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Noncontact three-dimensional mapping guides catheter ablation of difficult atrioventricular nodal reentrant tachycardia
International Journal of Cardiology 118 (2007) 154 – 163 www.elsevier.com/locate/ijcard
Noncontact three-dimensional mapping guides catheter ablation of difficult atrioventricular nodal reentrant tachycardia Pi-Chang Lee b , Ching-Tai Tai a , Yenn-Jiang Lin a , Tu-Ying Liu a , Bien-Hsien Huang a , Satoshi Higa a , Yoga Yuniadi a , Kun-Tai Lee a , Betau Hwang b , Shih-Ann Chen a,⁎ a
Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital and National Yang-Ming University, Taipei, Taiwan b Department of Pediatrics, Taipei Veterans General Hospital and National Yang-Ming University, Taipei, Taiwan Received 26 January 2006; received in revised form 24 May 2006; accepted 10 August 2006 Available online 4 October 2006
Abstract Background: Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common supraventricular tachycardia in adulthood. Although selective ablation of the slow AV nodal pathway can cure AVNRT, accidental AV block may occur. The details on the electrophysiologic characteristics, quantitative data on the voltage inside Koch's triangle, and the use of three-dimensional noncontact mapping to facilitate the catheter ablation of AVNRT associated with a high-risk for AV block or other arrhythmias have been limited. Methods and results: Nine patients (M/F = 5/4, 34 ± 23 years, range 17–76) with clinically documented AVNRT were included. All patients had undergone previous sessions for slow AV nodal pathway ablation but they had failed, because of repetitive episodes of complete AV block during the RF energy applications. Further, one patient had a complex anatomy and 4 patients were associated with other tachycardias, respectively. The electrophysiologic studies revealed that 4 patients had the slow–fast, 4 the slow–intermediate and one the fast–intermediate form of AVNRT. Noncontact mapping demonstrated two types of antegrade AV nodal conduction, markedly differing sites of the earliest atrial activation during retrograde VA conduction, and a lower range of voltage within Koch's triangle. The lowest border of the retrograde conduction region was defined on the map, and the application of the RF energy was delivered below that border to prevent the occurrence of AV block. The distance between the successful ablation lesions and the lowest border of the retrograde conduction region was significantly shorter in the patients with the slow–intermediate form of AVNRT than in those with the slow–fast form (5.5 ± 3.4 vs. 15 ± 7.6 mm; p b 0.05). After the ablation procedure, either rapid pacing or extrastimulation could not induce any tachycardia, and there was no recurrence during the followup (10.3 ± 5.4, 2 to 22 months). Conclusions: Noncontact mapping could effectively demonstrate the antegrade and retrograde atrionodal conduction patterns, electrophysiologic characteristics of Koch's triangle, and guide the successful catheter ablation in difficult AVNRT cases. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Atrioventricular nodal reentrant tachycardia; Catheter ablation; Noncontact three-dimensional mapping system
Atrioventricular nodal reentrant tachycardia (AVNRT) is well known to be the most common supraventricular tachycardia in adulthood. Although selective ablation of the slow AV nodal pathway can cure AVNRT [1], an accidental injury to the AV nodal tissue may happen during the radiofrequency ablation procedure. The information from three-dimensional noncontact mapping used to facilitate the ⁎ Corresponding author. Tel.: +886 2 2875 7156; fax: +886 2 2873 5656. E-mail address: [email protected] (S.-A. Chen). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.08.003
catheter ablation of AVNRT associated with a high-risk for AV block or other arrhythmias has been limited. Further, the details of the electrophysiologic characteristics and quantitative data of the voltage inside Koch's triangle are limited. The purpose of this study was to 1) utilize noncontact threedimensional mapping to define the antegrade and retrograde AV nodal conduction, 2) delineate the geometry of Koch's triangle and assess the electrophysiologic characteristics inside and outside Koch's triangle, and 3) guide the successful ablation of difficult AVNRT cases.
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1. Methods 1.1. Patients From March 2002 to December 2004, a total of nine patients (M/F = 5/4, 34 ± 23 years of age, range 17–76) with clinically documented AVNRT that underwent an electrophysiologic study and radiofrequency (RF) catheter ablation with the guidance of a noncontact three-dimensional mapping system at our institution were included (Table 1). All 9 patients had received previous sessions of slow AV nodal pathway ablation but failed, because of repetitive episodes of complete AV block during the RF energy applications or a complex anatomy in 1 patient (Case No.7, large coronary sinus ostium associated with a persistent left superior vena cava). Four patients (Cases No. 3, 4, 5 and 7) were associated with other types of tachycardias (1 with focal atrial tachycardia, 2 with atrial flutter, and 1 with ventricular tachycardia, respectively). An electrophysiologic study revealed that 4 patients had a slow–fast, 4 patients a slow–intermediate and 1 patient a fast–intermediate form of AVNRT. 1.2. Electrophysiologic study The details of conventional EP studies for AVNRT have been described in our previous publications [2,3]. With the percutaneous technique, a quadripolar electrode catheter was placed at the junction of the right atrium (RA) and superior vena cava for high right atrial electrogram recording and atrial stimulation. A second electrode catheter was positioned at the His bundle region to record the His bundle electrogram.
Table 1 Characteristics of the 9 patients with AVNRT Case Sex Age Type of Pattern of No. (y/o) AVNRT antegrade conduction
Earliest sites of retrograde conduction
Associated arrhythmias or complex anatomy
1 2 3 4
M F F M
17 28 38 30
S–I S–I S–F S–I
Pattern 1 Pattern 1 Pattern 1 Pattern 1
Middle KT Middle KT Upper KT Middle KT
5
M
20
F–I
Pattern 1
Middle KT
6 7
F F
71 50
S–I S–F
Pattern 2 Pattern 2
Middle KT Lower KT
8 9
F M
76 21
S–F S–F
Pattern 1 Pattern 1
Upper KT Bachmann bundle
– – Focal AT Typical CW, atypical AFL Idiopathic LV– VT – Persistent left SVC; Typical CW and CCW AFL – –
AFL: atrial flutter; AT: atrial tachycardia; AVNRT: atrioventricular nodal reentrant tachycardia; CCW: counterclockwise; CW: clockwise; F–I: fast– intermediate; KT: Koch's triangle; LV: left ventricle; S–F: slow–fast; S–I: slow–intermediate;SVC: superior vena cava; VT: ventricular tachycardia; +/−: yes/no.
