Characterizing the clinical implementation of a novel activation-repolarization metric to identify targets for catheter ablation of ventricular tachycardias using computational models

Fig. 1. Illustration of the RVI metric in normal conduction as well as in block. A) Activation sequence following an S2 beat that propagates throughout the tissue (S2 without block). Right panel: APs from the myocardium (red) and BZ (blue). The RVI at recording site i is given as the time difference between the RT(i) of the premature S2 beat and time of arrival of the S2 wavefront at the distal site AT(j). B) Activation sequence following an S2 beat with a shorter coupling interval leading to conduction block. The S2 beat blocks in the BZ where tissue is still refractory. The wavefront travels around the line of block and back towards the proximal site. Changes in the RVI at measurement site i value is illustrated by the thickness of the vertical gray bars which is large in normal propagation (A) and small in the case of block (B).

Fig. 2. Simulation results within the 2D computational model. A) Idealized infarct model consisting of: healthy myocardium (red); a circular region representing the BZ (gray); and two circular segments representing the necrotic scar (white). The BZ region contains an isthmus of 4 mm width separating the scars. B) Spatial distribution of Vm at the times the last S1 (t = 1020 ms) and S2 (t = 1240 ms) beats arrive at the isthmus' proximal mouth. C) Time course of Vm at recording sites (i) and (j) located at the myocardium and BZ inside the isthmus, respectively. D) ATs and RTs of the premature S2 beat.

Fig. 3. Simulation results within the BiV computational model. A) BiV model with a clipping plane view highlighting the endocardial surface of both right (RV) and left (LV) ventricles. Inset: intramural infarct anatomy with the delineation of one of the isthmuses within the scar. B) Activation sequence of the S2 beat following apical stimulation. C) Spatial distribution of Vm at different times illustrating conduction block of the S2 wavefront (t = 1300 ms); propagation through the isthmus highlighted in A) at t = 1400 ms; and the exit sites of the re-entry (t = 1460 ms).

Fig. 4. AT and RT calculation. ATs (red dots) and RTs (blue dots) obtained from: A) APs and B) electrograms computed following the last S1 beat and the S2 at recording site i in Fig. 2A. Electrogram of the premature S2 beat C) without noise and D) with noise. Dash lines represent projections of the AP time markers on the electrogram.

Fig. 5. The RVI metric applied to the 2D idealized infarct model. RVI maps constructed using three different interpolation methods: A) nearest neighbor; B) average; and C) minimum. Maps were constructed with search radius R of 4 mm (top panels), 8 mm (mid panels) and 16 mm (bottom panels).

Fig. 6. The RVI metric applied to the BiV scar anatomy model. RVI maps constructed using three different interpolation methods: A) nearest neighbor; B) average; and C) minimum. Maps were constructed with R = 2 mm (top panels) and R = 8 mm (bottom panels).

Fig. 7. Effects of Gaussian noise on RVI maps. RVI maps constructed with R = 4 mm and three different interpolation methods: A) nearest neighbor; B) average; and C) minimum. Lowest RVI value of each map is also shown.

Fig. 8. RVI maps computed on different electrode arrangements. A) Decapolar catheters placed parallel to the isthmus. B) Decapolar catheters placed perpendicular to the isthmus. C) Decapolar catheters arranged in a fan-like structure. D) Multipolar catheters placed randomly on the tissue surface. The minimum interpolation and R = 4 mm were used to compute RVIs.

Fig. 9. RVI maps computed on different electrode arrangements placed on the LV of the BiV scar anatomy model. A) Decapolar catheter inserted into the LV. B) Multipolar catheters placed randomly on the LV endocardium. Maps were constructed with R = 2 mm (left panels) and R = 8 mm (right panels). The minimum interpolation was used to construct the maps.

Fig. 10. RVI maps constructed using different pacing protocols. A) ATs and RVI map in steady-state S1 pacing at a BCL of 500 ms. B) ATs and RVI map in a premature S2 beat (coupling interval of 250 ms) without conduction block. The minimum interpolation and R = 4 mm were used to compute RVIs.

Fig. 11. AT and APD restitution properties of the 2D idealized infarct model. A) Differences between ATs of the S2 and S1 beats. B) Differences between APDs of the S2 and S1 beats.

Fig. 12. Effects of different electrophysiological properties of BZ tissue on the RVI metric. ATs and RVI maps following an S2 beat with a coupling interval of 250 ms in 2D infarct models with A) Slow conduction in the BZ; and B) Homogeneous tissue with same properties of the healthy myocardium.