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  • Title: Electrophysiological manifestations of the excitable gap of slow-fast AV nodal reentrant tachycardia demonstrated by single extrastimulation.
    Author: Lai WT, Lee CS, Sheu SH, Hwang YS, Sung RJ.
    Journal: Circulation; 1995 Jul 01; 92(1):66-76. PubMed ID: 7788919.
    Abstract:
    BACKGROUND: Although AV nodal reentrant tachycardia (AVNRT) is a well-known rhythm disorder, its anatomic substrate and electrophysiological mechanism remain to be defined. Previously, the description of the excitable gap (EG) of AVNRT was based on electrical stimulation performed from sites remote from the reentrant circuit. In the present study, we characterized the EG of AVNRT by atrial extrastimulation close to the putative reentrant circuit in the AV junction. METHODS AND RESULTS: In 16 patients (3 men, 13 women; mean age, 45 +/- 13 years) with inducible slow-fast AVNRT (mean cycle length, 353 +/- 52 ms), single extrastimuli with a 10-ms decrement in the premature coupling interval were delivered from the anterosuperior interatrial septum (fast pathway area) and the posteroinferior interatrial septum (slow pathway area) from late diastole until atrial refractoriness. An EG was considered present when resetting or termination of AVNRT was induced by single atrial extrastimulation. The study showed that the duration of the EG of AVNRT was wide, measuring 121 +/- 56 and 123 +/- 47 ms and occupying 33 +/- 11% and 34 +/- 9% of the tachycardia cycle length during single extrastimulation from the slow pathway area and the fast pathway area, respectively. The resetting pattern most commonly manifested as the sum of the coupling interval and the return cycle being less than a fully compensatory pause (two times the basic tachycardia cycle length). However, patterns equal to and greater than a fully compensatory pause were also observed. Of note, in 2 of the 16 patients, atrial extrastimulation from either the fast or slow pathway area also affected the preceding tachycardia cycle length (HH interval), indicating alteration of the anterograde input. In all patients, the curve derived from plotting the coupling interval of extrastimuli against the return cycle during resetting exhibited an "increasing" pattern. The mode of tachycardia termination usually occurred when the premature atrial impulse was orthodromically blocked in the anterograde slow pathway. CONCLUSIONS: The EG of slow-fast AVNRT is relatively wide, as demonstrated by single atrial extrastimulation from the interatrial septum near the AV junction. Overall, the electrophysiological manifestations of the EG of AVNRT are very similar to those described in AV reciprocating tachycardia incorporating an accessory connection. These findings lend further support to the notion that, in humans, AVNRT involves a reentrant mechanism with a wide excitable gap.
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