Abstract The May Measurement Month (MMM) campaign was conducted in the Philippines in 2023 to raise awareness of the importance of raised blood pressure (BP). Adults aged ≥ 18 years were recruited via opportunistic/convenience sampling at various screening sites. Three seated BP readings were taken on each participant, and a questionnaire collected information on demographics, lifestyle factors, and comorbidities. Hypertension was defined as a systolic BP ≥140mmHg and/or diastolic BP ≥90mmHg or being on BP-lowering medication. Controlled BP was defined as being on BP-lowering medication with a BP <140/90mmHg. In total, 33,190 were screened, with a mean age of 45.6 years and 58.9% were female. Of all participants, 11,421 (34.4%) had hypertension, of whom 4,177 (36.6%) were aware, and 4,058 (35.5%) were on antihypertensive medication. Of those on antihypertensive medication, 2,088 (51.5%) had controlled BP, and of all participants with hypertension, 18.3% had controlled BP. The MMM campaign in the Philippines identified a substantial number of participants with untreated or inadequately treated hypertension. This group of patients represent a missed opportunity for prevention of complications, hence the need for improved awareness through establishment of year-round hypertension screening programs and the use of at least two or more first-line antihypertensive drugs to achieve good BP control as recommended by guidelines.
Abstract The May Measurement Month (MMM) campaign was conducted in the Republic of Ireland and the United Kingdom in 2023 to raise awareness of raised blood pressure (BP). Adults aged ≥18 years were recruited through convenience sampling at hospitals, general practice surgeries, community pharmacies, universities, gyms, and other public places. Three seated BP readings were taken for each participant, and a questionnaire collected information on demographics, lifestyle factors, and comorbidities. Hypertension was defined as a systolic BP ≥140mmHg or diastolic BP ≥90mmHg or being on BP-lowering medication. Controlled BP was defined as being on BP-lowering medication with a BP <140/90mmHg. Multiple imputation was used to estimate one or two missing BP readings. In total, 2,201 were screened, with a mean age of 51.9 years and 51.2% were female. Of all participants, 821 (37.3%) had hypertension, of whom 393 (47.9%) were aware, and 300 (36.5%) were on antihypertensive medication. Of those on antihypertensive medication, 152 (50.8%) had controlled BP, and of all participants with hypertension, 18.6% had controlled BP. Hypertension was more common in males, whilst awareness, antihypertensive medication use, and BP control were lower. Hypertension awareness and antihypertensive medication use were particularly low in adults aged <50 years. The MMM campaign in the Republic of Ireland and the United Kingdom identified substantial numbers of participants with untreated or inadequately treated hypertension. This evidence reinforces the urgent need for more effective hypertension detection and control strategies to abate the rising hypertension burden.
Abstract Background / Introduction Venous thromboembolism (VTE) is a major cause of morbidity and mortality in patients with cancer. Although international guidelines provide recommendations for acute treatment and secondary prevention, real-world implementation may vary across medical specialties, particularly in complex clinical scenarios. Purpose To evaluate real-world, specialty-based approaches to acute treatment and secondary prevention of VTE in patients with cancer. Methods We conducted a nationwide, cross-sectional survey among physicians in Turkiye using a structured questionnaire. The survey focused on VTE management beyond primary prevention and included questions on acute-phase anticoagulant choice (first 10 days), secondary prevention duration and agent selection, criteria for extending anticoagulation up to 12 months, management of recurrent events under anticoagulation, and challenging clinical scenarios such as brain tumours, neurosurgical planning, severe renal impairment, thrombocytopenia, and pregnancy. Specialty-based comparisons were performed using chi-square or Fisher’s exact tests, as appropriate. Results A total of 84 physicians participated, including 50 cardiologists (59.5%) and 34 oncologists (40.5%). Low-molecular-weight heparin (LMWH) was the most frequently selected anticoagulant for acute VTE treatment (72.6%), with no significant difference between specialties. Following the acute phase, secondary prevention duration was most commonly individualised (56.0%). Marked inter-specialty differences were observed in secondary prevention agent selection with cardiologists predominantly favouring direct oral anticoagulants and oncologists more frequently preferring LMWH. Extension of secondary prophylaxis to 12 months was mainly driven by persistence of VTE risk factors, such as active cancer or ongoing anticancer therapy (65.1%). Approaches to recurrent VTE under anticoagulation were heterogeneous. In patients with brain tumours scheduled for neurosurgery, prophylaxis strategies differed significantly between specialties (p≈0.02). In severe renal impairment, LMWH and unfractionated heparin were preferred, whereas use of direct oral anticoagulants was limited. In pregnancy, LMWH was overwhelmingly favoured (78.3%). Notably, 94.0% of respondents reported a need to further update their knowledge on VTE prevention and treatment in cancer. All of data presented in Table. Conclusion(s) LMWH remains the cornerstone of acute VTE treatment in patients with cancer, while secondary prevention strategies, particularly anticoagulant selection, show substantial specialty-based variability. Significant differences in selected high-risk scenarios and the high demand for education highlight an unmet need for multidisciplinary, guideline-aligned approaches to optimise VTE management in cardio-oncology practice.Table.