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A third electrode catheter was located at the right ventricular apex for recording and ventricular pacing. A 7F, deflectable decapolar electrode catheter with 2–5–2 mm interelectrode spacing (AF Division, St. Jude Medical, MN, USA) was introduced from the right internal jugular vein and placed into the coronary sinus for recording. A 9F sheath was placed in the right internal jugular vein to introduce a noncontact mapping catheter close to the tricuspid annulus and was connected to a three-dimensional mapping system (EnSite 3000 catheter and workstation, Endocardial Solutions, Inc., St. Jude Medical, St. Paul, MN, USA). 1.3. Noncontact three-dimensional mapping system The details of the noncontact mapping system have been described thoroughly before [4]. In brief, the system is comprised of an inflatable multielectrode array (MEA) catheter, reference patch electrode, amplifiers, and Silicon Graphics workstation. Raw data detected by the MEA streams into the Silicon Graphics workstation via amplifiers and a fiber optic link. Before deployment of the MEA and throughout the study thereafter, heparin was periodically administrated to maintain the activated clotting time between 250 and 300 s. The MEA catheter was deployed over a 0.032in. J-tipped guide wire, advanced to the right ventricular outflow tract (RVOT), and inflated for mapping and navigation. A 4 mm-tip electrode catheter (Mansfield, Boston Scientific, Co., CA, USA) was used for radiofrequency ablation. The system could navigate any electrode catheter in relation to the MEA using a “locator” signal, which was used to construct a three-dimensional anatomical chamber model, providing a geometry matrix for the inverse solution, and to display and track the position of the catheter on it. Using mathematical techniques to process the potentials detected by the MEA, the system simultaneously reconstructs more than 3000 unipolar electrograms and displays them on the chamber model. The electrograms are displayed as isopotential maps with a color range representing the voltage amplitude. Consequently, a wavefront was defined as a discrete front of endocardial depolarization presenting as a region with a negative polarity. 1.4. Validation of the noncontact electrogram Contact electrograms were recorded from 20 randomly chosen locations around the chamber during sinus rhythm. The EnSite navigation signals were simultaneously recorded from each site for a geometric annotation of the location and generation of virtual electrograms that could be compared with the associated contact electrograms. Simultaneous recording of the bipolar and unipolar electrograms from the distal tip of the contact catheter was performed. Signals from both the contact and noncontact electrograms were filtered with a bandwidth of 2–300 Hz. The electrogram morphology, activation time difference, and electrogram voltage between the contact and noncontact electrograms which were taken
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Fig. 1. Noncontact three-dimensional mapping of the antegrade conduction during sinus rhythm in Case No. 2. Panels A1 to D1 (left panel) show the sequential isopotential maps in the right anterior oblique view during sinus rhythm. Panels A2 to D2 (right panel) show the sequential isopotential maps in the left posterior oblique view during sinus rhythm. The color scale for each isopotential map has been set so that white indicates the most negative potentials and blue indicates the least negative potentials. During sinus rhythm, the activation wavefronts from the sinus node separate into two components: anterior and posterior portions (Panel A1). The anterior wavefront quickly propagates through the anterior portion of the right atrium downward (Panel B1 and C1), and joins with the posterior wavefront in the isthmus region (Panel D1). Another posterior wavefront rapidly spreads along the CrT (Panel A2), propagates down through the isthmus (Panel B2), then retrogradely spreads to the septal region with a slower conduction velocity as compared to that along the CrT (Panel C2), and enters the AV nodal region via the posterior “slow” pathway input (Panel D2). CrT: Crista terminalis; CSO: coronary sinus ostium; His: His bundle region; IVC: inferior vena cava; RAA: right atrial appendage; SVC: superior vena cava; TV: tricuspid valve annulus.
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Fig. 2. Noncontact three-dimensional mapping of the antegrade conduction of the slow pathway during atrial pacing with a 320 ms pacing coupling interval in Case No. 6. Panels A1 to D1 (left panel) show the sequential isopotential maps in the right anterior oblique view during atrial pacing. Panels A2 to D2 (right panel) show the sequential isopotential maps in the left posterior oblique view during atrial pacing. The color scale for each isopotential map has been set so that white indicates the most negative potentials and blue indicates the least negative potentials. The sequence of the anterior wavefront was similar to that in Case No. 2 (Panels A1 to D1). However, the propagation of the posterior wavefronts is separated by the tendon of Todaro (panels A2 and B2), descends along the CrT and isthmus (Panel C2) and approaches the AV nodal region via the posterior “slow” pathway input (Panel D2).
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Fig. 3. In the left posterior oblique view, the sites of the earliest retrograde atrial activation were illustrated by shortening the coupling interval of the ventricular extrastimulation (Panel A: 400 ms; Panel B: 360 ms; Panel C: 320 ms) during a fixed ventricular pacing cycle length (S1S1 = 500 ms) in Case No. 3. Notice the site of the earliest atrial activation shifts gradually from the apex of Koch's triangle near the AV node–His bundle junction (fast pathway area) with a longer coupling interval, to a site posterior to the AV node near the orifice of the coronary sinus (slow pathway area) with a shorter coupling interval.
from the same endocardial sites were compared by using a well-described template comparison algorithm [5–8]. 1.5. Unipolar voltage analysis In all patients, the mean peak negative voltage (PNV) was analyzed from the negative unipolar electrograms, which were obtained from virtual sites equally distributed inside and outside Koch's triangle respectively; off-line software was utilized to analyze these data. Moreover, we divided Koch's triangle into three equal components to analyze and compare the mean unipolar PNV from the top of the His bundle area to the bottom of the coronary sinus ostium: upper, middle and lower one-third. Analysis was performed during sinus rhythm and right atrial pacing with pacing cycle lengths (CL) of 600 and 300 ms. The mean PNV inside and outside Koch's triangle was compared during various rhythms to investigate the substrate characteristics. A separate, off-line computer analysis program was used to analyze the distribution of the distance from the virtual sites to the balloon center for validation of the accuracy of the reconstructed electrograms. A standard feature on the noncontact mapping system was used to export all raw virtual and contact electrogram data to the off-line computer analysis program. The reason for using the PNV to represent the voltage data is described in the Discussion section. 1.6. Radiofrequency catheter ablation After completion of the basic electrophysiologic study, we determined the earliest atrial activation area of the retrograde conduction using ventricular extrastimulation. To document the sequential retrograde atrial activation using an Ensite system, we delineated the area of the retrograde VA conduction (including the possibility of retrograde fast and retrograde intermediate pathways). We avoided any application of the RF energy in this area to prevent the occurrence of permanent AV block when guiding the slow pathway ablation if the target site and retrograde VA conduction site were noted simultaneously at the same site. The RF energy was delivered while mon-
itoring the temperature at the catheter tip, which was limited to a maximum temperature of 50–55 °C. If accelerated junctional rhythm occurred, the RF energy was continued for 30 s along with rapid atrial pacing. Programmed stimulation after the ablation was repeated with and without the infusion of isoproterenol. Successful ablation was defined as either no AVNRT inducible or induction of a maximum of one AV node echo beat during an infusion of isoproterenol. 1.7. Follow-up evaluation After the procedure, the patients were monitored for 24 h in the intensive care unit prior to discharge. Each patient came back to the clinic every 2 weeks in the first month, then every 3 months in the first year, and every 6 months in the following years. 1.8. Statistical analysis All parametric data of the continuous variables were expressed as the mean ± SD. The data of the clinical and electrophysiologic characteristics between two different patient groups were compared using the Student's t-test. The data of the clinical and electrophysiologic characteristics among 3 or more patient groups were compared using one way ANOVA. The proportions and rates of the incidence between these 2 groups were compared by the Chi-square test with Yates' correction. For validation of the mapping accuracy, the correlation between the contact and noncontact electrograms was explored by calculating the Pearson's correlation coefficients and using the Bland–Altman technique for agreement. Statistical significance was defined as a p value b 0.05. 2. Results 2.1. Antegrade atrial conduction There were two different propagation patterns of the antegrade atrial conduction in our 9 patients. During sinus
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directly enter the apex of Koch's triangle, but instead descended along the tendon of Todaro of Koch's triangle, and approached the AV nodal region via the posterior “slow” pathway input (Fig. 2). 2.2. Retrograde atrial conduction
Fig. 4. A frequency distribution curve of the peak unipolar negative voltage was demonstrated outside and inside Koch's triangle during sinus rhythm. Notice 5.8% of the PNV values less than −0.27 mV were outside Koch's triangle (A) and 11.5% of the PNV values less than −0.27 mV were inside Koch's triangle (B).
