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  • br Discussion We successfully prevented the

    2019-05-16


    Discussion We successfully prevented the initiation of AF without inhibiting the AF-triggering APB, and eliminated the AF-triggering APB located close to the sinus node without damage to sinus node function. Nifekalant is an IKr antagonist that prolongs the duration of myocardial nuclear receptors and prevents the initiation and persistence of arrhythmias, including AF, by the mechanism of reentry and triggered activity [1]. However, it does not directly affect myocardial depolarization, and therefore does not decrease the frequency of APBs that are initiated by abnormal automaticity, such as isoproterenol-induced APB. The successful elimination of non-PV AF-triggering APBs would improve the clinical outcome of AF ablation [2]. However, this can be challenging because APBs are rarely provoked, even after administration of isoproterenol. In addition, the administration of isoproterenol can easily result in the initiation of AF triggered by the APBs, which can hinder precise contact activation mapping. However, our observations can improve the clinical outcomes of ablation in patients with non-PV APBs, which initiate AF.
    Conflict of interest
    Financial support
    Introduction Ebstein׳s anomaly, characterized by apical displacement of the posterior and septal leaflets of the tricuspid valve, accounts for <1% of all congenital heart diseases [1]. Approximately 20–30% of patients with Ebstein׳s anomaly have atrioventricular reciprocating tachycardia (AVRT) due to an atrioventricular accessory pathway [2,3]. Radiofrequency catheter ablation is a curable approach for symptomatic accessory pathways. However, in patients with Ebstein׳s anomaly, accessory pathway ablation is associated with a low success rate and increased risk of recurrence [4–6]. This is because it is difficult to identify the precise location of the atrioventricular junction [4,6].
    Case report A 50-year-old woman was referred to our hospital for radiofrequency catheter ablation of a paroxysmal supraventricular tachycardia. A 12-lead surface electrocardiogram revealed ventricular pre-excitation associated with type B WPW syndrome. A chest radiograph revealed cardiomegaly with a cardiothoracic ratio of 57% and normal pulmonary vascular markings. Two-dimensional echocardiography demonstrated enlargement of the right atrium, apical displacement of the septal leaflets of the tricuspid valve by 16.3mm/body surface area, severe tricuspid regurgitation, no shunt flow, and normal left ventricular function (Fig. 1). The diagnosis of Ebstein׳s anomaly with type B Wolff–Parkinson–White syndrome was confirmed.
    Discussion Catheter ablation of accessory pathways has a lower success rate and higher risk of recurrence in patients with Ebstein׳s anomaly than in those with structurally normal hearts. Moreover, the need for repeat procedures is common [4–7]. The success rates relative to patients and accessory pathways are reported to be 76–88% and 82–91%, respectively [4,7]. Several factors are responsible for the low success rate of accessory pathway ablation in patients with Ebstein׳s anomaly [4–6]. First, up to 50% of patients with Ebstein׳s anomaly have multiple accessory pathways [4,6]. The presence of multiple accessory pathways may complicate the localization of accessory pathways. Second, most accessory pathways are located along the atrialized right ventricle [4–6]. The local activation potentials recorded along the atrialized ventricle reveal continuous fragmented electrical nuclear receptors activity with multiple spikes in 53% of patients [4]. Because of these abnormal potentials, it is difficult to distinguish an atrial electrogram from a ventricular electrogram, and localize the atrioventricular junction. The success rate of accessory pathway ablation is lower in patients with an abnormal electrogram than in those without an abnormal electrogram (55% and 100%, respectively) [4]. Finally, the catheter stability is often impaired by a large right atrium, tricuspid insufficiency, and downward displacement of the tricuspid valve.