Exploratory Evaluation of Cardiac Fatty Acid-Binding Protein (H-FABP), Troponin I, NT-proBNP, Echocardiography, and Holter Monitoring for the Assessment of Doxorubicin-Induced Cardiac Damage in Dogs.

Doxorubicin-induced cardiotoxicity is an important concern in veterinary oncology, and early detection of myocardial injury remains clinically challenging. This exploratory pilot study described changes in cardiac fatty acid-binding protein (h-FABP), cardiac troponin I (cTnI), NT-proBNP, conventional echocardiographic variables, and 24-h Holter-derived heart rate variability parameters in dogs with hemangiosarcoma treated with doxorubicin. Fourteen dogs were prospectively evaluated before treatment initiation and one week after the third doxorubicin dose, corresponding to a cumulative dose of 90 mg/m2. The study did not include a control group, a predefined cardiotoxicity endpoint, or diagnostic-performance analysis. Plasma biomarkers, echocardiographic parameters, ventricular arrhythmic events, and Holter-derived time- and frequency-domain heart rate variability variables were compared between both time points. Cardiac troponin I increased significantly after three doxorubicin doses, from a median of 0.05 ng/mL to 0.15 ng/mL (p = 0.002). In contrast, h-FABP did not change significantly, with median values of 2.43 ng/mL at baseline and 2.62 ng/mL after treatment (p = 0.27). NT-proBNP also showed no significant change (p = 0.87). Among echocardiographic variables, E-point septal separation, fractional shortening, ejection fraction, LA/Ao, and LVDd index did not change significantly. Ventricular arrhythmic events were infrequent and were described descriptively, whereas Holter-derived HRV variables did not show statistically significant differences between time points. In this exploratory cohort, cTnI increased after three doxorubicin doses, whereas h-FABP and NT-proBNP did not change significantly at the evaluated time point. Because h-FABP was measured one week after treatment, its potential short-term post-infusion release cannot be assessed. Larger studies with serial early sampling, predefined cardiotoxicity endpoints, appropriate control groups, and adjusted statistical analyses are required.