Supraventricular tachycardia with VA Linking: What is the mechanism?

Abstract

A 72-year-old male with chronic right bundle branch block underwent diagnostic electrophysiologic study because of the recurrent symptomatic supraventricular tachycardia (SVT). Atrio-His and His-ventricular intervals measured 115 ms and 58 ms, respectively. Programmed atrial extrastimulation elicited dual atrio-ventricular (AV) node physiology; VA conduction was absent. A single atrial extrastimulus-induced SVT after an AH jump (Figure 1). Attempts to entrain tachycardia from the ventricle resulted in AV dissociation. The response to atrial overdrive pacing (AOP) from the high right atrium (HRA) and coronary sinus (CS) is shown in Figure 2. On the basis of the figures, what is the mechanism of tachycardia? DISCUSSION Supraventricular tachycardia shows midline atrial activation earliest at the His bundle region. Simultaneous atrioventricular activation and spontaneous periods of AV nodal Wenckebach block exclude orthodromic reciprocating tachycardia (ORT). Tachycardia induction after an AH jump, simultaneous atrioventricular activation, and earliest atrial activation at the His bundle suggest typical atrioventricular nodal reentrant tachycardia (AVNRT). Absent VA conduction with the inability to entrain tachycardia from the ventricle and persistence of tachycardia during AV block can be explained by retrograde and antegrade block in the lower common final pathway, respectively. Differential AOP from the HRA and CS produce "AHA" responses excluding junctional tachycardia and show VA linking (ΔVA = VA (CS) − VA (HRA) = 2ms) despite generating different AH intervals. VA linking indicates an AV nodal dependent tachycardia, and combined with the other aspects of this case favors AVNRT whereas seemingly excluding AT. 1,2 Despite these findings, however, the absence of VA conduction and the presence of AV nodal block are each individually uncommon during AVNRT and together raise suspicion for atrial tachycardia (AT). Evaluation of the P wave during periods of AV block (Figure 1, arrow) reveal a biphasic morphology in lead aVF (negative/positive) incompatible with typical AVNRT and characteristic of AT arising from the noncoronary cusp (NCC) of the aortic valve. 3,4 In this case, NCC AT (causing earliest atrial activation at the His bundle region) in the presence of dual AV nodal physiology and sustained slow pathway (SP) conduction (causing simultaneous atrioventricular activation) mimics typical AVNRT. 5 Repetitive retrograde concealment from SP into fast pathway (FP) perpetuates sustained SP conduction during ongoing AT. The apparent VA linking with differential AOP is best explained by SP conduction and the induction of typical (slow-fast) AV nodal echoes, which themselves (rather than atrial pacing per se) re-induce AT (particularly given the close proximity between the FP and NCC). With the diagnosis of NCC AT, the patient underwent successful ablation using a retrograde transaortic approach, but then easily developed sustained AVNRT manifesting multiple AV nodal pathways (Figure 3). In contrast to AT where the tran...

Diastolic potentials manifest the extension of a slow pathway to the inferolateral right atrium during fast-slow atrioventricular nodal reentrant tachycardia

“…In such cases, evaluation of VA linking is a helpful and accurate method for discrimination, although some pitfalls have been reported. 2 , 3 In our case, positive VA linking was reproducibly observed, indicating diagnostic significance of the AVNRT. Although adenosine-sensitive AT could not be completely excluded despite some controversy, we considered the most likely diagnosis of SVT2 to be fast-slow AVNRT with retrograde LCP block by placing importance on the positive VA linking and for the following reasons.…”