Localization of the Site of Origin of Postinfarction Ventricular Tachycardia by Endocardial Pace Mapping

Background. The purpose of this study was to assess the value of body surface mapping and the standard 12-lead ECG in localizing the site of origin of postinfarction ventricular tachycardia (VT) during endocardial pace mapping of the left ventricle. Methods and Results. Simultaneous recordings of 62-lead body surface QRS integral maps and scalar 12-lead ECG tracings were obtained in 16 patients with prior myocardial infarction during a total of 26 distinct VT configurations and during subsequent left ventricular catheter pace mapping at 9 to 24 different endocardial sites. Anatomic pacing site locations were computed by means of a biplane cineradiographic method and plotted on a polar projection of the left ventricle. The QRS integral map and the QRS complexes of the 12 standard leads of eachVT morphology obtained in a particular patient were compared independently with the different paced QRS integral maps and paced QRS complexes of the 12-lead ECG generated in that same patient. The stimulus site locations of the best matching paced QRS integral map and paced QRS complexes of the 12-lead ECG were indicated on the polar projection and subsequently compared with the endocardial location of the corresponding site ofVT origin identified during intraoperative (surgical ablation) or catheter activation sequence mapping (catheter ablation). The localization resolution of pace mapping was established separately for each electrocardiographic technique by computing the size of endocardial areas with similar morphological features of the QRS complex. Pace mapping advocated with body surface mapping or the 12-lead ECG enabled adequate reproduction of theVT QRS morphology in 24 of 26 VTs (92%) and 25 of 26 VTs (96%), respectively. Activation sequence mapping identified the site of origin in 12 of 26 previously observedVT configurations (46%). Ten and 11 VTs were localized by activation sequence mapping and pace mapping combined with body surface mapping or the 12-lead ECG, respectively. Pace mapping applied with body surface mapping identified the site of origin correctly (distance .2 cm) in 8 of 10 compared VTs (80%); an adjacent site (distance between 2 and 4 cm) or a disparate site (distance >4 cm) was identified in the remaining 2 of 10 VTs (20%). Pace mapping used with the 12-lead ECG localized the site of origin correctly in 2 of 11 VTs (18%); the site of origin was identified correctly next to an additional adjacent site in 5 of 11 VTs (55%); and an adjacent site or a disparate site was found in 1 of 11 VTs (9%vo) and 2 of 11 VTs (18%), respectively. The difference in localization accuracy of both electrocardiographic techniques was statistically significant (P=.02). The mean size of endocardial areas where a comparable QRS morphology was obtained during pace mapping was 6.0±4.5 cm2 with the application of body surface mapping and 15.1+±12.0 cm2 with the use of the 12-lead ECG. Conclusions. These results demonstrate that application of the 62-lead instead of the 12-lead ECG during endocardial pace mapping enhances the localization resolution of this mapping technique and enables more precise identification of the site of arrhythmogenesis in the majority of compared postinfarctionVT episodes. (Circulation. 1993;88[part 1]:2290-2306.)