Distinct biomarker patterns were observed across malignancy subgroups, with higher hs-cTnT increases in breast cancer, more prominent NT-proBNP elevation in lymphoma, and higher sST2 values in lung cancer.
Abstract
Cardiotoxicity associated with antineoplastic therapies remains an important clinical challenge in modern oncology. Early identification of subclinical cardiac injury may improve cardiovascular surveillance and long-term outcomes in cancer patients. This prospective observational cohort study included 90 adult patients with breast cancer, lymphoma, or lung cancer receiving potentially cardiotoxic therapy. Patients with clinically manifest heart failure, severe arrhythmias, advanced renal disease, recent acute myocardial infarction, untreated severe valvular disease, or other major cardiovascular comorbidities were excluded. High-sensitivity cardiac troponin T (hs-cTnT), NT-proBNP, and soluble ST2 (sST2) were measured at baseline, during treatment, at therapy completion, and at late follow-up. Non-parametric tests were used for repeated-measures and subgroup comparisons. Significant temporal variations were observed for all biomarkers. hs-cTnT increased from 5 [3–8] ng/L at baseline to 15 [10–25] ng/L at T2, while NT-proBNP increased from 120 [80–190] pg/mL to 210 [150–320] pg/mL. sST2 demonstrated a delayed elevation and remained increased at follow-up. Distinct biomarker patterns were observed across malignancy subgroups, with higher hs-cTnT increases in breast cancer, more prominent NT-proBNP elevation in lymphoma, and higher sST2 values in lung cancer. Serial biomarker assessment may provide complementary information on myocardial injury, ventricular stress, and fibrotic remodeling during cancer therapy. The observed biomarker trajectories are suggestive of different biological processes involved in therapy-related cardiotoxicity, but they should be interpreted in conjunction with imaging findings and clinical outcomes.
Cardiotoxicity remains a major limitation of contemporary anticancer therapies. Sodium–glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated cardiovascular benefits, including reduced heart failure hospitalizations, and emerging evidence suggests potential additional benefits in oncology populations. Accurate baseline cardiovascular risk stratification and early initiation of cardioprotective therapy are essential for preventing cancer therapy–related cardiovascular toxicity (CTR-CVT).
We prospectively evaluated 256 patients with breast or lung cancer prior to initiation of anticancer therapy. Baseline cardiovascular assessment included echocardiography with biplane left ventricular ejection fraction (LVEF), global longitudinal strain (GLS), diastolic function, and measurement of cardiac biomarkers (troponin and NT-proBNP). Cardiovascular history, demographic data, and risk factors were collected. CTR-CVT risk was assessed using the HFA-ICOS Cardio-Oncology risk assessment tool.Seventy patients (29 men, 41 women; mean age 69.6 ± 8.0 years) were classified as high risk and initiated on cardioprotective therapy. Forty-seven patients (67.1%) received angiotensin-converting enzyme inhibitors, beta-blockers, statins, and SGLT2 inhibitors (SGLT2i group). Twenty-three patients (32.9%) had contraindications to SGLT2i therapy and received standard cardioprotective treatment. Outcomes were assessed at 6 months.
At 6-month follow-up, no statistically significant changes in systolic or diastolic function were observed in either group. In the SGLT2i group, LVEF and GLS remained stable between baseline and follow-up (median LVEF 60.0% vs. 53.0%, p>0.05; GLS −18.9% vs. −16.8%, p>0.05). Renal function showed a modest numerical decline (median eGFR 80.0 vs. 62.0 ml/min/1.73 m², p>0.05). In patients not receiving SGLT2i, no significant changes were detected in LVEF or GLS, while a numerically greater decline in renal function was observed (median eGFR 95.0 vs. 49.0 ml/min/1.73 m², p>0.05). Diastolic parameters remained stable in the SGLT2i group, whereas a numerical increase in E/e′ medial was observed in the non-SGLT2i group. No heart failure–related hospitalisations or cardiovascular deaths occurred.
