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).