Abstract Introduction Hematopoietic stem cell transplantation (HSCT) is an effective treatment option for haematological malignancies (HM), although it involves potentially cardiotoxic therapies. Cardiotoxicity is currently defined mainly by reduction in left ventricular ejection fraction (LVEF) and/or global longitudinal strain (GLS), which may occur after earlier subclinical myocardial changes have already developed [1]. While transthoracic echocardiography is the first-line modality, its sensitivity for early subclinical myocardial changes may be limited. Cardiac magnetic resonance (CMR) enables more comprehensive assessment of ventricular function, deformation and geometry, yet data on CMR-detected subclinical myocardial remodelling after HSCT remains limited [2]. Purpose To evaluate subclinical myocardial remodelling before and one year after HSCT using CMR-derived functional, deformation and geometric parameters. Methods Thirty-nine patients with HM undergoing HSCT were prospectively enrolled. CMR was performed before HSCT and at one-year follow-up using a 3T scanner. Left ventricular (LV) and right ventricular (RV) volumes, systolic function longitudinal and circumferential strain, ventricular geometry and mitral valve-LV (MV-LV) coupling parameters were assessed. Statistical analysis was performed using IBM SPSS 29.0. Paired comparisons between baseline and one-year follow-up were performed, with correlation and subgroup analyses based on baseline values, sex and age. The study protocol was approved by our Regional Biomedical Research Ethics Committee. Results The study population had a median age of 61 years (range 18-74). Of the 39 patients included, 21 were men (53.8%) and 18 were women (46.2%). LVEF, LV geometry, volumes, GLS and circumferential strain did not change significantly. MV-LV coupling analysis demonstrated an increase in MV end-systolic area (p=0.015) and a greater systolic circumferential strain dispersion at the mitral level (p=0.021). Overall mitral annular circumferential strain remained unchanged, but patients with worse baseline values exhibited significantly greater deterioration (p=0.033), indicating heterogeneous MV-LV coupling response. RV remodelling was characterized by a deterioration in RV GLS (p=0.023) and an increase in RV ESL (p=0.039), with basal diameter changes affecting patients with smaller baseline values (p=0.005). Changes in mitral annular circumferential strain correlated with changes in RV GLS (ρ=0.727, p<0.001). Increasing age was associated with greater LV GLS deterioration over time (ρ=0.54, p<0.001). Conclusions Despite preserved ventricular volumes and global systolic function, CMR revealed early and heterogeneous subclinical myocardial remodelling one year after HSCT, involving MV-LV coupling and RV function. These findings suggest selective vulnerability of myocardial mechanics not detected by conventional functional parameters.
Abstract Introduction Myeloproliferative neoplasms (MPN) are clonal hematopoietic stem cell disorders that include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). These conditions are characterized by increased thrombotic and hemorrhagic risks, posing potential concerns for patients undergoing transcatheter aortic valve replacement (TAVR). However, comprehensive data regarding the safety and in-hospital outcomes of TAVR in patients with MPN remain limited. Purpose We aimed to evaluate the in-hospital outcomes of TAVR among patients with MPN compared to those without MPN using a propensity score-matched cohort. Methods The National Inpatient Sample database from 2016 to 2022 was queried to identify all adult TAVR hospitalizations. Baseline characteristics, procedural outcomes, and in-hospital complications were compared between patients with and without MPN. Propensity score matching (PSM) was implemented to adjust for baseline differences between MPN and non-MPN groups. The primary outcome was in-hospital mortality. Secondary outcomes included stroke/transient ischemic attack, acute myocardial infarction, major bleeding, acute kidney injury, atrial fibrillation, pacemaker implantation, heart failure, length of stay, and total hospital charges. Results Our study included 94,888 TAVR hospitalizations, with 262 (0.28%) patients having MPN. Following propensity score matching, 252 MPN patients were matched 1:1 with 250 non-MPN controls. Baseline characteristics were well-balanced after matching, with mean age 79.7±0.5 years in the MPN group versus 80.3±0.5 years in controls (p=0.344). In-hospital mortality rates were identical between groups (1.6% vs 1.6%, p=0.991). There were no significant differences in stroke/TIA (4.0% vs 3.6%, OR 0.81, 95% CI 0.26-2.53), acute myocardial infarction (2.0% vs 2.0%, OR 0.68, 95% CI 0.18-2.62), major bleeding (1.6% vs 2.4%, OR 0.72, 95% CI 0.17-3.05), acute kidney injury (12.7% vs 10.8%, OR 1.14, 95% CI 0.63-2.06), atrial fibrillation (38.9% vs 36.8%, OR 1.07, 95% CI 0.72-1.59), or pacemaker implantation (6.0% vs 6.4%, OR 0.97, 95% CI 0.49-1.95). Length of stay (difference +0.38 days, p=0.307) and total hospital charges (difference +$2,833, p=0.806) were also comparable between groups. Conclusion Our study demonstrated that patients with MPN undergoing TAVR had comparable in-hospital mortality and major complication rates compared to matched controls without MPN. These findings suggest that MPN should not be considered a contraindication to TAVR in appropriately selected patients. Further research is needed to evaluate long-term outcomes and identify optimal antithrombotic strategies in this population.
