Abstract 2235: Analysis of the Anatomical Tachycardia Circuit in Verapamil-sensitive Atrial Reentrant tachycardia Originating From the Vicinity of the Atrioventricular Node
Background: Less information exists regarding the anatomical tachycardia circuit of verapamil-sensitive atrial reentrant tachycardia originating from the atrioventricular (AV) node vicinity (V-AT).
Methods and results: To define the tachycardia circuit of the V-AT, single extrastimuli were delivered during tachycardia to 8 sites of the intraatrial septum: the ealiest atrial activation site; His bundle (HB) site; 3 arbitrarily divided sites on the AV junction extending from the HB site to the coronary sinus ostium (CSOS)(sites S, M and I); the superior, inferior, posterior and posteroinferior portions of the CSOS (S-CSOS, P-CSOS and PI-CSOS, respectively); and the CSOS in 8 patients with V-AT. At each site, the longest coupling interval (LCI) which reset the tachycardia and the subsequent return cycle (RC) were measured. The mean tachycardia cycle length (TCL) was 399 ± 65 ms. The LCI at the EAAS, HB site, site S, M and I, CSOS, I-CSOS, S-CSOS, P-CSOS and PI-CSOS were 389 ± 65, 366 ± 71, 363 ± 71, 353 ± 70, 350 ± 76, 333 ± 69, 340 ± 66, 330 ± 67, 303 ± 62 and 303 ± 64 ms, respectively, and the subsequent RC were 399 ± 65, 424 ± 67, 425 ± 60, 433 ± 64, 435 ± 57, 455 ± 65, 446 ± 73, 453 ± 76, 481 ± 70 and 483 ± 70 ms, respectively. The LCI at the EAAS was significantly longer than the LCI at the HB site, site S, M and I, CSOS, I-CSOS, S-CSOS, P-CSOS and PI-CSOS, respectively (p < 0.05 for HB site and p < 0.002 for site S, M and I, CSOS, I-CSOS, S-CSOS, P-CSOS and PI-CSOS, respectively). The RC at the EAAS did not differ from the TCL, whereas, those at the HB site, sites S, M and I, CSOS, I-CSOS, S-CSOS, P-CSOS and PI-CSOS were significantly longer than the TCL (p < 0.01). Furthermore, single extrastimulus delivered from the sites inferior to the HB site advanced the His potential without resetting the V-AT in 5 patients in whom the AV block was not observed during V-AT, suggesting that AV nodal conducting tissue is not involved in the tachycardia circuit.
Conclusion: It was shown that the atrial tissue within the Koch’s triangle extending from the HB site to PI-CSOS including the AV nodal conducting system is not involved in the tachycardia circuit in the V-AT. The verapamil-sensitive atrial tissue close to the AV node, but not the AV nodal tissue which contribute to AV conduction, forms the tachycardia circuit of the V-AT.