Transcoronary ethanol ablation of experimental ventricular tachycardia after epicardial ice mapping and localizing

Thirty-seven reproducible ventricular tachycardias (VTs) were induced in 19 dogs after the onset of myocardial infarction. The site of origin of VT was localized in 19 (59%) of 32 VTs by ice epicardial mapping. After 0.3-1.2 ml of 95% ethanol was injected into a small coronary artery supplying the arrhythmogenic area, VT was no longer inducible in 10 of 14 dogs. Intramyocardial ethanol (1-3 ml) was injected into the site of origin of VT in 9 dogs including 4 with VTs reinduced after intracoronary ethanol. Six of these VTs were not reinduced. Thus, the total efficacy rate was 84%. In 7 dogs, after injection of 0.4-1.2 ml (mean 0.5 ml) of 95% ethanol into a small normal coronary artery, the extent of the changes in ECG, CK-MB and pathology was found to be related to the size of myocardial damage and to the dose of ethanol. The smaller the dose of ethanol was given and the more distal the branch of coronary artery into which the ethanol was injected, the smaller the myocardial damage was. The data demonstrated that intracoronary or intramyocardial injection of ethanol may ablate the experimental VT induced by programmed heart stimulation in dogs after myocardial infarction, indicating that this approach may be useful and meaningful in some selected instances. However, it is necessary to limit the myocardial damage as far as possible.