What is the mechanism of this narrow QRS tachycardia in a patient with type‐A Wolff‐Parkinson‐White (WPW) syndrome?

A 52-year-old woman who had been previously diagnosed with type-A Wolff-Parkinson-White (WPW) syndrome was referred to our hospital for catheter ablation of a narrow QRS tachycardia. Figure 1A,B show the 12-lead electrocardiograms 1 year prior and recently, respectively. Multielectrode catheters were positioned in the high right atrium (HRA), His bundle (HB) region, coronary sinus (CS), and right ventricle (RV) apex. The baseline atrio-His (AH) and His-ventricular (HV) intervals were 90 and 38 ms, respectively. During an isoproterenol administration, a clinical narrow QRS tachycardia with a tachycardia cycle length of 242 ms and ventriculo-atrial interval of 62 ms was induced without an AH jump during atrial extrastimulus pacing (Figure 1C). What are the potential differential diagnoses? We also applied a couple of scanned extrastimuli (Figure 2A–C). What is the final diagnosis? Differential diagnoses of narrow QRS tachycardias include atrial tachycardia (AT), orthodromic reciprocating tachycardia (ORT), and atrioventricular nodal reentrant tachycardia (AVNRT).1 The prior episode of a type-A WPW syndrome and the earliest atrial activation site (EAAS) during the tachycardia being observed in the distal CS (dCS) suggested an ORT via a left lateral (LL) accessory pathway (AP). However, the CS activation sequence exhibited a reverse chevron pattern, with an equally early electrogram in the proximal CS (pCS) (Figure 1C). Based on this CS sequence, the LLAP may have been a bystander, because a simple ORT via an LLAP would exhibit a distal-to-proximal CS sequence. In this tracing, the differential diagnoses would have been AT, AVNRT, or ORT via another septal AP with a bystander LLAP. A scanned left ventricular (LV) extrastimulus advanced the subsequent atrial electrogram with the same sequence and terminated the tachycardia without ventricular capture (Figure 2A), excluding AT and suggesting an ORT via another AP rather than AVNRT with a bystander LLAP. A single atrial extrastimulus from the EAAS on the lateral aspect of the left atrium advanced the subsequent atrial electrogram but failed to reset the tachycardia, indicating a bystander LLAP (Figure 2B). Further decreasing the coupling interval of the atrial extrastimulus advanced the pCS electrogram by 36 ms but still failed to reset the tachycardia (Figure 2C). Summarizing these observations, ORT via a posteroseptal AP with a bystander LLAP was diagnosed. Despite the elimination of the bystander LLAP by a radiofrequency application, the tachycardia persisted with the same cycle length but with a shift in the EAAS and the proximal-to-distal CS sequence. RV overdrive pacing during the tachycardia terminated it but reset the atrial timing within the transition zone, supporting a diagnosis of ORT.1 The radiofrequency application in the EAAS located on the left posteroseptum successfully eliminated the other AP, and no further tachycardia was induced. This case provided some clinical insight. If the CS activation sequence had been eccentric but not straight, electrophysiologists should be aware of the potential presence of multiple APs. Furthermore, the main discussion would center on whether the left posteroseptal AP was an atrioventricular AP or a nodoventricular pathway connected to the leftward inferior extension of the atrioventricular node. Recently, the nodoventricular pathway has been well characterized,2-4 but a left-sided nodoventricular pathway is rare.5 Evidence supporting it was a nodoventricular pathway was that an early atrial extrastimulus failed to reset the tachycardia despite the advancement of the earliest pCS electrogram by 36 ms, indicating that the atrium was not involved in the tachycardia circuit (Figure 2C). However, the interpretation of the absence of a tachycardia reset has some pitfalls. First, the reset might be concealed if the prematurity of the atrial extrastimulus matches the decremental conduction in the atrioventricular node. Nonetheless, this compensation is less likely in this case because several atrial extrastimuli with different coupling intervals failed to reset the tachycardia. Second, there was a possibility that the atrial extrastimulus failed to reset the true EAAS, even though the earliest pCS electrogram was advanced. In that scenario, the atrium could still be part of the circuit, raising the possibility of an ORT via a posteroseptal atrioventricular AP. In contrast, the evidence supporting an atrioventricular AP was the absence of a decremental property of the retrograde conduction upon the scanned LV extrastimulus (Figure 2A). A nodoventricular pathway is typically connected to the slow pathway. Therefore, the tachycardia is generally delayed after a ventricular extrastimulus due to the decremental property of the nodoventricular pathway or slow pathway. Further evidence supporting an atrioventricular AP was that the AP was eliminated by an RF application on the LA endocardium. However, similarly, in a recent publication, a left-sided nodoventricular pathway was eliminated by an RF application on the mitral annulus. The authors concluded that the nodoventricular pathway had a branch bystander to the contiguous atrium.5 Based on those findings, it would be challenging to definitively distinguish between a posteroseptal atrioventricular AP and a nodoventricular pathway. Performing atrial overdrive pacing during the tachycardia might have been beneficial for a differential diagnosis.6 We are grateful to the physicians we connected with via #EPUniversity on Twitter. We thank Mr. John Martin for his assistance with the English proofreading of the manuscript. The authors declare no conflicts of interest. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.