PMC5067789_01
Electroanatomical mapping. Left ventricular posterior views of epicardial mapping (A) and endocardial/epircardial map (B). The earliest epicardial activation site during ventricular tachycardia (A, marked by a white arrow) shows the site where VT has been interrupted, and brown tags (A and C) indicate the ablation site on the LAVA potentials. A white circle (C) indicates voltage mapping during sinus rhythm (C) with isolated delayed potential around the ablation area.
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fig0005
After VT was induced (QRS morphology is identical to spontaneous ventricular arrhythmia), this isolated delayed potential became mid-diastolic and pre-systolic (180 ms before QRS complexes) (Fig. 1).
A twelve-lead ECG during ventricular tachycardia. Note the right bundle-branch morphology of the QRS complex (A). Findings during epicardial mapping during ventricular tachycardia show the presence of presystolic or mid-diastolic fragmentation (B). Panel (C) shows that the isolated potential in the epicardium occurs approximately 180 ms before the QRS complex during VT. Ablation at the epicardial site terminates ventricular tachycardia. In this area, during sinus rhythm it is possible to observe local abnormal ventricular activities (LAVA) potentials (white arrows). LAVA was defined as electrograms from poorly coupled surviving myocardial fibers with the following features: (1) sharp, high-frequency ventricular potentials distinct from the far-field ventricular electrogram; (2) occurring anytime during or, more frequently, after the far-field ventricular electrogram during sinus rhythm; and (3) sometimes displaying double or multiple high-frequency signals separated by very low-amplitude signals or an isoelectric interval. The complete elimination of LAVA would lead to a reduction in arrhythmia-free survival.
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Several additional radiofrequency applications were placed in close proximity adjacent to this site on local abnormal ventricular activities (LAVA) potentials (Fig. 2).