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.
