Circulation, Vol 87, 216-229, Copyright © 1993 by American Heart Association
PS Chen, PL Wolf, YM Cha, BB Peters and SL Topham
BACKGROUND. In Langendorff-perfused hearts and in hearts on cardiopulmonary
bypass, chemical ablation of the subendocardium of both ventricles
decreases ventricular vulnerability to fibrillation. It was hypothesized
that the effects of ablation are a result of the elimination of the
subendocardial Purkinje fiber network. This hypothesis has been supported
by recent observations that the supernormal excitability that is
demonstrable in the Purkinje fibers is associated with arrhythmogenesis.
METHODS AND RESULTS. We tested this hypothesis on 10 open-chest dogs by
evaluating the strength-interval curves of anodal and cathodal stimulation
with the assistance of computerized mapping techniques. The ventricular
fibrillation threshold was also determined. The same test was then
performed after chemical ablation of the subendocardium of either the right
ventricle (six dogs) or both ventricles (four dogs). Anodal supernormality
was consistently demonstrated in all the dogs studied both before and after
subendocardial ablation. The ventricular fibrillation thresholds were 23
+/- 5 mA both before and after right ventricular subendocardial ablation (p
= NS). The ventricular fibrillation thresholds before and after
biventricular subendocardial ablation were 25 +/- 3 and 22 +/- 10 mA,
respectively (p = NS). CONCLUSIONS. We conclude that 1) subendocardial
ablation does not decrease ventricular vulnerability when the heart is in
situ and is not on cardiopulmonary bypass and 2) anodal supernormal
excitability can be demonstrated in ventricles without a subendocardial
Purkinje fiber network.
ARTICLES
Effects of subendocardial ablation on anodal supernormal excitation and ventricular vulnerability in open-chest dogs
Department of Medicine, UCSD Medical Center.
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