• 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • Sustained AT Fig b B was induced


    Sustained AT2 (Fig. 1b(B)) was induced during pacing from the coronary sinus. The 3D activation map and the entrainment mapping including PPI from the CTI identified AT2 as a macroreentrant tachycardia circling counter-clockwise around the TA. AT2 was eliminated by CTI ablation. Sustained AT3 (Fig. 1b(C)) was induced during pacing from the coronary sinus. In AT1 and AT2, a sufficient number of points (AT1, 309; AT2, 442) were acquired to determine the circuit during the AT. However, in AT3, the activation sequence could not cover the TCL, in spite of acquiring a sufficient number of points (696). As shown in Fig. 3(a), the 3D activation map roughly suggested that the wavefront propagated centrifugally from the middle of the posterolateral wall, or propagated clockwise through the right septum around the SVC and the low-voltage area on the posterolateral wall. In the entrainment pacing, the PPI from the 3 sites around the low voltage area was identical to the TCL (Fig. 3(a)), and AT3 was identified as macroreentrant tachycardia, not focal AT. As shown in the voltage map, the fractionated potential shown in the middle of the low-voltage area suggested a zone of slow conduction critical for the perpetuation of the circuit. It suggested that the upper wavefront from this slow conduction propagated clockwise around the low-voltage area and the lower one terminated on the lower posterolateral wall due to the scar from IVC cannulation. Finally, a slow potential, with onset of 46 ms before the earliest atrial potential, was recorded with the ablation catheter at the site of the estimated slow conduction (Fig. 3(b)). In addition, 2 pre-potentials were recorded ahead of the slow potential. The first pre-potential was demonstrated 147ms earlier than the atrial potential at the distal electrode of the coronary sinus, which is defined as the reference atrial potential on the 3D activation map. In accounting for this local activation time, the window of activation time of AT3 was covered and became equal to the TCL (215ms). Radiofrequency waves were delivered at this site, and AT3 was terminated. We ensured that this site was not too close to sinus ccr2 inhibitor before ablation in sinus rhythm. An ablation line was made across the arrhythmogenic channel between the bottom of the low voltage area and the lower double potential. No tachycardia could be induced by either extra-stimulation or rapid atrial pacing (up to 300/min). At the end of the session, we confirmed that no sinus node dysfunction was present. So far, the patient has been free from palpitations for 6 months. No tachy or bradyarrhythmia has been documented, even in the Holter ECG.
    Discussion In this patient with a surgically repaired DORV, 3 macroreentrant ATs (AT1–AT3) were diagnosed and eliminated successfully. Macroreentrant right AT occurs commonly after surgical correction of CHD [1–4]. The mechanism often suggested is re-entry around surgical scars and/or anatomic barriers [5]. The circuits we assumed for the 3 macroreentrant tachycardias are shown in Fig. 4. The ATs were identified circling around an incisional line on the free wall of the right atrium (AT1), the tricuspid annulus (AT2), and a low voltage area in the lateral wall including the right septum (AT3). Isthmus-dependent atrial flutter, like AT2, and intra-atrial reentrant tachycardia, like AT1 and AT3, are the most common mechanisms of atrial reentrant tachyarrhythmias in patients with surgically corrected CHD, and they frequently coexist. The surface ECG is an inefficient tool for identifying patients with coexistent arrhythmias. It has been reported that coexistent isthmus-dependent atrial flutter and intra-atrial reentrant tachycardia were found in 44% of the patients examined, while intra-atrial reentrant tachycardia alone was inducible in 37% of the patients, and isthmus-dependent atrial flutter alone in 19% [5]. Accurately understanding arrhythmogenic substrate and the anatomical construction (catheters, incision, and low voltage areas) appears to be important to assist with catheter ablation of periatriotomy circuits in CHD, as reported elsewhere [7–9]. The 3D voltage map (Fig. 1(a)) methodically performed during AT was helpful in this case. An electroanatomical map with a very high density enabled us to accurately localize the entire reentrant circuit and the arrhythmogenic channels, especially in AT1 and AT2. In addition to that, the CARTO3 map was able to accurately indicate the position of the catheters and the anatomical construction. As shown in Fig. 2(b), Genetic code was easy to detect the activation around surgical scars and/or anatomic barriers. It has been reported that ccr2 inhibitor electroanatomical mapping is useful to delineate a tachycardia isthmus in periatriotomy circuits [7–9]. Accuracy in three-dimensional reconstruction of CARTO3 may also be more useful to understand anatomical construction and macroreentrant circuits.