Demonstration of anatomic reentrant circuit in verapamil-sensitive atrial tachycardia originating from the atrioventricular annulus other than the vicinity of the atrioventricular node.
The mechanism and tachycardia circuit of verapamil-sensitive atrial tachycardia originating from the atrioventricular annulus (AVA-AT) other than the atrioventricular node vicinity are not well clarified. In 23 patients, we examined the mechanism and anatomic tachycardia circuit of AVA-AT. While recording the atrial electrogram at the earliest atrial activation site (EAAS) during tachycardia, rapid atrial pacing at a rate 5 beats/min faster than the tachycardia rate was delivered from multiple sites of the right atrium (RA) to demonstrate manifest entrainment and define the direction of proximity of slow conduction area (SCA) of reentry circuit. When EAAS was orthodromically captured, radiofrequency energy was delivered starting at a site 2 cm away from the EAAS in the direction of entrainment pacing site. Then application site was gradually advanced toward the EAAS until termination of tachycardia to define the entrance of SCA of reentry circuit. Manifest entrainment was demonstrated in all AVA-ATs. The EAAS, distributed along the tricuspid annulus from 3- to the 12-o'clock position, was orthodromically captured by pacing delivered from high anterolateral RA (n = 6), high anteroseptal RA (n = 7), high posteroseptal RA (n = 3), low anterolateral RA (n = 6), and coronary sinus ostium (n = 1). Radiofrequency energy delivery to the site, 10.4 ± 2.4 mm proximal to the EAAS where the atrial electrogram was observed 13.9 ± 5.7 ms later than the EAAS, terminated AVA-AT immediately after the onset of energy delivery (2.9 ± 1.1 seconds). In conclusion, it was shown that the AVA-AT is organized as reentry involving the verapamil-sensitive SCA with its entrance and exit at different distinct locations.
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. Electronic address: yyamabe@kumamoto-u.ac.jp.
Hiroshige
H
Yamabe
Department of Cardiology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Ken
K
Okumura
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Junjiroh
J
Koyama
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Hisanori
H
Kanazawa
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Tadashi
T
Hoshiyama
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Hisao
H
Ogawa
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001283:Atrioventricular Node; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D017115:Catheter Ablation; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006325:Heart Atria / Q000503:physiopathology* / Q000601:surgery; D006329:Heart Conduction System / Q000187:drug effects* / Q000503:physiopathology / Q000601:surgery; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D013611:Tachycardia, Atrioventricular Nodal Reentry / Q000503:physiopathology / Q000628:therapy*; D016896:Treatment Outcome; D014700:Verapamil / Q000627:therapeutic use*
D000889:Anti-Arrhythmia Agents; D014700:Verapamil