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    • In Case we demonstrated dual

    2019-04-29

    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 kinase inhibitors 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. After overdrive pacing, excitation that is one lap behind (the second beat after the stimulus) is caused by several mechanisms. One is the prolonged conduction time that is longer than the TCL due to a long conduction pathway and/or slow conduction. The other is the dual-loop reentry [12]. The excitation wavefront induced by the overdrive stimulation entered one circuit after going around the other, so the penetration to the other reentry circuit became the second beat after the stimulus. Entrainment mapping using the activation sequence of the last captured beat is very useful for clarifying the complex relation of these reentrant circuits. The fourth criterion of reentry requires entrainment with shorter pacing cycle lengths in order to detect antidromic penetration into the reentrant circuit [13]. In Cases 1 and 2, entrainment with a shorter pacing cycle length demonstrated antidromic penetration to the circuit and changed the activation sequence of the last captured beats depending on the functional relation of reentrant circuits. However, it is sometimes difficult to determine changes induced by antidromic penetration, because the entrainment at shorter cycle lengths risks termination of the tachycardia and a catheter must be positioned precisely where antidromic penetration changes.
    Conflicts of interest
    Acknowledgments
    Introduction Patients with ischemic cardiomyopathy are at an increased risk for serious ventricular arrhythmias and sudden cardiac death (SCD). Epidemiological studies indicate that more than 50% of cardiac deaths are sudden [1,2]. Antiarrhythmic drugs (AAD) do not reduce mortality in these patients [3–7]. Although earlier trials used programmed electrical stimulation (PES) for risk stratification [6–8], more recent data demonstrate the benefit of implantable cardiac defibrillators (ICDs) to treat patients with severely reduced left ventricular ejection fractions (LVEF) without performing PES [7,9]. However, as many patients will never have any ICD treatment, further risk stratification is required. The MADIT I and II studies included PES before randomization to ICD or medical therapy (PES was not mandatory but encouraged in MADIT II and was performed in 80% of the patients). In the MUSTT study, a registry of all patients recruited was maintained, and included those patients who did not experience abnormal rhythms induced during PES (non-inducible patients). Buxton et al. showed that with no antiarrhythmic therapy, the non-inducible patients had better prognosis than inducible patients [10]. However, the mortality rate of both groups was still high, and the non-inducible patients might still benefit from ICD. The purpose of this study was to evaluate the efficacy of PES for risk stratification based on mortality for inducible patients treated with ICD vs. non-inducible patients in a “real-world” registry.