Role of activation signatures in re-entrant ventricular tachycardia circuits.

INTRODUCTION: Development of a rapid means to verify the ventricular tachycardia (VT) isthmus location from heart surface electrogram recordings would be a helpful tool for the electrophysiologist.

METHOD: Myocardial infarction was induced in 22 canines by left anterior descending coronary artery ligation under general anesthesia. After 3-5 days, VT was inducible via programmed electrical stimulation at the anterior left ventricular epicardial surface. Bipolar VT electrograms were acquired from 196 to 312 recording sites using a multielectrode array. Electrograms were marked for activation time, and activation maps were constructed. The activation signal, or signature, is defined as the cumulative number of recording sites that have activated per millisecond, and it was utilized to segment each circuit into inner and outer circuit pathways, and as an estimate of best ablation lesion location to prevent VT.

RESULTS: VT circuit components were differentiable by activation signals as: inner pathway (mean: 0.30 sites activating/ms) and outer pathway (mean: 2.68 sites activating/ms). These variables were linearly related (p < .001). Activation signal characteristics were dependent in part upon the isthmus exit site. The inner circuit pathway determined by the activation signal overlapped and often extended beyond the activation map isthmus location for each circuit. The best lesion location estimated by the activation signal would likely block an electrical impulse traveling through the isthmus, to prevent VT in all circuits.

CONCLUSIONS: The activation signal algorithm, simple to implement for real-time computer display, approximates the VT isthmus location and shape as determined from activation marking, and best ablation lesion location to prevent reinduction.