  Rotors are functional reentry sources identified in clinically relevant
cardiac arrhythmias, such as ventricular and atrial fibrillation. Ablation
targeting rotor sites has resulted in arrhythmia termination. Recent clinical,
experimental and modelling studies demonstrate that rotors are often anchored
around fibrotic scars or regions with increased fibrosis. However the
mechanisms leading to abundance of rotors at these locations are not clear. The
current study explores the hypothesis whether fibrotic scars just serve as
anchoring sites for the rotors or whether there are other active processes
which drive the rotors to these fibrotic regions. Rotors were induced at
different distances from fibrotic scars of various sizes and degree of
fibrosis. Simulations were performed in a 2D model of human ventricular tissue
and in a patient-specific model of the left ventricle of a patient with remote
myocardial infarction. In both the 2D and the patient-specific model we found
that without fibrotic scars, the rotors were stable at the site of their
initiation. However, in the presence of a scar, rotors were eventually
dynamically anchored from large distances by the fibrotic scar via a process of
dynamical reorganization of the excitation pattern. This process coalesces with
a change from polymorphic to monomorphic ventricular tachycardia.
