Cardiotoxicity following anthracycline-based chemotherapy is becoming a critical clinical burden, leading in time to heart dysfunction such as arrhythmia and heart failure. The purpose of this computational study is to better understand the structure-function interaction and subtle longitudinal changes in the presence of progressive fibrosis induced by chemotherapeutic drugs such as doxorubicin, DOX. Specifically, here we investigated via simulations how the cardiac action potential wave propagates in the presence of collagenous fibrotic clusters generated by this drug. For this, we built isotropic and anisotropic 3D left ventricular (LV) models from in vivo contrast-enhanced MRI data (1.4mm isotropic resolution) acquired in n=2 pigs pre-DOX and post-DOX therapy (at weeks 5 in one pig, at weeks 9 in the other pig). For computations, we employed a modified biophysical Mitchell-Schaeffer model with a fast GPU-based Lattice-Boltzmann numerical method (which runs directly on MR images Cartesian grid). Overall, our results showed that several key parameters (fibrosis density, tissue conductivity, action potential duration, anisotropy) independently contribute to the perturbation of the electrical wave propagation. Future work will focus on simulating potentially lethal arrhythmia in hearts subjected to DOX therapy.