In this 6-month longitudinal analysis of oncologic patients at high risk of CTR-CVT, inclusion of SGLT2 inhibitors in a cardioprotective regimen was not associated with adverse cardiac effects. Although statistical significance was not reached, trends toward more stable cardiac and renal parameters were observed. These findings are hypothesis-generating and support further investigation of SGLT2 inhibitors in cardio-oncology.Table showing the following parameters
M. Samardjieva, I. Simova, V. Petrusheva et al.· European Heart Journal, Supp...· 0 citations
Anthracyclines remain a cornerstone of breast cancer therapy but carry a significant risk of cancer therapy-related cardiac dysfunction (CTRCD). This study evaluates the incidence of CTRCD in an Indonesian setting using the latest 2022 ESC Cardio-Oncology guidelines, focusing on subclinical markers such as high-sensitivity Troponin I (hs-cTnI), Global Longitudinal Strain (GLS) and Mechanical Dispersion (MD).
This retrospective analytical cohort study involved 98 breast cancer patients treated with anthracyclines at a national referral hospital in Indonesia from July 2018 to February 2020. Clinical assessments, hs-cTnI, and echocardiography (LVEF, GLS, and MD) were performed at baseline, 1, 3, and 6 months. CTRCD was defined per the 2022 ESC criteria.
CTRCD occurred in 74.5% of patients, predominantly as asymptomatic mild cases (63.26%). While symptomatic CTRCD was relatively low (7.14%), asymptomatic dysfunction was detected as early as one-month post-chemotherapy. A significant progressive decline was observed in LVEF (68.2 ± 6.2% to 61.3 ± 8.8%,
p
< 0.001) and GLS (-19.7 ± 2.9% to -17.1 ± 3.5%,
p
< 0.001). Notably, mechanical dispersion significantly increased over time (
p
= 0.029), and median hs-cTnI surged from 1.6 ng/L to 82.2 ng/L (
p
< 0.001) by month 6.
The high incidence of asymptomatic CTRCD underscores the inadequacy of relying on clinical symptoms alone. Integration of hs-cTnI, GLS, and mechanical dispersion monitoring is may be essential for early detection and enables timely cardioprotective intervention.
The regression analyses suggest that this phenotype is multifactorial, with echocardiographic indices capturing the functional component and circulating biomarkers reflecting complementary aspects of the underlying biological response.
A. Farcaș, C. Goidescu, M. Stoia et al.· Medicina· 0 citations
Cardio-oncology has emerged as a critical discipline in modern medicine due to the growing population of cancer survivors and the increasing recognition of cardiovascular disease as a major cause of morbidity and mortality in this population. While there have been significant advances in chemotherapy such as advances in chemotherapy, targeted therapies, immunotherapies, and radiation therapy, these treatments are linked to a wide range of cardiovascular toxicities such as myocarditis, arrhythmias, and progressive fibrotic remodeling. These toxicities tend to be caused by interrelated and multifactorial cellular processes including endothelial damage, immunological dysregulation and mitochondrial dysfunction. Therefore, early diagnosis of subclinical harm using multimodal surveillance strategies integrating clinical risk assessment, specialized clinical imaging, and circulating biomarkers has replaced reactive care of overt cardiotoxicity in modern cardio-oncology. Echocardiographic techniques such as longitudinal strain, with the help of biomarker-guided surveillance of natriuretic peptides and cardiac troponins, have made the early detection of cardiac dysfunction more effective. However, the current prediction risk models are still constrained and limited by their dependence on static clinical variables and their partial integration of biological mechanisms. This review examines the current methods for risk stratification and surveillance throughout the cancer care continuum, including baseline assessment, monitoring during active therapy, and long-term survivorship surveillance. Future approaches for tailored cardiovascular care are also highlighted, including new advances in precision cardio-oncology such as multi-omics profiling, molecular biomarkers, artificial intelligence, and mechanism-guided preventative strategies. Therefore, advancing biologically informed and risk-adapted monitoring frameworks may enhance early diagnosis, maximize cardioprotective measures, and lower long-term cardiovascular consequences.
Aryan Gajjar, S. Shah, A. Gajjar et al.· Biomedicines· 0 citations
Anthracyclines remain a cornerstone of therapy for lymphoproliferative diseases eratie(LPD) but are associated with cardiovascular toxicity (CVT). While myocardial injury is well studied, anthracycline-induced vascular toxicity and endothelial dysfunction as early manifestations of cardiovascular damage remain insufficiently explored, particularly in patients with low or intermediate baseline CVT-risk, who do not meet criteria for cardioprotective therapy according to current guidelines. Identification of early biomarkers of subclinical vascular injury is, therefore, of major importance in cardio-oncology.