rhythm, the antegrade atrial conduction was demonstrated correspondingly to have two distinct wavefronts in 7 cases (Pattern 1): anterior and posterior portions. The anterior one quickly went propagated into the apex of the Koch's triangle, then through the anterior wall of the right atrium and joined with the posterior wavefront in the isthmus region (Fig. 1; left panels, A1–D1); another posterior wavefront rapidly conducted along the crista terminalis (CrT) and entered the summit of Koch's triangle, propagated through the isthmus, and turned around to approach the AV nodal region via the posterior “slow” pathway input (Fig. 1; right panels, A2–D2). In two cases (Nos. 6 and 7; Pattern 2) the antegrade atrial activation with a short pacing CL was slightly different from that with a long pacing CL. By using atrial pacing with a shorter CL, the propagation of the wavefronts could not
The retrograde atrial activation was evaluated both during the tachycardia and ventricular pacing. The earliest site of the retrograde atrial activation was situated at the apex of Koch's triangle (fast pathway area, n = 2), coronary ostium region (slow pathway area, n = 1), and interatrial septum close to the foramen ovale (Bachmann bundle, n = 1) in 4 patients with the slow–fast form of AVNRT; and between the area of the fast pathway and coronary sinus ostium (so-called intermediate pathway) in 1 patient with the fast–intermediate and 4 patients with the slow–intermediate form of AVNRT. In patient No. 3 with retrograde dual AV nodal pathways, the site of the earliest atrial activation was usually situated in two different locations during ventricular pacing: the apex of Koch's triangle near the AV node–His bundle junction (fast pathway area) with a longer pacing CL, and posterior to the AV node near the orifice of the coronary sinus (slow pathway area) with a shorter pacing CL. In this particular patient, the earliest retrograde atrial activation gradually shifted from the fast pathway region to the slow pathway region with a shortening of the pacing CL rather than a sudden shift (Fig. 3). In case No. 7, the earliest retrograde atrial activation of the fast pathway was unusually low, and located adjacent to the coronary sinus ostium (the typical slow pathway region). The antegrade slow pathway was situated oppositely at the apex of Koch's triangle near the AV node–His bundle junction. After successful ablation of the antegrade slow pathway, there was no AH jump during right atrial extrastimulation. Coronary sinus venography demonstrated a large coronary sinus ostium and persistent left superior vena cava. 2.3. Validation of the noncontact electrograms and voltage distribution The agreement analysis of the voltage and time difference indicated that only 6% and 9% of all recording sites were outside of one standard deviation, respectively. The average distance from the balloon center to Koch's triangle was 27.4 ± 9.1 mm (range from 9.8 to 42 mm). A histogram of the PNV frequency distribution was obtained from a total of 5090 electrograms inside and outside Koch's triangle. According to the unipolar voltage frequency distribution curve, 5% of the PNV values were less negative than −0.27 mV during sinus rhythm. During sinus rhythm, the distribution of the unipolar voltage demonstrated 11.5% of the PNV values less than −0.27 mV were located inside Koch's triangle and 5.8% of the PNV values less than −0.27 mV were located outside Koch's triangle ( p b 0.001) (Fig. 4). The mean unipolar PNV inside Koch's triangle (obtained from 48± 6 mapping sites in each patient) was significantly less
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Fig. 5. Geometric anatomy associated with the activation routes of the retrograde VA conduction in Case No. 2 (upper panel) and Case No. 6 (lower panel) is demonstrated in the left posterior oblique view. Notice that the position of the retrograde conduction routes were both uncommonly low so that transient heart block could easily happen during the previous session of radiofrequency catheter ablation. To avoid the retrograde conduction routes, radiofrequency energy (deep brown dots) was delivered under surveillance of the precise geometric mapping in both cases. Abbreviation: CSO: coronary sinus ostium; FO: foramen ovale; IVC: inferior vena cava; RAA: right atrial appendage; SVC: superior vena cava; TT: tendon of Todaro; TV: tricuspid valve annulus.
negative than the voltage outside Koch's triangle, whether during sinus rhythm (−0.79 ± 0.39 vs. −1.30 ± 1.03 mV; p b 0.001), right atrial pacing with a 600 ms CL (−0.79 ± 0.48 vs. −1.34± 1.33 mV; p b 0.001) or right atrial pacing with a 300 ms CL (− 0.63 ± 0.28 vs. − 1.35 ± 0.94 mV; p b 0.001). The PNV inside Koch's triangle was less negative during shorter right atrial pacing CLs compared to longer pacing CLs (− 0.63 ± 0.28 vs. − 0.79 ± 0.48 mV; p b 0.001) and sinus rhythm (− 0.63 ± 0.28 vs. − 0.79 ± 0.39 mV; p b 0.001; p b 0.001). The ratio of the mean PNV inside Koch's triangle to the maximal PNV of the global right atrium was 21.6 ± 9.0% during sinus rhythm, 18.3 ± 7.3% during right atrial pacing with a 600 ms CL, and 15.6 ± 5.8% during right atrial pacing with a 300 ms CL ( p b 0.001). During both sinus rhythm and right atrial pacing, the mean unipolar PNV in the lower one-third of Koch's triangle was less negative than that in the upper one-third (−0.67 ± 0.21 vs. −1.45 ± 0.43, p b 0.001; −0.78 ± 0.35 vs. −1.59 ± 0.38 mV, p b 0.001) and middle one-third (−0.67 ± 0.21 vs. −1.07 ± 0.29, p b 0.001; −0.78 ± 0.21 vs. −0.99 ± 0.62 mV, p b 0.05) of Koch's triangle in these patients. 2.4. Results of the radiofrequency catheter ablation Using sequential ventricular extrastimulation, we delineated the earliest atrial activation area of the retrograde conduction (Fig. 5). In 3 of our patients (Cases No. 2, 6
and 7), the location of the retrograde conductions area was observed to be uncommonly low so that transient heart block could be easily induced during the previous session of the RF catheter ablation, even when the ablation site was at the usual target location. Based on the geometric mapping, we were able to avoid applying the RF energy on the retrograde conduction routes. Accelerated junctional rhythm without AV block in 8 patients was demonstrated during the successful radiofrequency catheter ablation. Prolongation of the PR interval (from 150 to 230 ms) occurred in 1 patient during the first RF energy application (a total of 8 s) because the ablation lesion was just on the border of the fast pathway region in that case (Fig. 5; lower panel). After the ablation procedure, neither rapid pacing nor extrastimulation could induce any tachycardia with or without an isoproterenol infusion. The distance between the successful ablation lesions and the lowest border of the retrograde conduction area was significantly shorter in the patients with the slow–intermediate form of AVNRT than in those with the slow–fast form of AVNRT (5.5 ± 3.4 vs. 15 ± 7.6 mm; p b 0.05). The successful ablation site in the patient with the fast–intermediate form of AVNRT was located significantly higher than that in the other patients. After the ablation procedure, no tachycardia could be induced by either rapid pacing or extrastimulation in all these cases. There was no recurrence noted during the follow-up period (10.3 ± 5.4, 2 to 22 months).