Abstract Background Pathological findings, such as infiltration of T cells into myocardial tissue are useful in diagnosing immune checkpoint inhibitor-associated myocarditis (irMyocarditis). However, there is a lack of evidence regarding the infiltration of macrophages (CD68- or CD163-positive cells) in irMyocarditis and the correlation between the severity of macrophage infiltration and the prognosis of the patients with irMyocarditis remains to be elucidated. Purpose The objective of this study is to quantitatively assess the severity of macrophage infiltration by mechanically counting the number of CD68- or CD163-positive cells in myocardial specimens from the patients with irMyocarditis and to elucidate how the severity of macrophage infiltration correlates with the prognosis of the patients with irMyocarditis. Methods This multicentre retrospective observational study included 37 patients diagnosed with irMyocarditis. Myocardial specimens were immunostained using antibodies against CD68 or CD163, then, the number of positive cells was automatedly counted using a bioimage analysis software. We evaluated the number of cells per high power field (HPF) as both the average among the whole tissue and the hotspot, the HPF where the density of cells was highest in the tissue. The primary outcome of this study was major adverse cardiovascular events (MACE), a composite outcome of cardiovascular death, ventricular tachyarrhythmia, and complete atrioventricular block, and the secondary outcomes were acute decompensated heart failure (ADHF) and immune related adverse events (irAEs) in organs other than the heart. Results The number of infiltrating macrophages was significantly greater in the group of patients with MACE compared with the group of patients without MACE for CD68- or CD163-positive cells. This significant difference was observed both in the average of whole tissue and in the hotspot. The median of CD68-positive cells in the hotspot was 250 cells/HPF in MACE(+) group whereas 34 cells/HPF in MACE(-) group (p=0.012). The median of CD163-positive cells in the hotspot was 234 cells/HPF in MACE(+) group whereas 22 cells/HPF in MACE(-) group (p=0.0044) (Figure 1). When we defined the outcomes as the composite of MACE or ADHF, the median of CD163-positive cells in the hotspot was significantly greater in MACE/ADHF(+) group than in MACE/ADHF(-) group (73 cells/HPF vs. 17 cells/HPF; p=0.001)(Figure 2). We also evaluated CD163/CD68 ratio to investigate how the macrophage composition, M1- or M2-dominant, affects the prognosis of the patients with irMyocarditis. As a result, the patients who developed noncardiac irAEs following the onset of irMyocarditis had significantly lower CD163/CD68 ratio than the patients without noncardiac irAEs (0.08 vs. 0.68; p=0.046). Conclusion Quantitative assessment of infiltrating macrophages could provide clues for predicting the prognosis, such as MACE, ADHF, or following irAEs, in the patients with irMyocarditis.Figure 1 Figure 2
Abstract Background Cancer therapy-induced cardiotoxicity, particularly that associated with immunotherapy, is hard to diagnose and manage because current methods lack molecular specificity and are unable to detect early cardiac injury. Mitochondrial dysfunction underlies cardiotoxicity from conventional therapy, whereas T-cell infiltration drives immunotherapy-associated myocarditis. [¹⁸F]F-AraG is a PET tracer that allows noninvasive visualization of mitochondrial biogenesis in cardiomyocytes and activated T cells, enabling early detection of cardiotoxicity associated with cancer therapies, including immune checkpoint blockade (Figure 1). Purpose To evaluate whether [¹⁸F]F-AraG PET can serve as an early imaging biomarker of treatment-related mitochondrial alterations in the myocardium. Methods Doxorubicin-treated mice were used to model chemotherapy-induced cardiac injury. Early myocarditis detection was evaluated using [¹⁸F]F-AraG PET/CT in poly I:C–treated and experimental autoimmune myocarditis (EAM) mouse models. To assess the translational potential of [¹⁸F]F-AraG PET for assessment of off-target cardiac effects, 26 healthy subjects underwent PET imaging to establish physiological myocardial uptake. Seven patients with stage III melanoma and ten with advanced NSCLC were scanned before and after one infusion of immunotherapy. Myocardial uptake (SUVmax, SUVmean, SUVtotal) was quantified in the left (LV) and right (RV) ventricles, with regional LV analysis using a 17-segment model. Myocardial tracer uptake was compared with ECG findings in two patients with head and neck (H&N) cancer who had available ECG data. Associations between tracer uptake, mitochondrial DNA content, and PGC-1α expression were evaluated. Results Cardiac [¹⁸F]F-AraG uptake decreased after doxorubicin treatment (6.4 vs 4.5 %ID/cc, p<0.0001) alongside reductions in mitochondrial DNA copy number. In contrast, uptake increased in myocarditis models (poly I:C: 6.4 vs 9.9 %ID/cc, p<0.0001; EAM: 7.2 vs 9.9 %ID/cc, p=0.007) (Figure 1). Healthy human myocardium showed consistent, spatially uniform uptake (SUVmean COV: 11.2% LV, 12.3% RV), with higher LV uptake corresponding to greater mitochondrial content and PGC-1α expression. Previously treated patients with NSCLC demonstrated higher baseline LV uptake than controls (SUVmean 4.27 vs 3.47, p=0.01). Although mean post-immunotherapy changes were modest, >20% ventricular uptake increases occurred in 4/7 melanoma and 4/10 NSCLC patients; focal increases >40% in regional analysis were observed in 3/7 and 3/10 patients, respectively. Altered uptake patterns were associated with ECG abnormalities in patients with H&N. Conclusion [¹⁸F]F-AraG PET detects therapy-associated mitochondrial changes in the myocardium following cancer treatment. These findings support its potential utility as a noninvasive imaging approach for early evaluation of therapy-induced cardiac effects and anti-tumor immunity to guide patient care (Figure 2).
