Cardiotoxicity induced by contemporary oncologic therapies: early biomarkers and practical clinical algorithms

Abstract

Background. Anticancer therapies (anthracyclines, anti-HER2 agents, PD-1/PD-L1 inhibitors) reduce cancer-related mortality; however, they are associated with cardiotoxicity. According to the ESC guidelines, hs-cTn and NT-proBNP are considered reliable biomarkers for the early detection of subclinical myocardial injury. Objective(s). To evaluate cardiac biomarkers for the early identification and monitoring of cardiotoxicity caused by contemporary oncologic treatments, employing current clinical algorithms. Materials and methods. A narrative literature synthesis was conducted through the analysis of scientific articles indexed in international electronic databases (PubMed, Scopus, ScienceDirect, ESC Library), published between 2020-2025. Clinical studies, guidelines, and meta-analyses addressing the utility of cardiac biomarkers in detecting cardiotoxicity were included. Results. Antineoplastic agents induce dose-dependent cardiotoxicity through topoisomerase II inhibition and increased reactive oxygen species, causing cardiomyocyte vacuolization, myofibril loss, and apoptosis. Microcirculatory disturbances, endothelial injury, arterial thrombosis, and dyslipidemia contribute to left ventricular dysfunction, ischemic heart disease, and myocardial necrosis. Cardiac biomarkers (hs-cTn, proBNP) enable initial cardiovascular risk assessment and early toxicity monitoring during therapy. Emerging markers such as ST2 and GDF-15 provide additional prognostic value, although they are not yet widely implemented. Conclusion(s). Comprehensive laboratory and imaging assessments, including cardiac biomarkers, lipid profiles, and echocardiography, enable precise stratification of cardiotoxicity risk induced by antineoplastic therapy, facilitating early intervention and reducing cardiovascular morbidity.