Irregular Narrow QRS Tachycardia: What Is the Mechanism?

A 72-year-old female underwent an electrophysiological study for a paroxysmal narrow irregular tachycardia refractory to beta-blockers and bepridil, which had been diagnosed along with paroxysmal atrial fibrillation (PAF) using a wearable device (Figure 1A). A few years prior, the patient had undergone pulmonary vein isolation for PAF and slow pathway ablation for typical and atypical atrioventricular (AV) nodal reentrant tachycardia (AVNRT). Her clinical examination and echocardiographic findings were unremarkable, except for the presence of a bicuspid aortic valve. Irregular narrow QRS tachycardia with a cycle length of 520–560 ms was induced by atrial overdrive pacing (Figures 1B, 2, and 3). This tachycardia was reproducibly terminated by a rapid injection of 10 mg of adenosine triphosphate. What was the possible diagnosis of this tachycardia, and how do you differentiate it? Before the electrophysiological study, the irregular tachycardia was diagnosed as AF (Figure 1A). However, intracardiac electrocardiography revealed narrow QRS tachycardia with more ventricular activation than atrial activation (Figures 2 and 3). During tachycardia, P-waves were observed at regular intervals, and the P-wave morphology was similar to that during sinus rhythm, suggesting complete ventriculoatrial (VA) dissociation (Figure 1B). Therefore, atrial tachycardia, orthodromic reciprocating tachycardia using the AV accessory pathway, and AF were excluded. The possible diagnoses of this narrow QRS tachycardia with VA dissociation were AVNRT with an upper common pathway block, junctional tachycardia, orthodromic reciprocating tachycardia using a concealed nodoventricular or nodofascicular pathway, ventricular tachycardia originating from the His-Purkinje system, or intra-Hisian reentry. In the electrophysiological study, the atrio-Hisian and His-ventricular (HV) intervals were 112 and 60 ms, respectively, during sinus rhythm. Although this patient had undergone radiofrequency ablation targeting the anatomical and retrograde slow pathways in the previous session, triple antegrade AV nodal pathways were identified during programmed atrial extra-stimulation. Retrograde conduction was absent even after isoproterenol infusion. Tachycardia was induced by programmed atrial and ventricular stimulations. Although fluctuations in the HH and VV intervals were observed, the HV interval during tachycardia was 60 ms, which was the same as that during sinus rhythm. VA dissociation persisted even after isoproterenol administration. Atrial premature depolarization during tachycardia is one of the maneuvers to differentiate between AVNRT and junctional tachycardia [1, 2]. Padanilam et al. showed that premature atrial contractions delivered before the next expected His depolarization advanced the immediate His with continuation of tachycardia in all nine cases (100%) with junctional tachycardia [1]. Figure 2 shows the response to sinus rhythm penetrated before His depolarization when the fluctuation of the tachycardia was relatively stable. Sinus beats that occurred before His depolarization did not perturb tachycardia, which was inconsistent with junctional tachycardia. Focusing on the phase of tachycardia fluctuation, atrial excitation by the sinus rhythm occurring around the His refractory period consistently extended the timing of the immediate and next His excitations (Figure 3). This phenomenon suggests that the AV node is part of the circuit [1]. Atrial excitation from the sinus beats might enter the tachycardia circuit and switch to different anterograde conductions, thereby extending the next His excitation. However, this could also be explained by tachycardia termination and initiation by a double atrial response. Concealed nodoventricular or nodofascicular tachycardia was considered less likely due to the very long postpacing interval (PPI) observed after overdrive pacing from the right ventricular apex (782 ms; PPI = tachycardia cycle length + 220 ms). These findings collectively support the diagnosis of AVNRT; therefore, we decided to target the slow pathway using cryoablation. We eliminated all slow pathways after cryoablation of the anatomical slow pathway and roof of the coronary sinus ostium. Tachycardia was not observed. After a follow-up period of 8 months, the patient remained asymptomatic. The patient had been diagnosed with AF for a long time because of irregular tachycardia. Multiple AV nodal pathways can lead to variable RR intervals, mimicking AF [3]. Irregular tachycardia with VA dissociation made it difficult to use pacing maneuvers to clarify tachycardia mechanisms. This case highlights the importance of incorporating electrophysiological information in such situations. This work was supported by JSPS KAKENHI (grant number JP24K11205). This study was conducted in accordance with The Code of Ethics of the World Medical Association (Declaration of Helsinki). Informed consent was obtained from the patient to report the case and the images. The authors declare no conflicts of interest. The data underlying this article will be shared upon reasonable request from the corresponding authors.