gms | German Medical Science

Question: Recent findings on atrial fibrillation (AF) suggest that a single or a few stable rotors, mainly located in the pulmonary vein region, can act as a driving source of the arrhythmia. Periodic activation emanating from the rotors converts into a chaotic pattern via fibrillatory conduction as activation propagates across the atrial wall. It is likely that tissue heterogeneities favor this mechanism and can cause spiral wave breakup or spiral wave drift. The aim of this study was to illuminate these effects in a computer model.

Method Used: Cardiac activity was described by the monodomain approach using an atrial ionic current model. Geometrical models, consisting of a single bundle connected to a rectangular tissue model, were generated (Figure 1A [Fig. 1]). A mother rotor was initiated at two positions, distant and close to the bundle.

Results: In a model without bundle the tip of the spiral wave had a regular, stationary but meandering trajectory. When the bundle (representing additional load) was included into the model, different effects could be observed: A bundle distant to the rotor had only little influence on the spiral wave tip motion. Rather, local conduction delay or even functional block was seen when a propagation front crossed the bundle (Figure 1B [Fig. 1]). When block occurred, the wavefront split up into two wavelets which remained for up to 12 ms before they terminated again. This confirms experimental results on AF where short-lived spiral rotors were hypothesized to be the underlying mechanism for chaotic activity. When the spiral mother rotor was close to the bundle, the additional load induced a drift of the rotor towards the bundle. In this case the spiral wave anchored after about 1s of simulated time (Figure 1C [Fig. 1]).

Conclusion: The simulations show that our computer model of a single bundle connection, independent of the specific geometry used, is capable of reproducing breakup or anchoring of regular spiral waves.