Abstract Introduction In advanced stage breast cancer, conventional chemotherapy is one of the most commonly used therapeutic options; however, it is associated with a potential risk of cardiotoxicity. Although the cardiotoxic effects of anthracyclines on the left ventricular function have been well studied, alterations of the right ventricle continue to be controversial. The assessment of conventional echocardiographic parameters remains the first-line imaging approach for evaluating and monitoring longitudinal right ventricular function. Purpose The purpose of this study was to evaluate the early effects of anthracycline-based chemotherapy on right ventricular function in newly diagnosed breast cancer patients at low risk for cardiotoxicity. Methods This prospective study included 31 newly diagnosed breast cancer patients at low risk for cardiotoxicity who were treated with anthracycline-based chemotherapy. Baseline cardiovascular risk assessment was conducted according to established evidence-based risk stratification proformas for anthracycline cardiotoxicity. All patients received four cycles of chemotherapy. Transthoracic echocardiography was performed prior to anthracycline initiation, after the fourth (last) cycle, and 12 months after treatment completion. Variables included right heart parameters such as right ventricular (RV) end-diastolic and outflow tract dimensions, tricuspid annular plane systolic excursion (TAPSE), RV fractional area change (FAC%), Tissue Doppler systolic RV velocity (RVs’) and systolic pulmonary artery pressure. Results Right ventricular (RV) outflow tract dimensions increased by the end of the treatment protocol and persisted up to one year; however, statistical significance was observed only at the end of follow-up (III) compared with both baseline (I) and end-of-treatment (II) values (27,97±4,48 vs. 30,42±2,27, III vs. I (>) p=0,005; III vs. II (>) p=0,0001). RV end-diastolic dimensions although increasing, showed no significant change during follow-up. TAPSE and RVs′ demonstrated a significant reduction, with statistical significance evident at the end of follow-up compared with both baseline and end-of-treatment values. (22,42±2,80 vs. 21,19±2,04, III vs. I (<) p=0,029, III vs. II (<) p=0,028 and 14,00±1,69 vs. 13,03±1,37, III vs. I (<) p=0,002; III vs. II (<) p=0,001 respectively). No significant changes were observed in RV FAC% or systolic pulmonary artery pressure during treatment or at one-year follow-up. Conclusion Although right ventricular dysfunction is not considered in the universal definition of cardiotoxicity, the right heart may undergo significant deteriorations. Our analysis demonstrated a significant decline in right ventricular function during anthracycline-based cardiotoxic therapy and persisting up to one year after treatment completion, even in patients with low cardiotoxic risk, despite changes being subclinical and largely within normal ranges.
Abstract Introduction The rapid evolution of oncologic therapies and the growing population of long-term cancer survivors are driving a substantial increase in cardiovascular complications related to cancer treatment. As the number of cardio-oncology patients is expected to rise markedly in the coming decades, comprehensive training in this interdisciplinary field has become essential. This educational need is reinforced by the recent publication of the first Cardio-Oncology Core Curriculum by the European Society of Cardiology. Despite increasing efforts to train physicians and health-care professionals, systematic early exposure to cardio-oncology within undergraduate medical education is still lacking. Methods and results To address this gap, we established a structured cardio-oncology elective for medical students at a large university hospital with dedicated expertise in the field. The module was designed as a multi-layered curriculum integrating the four key components (i) theoretical instruction, (ii) practical and bedside teaching, (iii) exposure to cardio-oncology basic science, and (iv) oral examination based on student case presentations (Picture 1). The theoretical component provides a seminar-based comprehensive overview of basic cardio-oncology-principles guided by a classical cardio-oncology patient trajectory. This includes pre-treatment cardiovascular risk assessment, mechanisms and clinical presentation of therapy-related cardiotoxicity as well as survivorship care. Special sessions emphasize on cardiotoxic chemotherapies and targeted agents as wells as cardio-oncologic considerations in valvular disease and amyloidosis. Practical teaching focuses on structured clinical bedside anamnesis and examination of cardio-oncology patients as well as fundamentals of echocardiography and chemotherapy. A dedicated session introduces students to contemporary basic molecular science aspects of cardio-oncology, fostering early understanding of translational mechanisms relevant to the field. The module concludes with an oral examination in which students present and discuss a clinical case to demonstrate applied knowledge. Conclusions To our knowledge, this represents one of the first reports of a structured undergraduate cardio-oncology elective integrated into a medical school curriculum. This pilot program provides a framework for future refinement and expansion of cardio-oncology teaching at the undergraduate level, equipping the next generation of physicians for the evolving challenges at the intersection of oncology and cardiovascular medicine.Design of a cardio-oncology elective (1)
Abstract Background Cancer survivors remain at increased risk of coronary events even when obstructive coronary disease is mild. A key gap in routine care is detecting ongoing vascular inflammation, particularly after chest radiotherapy. Pericoronary adipose tissue attenuation on coronary computed tomography angiography (CCTA) is a practical imaging marker of coronary inflammation. Purpose To determine whether chest radiotherapy is associated with higher pericoronary fat attenuation on CCTA, and whether this inflammatory signal relates to high-risk plaque phenotype. Methods We retrospectively analyzed consecutive adults undergoing clinically indicated CCTA between 2021–2025. Cancer survivors were stratified into prior chest radiotherapy versus no radiotherapy and compared with age- and sex-matched non-cancer controls. Pericoronary fat attenuation was measured as mean attenuation (Hounsfield units) around the proximal right coronary artery. Coronary stenosis severity (CAD-RADS) and high-risk