Abstract
Introduction: Recent work has shown that the transition from persistent to permanent AF in goats coincides with an increase in fibrosis in the outer millimeter of the atrial wall. Macroscopically this leads to reduced electrical conductivity orthogonal to the dominant fiber orientation. A causal relation has not been established yet. Our purpose was to test if subepicardial fibrosis can explain the increased incidence of epicardial breakthroughs, which is also observed in permanent AF.
Methods: We constructed a detailed geometry of the human atria including all major bundle structures and two layers of fiber orientation. Computer simulations were run with a mesh of 0.2 mm resolution and an ionic current formulation specific for the human atrial myocyte. Subepicardial fibrosis was modeled by assigning zero transverse conductivity to a random selection of model elements. Simulations were performed with 0, 50, and 70% affected elements. Fibrillation was induced with incremental rapid pacing. Simulations were repeated with 10 different pacing locations, for a total of 30 simulations of 5 seconds each. We tested in the first place whether AF was induced by this protocol. In those simulations where fibrillation occurred, we computed the number of waves, number of phase singularities, percentage dyssynchrony, and number of breakthroughs in the 3 seconds after pacing.
Conclusion: Subepicardial fibrosis can account for an increased susceptibility for AF as well as for the remarkable increase in epicardial breakthrough observed in experimental studies.
Conflict of interest: none
