Characteristics, circuit, mechanism, and ablation of reentry in the rabbitatrioventricular node

Introduction: The circuitry underlying AV nodal reentry remains debated. We developed a model of AV nodal reentry and assessed the role of nodal input s, compact node, and its posterior nodal extension (PNE) in this phenomenon . Methods and Results: A fine scanning of short coupling interval range with an atrial premature beat consistently initiated slow-fast AV nodal reentran t beats that occurred 37 +/- 31 msec (mean +/- SD) after His-bundle activat ion in 11 of 16 consecutive rabbit heart preparations. The repeated testing (>40 times) of a chosen coupling interval within reentry window (6 +/- 9 m sec, n = 11) yielded reentrant intervals that varied by 2 +/- 1 msec (mean SD for 40 beats +/- SD, n = 11). The breakthrough point of reentrant activa tion, as assessed from four perinodal sites, varied in different preparatio ns from diffuse (4) to anterior (1), medial (3), or posterior (3); mean ree ntrant interval did not differ between perinodal sites. Antegrade perinodal activation pattern did not differ at reentrant versus nonreentrant couplin g intervals and thus was not a primary determinant of reentry. A PNE ablati on (n = 4) interrupted the slow pathway conduction and prevented reentry wi thout affecting antegrade perinodal activation or fast pathway conduction. Conclusion: A reproducible model of AV nodal reentrant beats was developed and used to study underlying circuitry. The AV nodal reentry involves unalt ered antegrade perinodal activation, slow PNE conduction and retrograde bro ad invasion of perinodal tissues starting at a preparation-dependent breakt hrough point. A PNE ablation abolishes the reentry.