Effects of subendocardial ablation on anodal supernormal excitation and ventricular vulnerability in open-chest dogs.

Abstract

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. 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). 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.