy: a cross-sectional analysis of clinical practice guidelines.","authors":"Joshua Ayoson, Nadine Schneider, Nina Müller, Brian Casanova, Rodi Tomar, Lina Kleijkers, Luca Siragusa, Sacha I Rothschild, Katharina Gut-Fischer, Maria M Wertli, Eva Haegler-Laube","doi":"10.1186/s40959-026-00493-z","DOIUrl":"https://doi.org/10.1186/s40959-026-00493-z","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background/objective: &lt;/strong&gt;Cardiovascular disease (CVD) is a major and potentially life-threatening late effect in cancer survivors, in some populations surpassing the risk of cancer recurrence as a leading cause of mortality. The aim of this study was to compare and critically appraise existing guidelines on CVD in cancer survivorship and to synthesize evidence-informed recommendations for the management of cardiovascular health in this population.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A systematic search was conducted on 16 January 2025 across PubMed, the Cochrane Library, and professional society websites. We included guidelines from professional oncology societies addressing CVD management in adult cancer survivors, published in English between 2000 and 2024. Guideline quality was assessed using the Appraisal of Guidelines for Research and Evaluation II (AGREE II) instrument. Recommendations, levels of evidence, and strengths of recommendations were extracted and standardized into the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) framework. Screening, grading, and data extraction were performed independently by two reviewers.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Of 524 screened references, twelve guidelines from seven professional societies met the inclusion criteria and were analyzed. Of the twelve guidelines, two were rated as high quality and ten as moderate quality. Risk stratification emerged as the foundation of follow-up care, with most guidelines considering baseline cardiovascular risk, type and cumulative dose of specific cancer therapy, and treatment-related cardiotoxicity. The ESC 2022 guideline proposed the most detailed tiered model (very high risk, early high risk, late high risk, moderate risk and low risk), while others such as ASCO 2017 and NCCN 2024 guidelines used simpler schemes based on anthracycline dose, age, or pre-existing CVD. Follow-up strategies, including surveillance, pharmacologic therapy, lifestyle counseling, and specialist referral were linked to risk category. However, substantial variation existed in the timing and frequency of cardiac imaging, use of biomarkers, and thresholds for initiating cardio-protective medication. Lifestyle modification and multidisciplinary care were consistently recommended, but detail and supporting evidence varied across guidelines. Structured implementation of cardio-oncology rehabilitation models was limited. Pregnancy-related cardiovascular surveillance and long-term implications of novel oncologic therapies were inconsistently addressed. Several recommendations were strongly endorsed despite limited prospective outcome data, highlighting a gap between recommendation strength and evidence level.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;In long-term survivorship, CVD represents a major determinant of morbidity and mortality beyond cancer surveillance. In this analysis, there was a consensus across guidelines on the central role of risk stratificatio","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neck adiposity on standard oncologic CT predicts radiation-induced carotid disease in oropharyngeal cancer.","authors":"Efthymios Triantafyllou, Dhawal S Bandrey, Bhumiben Patel, Patrik J Van-Bergen, Gabrielle N Mbagwu, Jennifer Shen, Taher K Kapadia, Juhee Song, Jun-Ichi Abe, Amy C Moreno, Mohamed A Naser, Katherine A Hutcheson, David I Rosenthal, Shaden Khalaf, Cezar Iliescu, Anita Deswal, Elie Mouhayar, Clifton D Fuller, Efstratios Koutroumpakis","doi":"10.1186/s40959-026-00486-y","DOIUrl":"https://doi.org/10.1186/s40959-026-00486-y","url":null,"abstract":"","PeriodicalId":9804,"journal":{"name":"Cardio-oncology","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}