Precision Monitoring Strategies for Chemotherapy-Induced Cardiotoxicity: A Review of Molecular Indicators for Early Detection and Risk Stratification

Chemotherapy-induced cardiotoxicity (CIC) is an increasingly recognized complication in cancer survivors, particularly with anthracyclines, human epidermal growth factor receptor 2 (HER2) inhibitors, vascular endothelial growth factor (VEGF) inhibitors, and immune checkpoint inhibitors. CIC may present acutely, chronically, or as a delayed condition, with phenotypes ranging from asymptomatic myocardial dysfunction to heart failure, arrhythmias, and myocarditis. This narrative review aimed to summarize the latest evidence on the pathogenesis of CIC and evaluate traditional and emerging biomarkers for early detection and risk stratification. We comprehensively reviewed the literature related to the pathogenesis and biomarkers of CIC, focusing on studies that examined oxidative stress, DNA damage, mitochondrial dysfunction, inflammation, and immune activation. The five most frequently reported mechanisms in CIC toxicity were oxidative stress, DNA damage, mitochondrial dysfunction, inflammation, and immune activation. Traditional biomarkers, such as cardiac troponin and natriuretic peptides, have been shown to aid in early detection; however, these biomarkers are limited by specificity and timing. Emerging biomarkers, including inflammatory cytokines, fibrosis-related proteins, extracellular vesicles, and non-coding RNAs, demonstrate greater sensitivity and potential for earlier risk stratification. However, study heterogeneity and limited validation across populations hinder clinical translation. Thus, integrating biomarkers with imaging modalities and standardized protocols may enhance personalized surveillance of CIC toxicity. Large prospective studies and standardized frameworks are essential. Hence, a multiparametric approach combining molecular, functional, and computational tools may define future precision monitoring for CIC toxicity.