Skip to main content
. Author manuscript; available in PMC: 2007 Sep 27.
Published in final edited form as: Q Rev Biophys. 2006 Jul 19;39(1):57–116. doi: 10.1017/S0033583506004227

Fig. 25.

Fig. 25

Mechanisms of ECG changes caused by the 1795insD mutation. (a) Stylized ECG defining the different deflections, waves and intervals. (b) Cellular mechanism of ST elevation and T-wave inversion. At fast rate, loss of dome or coved dome in epicardial cells creates a voltage gradient (▽Vm, blue arrows) between these cells (bold line) and M cells (thin line) during the AP plateau, leading to ST-segment elevation on the ECG [blue arrow in (a)]. Greatly prolonged notch in a coved-dome epicardial AP could delay its repolarization beyond that of M cell, thus reversing the normal gradient (normally, M cells have the longest APD and repolarize last) as indicated by the green arrow in (b), possibly leading to T-wave inversion [green arrow in (a)]. (c) Cellular mechanism of QT prolongation. At slow rate M-cell APD is prolonged by the mutation (red arrow). The delayed repolarization is reflected as QT prolongation on the ECG [red arrow in (a)]. [Simulation data in (b) and (c) are reproduced from Clancy & Rudy, 2002, with permission.]