In patients with surgically corrected
In patients with surgically corrected CHD, the anatomic position of the atriotomy scar as the arrhythmogenic substrate is commonly found in the free wall and not in the septum . The cause of this large area of low voltage (“atrial myopathy”) is unclear. Possible explanations include interruption of arterial supply and insufficient protection during cardioplegia. The multiple dense scars may result from the atriotomy, cannulation sites, conduit sites, and other surgical trauma . AT3 was identified as a macroreentrant tachycardia circling through the right septum around the SVC and the large area of low voltage in the lateral wall. In the electroanatomical map, the activation sequence could not cover the TCL in spite of acquiring a sufficient number of points. This is because the assessment of local electrograms, especially in low voltage areas, was incorrect. As noted, in cases of surgically corrected CHD, large areas of low voltage are not always consistent with surgical trauma (incisions or cannulation sites) . To identify the mechanism of the circuits of AT3, it met inhibitor was useful to assess local electrograms carefully in combination with conventional mapping techniques. The circuit we assumed for AT3 is shown in Fig. 4. The circuit is not definitive in AT3. As our mapping and measurement of the PPI from the sites around the SVC, especially around the right septum and the junction between RA and SVC, was insufficient, we could not correctly identify whether the circuit of AT3 included the SVC or not. Considering our results from the activation map and the PPI, we assumed that AT3 was propagated clockwise around the SVC and the low-voltage area on the posterolateral wall through the right septum. The so-called “dual-loop” or “8-shaped” atrial re-entry circuit described late after correction of CHD were not found in vestigial structures case [6,12,13].
Entrainment pacing was used to confirm that the tissue generating the isolated diastolic atrial potential was located within the reentrant circuit. In one series of patients with macro-right ATs following surgical repair of CHD, ablation of the isolated potentials successfully eliminated at least 1 of the ATs in 73% of the patients. However, AT recurred in 53% of these patients (mean time to recurrence 4.1 months). The use of well-referenced electroanatomical mapping to delineate the arrhythmogenic substrate clearly indicated to us the feasibility of successful ablation [14,15]. In addition, accuracy in 3D reconstruction with CARTO3 allowed us to understand the anatomical construction (catheter sites, incision, and low voltage areas) and macroreentrant circuits. Because the reentrant circuits commonly have some relationship with large areas of low voltage suggesting “atrial myopathy”, the assessment of local electrograms in low voltage areas is essential . Therefore, conventional mapping techniques were also necessary to identify the mechanism of the tachycardias and to eliminate all tachycardias successfully. This case demonstrates that the use of a combined conventional and electroanatomical mapping technique, such as CARTO3, can be helpful for identification of the critical isthmus for catheter ablation of macroreentrant AT in patients with surgically corrected CHD.
Conflict of interest