Early Biochemical, Oxidative-Stress, Inflammatory, and Clinical Features of Anthracycline-Associated Cardiac Injury and Dysfunction in Patients with Breast Cancer: A Prospective Clinical Toxicology Study

<jats:p>Background: Anthracycline-associated cardiac injury remains an important limitation of breast-cancer chemotherapy. This study characterized early cardiac, oxidative-stress, antioxidant, inflammatory, and clinical findings observed during the same post-cycle-two assessment window. Methods: This prospective clinical toxicology study included 150 women with breast cancer receiving anthracycline-containing chemotherapy. Measurements were obtained at baseline and after the second cycle. A composite early cardiac injury/cancer therapy-related cardiac dysfunction (CTRCD) classification comprised biomarker-defined myocardial injury without clinical dysfunction (n=10) and clinical CTRCD (n=32). Because post-cycle-two biomarkers and cardiac status were assessed concurrently, these biomarkers were analyzed descriptively and were not modeled as temporal predictors or evaluated by receiver operating characteristic analysis. Univariable logistic regression was restricted to baseline clinical factors. Results: Forty-two participants met the composite classification and 108 did not. Baseline left ventricular ejection fraction (LVEF) and most baseline biomarkers were comparable, although baseline C-reactive protein (CRP) was higher in the composite group (8.56±5.92 vs 5.94±3.93 mg/L; P=0.010). After cycle two, the composite group had larger increases in troponin, N-terminal pro-B-type natriuretic peptide (NT-proBNP), creatine kinase-MB, lactate dehydrogenase, malondialdehyde, CRP, interleukin-6, and tumor necrosis factor-α, together with greater declines in LVEF, superoxide dismutase, glutathione peroxidase, catalase, and reduced glutathione (all change-score comparisons P&lt;0.001). Hypertension (OR 2.87, 95% CI 1.36–6.06) and baseline LVEF &lt;60% (OR 2.53, 95% CI 1.17–5.50) were associated with the composite classification in univariable analyses. Conclusions: Early anthracycline-associated cardiac injury and dysfunction were accompanied by a concurrent multi-pathway profile of myocardial injury, wall stress, oxidative imbalance, antioxidant depletion, and inflammation. These findings support hypothesis-generating, multimodal surveillance research, but they do not establish temporal prediction or independent diagnostic performance for biomarkers measured during the same assessment window.</jats:p>