Aug 2026· Medicina· Vol 62, pp. 1634· 0 citations· 16 references
TL;DR
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.
Abstract
Background and Objectives: Although modern oncologic therapies have substantially improved cancer survival and overall prognosis, they have also led to an increasing burden of cardiovascular toxicity. Preventing severe complications such as heart failure and death remains a major priority, while maintaining the need for effective and potentially curative cancer therapy. Careful patient monitoring and early detection of cardiovascular complications may allow the timely implementation of cardioprotective strategies and treatments that could delay or prevent myocardial toxicity. Materials and Methods: A total of 92 women with breast cancer were enrolled in a prospective observational cohort study. All patients received an anthracycline-based chemotherapy regimen, cyclophosphamide, docetaxel and trastuzumab. Biomarker assessment, including NT-proBNP, high-sensitivity cardiac troponin I (hs-cTnI), Gal-3, and GDF-15, was performed at baseline and at the initiation of trastuzumab-based therapy. A comprehensive diastolic function assessment was performed, including transmitral Doppler flow parameters and tissue velocities. Patients were followed for 12 months, and all cardiovascular events occurring during the follow-up period were recorded. Results: Biological and ecocardiographic parameters were analyzed and multiple models of prediction were made. To identify predictors of estimated left ventricular filling pressure (eLVFP), stepwise multiple linear regression analyses were performed, and four significant predictors of left ventricular end-diastolic filling pressure were identified: one echocardiographic parameter (baseline LV filling pressure) and three biological variables (changes in Gal-3, GDF-15, and hs-cTnI levels after treatment). The overall regression model was highly significant (p < 0.001) and explained 77.07% of the variance in the dependent variable. Gal-3 was the strongest predictor of left ventricular filling pressure (p < 0.001). Conclusions: 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. This multimodal approach may therefore help identify patients with early treatment-related cardiac changes and potentially those at increased risk of subsequent CTRCD, particularly during a period when conventional LVEF-based surveillance may still appear reassuring.
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
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.
L. Kajanto, D. Stănculeanu, Anca Chisoi et al.· Cardio-Oncology· 0 citations
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
Current cardio-oncology surveillance strategies are primarily focused on patients with high or very high baseline cardiovascular (CV) toxicity risk. Patients with initially low risk are generally considered a clinically favorable group and therefore undergo less intensive monitoring. This approach may lead to underestimation of early, clinically silent vascular alterations developing during chemotherapy.
To assess changes in lipid profile parameters in oncohematological patients with low baseline cardiovascular toxicity risk and to determine their value for identifying early subclinical vascular toxicity and substantiating early initiation of cardioprotective therapy.
This study included 59 patients with B-cell hematological malignancies. According to ESC guidelines on cardio-oncology (2022), patients were stratified into low/moderate (n=42) and high/very high (n=17) CV toxicity risk groups. Lipid profiles were assessed at baseline and after three cycles of chemotherapy. Patients in the high/very high-risk group received standard cardioprotective therapy, including ACE inhibitors/ARBs, beta-blockers, and statins.
The median age in low risk group was 51.5 years [41.75; 63.00] (50% men), in high/very high risk group was 72 years [65.00; 75.00] (47.1% men). Most patients in both groups had traditional CV risk factors: obesity (n=11, 19%), smoking (n=12, 20%), diabetes mellitus (n=8, 13%), hypertension (n=24, 41%), and dyslipidemia (n=30, 51%), 8 patients in high/very high risk group were diagnosed with CAD. In patients with low and moderate baseline CV risk, a statistically significant deterioration in lipid profile was observed during chemotherapy, including increases in total cholesterol (4.54 vs. 5.43 mmol/L), low-density lipoprotein cholesterol (3.1 vs. 3.95 mmol/L), and triglycerides (0.86 vs. 1.01 mmol/L). All changes were highly significant (p<0.01). These findings are consistent with the development of subclinical endothelial dysfunction and early vascular toxicity, despite the absence of overt clinical manifestations of vasculotoxicity. In contrast, no significant changes in lipid parameters were observed in the high and very high-risk group, despite a greater baseline cardiovascular burden.
Patients with low baseline cardiovascular toxicity risk may develop early metabolic signs of subclinical vascular toxicity at the initial stages of chemotherapy. Dynamic assessment of lipid profile represents a simple and clinically applicable tool for early detection of vascular injury. The absence of high baseline cardiovascular risk does not preclude early vascular toxicity, supporting the rationale for considering earlier initiation of cardioprotective therapy in this patient population.
R. Alieva, K. Fozilov, M. Yakhyoeva 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.
A simplified risk score based on readily available clinical and echocardiographic variables for predicting anthracycline-related cardiotoxicity and the RE-ACT score provides additional post-treatment prognostic value is developed and validated and supports a practical 2-step strategy for personalized surveillance in cardio-oncology.
D. Cardinale, Nicola Cosentino, Chiara Morocutti et al.· JACC CardioOncology· 1 citation