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3. Discussion 3.1. Major findings To the best of our knowledge, this study was the first use of noncontact mapping to guide the successful ablation in difficult AVNRT cases associated with a high risk of AV block or other atrial arrhythmias. This study characterized two different patterns of the antegrade conduction and identified the earliest site of the retrograde conduction during sinus rhythm and decremental pacing. Furthermore, Koch's triangle demonstrated a significantly lower voltage than the rest of the right atrium, and the lower one-third of Koch's triangle demonstrated a significantly lower voltage than the rest of Koch's triangle. 3.2. Concept of AV nodal reentrant tachycardia 3.2.1. Antegrade AV nodal inputs The input hypothesis of the AV node has been previously proposed by several investigators [9,10]. However, there has been no evidence for the presence of a distinct anterior input into the AV node. Based on the optical mapping data and microelectrode recording, the previous study proposed a model for AV nodal impulse propagation [11]. The impulse appeared to conduct rapidly over the atrial tissue and slowly toward the AV node through the transitional zone surrounding the AV node. All of the atrial tissue enveloping Koch's triangle delivered impulses to the AV node, strongly suggesting that multiple nondiscrete AV nodal inputs were present. Some investigators arbitrarily divided these nondiscrete AV nodal inputs into the so-called fast pathway, slow pathway, and intermediate pathway. McGuire et al. suggested that the atrionodal connection closest to the His bundle was the preferred route of conduction through the AV node during normal AVor VA conduction, and that part of slow AV nodal pathway may lie outside the compact AV node [12,13]. Previous animal studies demonstrated that the antegrade conduction over the slow pathway existed in all normal hearts with or without AVNRT, but did not become manifest because propagation over the fast pathway reached the AV node first [11,14]. In the present study, 7 cases had similar patterns of the antegrade conduction no matter whether it was before or after the “jump” phenomenon. This finding was similar to the previous studies that suggested that no direct relationship existed between the “jump” and AV nodal input pathways [11,15]. This finding may be explained by the abrupt conduction delay within the AV node through the same atrionodal input. However, the propagation of the wavefronts in the other two cases could not spread directly toward the apex of Koch's triangle during atrial pacing with shorter CLs, but instead appeared to approach the AV nodal region via the posterior “slow” pathway input. This particular phenomenon may be caused by: 1) previous ablation lesions, 2) local fibrosis due to the older age or, 3) local functional block due to a negative balance of the source and sink [12,13,16].
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3.2.2. Retrograde AV nodal conduction This study demonstrated that the sites of the earliest retrograde atrial activation were conspicuously located at different sites among our patients with slow–fast, slow– intermediate and fast–intermediate forms of AVNRT. McGuire et al. had demonstrated the retrograde conduction with high-resolution mapping by using sixty electrodes during open-heart surgery [17]. However, another previous study by Anselme et al. showed that retrograde atrial activation over the fast pathway was heterogeneous within Koch's triangle and the coronary sinus during different modes of activation [18]. They emphasized that some challenging cases with complete heart block during the energy delivery may be caused by the anatomic heterogeneity and potentially dynamic properties of retrograde AV nodal conduction. To the best of knowledge, the present study is the first study to investigate the retrograde conduction by using high-resolution noncontact mapping in different types of AVNRT. Furthermore, the sites of the earliest retrograde atrial activation gradually shifted from the fast pathway region to the slow pathway region during shortened pacing CLs, rather than a sudden shift in the patients with retrograde dual AV nodal pathways. This phenomenon may imply that 1) the VA interval prolongation during shortened pacing CLs may be caused by a conduction delay inside the AV node or by a change in the location of the exit sites from the AV node; and 2) anisotropic conduction and the distributed cell layers inside Koch's triangle may contribute to the VA conduction delay. Previous studies demonstrated that functionally fast AV nodal pathways may be located in the posteroseptal right atrium, where slow pathway modification is performed [19]. In case No. 7 in the present study, the earliest retrograde atrial activation of the fast pathway was unusually low (adjacent to the coronary sinus ostium) while the antegrade slow pathway was oppositely situated at the top of Koch's triangle. Failure to recognize the presence of posterior fast AV node pathways may account for sporadic occurrences of AV block, complicating the ablation in patients with AVNRT. Coronary sinus venography demonstrated a large coronary sinus ostium and a persistent left superior vena cava. A large coronary sinus may have contributed to the complicated atrionodal input in that case. 3.2.3. Koch's triangle and the electrogram voltage Simultaneous intracellular and extracellular electrograms showed that the downstroke of the unipolar electrogram indicated the local activation [20]. Furthermore, the sections of the unipolar electrogram occurring before or after the downstroke of the deflection are caused by activation fronts distant from the recording sites [21], and the fundamental advantage of applying the unipolar electrograms also demonstrates that the voltages of the unipolar recording do not vary with the direction of the electrode axis as those of the bipolar recordings. Previous studies also indicated that the peak-to-peak voltages of the unipolar electrogram are
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determined primarily by the distant excitation waves instead of the local activation [22,23]. Previous studies demonstrated at least two distinct groups of atrionodal connections that may result from different cell types and anisotropic conduction [2,17,24,25]. McGuire et al. used a high-density plaque electrode, introduced during openheart surgery, to simultaneously acquire a large number of signals from a defined region. They demonstrated double potentials and fragmented potentials inside Koch's triangle [2,25]. Thus, the electrogram characteristics inside Koch's triangle would be expected to display a relatively lower range of voltages. In the present study, we demonstrated a similar result in the isopotential maps and virtual electrograms that were exported and analyzed from the noncontact mapping system. Koch's triangle did reveal a lower range of voltages as compared to outside Koch's triangle during sinus rhythm and atrial pacing, possibly due to the transitional cell distribution including multiple layers and anisotropic conduction. Furthermore, the lower one-third of Koch's triangle demonstrated the lowest voltage zone in our patients. In previous studies, this region was composed of a posterior extension to the AV node which included AV junctional cells and muscle fibers parallel to the tricuspid valve annulus [24,26]. The AV junctional cells in the posterior extension appear to participate in the slow pathway conduction and resemble nodal cells in their cellular electrophysiology, response to adenosine, and lack of connexin-43 [24]. In addition, the non-uniform distribution of the muscle fibers contributed to the slow conduction and low voltage. The specific electrophysiologic characteristics in the lower one-third of Koch's triangle could provide supplementary information to identify the slow pathway region and to guide the RF ablation of AVNRT. According to the previously published literature from this laboratory, there is a high correlation between the contact and noncontact electrograms when the distance from the mapping sites to the balloon center is less than 38 mm [27]. In our study group, the average distance from the balloon center to Koch's triangle for each patient was 27.4 ± 9.1 mm. 3.2.4. Catheter ablation Treatment of patients with AVNRT by ablation of the slow AV nodal pathway typically has a high success rate and a low complication rate, but inadvertent AV block may sometimes occur. Previous studies demonstrated that functionally fast AV nodal pathways might be located in the posteroseptal right atrium, where slow pathway modification is performed conventionally [19]. In those studies, RF ablation of the retrograde fast pathway affected the antegrade fast pathway, and the location of the antegrade and retrograde fast pathways may be anatomically similar [28,29]. In this study, we additionally characterized the sequential nature of the retrograde atrial activation route and thereby avoided the occurrence of AV block. Recognition of the activation route of retrograde conduction and acquisition of a precise 3D geometry may help avoid inadvertent AV block in certain difficult cases undergoing RF catheter ablation of AVNRT. In the present study, two patients failed the ablation in the previous ablation
sessions because of repeated episodes of AV block during the RF energy applications, however, they did not have highdegree AV block in the present study. In the conventional ablation treatment approach using only fluoroscopy, the successful ablation site of the slow pathway is usually located in the bottom one-third of Koch's triangle (near the coronary sinus ostium) and far from the usual AV node. However, in some particular cases, inadvertent AV block may occur when the region of the slow pathway is located in the middle or even the top onethird of Koch's triangle. The atrionodal input in those cases was remarkably different from that in the typical cases, possibly due to a peculiar distribution of the AV nodal cells and coronary sinus structure. Therefore, detailed localization of the retrograde fast pathway exit site and angiographic imaging of the coronary sinus anatomy may be necessary in some difficult cases before the catheter ablation of AVNRT. 4. Limitations Because this study group only included the difficult AVNRT cases, more studies need to characterize in more detail the atrial conduction into and out of Koch's triangle and to more fully assess the clinical relevance. The AV node proper may present signals as low voltage potentials that are even smaller and may be below the sensitivity of the noncontact recording, however, the feasibility of recording these potentials has not yet been evaluated. 5. Conclusion Noncontact three-dimensional mapping can identify the atrionodal inputs of the antegrade and retrograde conduction, demonstrate the geometry of Koch's triangle, and assess the electrophysiologic characteristics inside and outside of Koch's triangle. The precise geometry acquired by the noncontact mapping system may help avoid inadvertent AV block in some difficult cases undergoing catheter ablation of AVNRT. References [1] Jackman WM, Beckman KJ, McClelland JH, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med 1992;327:313–8. [2] Tai CT, Chen SA, Chiang CE, et al. Multiple antegrade atrioventricular node pathways in patients with atrioventricular node reentrant tachycardia. J Am Coll Cardiol 1996;28(3):725–31. [3] Tai CT, Chen SA, Chiang CE, et al. Complex electrophysiological characteristics in atrioventricular nodal reentrant tachycardia with continuous atrioventricular node function curves. Circulation 1997;95 (11):2541–7. [4] Tai CT, Huang JL, Lin YK, et al. Noncontact three-dimensional mapping and ablation of upper loop reentry originating in the right atrium. J Am Coll Cardiol 2002;40(4):746–53. [5] Schilling RJ, Peters NS, Davies DW. Simultaneous endocardial mapping in the human left ventricle using a non-contact mapping catheter: comparison of contact and reconstructed electrograms during sinus rhythm. Circulation 1998;98:887–98.
