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  • A quadripolar mapping catheter was placed along the RV septu


    A quadripolar mapping catheter was placed along the RV septum, and a 3.5mm bidirectional open irrigated mapping catheter (ThermoChool SF®, Biosense Webster, Johnson׳s & Johnson׳s, Diamond Bar, CA, US) was inserted retrogradely into the LV. An electroanatomical substrate map created using the CARTO3® system (Biosense Webster, Johnson׳s & Johnson׳s, Diamond Bar, CA, US) was obtained during constant sinus-triggered LVP (via the LV device lead). Pacing was necessary due to the absence of a spontaneous ventricular rhythm; LVP was preferred to enhance delayed septal activation. Thresholds for the bipolar substrate map were set at 1.5mV and 0.5mV to discriminate respectively healthy tissue and “dense” scar, as γ-Secretase inhibitor IX manufacturer typically set up for ventricular substrate mapping. A large area of the anterior, septal, and apical scar was reconstructed without evident LPs. The RV substrate map revealed low amplitude potentials at the apical septum, again without LPs (Fig. 2a, b). Changing the site of RV septal pacing did not influence the NSVT occurrence or morphology, despite a different interval between the spike and NSVT onset; reproducibility was demonstrated by temporary switching to LV stimulation (Fig. 1B). Notably, the ICD bipolar morphology (tip-ring) of the NSVTs closely matched the clinical VTs (see Supplemental material, SM1). A biventricular activation map of the induced NSVTs was then performed, which confirmed a centrifugal activation originating from the infero-apical interventricular septum to both ventricles (see Fig. 2c) without significant anticipation on both sides of the septum. The best pacemap QRS concordance was 11/12 on both sides of the septum (a discordant V1 is evident; see Supplemental material, SM2); a unipolar electrogram was also suboptimal for ectopic origin at the same sites. Further careful mapping at the LV exit allowed to find a single site showing a late potential after a paced RV complex, followed by a low-amplitude, highly fragmented diastolic potential occurring 90ms before the NSVT onset (Fig. 3). At this site, a single radiofrequency (RF) energy application interrupted the occurrence of NSVTs after 4.6s (see Supplemental material, SM3); at the end of the RF application, a very late potential was recorded at the same site (see Supplemental material, SM4). After 30min, non-inducibility was confirmed by multisite RV pacing, and the procedure was concluded. The subsequent hospital stay was uneventful, except for the occurrence of atrial fibrillation, which was treated with external cardioversion. A predischarge device check revealed a nearly complete abolition of ventricular extra beats, with a substantial increase of the CRT stimulation rate. The patient remained free from recurrence in the following 3 months.
    Discussion It has been already evidenced that RV backup pacing in patients implanted with an ICD can rarely induce VT [6], with an association between the RVP rate and the induced VT risk. However, the negative influence of chronic RV pacing on ventricular function might have worsened the arrhythmic burden in these patients as well as influencing the progression of heart failure symptoms. Our findings are highly suggestive of a concealed localized reentry, with unidirectional block and double exit as the underlying mechanism established in conjunction with the progression of the myocardial disease. We propose a possible schematic explanation of the arrhythmia mechanism in Fig. 4. Localized reentry has been suggested for idiopathic VTs arising in the Purkinje network [7]. Concerning structural heart disease, possible localized, re-entrant VTs have been reported in RV arrhythmogenic cardiomyopathy [8] and in experimental infarctions [9]; however, continuous electrical activity has also been recorded at successful RF ablation sites in those cases. Therefore, a functional nature of reentry cannot be excluded.
    Conflict of interest