plaque features (low attenuation plaque, positive remodeling, spotty calcification, napkin-ring sign) were recorded. A subset with complete blood count within ±30 days was used to examine associations with neutrophil-to-lymphocyte ratio (NLR). Results A total of 318 patients were included (198 cancer survivors, 120 controls; mean age 53±11 years; 54% female). Among survivors, 76 (38%) had prior chest radiotherapy. Obstructive coronary disease was uncommon and comparable across groups (≥50% stenosis: 9% radiotherapy vs 7% no radiotherapy vs 8% controls; p=0.81). Pericoronary fat attenuation was higher (less negative) in radiotherapy survivors compared with non-radiotherapy survivors and controls (−69±7 vs −73±6 vs −75±6 HU; p<0.001). High-risk plaque features were more frequent in the radiotherapy group (21% vs 13% vs 10%; p=0.03). After adjustment for traditional risk factors, chest radiotherapy remained independently associated with higher pericoronary fat attenuation (β=+3.1 HU, p=0.002). In the CBC subset (n=210), higher NLR showed a modest association with higher pericoronary fat attenuation (r=0.24, p=0.01). Conclusion Chest radiotherapy is associated with a measurable CCTA inflammatory signature using pericoronary fat attenuation, even when stenosis severity is similar. This pragmatic CT-based marker may help identify cancer survivors with persistent vascular inflammation and higher plaque vulnerability, supporting more targeted preventive strategies.
Abstract Background – Emerging evidence has revealed that cardiovascular diseases (CVDs) identify individuals prone to developing cancer. However, the precise impact and which CVD is most associated with future cancer is not clear. Therefore, we present an up-to-date impact of CVD on cancer incidence and cancer-related mortality. Methods – A scoping review with a systematic approach was performed in adherence to the guidelines of Transparent Reporting of Systematic Reviews and Meta-analyses (PRISMA). Studies evaluating cancer incidence and mortality among individuals with pre-existing CVD or cardiovascular (CV) risk assessments were included. To categorize the data, sub-groups were created: 1) coronary artery disease, 2) atrial fibrillation, 3) congenital heart disease, 4) heart failure, 5) hypertension, 6) thrombosis, and 7) cardiovascular health indicators. Various predictor indices were plotted in forest plots to visualize effect of CVD or CV health indicators on cancer incidence and cancer-related mortality. Results – The search strategy and screening process yielded 47 full-text articles for data-extraction. All CVDs and CV health indicators demonstrated an overall elevated risk of future cancer or cancer-related mortality (Figure 1). In the current evaluation, atrial fibrillation, congenital heart disease and thrombosis presented the strongest associations. Additionally, sex differences were subtle but present, favoring women. Conclusion – This scoping review highlights that the manifold of CVD and CV health indicators increase the risk of new-onset cancer and cancer-related mortality. Together, these findings emphasize the need for awareness of future cancer in patients with CVD as well as further in-depth studies for proper comparisons.
Abstract Background Translating the 2022 ESC cardio-oncology recommendations into a structured clinical decision support tool may facilitate standardized cardiovascular assessment and risk-adapted monitoring in patients receiving potentially cardiotoxic cancer therapy. Purpose To develop and present a structured clinical decision support tool implementing ESC recommendations to assist clinicians in baseline cardiovascular (CV) risk stratification and stepwise monitoring during and after anthracycline and HER2-targeted therapy, including post-treatment risk reassessment. Methods The tool was developed in accordance with the 2022 ESC Cardio-Oncology Guidelines and the HFA-ICOS framework for baseline CV risk stratification, categorizing patients as low, moderate, high, or very high risk. The algorithm integrates routinely available clinical and treatment-related inputs, including patient characteristics, cardiovascular history, comorbidities, ECHO parameters, cardiac biomarkers, and cancer therapy-related factors. For anthracycline-treated patients, cumulative doxorubicin-equivalent dose is incorporated, with a threshold of ≥250 mg/m² triggering intensified monitoring. The application is based on a rule-driven, guideline-based algorithm that processes user-entered data and generates risk-adapted monitoring recommendations in real time. The tool provides therapy-specific, stepwise monitoring schedules before, during, and after cancer treatment and defines guideline-recommended clinical, imaging, and biomarker thresholds prompting escalation. Results The developed clinical decision support tool enables rapid and standardized baseline CV risk stratification (Figure 1) and automatically generates individualized, therapy-specific monitoring strategies across the entire treatment trajectory (Figure 2). For each patient, the tool transparently reports the rationale underlying risk category assignment and delivers actionable recommendations regarding the timing and frequency of ECG, echocardiography, and cardiac biomarker assessment. Predefined, guideline-based triggers for both asymptomatic and symptomatic cancer therapy-related cardiac dysfunction activate escalation pathways, including intensified monitoring, initiation of cardioprotective therapy, and multidisciplinary reassessment of oncological treatment. This structured approach supports consistent, reproducible clinical decision-making within routine cardio-oncology practice at the point of care. Conclusion This clinical decision support tool operationalizes ESC cardio-oncology recommendations into a reproducible and intuitive format suitable for everyday clinical practice. Standardization of baseline CV risk assessment and longitudinal monitoring may reduce inter-physician variability and facilitate earlier detection of subclinical myocardial dysfunction without introducing additional risk factors beyond current guideline recommendations.Figure 1 Figure 2