P.-C. Lee et al. / International Journal of Cardiology 118 (2007) 154–163 [6] Kadish A, Hauck J, Pederson B, et al. Mapping of atrial activation with a non-contact, multielectrode catheter in dogs. Circulation 1999;99:1906–13. [7] Ropella KM, Sahakian AV, Baerman JM, et al. The coherence spectrum. A quantitative discriminator of fibrillatory and nonfibrillatory cardiac rhythms. Circulation 1989;80:112–9. [8] Abboud S, Sadeh D. The use of cross-correlation function for the alignment of ECG waveforms and rejection of extrasystoles. Comput Biomed Res 1984;17:258–66. [9] Efimov IR, Fahy GJ, Cheng Y, et al. High-resolution fluorescent imaging does not reveal a distinct atrioventricular nodal anterior input channel (fast pathway) in the rabbit heart during sinus rhythm. J Cardiovasc Electrophysiol 1997;8:295–306. [10] Ho SY, Kilpatrick L, Kanai T, et al. The architecture of the atrioventricular conduction axis in dog compared to man: its significance to ablation of the atrioventricular nodal approaches. J Cardiovasc Electrophysiol 1995;6:26–39. [11] Wu J, Zipes DP. Mechanisms underlying atrioventricular nodal conduction and the reentrant circuit of atrioventricular nodal reentrant tachycardia using optic mapping. J Cardiovasc Electrophysiol 2002;13:831–4. [12] McGuire MA, Yip ASB, Robotin M, et al. Surgical procedure for the cure of atrioventricular junctional (“AV node”) reentrant tachycardia: anatomic and electrophysiologic effects of dissection of the anterior atrionodal connections in a canine model. J Am Coll Cardiol 1994;24:784–94. [13] McGuire MA, Robotin M, Yip ASB, et al. Electrophysiologic and histologic effects of dissection of the connections between the atrium and posterior part of the atrioventricular node. J Am Coll Cardiol 1994;23:693–701. [14] Lin LJ, Billette J, Medkour D, et al. Properties and substrate of SP exposed with a compact node targeted FP ablation in rabbit atrioventricular node. J Cardiovasc Electrophysiol 2001;12:479–86. [15] Otomo K, Wang Z, Lazzara R, et al. Atrioventricular nodal reentrant tachycardia: electrophysiological characteristics of four forms and implications for the reentrant circuit. In: Zipes DP, Jalife J, editors. Cardiac electrophysiology: from cell to bedside. Third Edition. Philadelphia: WB Saunders; 2000. p. 504–21. [16] Keim S, Werner P, Jazayeri M, et al. Localization of the fast and slow pathways in atrioventricular nodal reentrant tachycardia by intraoperative ice mapping. Circulation 1992;86:919–25. [17] McGuire MA, Bourke JP, Robotin MC, et al. High resolution mapping of Koch's triangle using sixty electrodes in humans with atrioventricular junctional (AV nodal) reentrant tachycardia. Circulation 1993;88:2315–28.
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[18] Anselme F, Hook B, Monahan K, et al. Heterogeneity of retrograde fast-pathway conduction pattern in patients with atrioventricular nodal reentry tachycardia: observation by use of simultaneous multisite catheter mapping of Koch's triangle. Circulation 1996;93:960–8. [19] Engelstein ED, Stein KM, Markowitz SM, et al. Posterior fast atrioventricular node pathways: implications for radiofrequency catheter ablation of atrioventricular node reentrant tachycardia. J Am Coll Cardiol 1996;27:1098–105. [20] Spach MS, Barr RC. Ventricular intramural and epicardial potential distributions during ventricular activation and repolarization in the intact dog. Circ Res 1975;37:243–57. [21] Jacques MT, de Bakker, Timothy AS, et al. Activation mapping: unipolar versus bipolar recording from Cardiac electrophysiology from cell to bedside. 2nd edition. W.B. Saunders company; 1995. p. 1068–78. [22] Damiano Jr RJ, Blanchard SM, Asano T, Cox JL, Lowe JE. Effects of distant potentials on unipolar electrograms in an animal model utilizing the right ventricular isolation procedure. J Am Coll Cardiol 1988;11:1100–9. [23] Blanchard SM, Damiano Jr RJ, Asano T, Smith WM, Ideker RE, Lowe JE. The effects of distant cardiac electrical events on local activation in unipolar epicardial electrograms. IEEE Trans Biomed Eng 1987;34:539–46. [24] Hocini M, Loh P, Ho SY, et al. Anisotropic conduction in the triangle of Koch of mammalian hearts: electrophysiologic and anatomic correlations. J Am Coll Cardiol 1998;31:629–36. [25] McGuire MA, de Bakker JM, Vermeulen JT, et al. Atrioventricular junctional tissue. Discrepancy between histological and electrophysiological characteristics. Circulation 1996;94:571–7. [26] James TN. The tendon of Todaro and the “triangle of Koch”: lessons from eponymous hagiolatry. J Cardiovasc Electrophysiol 1999;10:1478–96. [27] Lin YJ, Tai CT, Huang JL, et al. Characterization of right atrial substrate in patients with supraventricular tachyarrhythmias. J Cardiovasc Electrophysiol 2005;16:173–80. [28] Chen SA, Chiang CE, Tsang WP, et al. Selective radiofrequency catheter ablation of fast and slow pathways in 100 patients with atrioventricular nodal reentrant tachycardia. Am Heart J 1993;125:1–10. [29] Mazgalev TN, Tchou PJ. Surface potentials from the region of the atrioventricular node and their relation to dual pathway electrophysiology. Circulation 2000;101:2110–7.
