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.