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.
We previously reported that verapamil-sensitive atrial tachycardia (AT) originating from the vicinity of the atrioventricular (AV) node is due to reentry with a slow conduction area, and ablation at a site supposed to be an entrance to the slow conduction area is effective in eliminating the tachycardia. The purpose of this study was to define the mechanism and anatomic tachycardia circuit of this verapamil-sensitive AT originating from the AV annulus (AVA-AT) other than the AV node vicinity. For this purpose, we initially delivered rapid atrial pacing during AT from multiple sites of the atrium whether the manifest entrainment of AT is demonstrable. When the manifest entrainment with orthodromic capture of the earliest atrial activation site (EAAS), the exit point from the area of the slow conduction area of the reentry circuit, is demonstrated, the pacing site is considered to be proximal to the slow conduction area of the reentry circuit. After identification of a site proximal to the slow conduction area, radiofrequency energy was delivered to a site between the pacing site and the EAAS to identify the entrance of the slow conduction area of the reentry circuit in the same way as previously used for AT originating from the AV node vicinity. The use of this strategy of entrainment pacing and radiofrequency energy application techniques allowed the characterization of the mechanism and anatomic tachycardia circuit of AVA-AT.
Methods
The study subjects were 23 consecutive patients with AVA-AT who were referred for electrophysiological studies and radiofrequency catheter ablation ( Table 1 ). AT originating from the vicinity of the AV node was excluded from the study, because we reported reentry as the mechanism of this specific form AT and the effect of catheter ablation on it. Written informed consent was obtained from each patient. The protocol was approved by Kumamoto University Hospital Human Research Committee.
| Patient | Age/Sex | Tachycardia Cycle Length (ms) | Location of EAAS | Manifest Entrainment Pacing Site | Successful RF Site Relative to EAAS | Distance Between EAAS and Successful RF Site (mm) | Activation Time Between EAAS and Successful RF Site (ms) | Interval from RF Onset to Termination (ms) |
|---|---|---|---|---|---|---|---|---|
| 1 | 35/F | 370 | TA 4-o’clock | High anteroseptal RA | TA 3-o’clock | 15 | 20 | 3.5 |
| 2 | 37/F | 360 | TA 4-o’clock | High posteroseptal RA | TA 3-o’clock | 8 | 13 | 3.2 |
| 3 | 44/F | 340 | TA 5-o’clock | High posteroseptal RA | TA 4-o’clock | 8 | 10 | 2.5 |
| 4 | 47/M | 455 | TA 7-o’clock | High posteroseptal RA | TA 6-o’clock | 10 | 11 | 2.5 |
| 5 | 50/F | 280 | TA 4-o’clock | High anteroseptal RA | TA 3-o’clock | 10 | 28 | 2.7 |
| 6 | 51/M | 530 | TA 8-o’clock | High anterolateral RA | TA 9-o’clock | 8 | 18 | 3.9 |
| 7 | 57/M | 405 | TA 12-o’clock | Low anterolateral RA | TA 11-o’clock | 10 | 9 | 3.5 |
| 8 | 60/M | 495 | TA 8-o’clock | High anterolateral RA | TA 9-o’clock | 10 | 22 | 3.7 |
| 9 | 60/F | 420 | TA 5-o’clock | Low anterolateral RA | TA 6-o’clock | 10 | 10 | 3.5 |
| 10 | 62/F | 530 | TA 5-o’clock | Low anterolateral RA | TA 6-o’clock | 12 | 15 | 5.0 |
| 11 | 63/F | 500 | TA 7-o’clock | Low anterolateral RA | TA 8-o’clock | 13 | 20 | 3.5 |
| 12 | 66/F | 385 | TA 12-o’clock | Low anterolateral RA | TA 11-o’clock | 7 | 5 | 3.2 |
| 13 | 67/M | 440 | TA 4-o’clock | High anteroseptal RA | TA 3-o’clock | 10 | 10 | 2.2 |