Abstract Background Patients with prostate cancer commenced on androgen deprivation therapy (ADT) have increased cardiovascular (CV) risk. Despite this, CV risk is often under-recognised and under-treated upon ADT initiation. Dedicated cardio-oncology (CO) services may facilitate systematic CV risk assessment and optimisation in this high-risk population. Purpose To investigate the feasibility and early outcomes of CV risk optimisation through a dedicated CO clinic in patients with prostate cancer receiving ADT. Method Patients with prostate cancer treated with ADT were reviewed prospectively in the dedicated CO clinics at a Victorian tertiary cardiac centre between 01/07/23–30/06/25. Data from electronic records collected on baseline CV comorbidities, cardiac investigations, medication changes, new CV diagnoses/interventions, mortality and trends in CV risk markers. Results 16 patients with 23 reviews (mean age 75.9±9.7years, median follow up 6.1±4.7months) were included. Baseline CV comorbidities were common (94% hypertension, 63% dyslipidaemia, 63% diabetes, 56% heart failure, 50% ischaemic heart disease, 50% with smoking history). 94% patients have CV medication modifications (total 38 modifications – 34% heart failure therapies, 24% statins, 18% antiplatelets/anticoagulants). Coronary artery disease was diagnosed in 6/8 patients without a pre-existing history. 2/16 patients required revascularisation (one patient needing percutaneous coronary intervention and one patient with coronary artery bypass grafting). During follow-up, median reductions were observed in total cholesterol (11.6%), LDL-cholesterol (18.3%), systolic blood pressure (12.4%) and HbA1c (2.1%). There was one cardiac admission and one cardiac-related death during follow up. Conclusion CV risk is elevated in patients with prostate cancer treated with ADT. CV risk optimisation can be feasibly achieved through a dedicated CO clinic which may have benefits in reducing CV complications.
Abstract Background In patients receiving anthracycline therapy, a decline in FMD reflects the development of endothelial dysfunction and may represent an early vascular response preceding myocardial involvement. Nevertheless, whether early FMD changes can reliably predict subsequent asymptomatic left ventricular dysfunction remains an open question. Purpose To evaluate longitudinal changes in FMD according to baseline cardiovascular risk and to explore whether early FMD changes are associated with subsequent asymptomatic cancer-therapy-related cardiac dysfunction (CTRCD) during anthracycline therapy. Methods This prospective analysis included 71 women (mean age 55.4±11.2 years) receiving anthracycline-containing chemotherapy. Patients were stratified into a low-risk group (n=40) and a moderate-to-high-very high risk group (n=31)according to the HFA-ICOS risk assessment. Cardiovascular evolution, monitoring and definition of asymptomatic CTRCD followed the 2022 ESC cardio-oncology recommendations. FMD was measured at baseline (T0), after 4 cycles (T1), and after 8 cycles (T2) using a validated automated FMD analysis. Between-group difference and longitudinal changes in FMD were performed using appropriate non-parametric methods. The association between early FMD change and CTRCD was assessed using logistic regression with adjustment for baseline cardiovascular risk; an additional threshold analysis evaluated the upper quartile of early FMD decrease (≥0.70). Results Cumulative anthracycline dose was 225.0±44.5 mg/m² in the low-risk group and 209.1±45.1 mg/m² in the moderate-to-high-very high risk group. FMD values were consistently higher in the low-risk group than in the moderate-to-high-very high risk group at baseline (11.40% vs 7.80%; p<0.001), after 4 cycles (10.85% vs 7.10%; p<0.001), and after 8 cycles (10.60% vs 6.50%; p<0.001) (Figure 1). A significant decline in FMD over time was observed in both risk groups (p < 0.001). Asymptomatic LV dysfunction after 8 cycles occurred in 19/71 patients (26.7%), with no significant difference between risk groups. Early FMD decline was not associated with the occurrence of asymptomatic CTRCD in univariable analysis OR 1.06(95% CI 0.85-1.32) or after adjustment for baseline cardiovascular risk OR 1.09(95% CI 0.86-1.37). The threshold analysis (Early FMD decrease ≥0.70) also showed no difference in outcome frequency (p=0.699). Conclusions During anthracycline chemotherapy, FMD trajectories differ according to baseline cardiovascular risk, with consistently lower FMD values in patients with moderate-to-high risk. In this cohort, early decline in FMD was not associated with subsequent asymptomatic LV dysfunction, suggesting that endothelial dysfunction, while an early vascular response to chemotherapy, may not be sufficient as a stand-alone predictor of CTRCD.Figure 1
Abstract Background With advancements in cancer therapy and prolonged survival, the prevalence of concomitant cancer and atrial fibrillation (AF) is increasing. The interaction between antineoplastic agents and anticoagulants complicates clinical management, rendering bleeding risks unpredictable. Current bleeding risk scores (e.g., HAS-BLED) often lack cancer-specific variables, limiting their accuracy in this population. We aimed to develop and validate a novel nomogram to predict bleeding risk specifically for patients with cancer and AF. Methods We conducted a retrospective study of 972 patients with cancer and AF. Patients were randomly assigned to a training set and a validation set in a 7:3 ratio. Univariate and multivariate logistic regression analyses were performed to identify independent risk factors for bleeding. A nomogram was constructed using R software. The model's performance was compared with the HAS-BLED, HEMORR2HAGES, NBLDSCOR, and ORBIT scores using the Area Under the Receiver Operating Characteristic Curve (AUC). Decision Curve Analysis (DCA) was used to assess clinical utility. Results Bleeding events occurred in 173 patients (17.8%), with the gastrointestinal tract being the most common site. Multivariate analysis identified eight independent risk factors: age ≥75 years, anemia, history of bleeding, anticoagulant usage, vitamin K antagonist (VKA) therapy, concomitant antiplatelet therapy, advanced cancer stage, and anti-angiogenic therapy. The novel nomogram demonstrated robust discrimination with an AUC of 0.784 in the training set and 0.770 in the validation set. Compared to the HAS-BLED, HEMORR2HAGES, NBLDSCOR, and ORBIT scores, the new model showed a higher AUC and superior net benefit in the validation cohort. Conclusion We developed a novel bleeding risk prediction model for patients with cancer and AF that incorporates crucial cancer-specific factors, such as tumor stage and anti-angiogenic therapy. This nomogram outperforms traditional risk scores in predictive accuracy and offers a valuable tool for personalized anticoagulation decision-making in this high-risk population.