To assess the diagnostic and prognostic value of endothelin-1 (ET-1) for detection and progression of endothelial dysfunction in lymphoma patients with low and intermediate CVT-risk receiving anthracycline-based chemotherapy.
This prospective study included 37 patients with newly diagnosed LPDs (median age 46 [34–62] years) treated with anthracycline-containing chemotherapy. Baseline CVT-risk was assessed using HFA-ICOS scores; all patients were classified as low or intermediate risk and did not require cardioprotective therapy. Serum ET-1 levels were measured by ELISA before treatment initiation and after 3 chemotherapy cycles (cumulative anthracycline dose 270 mg/m²). Endothelial function was evaluated using digital photoplethysmography (ANGIOSCAN-01), assessing phase shift (PS) and occlusion index (OI). ROC analysis was performed to evaluate prognostic performance.
Baseline ET-1 levels were elevated and increased significantly after 3 cycles of chemotherapy (5.39 [4.6–7.21] vs 7.19 [5.9–11.6] pg/mL; p = 0.003). This was accompanied by a significant decline in endothelial function parameters: PS (normal >10 ms) decreased from 8.6 [7.2–10.2] to 6.3 [5.2–9.8] ms (p = 0.014), and OI (normal >1.8) decreased from 1.7 [1.4–1.9] to 1.5 [1.2–1.9] (p = 0.004). ROC analysis demonstrated good prognostic performance of ET-1 for endothelial dysfunction: AUC 0.772 for PS (95% CI: 0.582-0.962, p=0.031) and 0.743 for OI (95% CI: 0.532-0.954, p=0.048).
Endothelin-1 is a promising early diagnostic and prognostic biomarker of subclinical anthracycline-induced vascular toxicity in lymphoma patients with low and intermediate CVT-risk. ET-1 assessment may facilitate early risk reclassification and optimization of cardio-oncology surveillance strategies.
R. Alieva, K. Fozilov, M. Yakhyoeva et al.· European Heart Journal, Supp...· 0 citations
Heart failure (HF) in cardio-oncology patients during anticancer therapy is usually regarded as an accelerated form of classical HF, which restricts early diagnosis and timely pathogenetically based treatment. Myocardial decompensation in these patients appears to involve distinct molecular mechanisms detectable before overt HF, and metabolomic profiling may help identify a specific cardio-oncological HF phenotype.
To characterize the metabolomic profile of HF in cardio-oncology patients versus HF patients without cancer and assess its utility for early cardiotoxicity detection and justification of early personalized cardioprotective therapy.
The study enrolled 102 patients. The cardio-oncology group (Onco, n=59) included patients with hematological malignancies (34 lymphomas, 25 multiple myeloma) examined before treatment and after three cycles of anticancer therapy; baseline risk was stratified using ESC-ICOS tools (24 low, 17 intermediate, 12 high, 6 very high). Various forms of cardiotoxicity were documented in 15 patients (left ventricular dysfunction n=8, arterial hypertension n=4, arrhythmias n=2, pulmonary embolism n=1). The control HF group comprised 43 patients with chronic HF without cancer (left ventricular ejection fraction 56%, NT-proBNP >968 pg/mL). All patients underwent targeted metabolomic analysis.
Significant differences in metabolomic profiles were found between Onco and HF patients. Arginine levels were higher in the Onco group (89.15 ± 33.89 vs. 73.27 ± 17.84; p=0.002), while ADMA and homoarginine did not differ significantly. No intergroup differences were seen for tryptophan, kynurenine, or kynurenic acid, whereas quinolinic acid and tryptamine were higher in the Onco group (p<0.005 and p<0.011), indicating a shift of kynurenine pathway activity toward a pro-inflammatory branch. All analyzed markers of mitochondrial fatty acid oxidation (C14-OH, C16:1-OH, C18:1-OH, C18-OH, C5-DC, cytidine) differed significantly (p<0.05), consistent with more pronounced impairment of mitochondrial β-oxidation in the HF group.
HF in cardio-oncology patients exhibits a distinct metabolomic phenotype that differs from classical HF and reflects key pathogenetic mechanisms of myocardial injury, enabling detection of subclinical cardiotoxicity. Metabolomic profiling opens new possibilities for early, pathogenetically oriented, personalized cardioprotective therapy, including pharmacological strategies targeting these metabolic alterations.
R. Alieva, K. Fozilov, M. Yakhyoeva et al.· European Heart Journal, Supp...· 0 citations
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