Speech:

Model of Bipolar Electrogram Fractionation and Conduction Block Associated with Activation Wavefront Direction at Infarct Border Zone Lateral Isthmus Boundaries

Abstract
After myocardial infarction, an infarct border zone (IBZ) forms around the infarct region. The IBZ is an arrhythmogenic area where the electrical activation impulse slows and can travel along circuitous pathways. Ventricular tachycardia (VT) is a common heart arrhythmia, and is often caused by a double-loop reentrant circuit, in which two activation wavefronts propagate simultaneously around a common isthmus in the IBZ. It is possible to interrupt the circuit using radiofrequency catheter ablation during electrophysiologic study. However, correct targeting may be difficult due to the problem of identifying all arrhythmogenic regions responsible for the clinical tachycardias that occur in a particular patient, and because of hemodynamic compromise during VT, which precludes mapping of the heart surface. We have developed a method that can potentially be useful to detect arrhythmogenic regions from which VT can form, without the need for tachycardia induction or extensive electrophysiologic mapping.

A model was devised to explain both the functional electrical conduction block that occurs in the postinfarction heart, and that can be useful to explain electrogram fractionation, the appearance of multiple small deflections in the signal acquired from the heart surface at the IBZ. When the activation wavefront encounters a sharp change from lesser to greater conducting volume during propagation through the IBZ, the wavefront becomes convex and slows, due to the reduction in available current to activate viable tissue in the distal direction. For particularly large impedance mismatch, this can lead to very slow conduction, < 0.01 millimeters per millisecond, or even functional conduction block.

We have identified these conditions as occurring at the lateral boundaries present on either side of the isthmus, or diastolic pathway, of the reentrant VT circuit. At these locations, there is a sharp spatial change from thinnest to thicker IBZ. During double-loop reentrant VT, a loop of the circuit travels around each lateral boundary. Furthermore, because of the variability in thin-to-thick infarct border zone at the lateral boundaries, the electrical activation wavefront can become discontinuous, resulting in electrogram fractionation. By targeting radiofrequency catheter ablation energy across the isthmus from one lateral boundary to the other, it is possible to interrupt the circuit so that reinduction of VT is prevented, including those clinical tachycardias that are not readily mappable by current methods.

Most recently, we have shown how wavefront curvature can be used to describe reentry induction during premature excitation of the heart. The model suggests that only by applying an electrical stimulus from certain locations and at certain coupling intervals, will the conditions conducive to reentrant VT onset be achieved, and that based on the mechanism, the reentry morphology must always be in the form of a double loop. It is possible to improve the success rate for ablating clinical VT by more accurately predicting the locations where premature excitation will lead to successful induction of reentrant tachycardia using this model. It can also be shown, based on the model, that the size and shape of the reentrant VT isthmus is constrained to certain dimensions. These findings are potentially helpful for improved and rapid radiofrequency catheter ablation targeting of arrhythmogenic regions of the IBZ in patients with recurrent reentrant VT. It could go a long way toward the successful treatment of these patients without the need for follow-up study, as well as to reduce the fluoroscopy time needed for evaluation.