Abstract 11377: Demonstration of Manifest Entrainment in Verapamil-sensitive Atrial Tachycardia Originating from the Vicinity of the Atrioventricular Node: Consideration into the Mechanism and Anatomy of Tachycardia Circuit
Background: The mechanisms of the verapamil-sensitive atrial tachycardia originating from the vicinity of the atrioventricular node (V-AT) have not been well clarified.
Objectives: The purpose of this study was to define the mechanism and anatomical tachycardia circuit of V-AT using transient entrainment method.
Methods: Fourteen patients with V-AT (6 males and 8 females, mean; 69 years) were included in this study. After induction of the V-AT, endocardial mapping of the right atrium was performed by the non-contact mapping system (EnSite 3000) and the earliest atrial activation site (EAAS) during tachycardia was identified. While recording the contact atrial atrial electrogram at the EAAS, rapid atrial pacing, 5 beats/minute faster than the tachycardia rate, was delivered from the multiple sites of the right atrium to demonstrate the manifest entrainment. Rapid pacing was delivered from the multiple sites of the right atrium, including the high antero-lateral, hight postero-septal, low antero-lateral, low postero-septal right atrium, right atrial appendage, coronary sinus ostium and cavo-tricuspid isthmus.
Results: V-AT was induced and terminated by atrial rapid and extrastimulus pacing with an inverse relation between the coupling interval and return cycle and the EAAS was observed in the vicinity of the HB site in all patients. The mean tachycardia cycle length was 430±97 msec. Manifest entrainment was observed by the rapid atrial pacing delivered from the high antero-lateral right atrium in 5 patients, from the high postero-septal right atrium in 7 patients and from the right atrial appendage in 2 patient, respectively, and thus the atrial electrogram at the EAAS was captured orthodromically in all patients. However, manifest entrainment was not observed by the pacing delivered from coronary sinus ostium and from cavotricuspid isthmus in any of the patients. These suggest that the critical slow conduction area of the reentry circuit extends to the direction outside of the Koch's triangle.
Conclusions: The underlying mechanism of V-AT was due to reentry. The slow conduction area of the reentry circuit in V-AT, which is composed of calcium channel dependent-tissue, was suggested to extend from the EAAS to the direction outside of the Koch's triangle.
- © 2010 by American Heart Association, Inc.