Development of an automaton model of rotational activity driving atrial fibrillation

Background: Atrial fibrillation (AF) is difficult to treat effectively, owing to uncertainty in where to best ablate to eliminate arrhythmogenic substrate. A model providing insight into the electrical activation events would be useful to guide catheter ablation strategy. Method A two-dimensional, 576x576 node automaton was developed to simulate atrial electrical activity. The substrate field was altered by the presence of differing refractory period at varying locations. Fibrosis was added in the form of short, randomly positioned lines of conduction block. Larger areas of block were used to simulate ablation lesions. Anisotropy was imposed in a 2:1 ratio. A premature electrical impulse from one of four grid corners was utilized to initiate activation. Results: Rotational activity was uninducible when refractory patch dimensions were less than 20x20 mm. For larger refractory regions, a single premature stimulus was capable of inducing an average of 1.19 +/- 1.10 rotors, which often formed near the patch edges. A maximum of 5 rotors formed when refractory patch dimensions approached the size of the entire left atrial virtual field. Rotors formed along a refractory patch edge, after wavefront arrival was delayed at turning points or due to the presence of a fiber cluster of sufficient size. However, rotational activity could also occur around a large fiber cluster without the need of spatially variable refractoriness. When obstacles to conduction were lacking in size, nascent rotors drifted and either extinguished, or stabilized upon anchoring at a sufficiently large fiber cluster elsewhere in the field. Transient rotors terminated when traversing a region with differing refractory periods, if no obstacle to conduction was present to sufficiently delay wavefront arrival beyond the longest refractory period. Other rotors were annihilated when a nearby rotor with faster spin rate gradually interrupted the activation pathway. Elimination of anchors by removal, or by simulated ablation over a sufficient region, prevented rotor onset at a particular location where it would otherwise form. Conclusions: The presence of obstacles to conduction and spatial differences in refractory period are important parameters for initiating and maintaining rotational activity in this simulation of an atrial substrate.