Origin of the electrocardiographic U wave: effects of M cells and dynamic gap junction coupling.

Abstract

The electrophysiological basis underlying the genesis of the U wave remains uncertain. Previous U wave modeling studies have generally been restricted to 1-D or 2-D geometries, and it is not clear whether the U waves generated by these models would match clinically observed U wave body surface potential distributions (BSPDs). We investigated the role of M cells and transmural dispersion of repolarization (TDR) 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 junction conductivity, the ECG with static gap junctions did not exhibit a U wave. In the 3-D model, TDR was necessary to account for the clinically observed potential minimum in the right shoulder area during the U wave peak. Peak T wave simulations were also run. Consistent with at least some clinical findings, the U wave body surface maximum was shifted to the right compared to the T wave maximum. We conclude that TDR can account for the clinically observed U wave BSPD, and that dynamic gap junction conductivity can result in realistic U waves generated by M cells.