Tunnel propagation following defibrillation with ICD shocks: hidden postshock activations in the left ventricular wall underlie isoelectric window

Abstract

Background: After near-defibrillation threshold (DFT) shocks from an implantable cardioverter-defibrillator (ICD), the first postshock activation that leads to defibrillation failure arises focally after an isoelectric window (IW). The mechanisms underlying the IW remain incompletely understood.

Objective: The goal of this study was to provide mechanistic insight into the origins of postshock activations and IW after ICD shocks, and to link shock outcome to the preshock state of the ventricles. We hypothesized that the nonuniform ICD field results in the formation of an intramural excitable area (tunnel) only in the left ventricular (LV) free wall, through which both pre-existing and new shock-induced wavefronts propagate during the IW.

Methods: Simulations were conducted using a realistic three dimensional (3D) model of defibrillation in the rabbit ventricles. Biphasic ICD shocks of varying strengths were delivered to 27 different fibrillatory states.

Results: After near-DFT shocks, regardless of preshock state, the main postshock excitable area was always located within LV free wall, creating an intramural tunnel. Either pre-existing fibrillatory or shock-induced wavefronts propagated during the IW (duration of up to 74 ms) in this tunnel and emerged as breakthroughs on LV epicardium. Preshock activity within the LV played a significant role in shock outcome: a large number of preshock filaments resulted in an IW associated with tunnel propagation of pre-existing rather than shock-induced wavefronts. Furthermore, shocks were more likely to succeed if the LV excitable area was smaller.

Conclusion: The LV intramural excitable area is the primary reason for near-DFT failure. Any intervention that decreases the extent of this area will improve the likelihood of defibrillation success.

Fig. 1. Model geometry and dose-response curve

A, Rabbit ventricular geometry and ICD-like electrodes in anterior and basal views; RV catheter in red, active can in blue. B, Dose-response curve resulting from all defibrillation episodes.

Fig. 2. Main postshock excitable area is in the LV wall

A, V_m maps in apex-to-base cross-sections following 175-V shock. Time is counted from shock onset. Regions within circles are septal excitable areas. White arrows denote direction of propagation. B, Percentage of total excitable volume in the LV wall as a function of SS at shock-end (7ms, red) and 17ms postshock (black).

Fig. 3. Extent of LV preshock excitable area affects shock outcome

A, V_m maps following 50-V shock delivered when LV was mostly refractory. B, Shock outcome grid for four preshock states, each with <15% excitable tissue in LV wall. Shock outcome is denoted by symbols in the grid. C, Dose-response curves for episodes of shock delivery at preshock states with >15% (red) and ≤15% (black) excitable tissue in LV wall.

Fig. 4. Shock outcome grid

Pink denotes fibrillation re-initiation episodes following IW. Images at bottom represent epicardial preshock V_m maps. Breakthroughs following IW are on LV anterior (left) and posterior (right) epicardium, with one exception on RV epicardium (marked by “RV”). Red boxes indicate breakthroughs near LV apex. Episodes with the same postshock behavior as a function of SS (S or D) and initiating PA origin (I or II, denoting pre-existing or shock-induced PA, respectively) are grouped into columns. Labels at bottom indicate figures in which the corresponding behavior is examined.

Fig. 5. Behavior S with pre-existing initiating PA

A. Preshock V_m maps with filaments in pink. B–C. Shock-induced response and propagation of Pas following 25-V and 175-V shocks. Open triangles mark LV epicardium that is refractory after the 175-V shock. White arrows denote propagation direction. Transmural apex-to-base maps are shown larger than epicardial maps to better show intramural propagation. D. Epicardial and transmural Φe maps (top) and Φe traces (bottom) within (black, red) and outside (green, blue) the tunnel following the 175-V shock.

Fig. 6. Behavior D with pre-existing initiating PA

A. Preshock V_m maps with filaments in pink. B–C. Shock-induced response and propagation of Pas following 50-V and 175-V shocks. Symbols as in Fig.5.

Fig. 7. Behavior D with shock-induced initiating PA

A. Preshock V_m maps. No preshock filaments existed within LV. B–C. Shock-induced response and propagation of PAs following 50-V and 125-V shocks. Symbols as in Fig.5. D. Epicardial and transmural Φe maps (top) and Φe traces (bottom) within (blue, green) and outside (black, red) the tunnel following a 125-V shock.

Fig. 8. Behavior S with shock-induced initiating PA

A. Preshock V_m maps. B–D. Shock-induced response and propagation of PAs following 75V, 100V and 175V shocks. Symbols as in Fig.5. E. V_m traces at the site marked with *. Gray rectangle denotes shock duration. Inset (bottom) emphasizes the incremental elevation of V_m with increases in SS within 13-ms interval following shock-end (interval outlined with dashed line).