Author + information
- A.M. Greenspan,
- K.P. Joshi,
- I. Khurram and
- S.K. Mainigi
Contact tissue impedance mapping (CTIM) can differentiate focal atrial tachycardia (AT) from macro-reentry e.g. atrial flutter, and localized reentry e.g. AVNRT, by identifying a contiguous low impedance area (CLIA) only in AT. We suspect that the CLIA is related to triggered activity as suggested by its presence only in AT associated with sharp, short duration electrograms at the site of origin. We hypothesized that if the CLIA reflected a region of triggered activity (TA) due to after-depolarizations it should be present in premature ventricular complexes (PVC) that are mainly due to TA. To expand the utility of CTIM in analysis of arrhythmia mechanisms, we applied CTIM in patients with PVCs to determine if CLIA’s are present and help localize their ablation site.
Forty-one consecutive patients with 53 different PVCs,28 male (68%),19 with CHF(46%) ,with mean LVEF of42±16% were mapped via local activation time (LAT) and CTIM utilizing the Carto 3 and XP mapping systems, and a 4-mm tip ablation catheter. Maps were created by moving the catheter to approximately150 points in the ventricle. Pace mapping was used adjunctively to select the ablation site. Low impedance (Z) was defined as ≤ Z min + 10%x(Zmax- Zmin). Normal Z was defined as ≥ Zmin + 20%x(Zmax-Zmin).
The origin of the 53 PVCs were outflow tract (OT) -25, mitral annulus -9, LV papillary muscles (PAP) - 4, LV lateral wall - 4, tricuspid annulus- 3 , RV septum- 2, LV apex - 1 and 1 in aorto-mitral continuity. Forty-nine (93%) of the 53 PVCs had a CLIA and all had sharp normal voltage (>1.5 mV) narrow(<55ms) electrograms at the ablation site. In 19 (76%) of 25 OT PVC and in 17 (71%) of the 24 Non-OT PVCs the CLIA contained the ablation site, and in remaining 15 PVCs (29%) the CLIA were within 1.3±0.6cm (1.2±0.6 for OT PVC and 1.5±0.6 for non-OT PVC) of the ablation site. The mean distance of CLIA to the ablation site was 0.4±0.7cm and the average surface area of the CLIA was 6.1±3.5cm2. The size of the CLIA was directly proportional to its distance from the ablation site when it did not contain the ablation site. Four patients 2 with PAP PVC and 2 with mitral annular PVC had no CLIA, but all had highly fractionated, long duration (97-145 ms) low amplitude(<0.5mV) electrograms at the ablation site.
Most PVCs have associated CLIAs in the CTIM without fractionated long duration electrograms at the site of origin. The CLIAs either contain the successful ablation site or are in close proximity to it. It appears that the CLIA phenomenon seen in focal ATs is also seen in ventricular arrhythmias related to TA and can be utilized to localize the origin of PVCs.