Figure Legends
Fig. 1. The mapping results of two kinds of ATs and sinus rhythm in patient 2. A, Activation mapping shows a localized reentry run around the obstruct line formed by scars (black box). The DPs are shown near the scar line in the first AT (A 2). B, After ablation of the isthmus in the scars, AT converted to an RMAT depending on the LPV. The location where the DP showed normal potential in the second AT (B 2), and the white block line disappeared due to nearby atrial chronicle activation. There is a new white block line near the LAA (black box) and the location where the FP shown in AT1 (A 3) converted to a DP in AT2 (B 3). C, An FP covering nearly 1/3 of the CL was mapped between the LIPV and the scars in the mitral isthmus, and the AT converted to SR after ablation at this site. D, In sinus rhythm, the positions that showed potential conversion in different ATs showed normal potentials. There were two regions of the FCB in this patient that functioned in different mechanisms of ATs. AT= atrial tachycardia; CL=cycle length; DP=double potentials; FCB=functional conduction block; FP=fragmented potential; LAA=left atrial appendage; LPV=left pulmonary vein; RMAT= roof-dependent macroreentrant tachycardia; SR=sinus rhythm.
Fig. 2. The mapping results of three kinds of ATs in patient 3. AT1, activation mapping shows that the mechanism of the first was PMF. AT2, the AT1 converted to a localized reentry with multiple breakouts running around the obstruct line (black box) after ablation of the mitral isthmus. A DP showed near the white line. AT3, the AT2 converted to a localized reentry running around the LAA after ablation of the upper breakout, and the white block line disappeared, causing near atrial chronicle activation again. The DP converted to the normal potential again. The regions of the FCB were only shown in AT2 and maintained the localized reentrant circuit. There was a constant scar line near the LSPV (white line). AT= atrial tachycardia; CL=cycle length; DPs=double potentials; FCB=functional conduction block; FP=fragmented potential; LAA=left atrial appendage; PMF=perimitral flutter; LSPV=left superior pulmonary vein.
Fig. 3. The mapping results of four kinds of ATs in patient 7. AT1, activation mapping shows the double-loop MAT, and entrainment mapping suggests that a better PPI is related to the PMF. AT2, the double-loop MAT converted to PMF after ablation of the mitral isthmus, and an FCB region was present in the anterior wall (black box). A DP showed near the white line but not in AT1. AT3, for failure to block the mitral isthmus through a traditional ablation strategy, an anterior line was ablated as an alternative plan. After ablation, the AT2 converted to RMAT running around the LSPV, and the white block line disappeared, causing nearby atrium chronicle activation again. The DP converted to the normal potential again but with low voltage. AT4, activation mapping showed 26% of the TCL (70 ms) missing. PPI-TCL<20 ms at the left lateral ridge, posterior base of the LAA. PPI-TCL >20 ms in the septal MA and proximal and distal coronary sinus. AT was terminated to sinus rhythm after ablation in the base of the LAA near the left lateral ridge. The regions of the FCB are only shown in AT 2, and the relationship with this AT is not clear. AT= atrial tachycardia; CL=cycle length; DP=double potentials; FCB=functional conduction block; FP=fragmented potential; LAA=left atrial appendage; PMF=perimitral flutter; LSPV, left superior pulmonary vein; PPI= postpacing interval; TLC= tachycardia cycle length; RMAT= roof-dependent macroreentrant tachycardia.
Fig. 4 . The mapping results of two kinds of ATs in patient 4. AT1, activation mapping shows the double-loop MAT related to the scar in the anterior wall. There were two breakout pathways of the scar. AT2, after ablation of the lower breakout, the AT1 converted to AT2, which could be forecasted before the first ablation. The AT converted to sinus rhythm after ablation of the upper breakout. No FCB region could be seen during ablation.