Dynamical anchoring of distant Arrhythmia Sources by Fibrotic Regions via Restructuring of the Activation Pattern

TL;DR

This study demonstrates that fibrotic regions in cardiac tissue can dynamically attract and anchor distant arrhythmia sources, such as rotors, through a process of reorganization of activation patterns, influencing arrhythmia behavior.

Contribution

It reveals a novel mechanism where fibrotic scars actively attract rotors from a distance, not just serve as passive anchoring sites, advancing understanding of arrhythmia dynamics.

Findings

Fibrotic scars can dynamically anchor rotors from large distances.

Presence of scars changes arrhythmia from polymorphic to monomorphic tachycardia.

Dynamical reorganization of activation patterns mediates rotor anchoring.

Abstract

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.