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  • The PPI from the CS ostium

    2019-04-15

    The PPI from the CS ostium was close to the TCL, suggesting that the CS ostium was on the dominant circuit (Fig. 8B). During entrainment from the CS ostium, the last captured beat of the TA was the second beat after the stimulus, suggesting that the slow conduction area (crosshatch) was located distal to the site B and that the TA was not involved within the dominant circuit (Fig. 8B). At a pacing tnf alpha inhibitor length of 240ms, the last captured beat of the CS was the second beat, which changed to the first beat after shortening of the pacing cycle length to 220ms (Fig. 8C). This change could be explained by the antidromic penetration of the reentrant circuit by the shorter pacing cycle length (Fig. 8C, red line) [3]. The different response between the CS and the right atrium suggested the anatomically different exit sites from the dominant localized reentrant circuit to the right atrium and the CS. During entrainment from the CS ostium, TA1-2 was captured antidromically, suggesting the presence of clockwise conduction through the septal isthmus. The fractionated potential was observed at the roof of the CS ostium (Fig. 3), and all of the last captured beats became the first beat after the stimulus from the roof of the CS ostium, suggesting that the dominant reentry circuit was localized at the CS ostium. During entrainment, the preceding small electrogram (y) before stimulation artifact could be recognized (Fig. 3, upper). Therefore, the last stimulus captured both the potential just after the stimulus (x) and the next preceding potential (y) (Fig. 8D), likely because there was a gap between x and y potential, and x potential had a lower threshold than y potential. Although y potential was clear, it was difficult to determine the initial point of x potential because both y and x potentials showed continuous fractionated potential. If we define x potential as the latest component of the fractionated potential, PPI became 260ms, equal to TCL (Fig. 3, red arrow). The cause of fractionated potential in the CS is attributable to anisotropic conduction due to the complex anatomy of the CS muscular cuff [6,7]. Tonet et al. reported a patient with localized reentrant atrial tachycardia at the CS ostium [8]. Fragmented potential with longer duration of electrograms associated with significant conduction delay were recorded at the CS ostium. In Case 2, we demonstrated dual-loop reentry consisting of the TA and the superior trans-septal incision. The dual-loop reentry after open heart surgery has been well studied by three-dimensional electroanatomical mapping [1,9]. However, the dynamic relation of dual-loop reentry around the TA and the superior trans-septal incision was not clear [10]. In case 2, the prolonged PPI at the corridor between the TA and the superior trans-septal line suggested that the circuit around the superior trans-septal incision was not a dominant circuit (Fig. 8E). During entrainment from the TA circuit, shortening the pacing cycle length from 250ms to 230ms changed the activation sequence of the last captured beats after the stimulus because of the antidromic penetration (Fig. 8F and G, red line) to the circuit around the TA. Antidromic penetration to the circuit not only changed the excitation wave morphology but also shortened the return cycle compared to the TCL (Fig. 5, #). The deeper antidromic penetration through the TA entered the corridor between the TA and the trans-septal incision line. This activation showed a shortened return cycle despite the fact that the excitation wave forms were nearly the same as those during entrainment, because the captured activation sequence of the corridor was orthodromic (Fig. 8G). The common pathway of this dual-loop reentry between the TA and the trans-septal incision line was located posterior to the trans-septal incision line. In Case 3, we revealed dual-loop reentry around the TA and the longitudinal dissociation along the cavo-tricuspid isthmus. Lateral cavo-tricuspid isthmus ablation shortened TCL without termination. Before the lateral cavo-tricuspid isthmus ablation, clockwise conduction through the posterior isthmus (n) could not turn around the lateral edge of the longitudinal dissociation of the isthmus and was blocked by the counter-clockwise conduction (n−1) from the lateral TA (Fig. 6 upper left and arrow from ABL3-4 in lower panel). It is possible that the lateral cavo-tricuspid isthmus ablation changed the anisotropic conduction, the clockwise conduction through the posterior isthmus could turn around the lateral isthmus, and counter-clockwise conduction through the anterior isthmus returned to the CS ostium (Fig. 6, upper right). During entrainment from the right atrial free wall (TA17-18, site A), counter-clockwise activation of the right atrial free wall could enter the anterior isthmus and demonstrated a prolonged PPI (Fig. 7, upper). The last captured beats of the late component of the double potentials along the cavo-tricuspid isthmus were the second beat after the stimulus. Both the prolonged PPI and the delayed capture of the double potential suggested that the entrainment site was not on the dominant circuit. On the other hand, entrainment from the anterior cavo-tricuspid isthmus (site B) demonstrated the same PPI as the TCL and all of the last captured beats became the first beat after the stimulus (Fig. 7, lower). Localized atrial tachycardia from the septal isthmus and CS ostium has been reported by Yang et al. [11]. In Fig. 6, no double potentials in TA3-4 and TA5-6 could be observed because of an anterior shift in the TA catheter (a larger ventricular activation wave in TA 11-12 and TA13-14). In Fig. 7, as the TA catheter shifted to the posterior side (larger atrial activation wave in TA 11-12 and TA13-14), double potentials in TA3-4 and TA5-6 reflecting longitudinal dissociation of the isthmus could be recognized.