| 14 | 67/M | 355 | TA 11-o’clock | CS ostium | TA 12-o’clock | 11 | 15 | 0.25 |
| 15 | 68/M | 380 | TA 4-o’clock | High anteroseptal RA | TA 3-o’clock | 10 | 8 | 1.7 |
| 16 | 69/F | 360 | TA 6-o’clock | High anteroseptal RA | TA 5-o’clock | 10 | 11 | 4.0 |
| 17 | 71/M | 455 | TA 6-o’clock | High anterolateral RA | TA 5-o’clock | 11 | 10 | 1.6 |
| 18 | 72/M | 590 | TA 10-o’clock | High anteroseptal RA | TA 11-o’clock | 12 | 15 | 2.5 |
| 19 | 77/M | 370 | TA 6-o’clock | High anteroseptal RA | TA 5-o’clock | 9 | 10 | 1.0 |
| 20 | 78/F | 540 | TA 12-o’clock | High anterolateral RA | TA 11-o’clock | 8 | 13 | 2.9 |
| 21 | 78/F | 475 | TA 8-o’clock | High anterolateral RA | TA 9-o’clock | 15 | 7 | 4.0 |
| 22 | 79/M | 425 | TA 4-o’clock | Low anterolateral RA | TA 5-o’clock | 7 | 20 | 2.5 |
| 23 | 80/F | 415 | TA 5-o’clock | High anterolateral RA | TA 6-o’clock | 15 | 20 | 3.7 |
| Mean ± SD | 63 ± 13 | 429 ± 77 | 10.4 ± 2.4 | 13.9 ± 5.7 | 2.9 ± 1.1 |
Two 6Fr quadripolar electrode catheters (St. Jude Medical, St. Paul, Minnesota) were positioned in the His bundle region and the right ventricular apex. A 6Fr 20-pole electrode catheter (St. Jude Medical) was introduced into the coronary sinus (CS). Two 7Fr, 4-mm tip, deflectable, quadripolar electrode catheters with a 2-mm interelectrode distance (Biosense Webster, Inc., Diamond Bar, California, or Japan Lifeline, Tokyo, Japan) were advanced to the right atrium (RA) for atrial mapping, pacing, and ablation. Bipolar electrograms were filtered between 50 to 600 Hz and recorded along with the surface electrocardiogram using a polygraph (EP-WorkMate; EP MedSystems, Inc., Mt Arlington, New Jersey). Atrial and ventricular pacing were performed using a cardiac stimulator (SEC-4103; Nihon Kohden, Tokyo, Japan). AT was diagnosed using the standard criteria.
After right atriography in a biplane view, the RA was mapped during AT using a noncontact mapping system (EnSite 3000; St. Jude Medical) or contact mapping system (EnSite NavX; St. Jude Medical) to identify the EAAS. The electrogram at the EAAS was validated by contact bipolar and unipolar electrograms in all patients. During noncontact mapping, a 9Fr multielectrode array catheter was introduced from the right femoral 10Fr sheath into the RA, deployed over a 0.032-inch guidewire, and its distal tip was fixed in the right ventricular outflow. Details of the EnSite 3000 system were described previously.
The proximity of the slow conduction area of the reentry circuit was identified by the entrainment technique. While recording the contact atrial electrogram at the EAAS, rapid atrial pacing at a rate 5 beats/min faster than the tachycardia rate was delivered to demonstrate manifest entrainment and orthodromic capture of the EAAS. When the manifest entrainment with orthodromic capture of the EAAS was demonstrated, the pacing site was considered to be proximal to the slow conduction area of the reentry circuit. Rapid pacing was delivered from 8 sites on the RA: high anterolateral, high posterolateral, high anteroseptal, high posteroseptal, low anterolateral, low posterolateral, low posteroseptal RA, and CS ostium. Manifest entrainment was defined when constant fusion of P waves on the electrocardiogram was demonstrated except for the last entrained beat and when orthodromic capture with a long conduction time and antidromic capture with direct activation by pacing showing different electrogram morphology were both observed for the 1 paced beat during pacing.
