High Density Intramural Mapping of Post-Infarct Premature Ventricular
Background: Spontaneous ventricular premature contractions (PVCs) in the
post infarct milieu is assumed to be due to automaticity. However, the
mechanism has not been studied with appropriate mapping tools.
Objective: To study the mechanism of spontaneous PVCs with high density
intramural mapping in a canine model, to test the hypothesis that
post-infarct PVCs are due to re-entry rather than automaticity. Methods:
In 15 anesthetized dogs, using 768 intramural unipolar electrograms,
simultaneous recordings were made. After 30 mins of stabilization,
recordings were made during the first 10 minutes of ischemia, and
activation maps were constructed of individual beats. Acute ischemia was
produced by clamping the left anterior descending coronary artery
proximal to the first diagonal branch. The analysis was limited to the
activation pattern of spontaneous ventricular beats. Results: In all
experiments ST-T alternans occurred. In 8 of 15 dogs spontaneous
ventricular beats occurred. In all 8 of these experiment earliest,
ectopic activity occurred in the endocardium, well within the ischemic
zone. From there, activity spread rapidly along the subendocardium, with
endo-to epicardial spread along the non ischemic myocardium. Epicardial
breakthrough always occurred at the border of the ischemic myocardium.
In 3 dogs, delayed potentials were observed, which were earliest at the
ischemic epicardium and extended transmurally with increasing delay
towards the endocardium, where they culminated in a premature beat.
Conclusion: Graded responses that occur with each sinus beat
intramurally, when able to propagate from epicardium to endocardium is
the mechanism by which PVCs are generated in post-infarct myocardium.