Uniform slow conduction during sinus rhythm and low voltage/low voltage gradient ΔV/V characterize the VT isthmus...

Reentrant ventricular tachycardia (VT) properties require further elucidation.

To understand circuit mechanisms and improve ablation targeting.

In postinfarction VT patients undergoing electrophysiology study and catheter ablation, high-density endocardial electrogram contact mapping data was acquired during sinus rhythm (n = 6) and during VT (n = 12) and annotated by the system. Bipolar endocardial VT voltage was used to compute the voltage gradient, ΔV/V, at isthmus midline and at the lateral boundaries. Voltage was additionally represented as a depth as well as a color change, to better visualize level. Linear regression analysis was implemented to quantitate the sinus rhythm activation gradient along the isthmus long-axis midline, and along 3 other spokes originating from a last activation point.

The mean voltage along the isthmus long-axis was 0.234 ± 0.137 mV, vs 0.383 ± 0.290 mV aside boundaries (P < .001). The gradient ΔV/V along the isthmus long-axis was 0.425 ± 0.324, vs 0.823 ± 0.550 at boundaries (P < .001). Sinus rhythm activation was uniform (mean r² = 0.93 ± 0.05) and slow (∇ = 0.16 ± 0.03 mm/msec) along the spoke coinciding with isthmus long-axis midline, vs less uniform (mean r² = 0.32 ± 0.25) and rapid (∇ = 0.73 ± 0.62 mm/msec) along the other spokes (P < .001 and P = .003, respectively). Plotting r² vs ∇, parameters of isthmus vs nonisthmus spokes were clearly separable.

A low-voltage trench coincides with the VT isthmus, vs abrupt voltage increase at the lateral boundaries, which may contravene prior definitions of conducting channels. Sinus rhythm uniform slow conduction occurs at the VT isthmus location, preventing circuit disruption while enabling the formation of an excitable gap to perpetuate reentry.