An unusual case of tachycardia termination: What is the mechanism?

A 41-year-old man with no prior cardiac history and a history of regular narrow QRS tachycardia, presenting with frequent paroxysmal palpitations, was referred to our institution. The tachycardia was adenosine-sensitive, leading to the acute termination of the tachycardia. The baseline electrocardiogram was unremarkable. During an electrophysiology study (EPS), supraventricular tachycardia (SVT) was easily induced by ventricular extrastimuli. Figure 1 shows a single ventricular extrastimulus applied from the right ventricular apex (RVa) during the tachycardia, and this finding was reproducible. What is the mechanism of the observed response? What are the clinical implications? Focusing solely on the surface ECG findings, a deflection consistent with a retrograde P wave is observed at the terminal end of the QRS, although it is challenging to confirm. A very late coupled premature ventricular contraction (PVC) is applied, and it demonstrates evident QRS fusion. This must be by consequence “His refractory.” This PVC delays the subsequent QRS complex. Thus, one observes fusion and reset of the tachycardia, most consistent with macroreentry. The observation suggests that the retrograde limb of the circuit is an accessory pathway (AP).1 It is worth noting that the ability of a very late coupled PVC from the RV to reset the tachycardia implies that the RV is part of the circuit or has excellent access to it. Possible explanations for this include the presence of a right AP, right paraseptal AP, or a right nodoventricular AP.2, 3 The intracardiac tracings (Figure 1) reveal that the prevailing SVT is an orthodromic reciprocating tachycardia (ORT), and the retrograde limb is a left lateral AP with eccentric atrial activation.4 However, this has to be reconciled with the observation that a “very late” coupled PVC from the RV resets and terminates the SVT, making a left lateral AP quite unlikely, as it would require a closer coupled PVC from the RV to access the circuit. Figure 2 illustrates that the RVa PVC advanced the right atrial electrograms (EGMs) (His A-A 399 ms), but not the left atrial EGMs (CS 7-8 A-A 437 ms). Simultaneously, it caused a delay in the subsequent QRS and termination of the SVT. This is best explained by a second right atrioventricular or nodoventricular AP that did not participate directly in the SVT, as depicted in the schematic diagram (Figure 2). One also observes a reversal of polarity at the septal EGM consistent with a change in direction of the atrial wavefront at that site. The atrial activation wavefront after the PVC is thus fused between that coming from the distal left atrium (LA) whose timing is not affected by the PVC and that coming earlier from the right. The electrode coverage is unfortunately inadequate to pinpoint the onset of the right wavefront more precisely, and no accurate comment can be made on the location of the right AP (septal, right paraseptal or right AP). The cumulative evidence supports the existence of a “double loop” mechanism, in which the anterograde conduction occurs over the normal atrioventricular nodal (AVN) conduction, while retrograde conduction is over either the right or left AP. The left AP circuit activates the atrium ahead of the right AP, preventing the anterograde wave originating from the right AP from conduction into the AVN. However, the right AP still serves as a substrate for the double loop. When the PVC conducts retrogradely over the right AP, it enters the circuit and reveals the right loop. The advanced atrial activation via the right AP subsequently conducts with a long PR interval (HIS A-V 372 ms), likely over a slow AVN pathway, and the tachycardia terminates. Consequently, the right AP does not directly participate in the observed SVT (bystander), but it possesses the capability to reset and terminate it. It is important to note that the tracings do not exclude the possibility of a right nodoventricular connection. It is speculated that the premature atrial activation after the PVC prolonged AV node conduction preceding the last QRS of tachycardia, resulting in termination of the tachycardia after the last atrial event over the left AP. After mapping the left lateral AP during RV pacing, radiofrequency ablation was carried out. Retrograde conduction after ablation of the left was central and rate dependent and SVT could not be induced. It was thus decided at the time to terminate the study. Unfortunately, it left the question open as to whether retrograde conduction was occurring over a right paraseptal AV pathway or right nodoventricular difficult to engage at this point in the study but without apparent clinical importance. This case highlights some important clinical implications. In clinical practice, it can be tempting to focus solely on the observed SVT and target the obvious left AP for ablation, without further testing. However, this approach may not be advisable, as it could leave a right AP untouched, leading to the recurrence of an SVT related to it. Conducting a comprehensive diagnostic study does not significantly prolong the procedure and can reveal unexpected findings, such as the presence of a right AP in this case. This underscores the importance of thorough evaluation to ensure all relevant pathways are identified and targeted during ablation, reducing the risk of SVT recurrence. The authors declare no conflict of interest. The data that support the findings of this study are openly available in Authorea at https://www.authorea.com/users/630458/articles/650179-unusual-case-of-tachycardia-termination-what-is-the-mechanism.

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