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  • br Discussion In this case

    2019-05-15


    Discussion In this case report, we demonstrated the consistent fusion of P-waves during CS os pacing, except for the last captured beat, which was entrained but not fused, thereby satisfying the entrainment criteria [2,3]. The tachycardia could be induced with reproducible results by a single atrial extrastimulus within constant coupling intervals. An inverse relationship was found at tachycardia induction and entrainment pacing. The induced AT did not exhibit the warm-up phenomenon. All these findings indicate reentry as the mechanism of the AT. Adenosine-sensitive AT is usually focal in origin and arises from the region of the crista terminalis (inclusive of the sinus node), AV annulus, CS os, and various atrial sites [1,4–10]. Adenosine decreases the intracellular levels of cyclic adenosine monophosphate, resulting in the inhibition of the inward calcium current [11,12]. Thus, adenosine-sensitive reentrant AT is believed to involve calcium-channel-dependent substrates, such as those on the remnant or sleeve of AV nodal-like structures identified along the AV vicinity and AV annulus [1,5,10,13]. This type of AT characteristically occurs in the incessant, nonsustained repetitive pattern with oscillations in the A–A intervals [1,4], generally making it amphetamine sulfate difficult to demonstrate entrainment. In the present case, however, entrainment was clearly observed because the AT had a relatively stable rhythm and sufficient persistence. During pacing from both the CS os and the HIS, manifest entrainment was demonstrated. PPI was shorter in the HIS than the CS os, at each PCL. Similarity with the P-wave morphology of tachycardia was greater when obtained during entrainment from the HIS than when obtained during entrainment from the CS os. Consistent fusion in the atrial activation sequence was observed in the confined area around HIS 1-2 and HIS 3-4 (Fig. 5) during entrainment from the CS os. These findings indicate the proximity of the distal HIS to the exact microreentry circuit. As shown in this study, careful and precise observation is necessary to demonstrate entrainment, which is not always clear-cut in AT. Intrinsically, the P-wave is too subtle to reflect a small change in the morphology. In addition, it is not possible to prevent T-wave morphology from interfering with P-wave morphology during rapid atrial pacing. We focused on leads V1 and V2 (Fig. 2) because the influence of amphetamine sulfate the previous T-wave was minimized in those leads. We could not observe obvious changes in P-wave morphology when the CS os and the HIS pacing rates were increased. It might be more difficult to demonstrate progressive fusion of P-wave in focal reentrant AT because the interference by the previous T-wave is unavoidably increased. Progressive fusion of the atrial activation sequence also could not be detected. During atrial fusion, the local excitation is determined by whether the local myocardium was captured by the excitation from the entrainment pacing site or by the excitation from the site of exit of the reentry circuit. Therefore, the local excitation pattern should be “all-or-none,” as demonstrated by the distal HIS electrodes in this case (Fig. 5). The difference in the distribution of each local excitation pattern is reflected in P-wave morphology as a fusion. As demonstrated in Fig. 5, the atrial area captured by the excitation from the reentry circuit during entrainment pacing from the CS os might be relatively small and confined to the vicinity of the distal HIS. Therefore, to detect the progressive fusion of the atrial activation sequence, the spatial resolution afforded by the current electrode disposition would be too low. After the first report published by Iesaka et al. [1], the apex of the triangle of Koch has been identified as a specific site for the origin of focal AT [5–8]. Alternative radiofrequency delivered from the left interatrial septum or non-coronary aortic sinus of Valsalva has been demonstrated to effectively terminate AT, while avoiding the potential risk of inadvertent damage to the AV nodal conduction system [6–8,14–16]. However, the presumable mechanism and responsiveness to adenosine have not always been fully explained in any of the previous reports. In this report, we were able to explain the reentry mechanism through the demonstration of manifest entrainment (entrainment with fusion) by the pacing from the CS os. This finding was not consistent with those of Yamabe et al., who suggested that entrainment with fusion cannot be observed because rapid atrial pacing from the CS easily captures the earliest atrial electrogram antidromically [5]. They presumed that the reentry circuit of the AT is too small to permit the observation of manifest entrainment. In the present case, we did not perform three-dimensional electroanatomic mapping, and we could not observe concealed entrainment. Therefore, the precise reentry circuit and duration of the excitable gap could not be elucidated. However, our findings indicated that, at least, the reentry circuit of the present AT had sufficient size or an excitable gap to permit the advancement of the atrial electrograms by the pacing from an atrial activation site that was not the earliest.