Right atrial tachycardia with 2:1 intra‐atrial conduction

Abstract

a b s t r a c tIn a case of atrial tachycardia (AT) originating from the inferolateral right atrium, cycle length (CL) alternans was observed. Conduction at the longer CL was to the high right atrium (HRA), His bundle electrogram region (HBE), and coronary sinus (CS). Conduction at the shorter CL was to the HRA, with that to the HBE and CS blocked.& 2014 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved. Case reportA 54-year-old woman presented to our clinic with palpitation and shortness of breath. Six years previously, she underwent successful catheter ablation for focal atrial tachycardia (AT) originating from the base of the right atrial appendage and right side of the fossa ovalis. However, AT originating from the inferolateral right atrium (RA) could not be ablated. The patient later developed multiple sclerosis, and steroid therapy was started. However, the AT recurred 2 months after the initiation of steroid therapy. Catheter ablation was again performed. The RA voltage map during sinus rhythm (Fig. 1, left) revealed a low-voltage area in the inferolateral RA and scarring at the inferolateral RA adjacent to the tricuspid annulus. Focal AT (AT1; tachycardia cycle length [CL]: 442 ms, total right atrial activation time: 23 ms) at 136 beats/min that originated from the inferolateral RA adjacent and anterior to the scar (Figs. 1 and 2, right) was induced by programmed atrial pacing and successfully ablated. Programmed atrial stimulation was performed to confirm the success of the ablation, but AT was easily induced by rapid atrial pacing, and the site of the earliest site was shifted to the lateral side along the right atrial scar area. Additional ablation was performed at the earliest activation site. Therefore, ablation points formed a linear ablation line along the right atrial scar site. Finally, another focal AT (AT2) was induced. The earliest AT2 activation site (hereafter referred to as the ABL site) was located lateral to the AT1 site (Fig. 3), and the AT2 was characterized by the presence of slight CL alternans (Fig. 4). The AT2 of the longer CL (184 and 182 ms) was conducted to the high right atrium (HRA), His bundle electrogram (HBE) region, and proximal and distal coronary sinuses (CSp and CSd, respectively). However, the AT2 of the shorter CL (167 and 174 ms) was conducted to the HRA, but conduction to the HBE and CS was blocked. The reason that the AT2 conducted to the RA appendage (HRA) but showed 2:1 conduction to the HBE region and left atrium might be explained as follows: the multiple ablation points actually created the linear lesion formation from the anterolateral tricuspid annulus to the inferolateral right atrium (Fig. 3) along the scar area (Fig. 1, left); thus, the activated AT2 could not conduct to the septal RA and LA in a 1:1 fashion. The surface electrocardiogram obtained during AT2 showed fairly regular results but no obvious P wave, which is typical of atrial fibrillation. AT2 was seen during the point-by-point ablation of the re-induced AT; therefo...

Intra-Atrial Block: Definition and Relationship to Atrial Fibrillation and Other Adverse Outcomes

“…In 1977, our group demonstrated that IAB can be rate-related, as was shown in a case of simultaneous intra-atrial and intra-ventricular conduction defects that mimicked an intermittent trifascicular conduction disorder. [25] Others have shown that: (1) portions of the right atrium can be in sinus rhythm (protected by entrance block) while other portions and the left atrium can be in flutter-fibrillation; (2) similar phenomena can exist in the left atrium following ablation; (3) intra-atrial block may occur during atrial tachycardia though being absent during sinus rhythm; (4) intra-and inter-atrial dissociation can occur during atrial flutter or fibrillation, [26][27][28][29][30][31][32][33] and (5) second degree IAB can be produced with atrial stimulation at critical drive rates (in an era well before ablation) thus confirming rate-related potential. [34] In one patient, electrophysiologic testing of sinus node function in the small section of the right atrium that was in sinus rhythm revealed an underlying sinus node dysfunction, while the rest of the right atrium and the left atrium was in atrial flutter-fibrillation.…”

“…Of note, but perhaps not of surprise, the risk for developing AF appears greatest when IAB is most pronounced, as measured by P wave width or P wave dispersion. [11,[13][14]20,[26][27][28][29][30][31][32][35][36][37][38][39][40][41][42][43][44][45][46] Relatedly, there have been reports of an increased risk for thromboembolism in patients with IAB-both stroke and peripheral. [6] Third, in our experience, not infrequently IAB also accompanies sinus node dysfunction, thus likely indicating pathology of both the sinus node and surrounding atrial tissue.Interestingly, in at least one report, in patients with sick sinus syndrome and paroxysmal atrial fibrillation in whom right atrial pacing was instituted as part of preventive treatment for recurrent AF, the presence of IAB during sinus rhythm was associated with a higher incidence of recurrent AF than when IAB was absent.…”