Abstract
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.