Abstract Background Patients with cancer are at increased risk of atherosclerotic cardiovascular (ASCVD) events, yet guidelines provide limited guidance on risk stratification. Coronary artery calcium (CAC) on chest computed tomography (CT) scans routinely performed in oncology care may help identify high-risk patients. Objective To compare CAC volume quantified on contrast-enhanced chest CT scans versus dedicated non-contrast, ECG-gated cardiac CT scans. Methods Data were used from ITHACA, a prospective cohort study including adult patients with cancer who underwent both dedicated non-contrast, ECG-gated cardiac CT (reference) and routine contrast-enhanced, non-ECG gated chest CT. CAC volume was quantified on the reference scan using standard software, and on contrast-enhanced CT scans using manual annotation, with application of a scan-specific threshold to account for the presence of contrast by a standardized method (Figure 1). The correlation between CAC volume measured on contrast-enhanced scans and the reference scan was assessed using Spearman’s correlation. Secondary analyses included agreement by Bland-Altman analysis, risk categorization using regression-based volume thresholds (reflecting Agatston risk groups), and interclass correlation. Results A total of 103 contrast-enhanced CT scans from 56 patients were included. Median age was 67 (IQR 59-72), and 80% were male. Median time between reference and contrast-enhanced CT was 85 days (IQR, 44-147). Median CAC volume was 191.58 mm³ (IQR, 10.15–834.64) on non-contrast CT and 84 mm³ (IQR, 13–559) on contrast-enhanced CT, with 84% and 79% having a volume >0 mm³, respectively. A strong correlation was observed between volume on reference CT and manually annotated volume on contrast-enhanced CT (ρ=0.78, 95% CI 0.68-0.85) (Figure 2). Bland Altman analysis showed minimal systemic bias and no evidence of proportional bias. Interobserver reliability was excellent (intraclass correlation coefficient (ICC) = 0.98, 95% CI 0.96-0.98). Agreement in Agatston risk categories, assigned by applying regression-based volume thresholds to CAC volume, was substantial (Cohen’s kappa 0.76), with most discrepancies in patients with low CAC volume. Conclusion CAC volume measured on contrast-enhanced chest CT scans performed in routine cancer care strongly correlates with CAC volume on dedicated non-contrast cardiac CT. Further studies should focus on developing and validating methods for automated CAC quantification on contrast-enhanced scans.
Abstract Background The 2022 ESC Guidelines on cardio-oncology recommend measuring cardiac biomarkers, troponin and natriuretic peptides (e.g. NTproBNP), in patients initiating treatment with immune checkpoint inhibitors (ICI). The main goal is to stratify the risk of cardiovascular events. Nobody has verified the value of these biomarkers in predicting anticancer treatment efficacy and mortality. Purpose The aim of the study was to assess a value of troponin and NTproBNP levels determined before the start of cancer therapy with ICI in an assessment of anticancer treatment effectiveness expressed by time to treatment failure (TTF) and overall survival (OS). Methods TTF was defined as time from the beginning of treatment with ICI to a moment of premature termination due to a diagnosis of unacceptable toxicity, progression of cancer disease or all-cause death. OS included all-cause death as endpoint of observation. The study based on analysis of electronic data (Clininet) of the National Research Institute of Oncology. The inclusion criteria were: beginning of treatment with ICI in the period August 2016 - April 2025 diagnosis of melanoma or lung cancer or breast cancer or renal carcinoma (ICD-10: C43, C34, C50, C64) treatment with niwolumab or pembrolizumab or niwolumab+ipilimumab available results of troponin or NTproBNP determined by oncologists before cancer therapy with ICI. Results Among 3295 patients treated with ICI: 1411 (42,8%) and 1369 (41,5%) had evaluated troponin or NTproBNP, respectively. Among 1411 patients with available baseline troponin before ICI treatment: 1104 (78.2%) patients had value <14 ng/L and 307 (21.8%) had abnormal elevated value > 14 ng/L. Among 1369 patients with available baseline NTproBNP before ICI treatment: 680 (49.7%) patients had value < 125 pg/ml and 689 (50.3%) patients had abnormal elevated value > 125 pg/ml. The patients with pre-existing elevated troponin level had significantly shorter TTF (4.2 vs 9.1 months, log-rank p<0.0001) and OS (13.9 vs 38.7 months, log-rank p<0.0001). The patients with pre-existing elevated NTproBNP level had significantly shorter TTF (4.9 vs 10.8 months, log-rank p<0.0001) and OS (17.3 vs 54.3 months, log-rank p<0.0001). Conclusions Elevated cardiac biomarkers may help oncologists to predict an outcome of patients treated with ICI: a need for premature termination for any reason and all-cause mortality. The study clearly confirms the validity of the assessment of these biomarkers in all cancer patients before treatment with ICI.
