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  • br Discussion In this study AT originated in the

    2019-05-06


    Discussion In this study, AT originated in the orifice of the RAA in a patient with ARVC/D. The origins of these ATs were quite close, which is supported by similar P-wave morphology of each AT. The ATs could be ablated by multiple endocardial RF applications. In this case, the exact mechanism underlying the ATs was unclear because of the failure of detailed electrophysiologic testing. However, the activations of each AT spread from a single earliest point of activation, and each AT activation time did not cover >90% of the tachycardia atipamezole length. The termination by pacing and these activation features suggest that the mechanism of AT is micro-reentry or triggered activity. To the best of our knowledge, there have been no reports of AT combined with ARVC/D, and only a few reports have described atrial involvement in ARVC/D. In a single case, right atrial biopsies verified the presence of fibrotic replacement of the atrial myocardium in a patient with ARVC/D, sick sinus syndrome, and an atrioventricular conduction disturbance [2]. A previous report showed that patients with ARVC/D had not only prolonged interatrial conduction expressed as a longer P-wave duration but also significant abnormalities in the P-wave morphology [3]. Atrial involvement in ARVC/D was also noted in several animal models of the disease, that is, the loss of the atrial myocardium and the presence of bilateral, focal, fibrofatty atrial lesions in up to one-third of affected boxer dogs and cats [4,5]. Takemura et al. [6] found that the RA was electrically silent with no capture during electrical stimulation at all sites, except for small areas in the lower RA in a patient with ARVC/D. In fact, this patient had an extensive low voltage area throughout the RA, and the P-wave duration during atrial pacing was substantially prolonged after ablation (Fig. 1B). Furthermore, the AT in our patient originated from the low voltage zone (LVZ) or the border zone adjacent to the LVZ (Fig. 4). The LVZ contained low-amplitude and fractionated electrograms (pink dots in Fig. 3), suggesting slowed or anisotropic conduction through the diseased RA. These anatomic changes could be a potential source for the development of AT and may be related to the fibrotic replacement of the atrial myocardium in a patient with ARVC/D. The occurrence of AT in patients with ARVC is rare; however, care is warranted because AT may cause inappropriate ICD discharges in patients with ARVC/D.
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    Conflict of interest statement
    Case A 77-year-old man with symptomatic paroxysmal atrial fibrillation (AF) was referred for catheter ablation. In the electrophysiological study, three-dimensional (3D) geometries of the left atrium (LA) and pulmonary veins (PVs) were constructed with an EnSite NavX mapping system (St. Jude Medical Inc., St. Paul, MN, USA). After 5min of AF stabilization induced by rapid atrial pacing, dominant frequency (DF) maps were created with a DF software installed in NavX (sampling rate, 1200Hz; resolution, 0.14Hz; with a Hamming window function), using data obtained with a 20-pole circular mapping catheter (1.5mm interelectrode spacing, Livewire Spiral HP catheter, St. Jude Medical). The bipolar signals during 5s recordings were analyzed, and the highest peak frequency of the resulting spectrum was identified as the DF. On the DF map, high-DF sites were defined as sites with frequencies of >8Hz and in bright purple. High-DF sites were observed at the left inferior PV (LIPV); antrum of the left superior PV (LSPV); LIPV and right superior PV (RSPV); septal portion, roof, and floor of the LA; and mitral isthmus (Fig. 1). NavX and single Lasso catheter (Biosense Webster Inc., Diamond Bar, CA, USA)–guided extensive encircling ipsilateral PV isolation (EEPVI) was performed during AF with a 4-mm irrigated-tip radiofrequency (RF) ablation catheter (Safire BLU, St. Jude Medical; 25–30W, 41°C). During the EEPVI of the left PVs, the AF was terminated by RF deliveries at the posterior and anterior aspects of the LSPV antrum, but recurred immediately after these RF deliveries. After the creation of an entrance block into the left PVs, the AF became sustained; therefore, we then performed EEPVI of the right PVs. Such a termination and subsequent recurrence of AF occurred during the RF deliveries at the posterior aspect of the RSPV antrum. The AF eventually terminated during the ablation of the anterior aspect of the RSPV antrum, although the EEPVI of the right PVs was not completed (see the red ablation points in Fig. 1). 3D DF maps of the LA and PVs were merged offline with 3D CT images of the LA, PVs, and epicardial adipose tissue (EAT), which was reconstructed by assigning the Hounsfield units (−50 to −200) generally used for detecting adipose tissue. Interestingly, 3 of 4 AF termination sites were located at high-DF sites, which were all covered with EAT (Fig. 1). High-DF sites are known to be related to the center of focal-firing rotors or local reentry circuits [1]. In this case, termination of the AF by ablation and a subsequent immediate recurrence was repeatedly observed at 3 high-DF sites, which provided an insight for understanding the mechanism of high-DF sites. However, an RF delivery applied to the posterior aspect of the RSPV antrum without a high-DF site also terminated the AF. This could have been caused by a substrate modification and/or triggered firing from the left PVs because the AF termination at that site occurred after the EEPVI of the left PVs was completed. Moreover, we reported that high-DF sites corresponded to EAT sites [2]. Since EAT contains ganglionated plexi and secretes several inflammatory cytokines, it could be the substrate for the development of high-DF sites. Therefore, this phenomenon also presents atipamezole the insightful observation that EAT may be related to the development of dominant rotors maintaining AF; however, further prospective studies are needed to clarify this relation.