Session P84.3
Influence of Atrial Dilatation in the Generation of Re-Entries Caused by Ectopic Activity in the Left Atrium
CA Ruiz-Villa, C Tobón, JF Rodriguez, JM Ferrero,
F Hornero, J Saíz*
Universidad Politécnica de Valencia
Valencia, Spain
Clinical and experimental studies have shown that Atrial Fibrillation (AF) tends to perpetuate itself over time, generating structural and electrophysiological changes known as atrial remodeling. In some patients, atrial dilatation is associated with the maintenance of cardiac arrhythmias. In this work, the influence of atrial dilatation on the reentry activity induced by an ectopic beat applied at different points of the atrium is studied. We have developed two models of anatomically realistic 3D atrium of human heart: normal and dilated. In the normal model the dimensions of the basic anatomical axis were to the left atrium: 4.31 cm for antero-posterior axis, 4.49 cm for mediolateral axis and 4.11 cm for superior-inferior axis. To obtain the dilated atrial model, the main axis were increased. The dimension of the dilated model are: 5.09 cm for antero-posterior axis, 6.20 cm for mediolateral axis and 5.82 cm for superior-inferior axis. The models include realistic fiber orientation. Both models included the cell Nygren model with electrical remodeling, for electrophysiological effects. When an ectopic beat is applied in the center of the free wall of the left atria, a reentry with a vulnerable window of 8 ms was observed in dilated atria. However, in normal atria this reentry activity was not found. For an ectopic beat applied between the right pulmonary veins, the vulnerable window to reentry activity was higher in dilated atria than in normal atria (12 times). When the ectopic beat was applied between the left pulmonary veins, the vulnerable window to reentry activity was very similar in both atria (17 ms for normal and 18 ms for dilated atria). This study shows an important influence of atrial dilatation on the reentry activity induced by ectopic beats and thereby on AF.
(Abstract Control Number: 121)