Noncontact three-dimensional mapping guides catheter ablation of difficult atrioventricular nodal reentrant tachycardia Pi-Chang Lee b , Ching-Tai Tai a , Yenn-Jiang Lin a , Tu-Ying Liu a , Bien-Hsien Huang a , Satoshi Higa a , Yoga Yuniadi a , Kun-Tai Lee a , Betau Hwang b , Shih-Ann Chen a,⁎ a
Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital and National Yang-Ming University, Taipei, Taiwan b Department of Pediatrics, Taipei Veterans General Hospital and National Yang-Ming University, Taipei, Taiwan Received 26 January 2006; received in revised form 24 May 2006; accepted 10 August 2006 Available online 4 October 2006
Abstract Background: Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common supraventricular tachycardia in adulthood. Although selective ablation of the slow AV nodal pathway can cure AVNRT, accidental AV block may occur. The details on the electrophysiologic characteristics, quantitative data on the voltage inside Koch's triangle, and the use of three-dimensional noncontact mapping to facilitate the catheter ablation of AVNRT associated with a high-risk for AV block or other arrhythmias have been limited. Methods and results: Nine patients (M/F = 5/4, 34 ± 23 years, range 17–76) with clinically documented AVNRT were included. All patients had undergone previous sessions for slow AV nodal pathway ablation but they had failed, because of repetitive episodes of complete AV block during the RF energy applications. Further, one patient had a complex anatomy and 4 patients were associated with other tachycardias, respectively. The electrophysiologic studies revealed that 4 patients had the slow–fast, 4 the slow–intermediate and one the fast–intermediate form of AVNRT. Noncontact mapping demonstrated two types of antegrade AV nodal conduction, markedly differing sites of the earliest atrial activation during retrograde VA conduction, and a lower range of voltage within Koch's triangle. The lowest border of the retrograde conduction region was defined on the map, and the application of the RF energy was delivered below that border to prevent the occurrence of AV block. The distance between the successful ablation lesions and the lowest border of the retrograde conduction region was significantly shorter in the patients with the slow–intermediate form of AVNRT than in those with the slow–fast form (5.5 ± 3.4 vs. 15 ± 7.6 mm; p b 0.05). After the ablation procedure, either rapid pacing or extrastimulation could not induce any tachycardia, and there was no recurrence during the followup (10.3 ± 5.4, 2 to 22 months). Conclusions: Noncontact mapping could effectively demonstrate the antegrade and retrograde atrionodal conduction patterns, electrophysiologic characteristics of Koch's triangle, and guide the successful catheter ablation in difficult AVNRT cases. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Atrioventricular nodal reentrant tachycardia; Catheter ablation; Noncontact three-dimensional mapping system
Atrioventricular nodal reentrant tachycardia (AVNRT) is well known to be the most common supraventricular tachycardia in adulthood. Although selective ablation of the slow AV nodal pathway can cure AVNRT [1], an accidental injury to the AV nodal tissue may happen during the radiofrequency ablation procedure. The information from three-dimensional noncontact mapping used to facilitate the ⁎ Corresponding author. Tel.: +886 2 2875 7156; fax: +886 2 2873 5656. E-mail address: [email protected] (S.-A. Chen). 0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.08.003
catheter ablation of AVNRT associated with a high-risk for AV block or other arrhythmias has been limited. Further, the details of the electrophysiologic characteristics and quantitative data of the voltage inside Koch's triangle are limited. The purpose of this study was to 1) utilize noncontact threedimensional mapping to define the antegrade and retrograde AV nodal conduction, 2) delineate the geometry of Koch's triangle and assess the electrophysiologic characteristics inside and outside Koch's triangle, and 3) guide the successful ablation of difficult AVNRT cases.
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1. Methods 1.1. Patients From March 2002 to December 2004, a total of nine patients (M/F = 5/4, 34 ± 23 years of age, range 17–76) with clinically documented AVNRT that underwent an electrophysiologic study and radiofrequency (RF) catheter ablation with the guidance of a noncontact three-dimensional mapping system at our institution were included (Table 1). All 9 patients had received previous sessions of slow AV nodal pathway ablation but failed, because of repetitive episodes of complete AV block during the RF energy applications or a complex anatomy in 1 patient (Case No.7, large coronary sinus ostium associated with a persistent left superior vena cava). Four patients (Cases No. 3, 4, 5 and 7) were associated with other types of tachycardias (1 with focal atrial tachycardia, 2 with atrial flutter, and 1 with ventricular tachycardia, respectively). An electrophysiologic study revealed that 4 patients had a slow–fast, 4 patients a slow–intermediate and 1 patient a fast–intermediate form of AVNRT. 1.2. Electrophysiologic study The details of conventional EP studies for AVNRT have been described in our previous publications [2,3]. With the percutaneous technique, a quadripolar electrode catheter was placed at the junction of the right atrium (RA) and superior vena cava for high right atrial electrogram recording and atrial stimulation. A second electrode catheter was positioned at the His bundle region to record the His bundle electrogram.
Table 1 Characteristics of the 9 patients with AVNRT Case Sex Age Type of Pattern of No. (y/o) AVNRT antegrade conduction
Earliest sites of retrograde conduction
Associated arrhythmias or complex anatomy
1 2 3 4
M F F M
17 28 38 30
S–I S–I S–F S–I
Pattern 1 Pattern 1 Pattern 1 Pattern 1
Middle KT Middle KT Upper KT Middle KT
5
M
20
F–I
Pattern 1
Middle KT
6 7
F F
71 50
S–I S–F
Pattern 2 Pattern 2
Middle KT Lower KT
8 9
F M
76 21
S–F S–F
Pattern 1 Pattern 1
Upper KT Bachmann bundle
– – Focal AT Typical CW, atypical AFL Idiopathic LV– VT – Persistent left SVC; Typical CW and CCW AFL – –
AFL: atrial flutter; AT: atrial tachycardia; AVNRT: atrioventricular nodal reentrant tachycardia; CCW: counterclockwise; CW: clockwise; F–I: fast– intermediate; KT: Koch's triangle; LV: left ventricle; S–F: slow–fast; S–I: slow–intermediate;SVC: superior vena cava; VT: ventricular tachycardia; +/−: yes/no.
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A third electrode catheter was located at the right ventricular apex for recording and ventricular pacing. A 7F, deflectable decapolar electrode catheter with 2–5–2 mm interelectrode spacing (AF Division, St. Jude Medical, MN, USA) was introduced from the right internal jugular vein and placed into the coronary sinus for recording. A 9F sheath was placed in the right internal jugular vein to introduce a noncontact mapping catheter close to the tricuspid annulus and was connected to a three-dimensional mapping system (EnSite 3000 catheter and workstation, Endocardial Solutions, Inc., St. Jude Medical, St. Paul, MN, USA). 1.3. Noncontact three-dimensional mapping system The details of the noncontact mapping system have been described thoroughly before [4]. In brief, the system is comprised of an inflatable multielectrode array (MEA) catheter, reference patch electrode, amplifiers, and Silicon Graphics workstation. Raw data detected by the MEA streams into the Silicon Graphics workstation via amplifiers and a fiber optic link. Before deployment of the MEA and throughout the study thereafter, heparin was periodically administrated to maintain the activated clotting time between 250 and 300 s. The MEA catheter was deployed over a 0.032in. J-tipped guide wire, advanced to the right ventricular outflow tract (RVOT), and inflated for mapping and navigation. A 4 mm-tip electrode catheter (Mansfield, Boston Scientific, Co., CA, USA) was used for radiofrequency ablation. The system could navigate any electrode catheter in relation to the MEA using a “locator” signal, which was used to construct a three-dimensional anatomical chamber model, providing a geometry matrix for the inverse solution, and to display and track the position of the catheter on it. Using mathematical techniques to process the potentials detected by the MEA, the system simultaneously reconstructs more than 3000 unipolar electrograms and displays them on the chamber model. The electrograms are displayed as isopotential maps with a color range representing the voltage amplitude. Consequently, a wavefront was defined as a discrete front of endocardial depolarization presenting as a region with a negative polarity. 1.4. Validation of the noncontact electrogram Contact electrograms were recorded from 20 randomly chosen locations around the chamber during sinus rhythm. The EnSite navigation signals were simultaneously recorded from each site for a geometric annotation of the location and generation of virtual electrograms that could be compared with the associated contact electrograms. Simultaneous recording of the bipolar and unipolar electrograms from the distal tip of the contact catheter was performed. Signals from both the contact and noncontact electrograms were filtered with a bandwidth of 2–300 Hz. The electrogram morphology, activation time difference, and electrogram voltage between the contact and noncontact electrograms which were taken
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Fig. 1. Noncontact three-dimensional mapping of the antegrade conduction during sinus rhythm in Case No. 2. Panels A1 to D1 (left panel) show the sequential isopotential maps in the right anterior oblique view during sinus rhythm. Panels A2 to D2 (right panel) show the sequential isopotential maps in the left posterior oblique view during sinus rhythm. The color scale for each isopotential map has been set so that white indicates the most negative potentials and blue indicates the least negative potentials. During sinus rhythm, the activation wavefronts from the sinus node separate into two components: anterior and posterior portions (Panel A1). The anterior wavefront quickly propagates through the anterior portion of the right atrium downward (Panel B1 and C1), and joins with the posterior wavefront in the isthmus region (Panel D1). Another posterior wavefront rapidly spreads along the CrT (Panel A2), propagates down through the isthmus (Panel B2), then retrogradely spreads to the septal region with a slower conduction velocity as compared to that along the CrT (Panel C2), and enters the AV nodal region via the posterior “slow” pathway input (Panel D2). CrT: Crista terminalis; CSO: coronary sinus ostium; His: His bundle region; IVC: inferior vena cava; RAA: right atrial appendage; SVC: superior vena cava; TV: tricuspid valve annulus.
