Discussion
We have demonstrated with high density intramural mapping of post-infarct PVC, that transmural re-entry with graded responses that propagate in from epicardium to endocardium is the mechanism of PVC in our experimental model. Even though transmural re-entry has been demonstrated before, the graded response in myocardium from epicardium to endocardium during sinus rhythm culminating in PVC is a novel finding. In agreement with the results of the present study, earlier studies also showed that ectopic activity during acute ischemia originated in the sub-endocardium.(8,10,11) A role for the Purkinje system was suggested based on the argument that whenever sub-endocardial recordings showed Purkinje activity, the Purkinje spikes preceded myocardial deflections during premature beats and subsequent beats of a tachycardi and when hearts were paced via the electrode terminal from which Purkinje activity had been recorded, the epicardial activation pattern was the same as during the spontaneous premature beat. Janse et al, probably because the number of electrodes from which electrograms could be recorded simultaneously was too small (n=60), no evidence for transmural re-entry was found. (11)
Reentry within the intramural space has not been studied in ischemic PVCs for inability map the intramural space. The sampling rate needed to appropriately map Purkinje as detailed by Ideker (13) effectively sets up a conundrum for high resolution mapping of the intramural space as it is not possible to have such high sampling rate and adequate number of mapping channels.
In the present study, no Purkinje activity was recorded. This was most likely due to the sampling rate used (960 samples/sec). Janse et al could only record Purkinje activity when the sampling rate was raised to once per 0.5 ms and when the amplification factor was increased.(11) This could only be obtained at the cost of less electrodes from which activity could simultaneously be recorded. The advantage of the present study lies in the number of simultaneously recorded electrograms (768) so that the mechanism of intramural re entry could be detected. The disadvantage is the sampling rate precludes recording of Purkinje activity. Although the origin of PVC was within the ischemic sub endocardium, epicardial breakthrough occurred at the ischemic border, often at more than one separate front. Epicardial mapping alone would have erroneously indicated the border zone as the source.Transmural re-entry has been observed in different settings. In canine hearts with an evolving myocardial infarction, recordings from 232 cardiac sites revealed intramural re entry (14). In human hearts with a chronic myocardial infarction, transmural re entry was documented, (15) although in the latter study focal mechanisms were identified as well.