After identification of a site proximal to the slow conduction area, radiofrequency energy was delivered to a site between the pacing site and the EAAS to identify the entrance of the slow conduction area. Radiofrequency energy was delivered starting at a site 2 cm away from the EAAS in the direction of the rapid atrial pacing site. This was based on the hypothesis that the slow conduction area is present between the EAAS, the exit, and the pacing site showing manifest entrainment, being located proximal to the slow conduction area. We first delivered the energy at the site 2 cm away from the EAAS, because this site was speculated to be proximally close to entrance to the slow conduction area, based on the size of the slow conduction area in the reentry circuit of the AV nodal reentrant tachycardia, being 1 to 2 cm in length. A current of 15 to 20 W was delivered with the temperature limit set at 55°C using a radiofrequency energy generator (CABL-IT; Central Inc., Ichikawa, Chiba, Japan). When AT was not terminated within 5 seconds of energy application, the energy application was stopped. Then the energy application site was advanced in a stepwise fashion by 3 mm toward the EAAS under the guidance of EnSite anatomic map, until the tachycardia was terminated. The distance between the EAAS and successful ablation site was measured on the three-dimensional endocardial surface.
Values are expressed as mean ± SD.
Results
In all patients, AT was induced and terminated by atrial rapid and extrastimulus pacing, and an inverse relation between A1A2 and A2Ae was observed during the induction of AT by atrial extrastimulus pacing. The EAAS was observed along the tricuspid annulus ( Table 1 ). AT was terminated by intravenous verapamil (2.5 mg in 12 patients and 5 mg in 11 patients) before the electrophysiological study and by intravenous 5 mg adenosine triphosphate during the electrophysiological study in all patients.
Manifest entrainment associated with the orthodromic capture of the earliest atrial electrogram was demonstrated in all patients ( Table 1 ). In all patients, AT was terminated by the application of radiofrequency energy, which was delivered to the site proximal to the EAAS in the direction of the rapid pacing site where the manifest entrainment was observed. Table 1 lists the locations of successful ablation sites relative to the EAAS. The distance between the EAAS and the successful energy application site was 10.4 ± 2.4 mm (7 to 15; Table 1 ). The onset of atrial electrogram at the successful radiofrequency energy application site occurred 13.9 ± 5.7 ms later than that of EAAS ( Table 1 ). AT was terminated immediately after the onset of radiofrequency energy delivery (2.9 ± 1.1 seconds; Table 1 ). The mean number of radiofrequency applications required for successful ablation was 4 ± 2. Ablation was not associated with any complications.
Figure 1 shows the tracing during manifest entrainment in patient 7. The EAAS was in the 12-o’clock position of the tricuspid annulus in this patient. During pacing from the low anterolateral RA, not only EAAS but also high RA and CS recording sites were orthodromically captured via the long conduction interval ( solid arrow ). This was clearly shown in the last entrained beat as indicated by the rectangular dashed line in Figure 1 . All the electrograms at the EAAS, high RA, and CS sites showed morphologies identical to those during AT, and the cycle lengths of these orthodromically captured site electrograms were 385 ms, identical to the pacing interval and shorter than the AT cycle length (405 ms). In contrast, the atrial electrograms at the proximal low anterolateral RA occurred 30 ms earlier than those at CS 1-2 during pacing but 10 ms later than those at CS 1-2 during AT. Furthermore, the interval of the atrial electrogram at proximal low anterolateral RA just after pacing (420 ms) was longer than the pacing cycle length (385 ms), indicating the antidromic capture of the electrogram at proximal low anterolateral RA ( dashed arrow ). In addition, the surface P-wave morphologies in lead V 1 during pacing ( open arrow ) were different from those during tachycardia ( closed arrow ), indicating fusion of surface P wave during pacing except for the last captured beat. All these clearly demonstrate classic entrainment by the pacing from the low anterolateral RA.
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