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Fig. 2. Noncontact three-dimensional mapping of the antegrade conduction of the slow pathway during atrial pacing with a 320 ms pacing coupling interval in Case No. 6. Panels A1 to D1 (left panel) show the sequential isopotential maps in the right anterior oblique view during atrial pacing. Panels A2 to D2 (right panel) show the sequential isopotential maps in the left posterior oblique view during atrial pacing. The color scale for each isopotential map has been set so that white indicates the most negative potentials and blue indicates the least negative potentials. The sequence of the anterior wavefront was similar to that in Case No. 2 (Panels A1 to D1). However, the propagation of the posterior wavefronts is separated by the tendon of Todaro (panels A2 and B2), descends along the CrT and isthmus (Panel C2) and approaches the AV nodal region via the posterior “slow” pathway input (Panel D2).
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Fig. 3. In the left posterior oblique view, the sites of the earliest retrograde atrial activation were illustrated by shortening the coupling interval of the ventricular extrastimulation (Panel A: 400 ms; Panel B: 360 ms; Panel C: 320 ms) during a fixed ventricular pacing cycle length (S1S1 = 500 ms) in Case No. 3. Notice the site of the earliest atrial activation shifts gradually from the apex of Koch's triangle near the AV node–His bundle junction (fast pathway area) with a longer coupling interval, to a site posterior to the AV node near the orifice of the coronary sinus (slow pathway area) with a shorter coupling interval.
from the same endocardial sites were compared by using a well-described template comparison algorithm [5–8]. 1.5. Unipolar voltage analysis In all patients, the mean peak negative voltage (PNV) was analyzed from the negative unipolar electrograms, which were obtained from virtual sites equally distributed inside and outside Koch's triangle respectively; off-line software was utilized to analyze these data. Moreover, we divided Koch's triangle into three equal components to analyze and compare the mean unipolar PNV from the top of the His bundle area to the bottom of the coronary sinus ostium: upper, middle and lower one-third. Analysis was performed during sinus rhythm and right atrial pacing with pacing cycle lengths (CL) of 600 and 300 ms. The mean PNV inside and outside Koch's triangle was compared during various rhythms to investigate the substrate characteristics. A separate, off-line computer analysis program was used to analyze the distribution of the distance from the virtual sites to the balloon center for validation of the accuracy of the reconstructed electrograms. A standard feature on the noncontact mapping system was used to export all raw virtual and contact electrogram data to the off-line computer analysis program. The reason for using the PNV to represent the voltage data is described in the Discussion section. 1.6. Radiofrequency catheter ablation After completion of the basic electrophysiologic study, we determined the earliest atrial activation area of the retrograde conduction using ventricular extrastimulation. To document the sequential retrograde atrial activation using an Ensite system, we delineated the area of the retrograde VA conduction (including the possibility of retrograde fast and retrograde intermediate pathways). We avoided any application of the RF energy in this area to prevent the occurrence of permanent AV block when guiding the slow pathway ablation if the target site and retrograde VA conduction site were noted simultaneously at the same site. The RF energy was delivered while mon-
itoring the temperature at the catheter tip, which was limited to a maximum temperature of 50–55 °C. If accelerated junctional rhythm occurred, the RF energy was continued for 30 s along with rapid atrial pacing. Programmed stimulation after the ablation was repeated with and without the infusion of isoproterenol. Successful ablation was defined as either no AVNRT inducible or induction of a maximum of one AV node echo beat during an infusion of isoproterenol. 1.7. Follow-up evaluation After the procedure, the patients were monitored for 24 h in the intensive care unit prior to discharge. Each patient came back to the clinic every 2 weeks in the first month, then every 3 months in the first year, and every 6 months in the following years. 1.8. Statistical analysis All parametric data of the continuous variables were expressed as the mean ± SD. The data of the clinical and electrophysiologic characteristics between two different patient groups were compared using the Student's t-test. The data of the clinical and electrophysiologic characteristics among 3 or more patient groups were compared using one way ANOVA. The proportions and rates of the incidence between these 2 groups were compared by the Chi-square test with Yates' correction. For validation of the mapping accuracy, the correlation between the contact and noncontact electrograms was explored by calculating the Pearson's correlation coefficients and using the Bland–Altman technique for agreement. Statistical significance was defined as a p value b 0.05. 2. Results 2.1. Antegrade atrial conduction There were two different propagation patterns of the antegrade atrial conduction in our 9 patients. During sinus
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directly enter the apex of Koch's triangle, but instead descended along the tendon of Todaro of Koch's triangle, and approached the AV nodal region via the posterior “slow” pathway input (Fig. 2). 2.2. Retrograde atrial conduction
Fig. 4. A frequency distribution curve of the peak unipolar negative voltage was demonstrated outside and inside Koch's triangle during sinus rhythm. Notice 5.8% of the PNV values less than −0.27 mV were outside Koch's triangle (A) and 11.5% of the PNV values less than −0.27 mV were inside Koch's triangle (B).
