Figure 5: The relationship between the stimulation site and VT inducibility is illustrated using a computer model. In this model, unexcitable regions (black) create an asymmetrical channel, wider at the left-hand side, than at the right, creating anatomy that facilitates left to right conduction through the channel.19 Panel A. Simulations of the same stimulation sequence of stimuli were conducted to determine the range of sites over which re-entry was induced. Stimulation at sites along the blue line successfully induced VT, while stimulation from sites along the red line failed to do so. Panel B. Two separate simulations are shown with programmed stimulation applied at the ~11 o’clock (Stimulation Site 1 where no VT was induced) and 2 o’clock positions (Stimulation Site 2 where VT was induced). The leading edge of the excitation wavefront is black and the trailing edge of refractoriness fades to green - yellow. The last beat of the drive train (S1) at 300ms (panel a) and the onset and propagation of the extrastimulus beat (S2) at 220ms (panels b-e) are shown. With stimulation from Site 1 close to the broad end of the channel, the paced wavefronts encounter the ends of the channel with a timing that prevented reentry for all extrastimuli down to refractoriness. This is due to block of the S1 wavefront at the narrow end of the channel shortly before arrival of the S2 wavefront, such that the channel is refractory for the S2 wavefront. In contrast, Stimulation Site 2 is close to the narrow end of the channel. A premature stimulus encounters block at the narrow end, propagates to the entrance, then through the isthmus with sufficient time for the initial site of block to recover, and emerges from the channel producing the first reentrant beat.
Table 1: Clinical characteristics