title: Mother rotor anchoring in branching tissue with heterogeneous membrane properties.
abstract: Abstract Current understanding of atrial fibrillation is based on the co-existence of multiple re-entrant waves propagating randomly throughout the tissue. However, recent experimental results indicate that in many cases one or a small number of periodic, high-frequency re-entrant sources (mother rotors) can drive the arrhythmia. Owing to the high activation rate, mother rotors seem to be located in regions of shortened action potential duration. In this study a computer model of cardiac propagation was applied to investigate mechanisms leading to the formation and maintenance of such mother rotors. For this purpose, a region of short action potential duration was generated by varying the acetylcholine concentration across the tissue. A mother rotor initiated in the center of this region drifts away, and the activation terminates. If an additional heterogeneity such as a bundle is included into the model, a further drift mechanism directed to the bundle is observed and the rotor can be stabilized. Therefore, bundle insertions may play an important role in the maintenance of mother rotors. The influence of the driving rotor on the activation pattern was studied in a three-dimensional model of rectangular shape and a monolayer model of anatomically correct atrial geometry.
authors.affiliation: Institute of Biomedical Engineering, University for Health Sciences, Medical Informatics and Technology (UMIT), Hall i.T., Austria. leonhard.wieser@umit.at
authors.forename: Leonhard
authors.initials: L
authors.lastname: Wieser
authors.forename: Claudia N
authors.initials: CN
authors.lastname: Nowak
authors.forename: Bernhard
authors.initials: B
authors.lastname: Tilg
authors.forename: Gerald
authors.initials: G
authors.lastname: Fischer
mesh_terms: D000200:Action Potentials; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology*; D006325:Heart Atria / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008564:Membrane Potentials; D008955:Models, Cardiovascular; D032383:Myocytes, Cardiac