Differential Effects of Adenosine on Antegrade Fast Pathway, Antegrade Slow Pathway, and Retrograde Fast Pathway in Atrioventricular Nodal Reentry

Abstract

Adenosine has a potent negative dromotropic effect. However, comparative effects of adenosine on the three pathways of atrioventricular (AV) nodal reentry remain unclear. In this study, we sought to determine the effects of adenosine on the antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT). Twenty patients with common slow-fast AVNRT (mean cycle length 360 ± 49 ms) were studied. The effects of adenosine on the antegrade slow pathway and on the retrograde fast pathway conduction were determined during sustained AVNRT and constant right ventricular pacing at identical cycle lengths (mean 360 ± 49 ms), respectively. Incremental doses of adenosine were rapidly administered: initial dose of 0.5 mg, followed by stepwise increases of 0.5 or 1.0 mg given at 5-min intervals until termination of AVNRT or second-degree ventriculoatrial block occurred. After the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation, the effect of adenosine on the antegrade fast pathway conduction was evaluated. The dose-response curve of adenosine and the dose of adenosine required to produce AV or ventriculoatrial block among the representative three conduction pathways were compared. The dose-response curve for the effect of adenosine on the antegrade fast pathway lies to the left and upward to that of the effect of adenosine on the antegrade slow pathway which in turn lies to the left and upward to that of the retrograde fast pathway. The mean dose of adenosine required to produce conduction block at antegrade fast, antegrade slow, and retrograde fast pathways were 1.4 ± 0.5, 4.2 ± 1.6, and 8.5 ± 2.6 mg, respectively (p < 0.01). Adenosine has a differential potency to depress antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AVNRT. The depressant effect of adenosine on the antegrade fast pathway is more potent than that on the antegrade slow pathway which in turn is more potent than that on the retrograde fast pathway conduction.

Proarrhythmic effects of adenosine: a review of the literature

“…25 39 40 Adenosine is effective in terminating AV nodal re-entry tachycardias, but these have also been reported as having been induced by adenosine 41 ; indeed Curtis et al found that low dose adenosine could induce AV nodal re-entrant tachycardias in 9 of 16 patients who were known to experience this tachycardia. The effect of adenosine on the underlying dual AV node pathways in these patients was investigated, and in common with other workers, 42 adenosine was shown preferentially to block the fast antegrade pathway, thus allowing a re-entry circuit to develop. A similar response to adenosine has been observed when it was erroneously given to a patient with a sinus tachycardia (personal communication), who had presented to the emergency department with a history of recurrent palpitation; on three consecutive occasions a brief period of narrow complex tachycardia (probably AV nodal re-entry tachycardia) was induced, followed by return to sinus tachycardia.…”

Validation of dual atrioventricular nodal physiology in dual atrioventricular nodal non‐reentrant tachycardia via adenosine triphosphate injection during atrial pacing: A novel insight into the role of leftward inferior extension

“…24 Current literature notes that antegrade FP exhibits heightened sensitivity to ATP relative to antegrade SP. 25 In this specific case, ATP selectively inhibited antegrade FP, allowing the remaining antegrade SP to become more pronounced. We propose that ATP injection during atrial pacing could serve as a potential diagnostic tool for both DAVNNT and AVNRT patients.…”

Mahaim pathway tachycardia versus bystander ventricular tachycardia: A distinction without a difference

“…However, this alternative scenario is unlikely, since the anterograde slow AV nodal pathway is notably more sensitive to adenosine than the retrograde fast AV nodal pathway. 6 , 7 , 8 Therefore, in response to adenosine, NV-dependent ART would be expected to terminate in the anterograde limb (slow AV nodal pathway), not the retrograde limb. Accordingly, because of persistence of conduction over the slow AV nodal and NV pathways following termination of tachycardia, and because of the presence of fusion beats during tachycardia, we deduce that the tachycardia had an intra-Mahaim pathway origin and that termination of tachycardia with adenosine was due solely to its direct effects on the Mahaim pathway.…”