Fragmented, Long‐Duration, Low‐Amplitude Electrograms Characterize the Origin of Focal Atrial Tachycardia

Abstract

Focal atrial tachycardias (FAT) originate from areas with poor cell-to-cell coupling. Due to cellular uncoupling extracellular potentials become fractionated. The degree of fragmentation may be used to identify the site of origin of FAT prior to catheter ablation. We studied electrical fragmentation in relation to the distance to the site of earliest activity during FAT. Three-dimensional (3-D) electroanatomical activation/voltage maps obtained from patients (n = 15: 6 male, age 40 +/- 14 (19-72) years) referred for catheter ablation of FAT were analyzed. Bipolar atrial potentials (BP) were categorized according to the number of deflections. The peak-to-peak amplitude and the time interval between the first and last deflection (fractionation duration) of each BP were measured. Eighteen different atrial tachycardias (AT) (CL 346 +/- 109 [190-550]) msec were analyzed. The incidence of single potentials ranged from 30 to 81 (59 +/- 16)%. The occurrence of double and fractionated potentials < or = 2 cm of the site of earliest activity ("focal area") was higher compared to the remainder of the atria (67 +/- 22% vs 34 +/- 14%, P < 0.001). Focal area potentials were characterized by a longer duration (49 +/- 22 msec vs 34 +/- 17 msec, P < 0.001) and a lower peak-to-peak amplitude (0.51 +/- 0.43 [0.12-1.7] mV vs 0.94 +/- 0.69 [0.22-2.58] mV, P = 0.03). Fractionation was not associated with FAT cycle length (r =-0.26, P = 0.29) or left atrial diameter (r = 0.47, P = 0.30). Significant differences in fractionation, fractionation duration, and peak-to-peak-amplitude of atrial potentials between the focal area and the remainder of the atria exist. Fractionation and voltage mapping can be used, besides activation mapping, to identify the site of origin of FAT during catheter ablation.