Alternation of atrioventricular nodal conduction time during atrioventricular reentrant tachycardia: are dual pathways necessary?

INTRODUCTION

Alternation of atrial cycle length and AV nodal conduction time (NCT) is often observed during AV reentrant tachycardia. Both AV nodal dual pathway and rate-dependent function have been postulated to be involved in this phenomenon. This study was designed to determine the respective role of these two mechanisms in the alternation observed in an in vitro model of orthodromic AV reentrant tachycardia.

METHODS AND RESULTS

The tachycardia was produced by detecting each His-bundle activation and stimulating the atrium after a retrograde delay, thereby simulating retrograde pathway conduction, in six isolated rabbit heart preparations. After a 5-minute stabilization period at a fast rate, the retrograde delay was decremented by 2 msec every minute until nodal blocks occurred. We observed a sequential alternation of the cycle length and NCT in four preparations in the short retrograde delay range. The magnitude of the alternation gradually increased as the retrograde delay was decreased and reached 4.6 +/- 0.5 msec during 1:1 conduction. The alternation increased further just prior to termination of the tachycardia by an AV nodal block. None of the preparations showed discontinuous AV nodal recovery curves. Moreover, an electrode positioned over the endocardial surface of the node showed that the alternation developed distally to the nodal inputs, which are believed to constitute a major component of dual pathways. A mathematical model predicted the alternation from known characteristics of rate-dependent nodal functional properties.

CONCLUSIONS

NCT and cycle length alternation can arise during orthodromic AV reentrant tachycardia when the retrograde delay is sufficiently short. The characteristics of the alternation, presence of continuous recovery curves, intranodal location of the alternation, and mathematical modeling suggest that the alternation is predictable from the known functional properties of the AV node without postulating dual pathway physiology.