Abstract 2681: Mechanism of Electrocardiographic U Wave Body Surface Potential Distributions: A 3-D Modeling Study
Electrophysiological basis underlying the genesis of U wave has not been precisely elucidated. None of previous modeling studies were performed in a three-dimensional (3-D) model, and it is not clear whether the U-waves generated by these models would match the clinically observed U wave body surface potential distributions (BSPD). We investigated the role of M cell and transmural dispersion of repolarization (TDR) in the genesis of clinically observed U wave BSPD in a 2-D, fully ionic heart tissue slice model and a realistic 3-D heart/torso model. In the 2-D model, while a U wave was present in the ECG with dynamic gap junctions, the ECG with static gap junction did not exhibit a U wave. TDR was essential for creating clinically observed potential minimum at the base. In the 3-D model, TDR was necessary to account for the clinically observed basal shift of the maximum and potential minimum in the right shoulder on the U wave BSPD (Figure⇓). As in the 2-D model, when the heart tissue had isotropic conductivity and the resistance at the atrioventricular (AV) junction was set to infinity, the combined source distribution results in no current flow and therefore no U wave BSPD was observed. We conclude that not only TDR but also dynamic gap junction coupling between myocardial cells and the finite resistance of the tissue at the AV junction are critical in the genesis of clinically observed U wave BSPD.