Introduction
The inability to map the intramural space in humans has led to tacit acceptance of using either endocardial or epicardial data to determine targets for ablation and or deciding mechanism of post infarct Premature Ventricular Contraction (PVC). Though the significance of the intramural space in ventricular arrhythmogenesis has recently been highlighted by us and others (1-4), it has not been studied with high resolution mapping in post-infarct PVCs.
Additionally, the prevailing theory of post-infarct PVC has been attributed to purkinje depolarizations in the border zones (5) as the driver, setting up automaticity as dogma. However, if upstream mechanisms are not adequately evaluated, mapping data could easily be misinterpreted based on downstream endo/ epi cardial mapping findings. Potential mechanisms such as depolarization of non-ischemic myocardium close to the ischemic border by injury currents (6), or transmural re-entry have not been studied in detail. As such we devised a high density mapping scheme with 768 simultaneous intramural electrograms. As ST-T alternans and injury currents are best monitored by unipolar electrograms we elected to use an exclusive unipolar scheme developed by Downar to evaluate mechanism of spontaneous post-infarct PVCs (7-8).