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  • br Radiofrequency ablation Application of single radiofreque

    2019-05-04


    Radiofrequency ablation Application of single radiofrequency mCAP to the earliest atrial activation site during tachycardia terminated the tachycardia and restored sinus rhythm (Fig. 4). Because the local AF in the SVC continued, we confirmed that isolation of the SVC from the RA had been achieved (Fig. 4) using repeated intravenous administration of ATP (20mg). Dissociation between the mCAP SVC and RA was still achieved during administration of ATP, excluding the possibility of a dormant conduction between the SVC and RA.
    Discussion Studies have clarified that the major sources of atrial arrhythmias are located at the junction of the atria and thoracic veins, such as the pulmonary veins [6]. Initially, we speculated that the AT in our patient originated from the right superior pulmonary vein (RSPV). However, activation at the SVC–RA connection preceded the potentials in the RSPV. Recently, the SVC has been considered to be one of the major foci for initiating atrial tachyarrhythmias, such as AT and AF [1–4,7]. Several reports have demonstrated that the atrial muscle extending into the SVC is related to the arrhythmogenesis of the SVC [8–10]. SVC cadiomyocytes can depolarize spontaneously [8,9], and ectopic firings from the SVC could initiate and maintain AT and AF [1–4]. In addition to automaticity, reentry within the SVC has also been reported to be one of the involved mechanisms [2,11]. In the present case, the rhythm in the SVC locally exhibited AF, and we considered this to be the cause of the AT. Very few reports have described the occurrence of 2 different forms of atrial tachyarrhythmias observed in both the SVC and atrium. Conduction block at the SVC–RA junction may explain the 2 different rhythms observed in the SVC and atrium. Although conduction block at the junction between the pulmonary veins and left atrium has been reported, conduction block from the SVC to RA is not common [1,3,5,7,12]. Moreover, while the RA–SVC connection exhibited 1:1 conduction during sinus rhythm at 60bpm, the SVC–RA connection demonstrated 2:1 to 3:1 conduction block during AT (Fig. 2). We also examined the SVC–RA conduction pharmacologically. Intravenous ATP at a dose of 20mg accelerated the SVC–RA conduction, supporting the existence of an exit block. ATP has been widely used in AF ablation to unmask dormant pulmonary vein conduction [13,14]. The exact mechanism through which ATP facilitates pulmonary vein to left atrium conduction remains unclear [13–15]. Adenosine activates outward potassium current via the purinergic A1-receptor. Hyperpolarization of the cell membrane and shortening of the action potential/refractory period may facilitate electrotonic conduction [13,14]. Although there have been few reports describing the effects of adenosine on SVC–RA conduction, the same mechanisms are suggested [16]. The location of the SVC–RA connection was successfully documented by a multipolar circular mapping catheter and CARTO mapping. The Lasso catheter revealed that the SVC–RA connection was located at a posteroseptal site of the SVC–RA junction. The location of this site corresponded to location of the earliest activation visualized by CARTO mapping. These facts suggested that atrial activation spread through the SVC–RA connection at the septal site of the SVC–RA junction. Furthermore, application of single radiofrequency energy at this site successfully eliminated the tachycardia and restored sinus rhythm, and electrical isolation of the SVC was obtained. Several investigators reported that slow conduction between the SVC and RA was frequently observed at the superior part of the crista terminalis [12,17], but also reported this phenomenon at other sites [5,18]. Because only a few cases have been reported, we cannot assume that this is the most common site of slow conduction. In the present case, activation mapping of the tachycardia and successful ablation of the specific site (Fig. 4) revealed that a slow conduction zone was located at the superior part of the crista terminalis.