MECHANISMS UNDERLYING DIFFERENT SURFACE ECG MORPHOLOGIES OF RECURRENTMONOMORPHIC VENTRICULAR-TACHYCARDIA AND THEIR MODIFICATION BY PROCAINAMIDE

ECG Pleomorphism of Ventricular Tachycardia, Introduction: Distinct su rface ECG morphologies (ECGMs), from one episode to the next, of recur rent monomorphic ventricular tachycardia (VT) in the same patient comp licate endocardial catheter mapping and the success of ablative therap y, This study investigates the incidence and mechanisms of multiple EC GMs during recurrent monomorphic VTs in a canine model of experimental myocardial infarction (MI), Methods and Results: Computerized ECG ana lysis and simultaneous endocardial and epicardial activation mapping w ith a 64 bipolar electrode array were used to analyze the relation bet ween site of VT origin, local activation sequence, and surface ECGM in 72 VT episodes induced in 9 of 17 dogs with experimental MI, Pairwise comparisons of all VTs induced in the same animal were done in drug-f ree state (47 VTs) and after intravenous procainamide (25 VTs), In dru g-free state, VT pairs with similar surface ECGMs manifested endocardi al breakthrough sites (BSs) within a distance < 10 mm in 46 (100%) of 46 VT pairs compared to 43 (45%) of 95 VT pairs with different surface ECGMs (P < 0.0001), Of all 89 VT pairs with endocardial BSs within < 10 mm, similar endocardial activation patterns were found in 34 (74%) of 46 pairs with similar ECGMs in contrast to 6 (14%) of 43 pairs with different ECGMs (P < 0.001), Similar comparisons of VT pairs induced after intravenous procainamide administration showed that the endocard ial BSs were located within < 10 mm in 9 (75%) of 12 VT pairs with sim ilar and in 17 (49%) of 95 with different surface ECGMs, respectively (P = NS),Conclusions: In the same heart, similar surface ECGMs of recu rrent VT are highly predictive of closely spaced endocardial BSs in dr ug-free state, but not after procainamide administration, Nearly half of the VTs with different surface ECGMs still originate from closely s paced endocardial BSs but commonly manifest a change in the endocardia l activation spread from this site, Thus, assumptions about different mechanisms and sites of VT origin based on different surface ECGMs sho uld be made with caution.