Abstract Background Anthracycline-induced cardiotoxicity limits the therapeutic efficacy of cancer treatment and is characterized by mitochondrial dysfunction, oxidative stress, inflammatory activation, and cardiomyocyte apoptosis. The cardiomyocyte-intrinsic survival mechanisms that counteract these stress pathways remain incompletely defined. Methods Doxorubicin-induced cardiotoxicity was modeled using human induced pluripotent stem cell–derived cardiomyocytes and a murine model of anthracycline injury. Cardiomyocyte viability, mitochondrial structure and bioenergetics, oxidative stress, inflammatory signaling, and contractile function were assessed using high-content imaging, ultrastructural analysis, metabolic flux measurements, and functional assays. Transcriptomic profiling was performed to identify candidate survival regulators, followed by molecular, genetic, and functional validation in vitro and in vivo. Results Doxorubicin induced dose-dependent cardiomyocyte injury marked by reduced cell survival, increased apoptosis, mitochondrial ultrastructural disruption, impaired oxidative phosphorylation, excessive reactive oxygen species generation, and increased tumor necrosis factor–α secretion. In vivo, doxorubicin exposure resulted in reduced survival and progressive systolic and diastolic dysfunction accompanied by myocardial architectural disorganization and cardiomyocyte loss. Transcriptomic analysis identified TNFAIP8 as a doxorubicin-responsive gene whose expression was reduced in injured cardiomyocytes and myocardium. Loss of TNFAIP8 was sufficient to impair cardiomyocyte viability and phenocopied key features of doxorubicin-induced injury. Conversely, preservation of TNFAIP8 expression was associated with attenuation of oxidative stress–driven inflammatory signaling, reduced FGFR1 activation, and suppression of caspase-3–dependent apoptosis, accompanied by improved cardiomyocyte survival and contractile performance. Conclusions Doxorubicin-induced cardiotoxicity is driven by oxidative stress–associated inflammatory signaling that converges on destabilization of the cardiomyocyte survival factor TNFAIP8, thereby lowering the apoptotic threshold. Maintenance of TNFAIP8 defines a cardiomyocyte-intrinsic survival axis that preserves mitochondrial integrity, limits apoptotic activation, and protects cardiac structure and function under anthracycline stress.
Abstract Introduction Although post-transplant cyclophosphamide (PT-Cy) is currently widely used to prevent graft-versus-host disease (GvHD) following allogeneic hematopoietic stem cell transplantation (alloHSCT), concerns remain regarding its cardiotoxicity. Purpose The aim was to investigate the association between early cardiotoxicity occurring within the first 100 days post-transplant and PT-Cy. Methods We conducted a monocentric retrospective observational study including all consecutive patients who underwent alloHSCT at our Hospital between July 2011 and July 2023. The primary endpoint was a composite of early cardiotoxicity, including cardiovascular death, heart failure (HF), myocarditis, pericardial disease, electrical disorders, and acute arterial events. A propensity-score matching was performed to balance characteristics between patients who received post-transplant PT-Cy and those who did not. Predictors of early cardiotoxicity were analyzed using Fine-and-Gray subdistribution hazard models. Results Among 1,381 patients, 143 (10%) experienced early cardiotoxicity within 100 days post-transplant. The most frequent events were HF (53%), electrical disorders (20%), and pericardial disease (19%). Age (sHR 1.01; 95% CI: 1.00-1.03; p=0.028), prior HF (sHR 2.02; 95% CI: 1.04-3.93; p=0.037), prior cancer therapy–related cardiac dysfunction (sHR 4.24; 95% CI: 2.05-8.78; p<0.001), hypertension (sHR 1.54; 95% CI: 1.00-2.36; p=0.047), and PT-Cy (sHR 1.62; 95% CI: 1.07-2.44; p=0.022) were independently associated with early cardiotoxicity. After 1:1 propensity score–matching, the administration of PT-Cy remained associated with cardiotoxicity (HR=2.00; 95% CI: 1.05-3.80; p=0.035). Conclusions The administration of PT-Cy was independently associated with an increased risk of early cardiotoxicity, particularly HF. These results underscore the need for early cardiovascular risk assessment and tailored surveillance, particularly in patients receiving PT-Cy.Early cardiotoxicity Hematologic outcomes
