Circulation, Vol 80, 324-334, Copyright © 1989 by American Heart Association
CD Schuger, RT Steinman and MH Lehmann
Our purpose was to characterize the excitable gap during atrioventricular
nodal reentrant tachycardia (AVNRT) to elucidate the electrophysiologic
substrate of this clinically familiar microreentrant arrhythmia.
Accordingly, in 11 patients with classic slow-fast AVNRT (mean cycle
length, 342 +/- 41 msec), a single ventricular extrastimulus (V2) was
periodically delivered after a spontaneous tachycardia beat (V1) until
ventricular refractoriness was reached. With this technique, an excitable
gap was considered present when atrial preexcitation of at least 20 msec
could be achieved along with tachycardia resetting (noncompensatory pause
after V2). The range of V1V2 intervals that resulted in atrial
preexcitation constituted the preexcitation zone. Five patients (45%)
showed evidence of an excitable gap at baseline, with a maximal atrial
preexcitation achievable of 33 +/- 6 msec, representing 9 +/- 1% of the
tachycardia cycle length. Verapamil was then administered to all 11
patients with the purpose of slowing the anterograde tachycardia wavefront
before arrival of V2. This resulted in widening of the preexcitation zone
in three patients by a mean of 50 +/- 37 msec, with a corresponding
increase in maximal atrial preexcitation to 70 +/- 32 msec, or 16 +/- 4% of
AVNRT cycle length, and the appearance of atrial preexcitation in two
patients who lacked it during baseline. In the remaining six patients,
AVNRT was not sustained after verapamil or was too unstable for evaluation.
During baseline, V2A2 conduction time increased by only 5 +/- 3 msec
throughout the preexcitation zone, with values at the outer border
unchanged after verapamil, implying a fully excitable gap in the retrograde
limb. In all patients with a preexcitation zone, AVNRT was consistently
reset by V2, both at baseline and after verapamil, with a "flat" but mainly
"increasing" response pattern as V1V2 was shortened. Hence, a significant
number of patients with AVNRT have evidence of an excitable gap whose
demonstrability can be facilitated by pharmacologic intervention;
documentation of an increasing resetting response pattern, most apparent
after verapamil, provides new evidence for a reentrant mechanism in AVNRT;
and while not definitively proven, the presence of a fully excitable gap
during AVNRT is most consistent with a microreentry circuit that
incorporates an anatomic obstacle.
ARTICLES
The excitable gap in atrioventricular nodal reentrant tachycardia. Characterization with ventricular extrastimuli and pharmacologic intervention
Electrophysiology Laboratory, Wayne State University, Detroit, Michigan.
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