Regularly irregular tachycardia: What is the mechanism?

A 62-year-old woman without overt structural heart disease was referred to our hospital for ablation of a narrow QRS complex tachycardia (Figure 1A). A 12-lead electrocardiogram during sinus rhythm revealed no pre-excitation (Figure 1B). What is the mechanism of this regularly irregular tachycardia? Differential diagnoses of regularly irregular narrow QRS tachycardias include atrial flutter, double ventricular response, and orthodromic reciprocating tachycardia (ORT), atrioventricular nodal reentrant tachycardia (AVNRT) or atrial tachycardia (AT) with alternating antegrade atrioventricular nodal (AVN) pathways.1 No F wave excludes atrial flutter, and no sinus P wave preceding QRS excludes a double ventricular response. The tachycardia exhibits a 1:1 atrioventricular relationship with identifiable P waves following the QRS wave. In addition, the fixed RP interval despite the alternating PR interval suggests the presence of VA linking, which rules out AT. The retrograde limb appears to have less decremental properties, either a fast pathway (FP) or an accessory pathway (AP). Further interpretation reveals an alternating PR interval of approximately 120 and 250 ms, suggesting alternating anterograde conduction over the FP and slow pathway (SP). Because the FP is presumed to be an anterograde limb, the FP cannot be a retrograde limb of this tachycardia. Summarizing these observations, the ORT via an AP with alternating anterograde limb over FP and SP is most likely diagnosis. Multielectrode catheters were positioned in the high right atrium, His bundle region, coronary sinus (CS), and right ventricular (RV) apex. The baseline atrial-His and His-ventricular intervals were 94 and 42 ms, respectively. Ventricular extastimulus revealed eccentric retrograde atrial activation with the earliest activation of distal CS, which lacked decremental properties. Atrial burst pacing showed Wenckebach block at a pacing rate of 410 ms. A decrease in the atrial extrastimulus coupling interval at a basic pacing CL of 600 ms revealed AH interval jump at a coupling interval of 340 ms without any apparent pre-excitation, suggesting the presence of dual AVN pathways. A narrow QRS complex tachycardia with cycle length alternations of 294 and 420 ms was induced with AH jump. These alternations were contributed by AH interval alternations of 114 and 240 ms (Figure 2). After tachycardia cycle length (TCL) was fixed, RV overdrive pacing advanced the atrial timing within the transition zone, which was diagnostic of ORT via the left lateral AP (Figure 3).2 Based on the presence of the SP and significant alternations in the AH interval of 126 ms during ORT, the anterograde limb was presumed to alternate between the FP and SP. The AP was successfully eliminated by radiofrequency application at the 3 o'clock position of the mitral annulus. The SP ablation was not performed because no tachycardia was inducible after AP ablation. In patients with a manifest or concealed AP, the prevalence of coexisting dual AVN pathways has been reported to be 12%. Of these, FP and SP are used alternately in 18% of those in whom ORT is induced.3 This tachycardia can be induced only in the setting of TCL, and the refractory period of FP is approximate. This regularly irregular tachycardia provides us two clinical implications. First, when we encounter this tachycardia, the first step to reach the correct diagnosis would be to assess whether this alternation is due to alternation in PR interval or RP interval. Second, in the presence of a dual AV nodal pathway, ORT can be induced with AH jump, which may exhibit regularly irregular tachycardia behavior. I would like to express my deepest appreciation to my co-authors and patient. The patient has provided consent for publication. 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.