Dual Tachycardia Followed by Tachycardia With Atrioventricular Block: What Is the Mechanism and What Does It Prove?

A 30-year-old woman without any significant medical history was hospitalized with narrow complex tachycardia at a rate of 280 bpm that converted to sinus rhythm after the Valsalva maneuver (Figure 1). Upon emergency medical team arrival, she was awake and oriented. Baseline electrocardiogram (ECG) showed sinus rhythm at a rate of 98 bpm, with narrow QRS, and no signs of long QT, Brugada, or pre-excitation. Physical examination, blood tests, including thyroid function and transthoracic echocardiography, were all within normal limits. An electrophysiology study was then performed. Basic measurements demonstrated a normal AH interval of 85 ms and HV of 41 ms without signs of preexcitation. Ventricular pacing at a cycle length (CL) of 450 ms revealed 1:1 retrograde concentric and decremental atrial activation. Atrial pacing showed dual AVN physiology without evidence of preexcitation. The clinical tachycardia was consistently induced with atrial pacing following a single extra stimulus (Figure 2). Tachycardia CL was 280 ms, with concentric coronary sinus activation and variable VA of −15 to 0 ms. Two distinctive phenomena were noted during the SVT (Figures 3 and 4). What are the two unique findings that are shown in the tracing, and what do they prove? Baseline ECG (Figure 1) demonstrates short RP tachycardia (particularly noted in the chest leads) that is consistent with AVNRT, junctional tachycardia, AVRT, or atrial tachycardia with prolonged PR. Dual AVN physiology was observed, with no evidence of an accessory pathway. Narrow complex tachycardia was reproducibly initiated with VA of 0 ms and even slightly negative, demonstrating earlier retrograde activation of the atria than the ventricles during AVNRT (Figure 2). A unique phenomenon is shown in Figure 3 with dual tachycardias that occur simultaneously. Although the atria are in atrial fibrillation, as noted in the CS electrograms, the AVNRT circuit continues with constant H-H and V-V intervals of 300 ms. This is evident that the atria are not required for the perpetuation of AVNRT and rules out the possibility of atrial tachycardia as a potential mechanism of the SVT. A second unique phenomenon is demonstrated in Figure 4. Although the AVNRT circuit accelerates to a CL of 280 ms, a 2:1 infra-his AV block occurs. This demonstrates that the ventricles are not necessary for the maintenance of the tachycardia circuit and, at the same time, rules out the possibility of atrioventricular reciprocating tachycardia. The present case demonstrates two distinct phenomena during the perpetuation of atrioventricular nodal reentrant tachycardia (AVNRT). One of the ongoing controversies is whether the re-entrant circuit in AVNRT is entirely sub-atrial or intranodal, including the “upper and lower” final common pathways, or whether involvement of the atrium or His bundle is required. The presence of 1:1 conduction at rapid rates with a short V-A interval, short H-A interval that remains relatively fixed during SVT, and the results of surgical interventions suggest to some that the reentrant circuit involves tissue above and below the AVN 1. In the past, ablation of the “fast” pathway at the apex and “slow” pathway at the base of the triangle of Koch has suggested an anatomic construct in which the impulse goes from the fast pathway to the septal atrium, followed by sequential atrial activation to the slow pathway through which the AVN is engaged. This concept, together with the relatively easy re-establishment of AVNRT from the base of the Koch triangle, led some to infer atrial involvement in the circuit. On the other hand, some experimental and clinical data suggest that in most patients, AVNRT is a sub-atrial reentrant circuit 2, 3. Clinical observations during spontaneous SVT also support that the atrium and ventricle are not necessary for the reentrant circuit 4-6, demonstrated by initiation of AVNRT in the absence of an atrial echo; maintenance of AVNRT in the presence of either a changing V-A relationship, 2:1 retrograde or V-A block and/or A-V dissociation; resetting AVNRT without atrial activation; atrial pacing and entrainment of AVNRT with a longer A-H than during the tachycardia entrainment suggesting that little if any of the atrium is required. In this single case of AVNRT, we demonstrate how the atria and ventricles are not required for the perpetuation of the AV nodal reentry. At first, the tachycardia circuit was not affected by the simultaneous occurrence of atrial fibrillation and continued to be unaffected also in the presence of 2:1 atrioventricular block to the ventricles with minimal or no change in tachycardia CL, manifest by fixed A-A and H-H intervals. These two findings in the same patient illustrate the independence of the AV nodal reentry tachycardia from the atria and ventricles and support the intranodal location of the AVNRT circuit 7, 8. Ultimately, following successful slow pathway ablation, SVT was no longer induced. This article is dedicated to our late mentor, Mark E. Josephson, who truly believed that the atrium is unnecessary for the initiation and maintenance of A-V nodal re-entrant supraventricular tachycardia since 1976 8. The authors declare no conflicts of interest. All the relevant data are available in the manuscript itself.