rhythm, the antegrade atrial conduction was demonstrated correspondingly to have two distinct wavefronts in 7 cases (Pattern 1): anterior and posterior portions. The anterior one quickly went propagated into the apex of the Koch's triangle, then through the anterior wall of the right atrium and joined with the posterior wavefront in the isthmus region (Fig. 1; left panels, A1–D1); another posterior wavefront rapidly conducted along the crista terminalis (CrT) and entered the summit of Koch's triangle, propagated through the isthmus, and turned around to approach the AV nodal region via the posterior “slow” pathway input (Fig. 1; right panels, A2–D2). In two cases (Nos. 6 and 7; Pattern 2) the antegrade atrial activation with a short pacing CL was slightly different from that with a long pacing CL. By using atrial pacing with a shorter CL, the propagation of the wavefronts could not
The retrograde atrial activation was evaluated both during the tachycardia and ventricular pacing. The earliest site of the retrograde atrial activation was situated at the apex of Koch's triangle (fast pathway area, n = 2), coronary ostium region (slow pathway area, n = 1), and interatrial septum close to the foramen ovale (Bachmann bundle, n = 1) in 4 patients with the slow–fast form of AVNRT; and between the area of the fast pathway and coronary sinus ostium (so-called intermediate pathway) in 1 patient with the fast–intermediate and 4 patients with the slow–intermediate form of AVNRT. In patient No. 3 with retrograde dual AV nodal pathways, the site of the earliest atrial activation was usually situated in two different locations during ventricular pacing: the apex of Koch's triangle near the AV node–His bundle junction (fast pathway area) with a longer pacing CL, and posterior to the AV node near the orifice of the coronary sinus (slow pathway area) with a shorter pacing CL. In this particular patient, the earliest retrograde atrial activation gradually shifted from the fast pathway region to the slow pathway region with a shortening of the pacing CL rather than a sudden shift (Fig. 3). In case No. 7, the earliest retrograde atrial activation of the fast pathway was unusually low, and located adjacent to the coronary sinus ostium (the typical slow pathway region). The antegrade slow pathway was situated oppositely at the apex of Koch's triangle near the AV node–His bundle junction. After successful ablation of the antegrade slow pathway, there was no AH jump during right atrial extrastimulation. Coronary sinus venography demonstrated a large coronary sinus ostium and persistent left superior vena cava. 2.3. Validation of the noncontact electrograms and voltage distribution The agreement analysis of the voltage and time difference indicated that only 6% and 9% of all recording sites were outside of one standard deviation, respectively. The average distance from the balloon center to Koch's triangle was 27.4 ± 9.1 mm (range from 9.8 to 42 mm). A histogram of the PNV frequency distribution was obtained from a total of 5090 electrograms inside and outside Koch's triangle. According to the unipolar voltage frequency distribution curve, 5% of the PNV values were less negative than −0.27 mV during sinus rhythm. During sinus rhythm, the distribution of the unipolar voltage demonstrated 11.5% of the PNV values less than −0.27 mV were located inside Koch's triangle and 5.8% of the PNV values less than −0.27 mV were located outside Koch's triangle ( p b 0.001) (Fig. 4). The mean unipolar PNV inside Koch's triangle (obtained from 48± 6 mapping sites in each patient) was significantly less
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Fig. 5. Geometric anatomy associated with the activation routes of the retrograde VA conduction in Case No. 2 (upper panel) and Case No. 6 (lower panel) is demonstrated in the left posterior oblique view. Notice that the position of the retrograde conduction routes were both uncommonly low so that transient heart block could easily happen during the previous session of radiofrequency catheter ablation. To avoid the retrograde conduction routes, radiofrequency energy (deep brown dots) was delivered under surveillance of the precise geometric mapping in both cases. Abbreviation: CSO: coronary sinus ostium; FO: foramen ovale; IVC: inferior vena cava; RAA: right atrial appendage; SVC: superior vena cava; TT: tendon of Todaro; TV: tricuspid valve annulus.
negative than the voltage outside Koch's triangle, whether during sinus rhythm (−0.79 ± 0.39 vs. −1.30 ± 1.03 mV; p b 0.001), right atrial pacing with a 600 ms CL (−0.79 ± 0.48 vs. −1.34± 1.33 mV; p b 0.001) or right atrial pacing with a 300 ms CL (− 0.63 ± 0.28 vs. − 1.35 ± 0.94 mV; p b 0.001). The PNV inside Koch's triangle was less negative during shorter right atrial pacing CLs compared to longer pacing CLs (− 0.63 ± 0.28 vs. − 0.79 ± 0.48 mV; p b 0.001) and sinus rhythm (− 0.63 ± 0.28 vs. − 0.79 ± 0.39 mV; p b 0.001; p b 0.001). The ratio of the mean PNV inside Koch's triangle to the maximal PNV of the global right atrium was 21.6 ± 9.0% during sinus rhythm, 18.3 ± 7.3% during right atrial pacing with a 600 ms CL, and 15.6 ± 5.8% during right atrial pacing with a 300 ms CL ( p b 0.001). During both sinus rhythm and right atrial pacing, the mean unipolar PNV in the lower one-third of Koch's triangle was less negative than that in the upper one-third (−0.67 ± 0.21 vs. −1.45 ± 0.43, p b 0.001; −0.78 ± 0.35 vs. −1.59 ± 0.38 mV, p b 0.001) and middle one-third (−0.67 ± 0.21 vs. −1.07 ± 0.29, p b 0.001; −0.78 ± 0.21 vs. −0.99 ± 0.62 mV, p b 0.05) of Koch's triangle in these patients. 2.4. Results of the radiofrequency catheter ablation Using sequential ventricular extrastimulation, we delineated the earliest atrial activation area of the retrograde conduction (Fig. 5). In 3 of our patients (Cases No. 2, 6
and 7), the location of the retrograde conductions area was observed to be uncommonly low so that transient heart block could be easily induced during the previous session of the RF catheter ablation, even when the ablation site was at the usual target location. Based on the geometric mapping, we were able to avoid applying the RF energy on the retrograde conduction routes. Accelerated junctional rhythm without AV block in 8 patients was demonstrated during the successful radiofrequency catheter ablation. Prolongation of the PR interval (from 150 to 230 ms) occurred in 1 patient during the first RF energy application (a total of 8 s) because the ablation lesion was just on the border of the fast pathway region in that case (Fig. 5; lower panel). After the ablation procedure, neither rapid pacing nor extrastimulation could induce any tachycardia with or without an isoproterenol infusion. The distance between the successful ablation lesions and the lowest border of the retrograde conduction area was significantly shorter in the patients with the slow–intermediate form of AVNRT than in those with the slow–fast form of AVNRT (5.5 ± 3.4 vs. 15 ± 7.6 mm; p b 0.05). The successful ablation site in the patient with the fast–intermediate form of AVNRT was located significantly higher than that in the other patients. After the ablation procedure, no tachycardia could be induced by either rapid pacing or extrastimulation in all these cases. There was no recurrence noted during the follow-up period (10.3 ± 5.4, 2 to 22 months).
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3. Discussion 3.1. Major findings To the best of our knowledge, this study was the first use of noncontact mapping to guide the successful ablation in difficult AVNRT cases associated with a high risk of AV block or other atrial arrhythmias. This study characterized two different patterns of the antegrade conduction and identified the earliest site of the retrograde conduction during sinus rhythm and decremental pacing. Furthermore, Koch's triangle demonstrated a significantly lower voltage than the rest of the right atrium, and the lower one-third of Koch's triangle demonstrated a significantly lower voltage than the rest of Koch's triangle. 3.2. Concept of AV nodal reentrant tachycardia 3.2.1. Antegrade AV nodal inputs The input hypothesis of the AV node has been previously proposed by several investigators [9,10]. However, there has been no evidence for the presence of a distinct anterior input into the AV node. Based on the optical mapping data and microelectrode recording, the previous study proposed a model for AV nodal impulse propagation [11]. The impulse appeared to conduct rapidly over the atrial tissue and slowly toward the AV node through the transitional zone surrounding the AV node. All of the atrial tissue enveloping Koch's triangle delivered impulses to the AV node, strongly suggesting that multiple nondiscrete AV nodal inputs were present. Some investigators arbitrarily divided these nondiscrete AV nodal inputs into the so-called fast pathway, slow pathway, and intermediate pathway. McGuire et al. suggested that the atrionodal connection closest to the His bundle was the preferred route of conduction through the AV node during normal AVor VA conduction, and that part of slow AV nodal pathway may lie outside the compact AV node [12,13]. Previous animal studies demonstrated that the antegrade conduction over the slow pathway existed in all normal hearts with or without AVNRT, but did not become manifest because propagation over the fast pathway reached the AV node first [11,14]. In the present study, 7 cases had similar patterns of the antegrade conduction no matter whether it was before or after the “jump” phenomenon. This finding was similar to the previous studies that suggested that no direct relationship existed between the “jump” and AV nodal input pathways [11,15]. This finding may be explained by the abrupt conduction delay within the AV node through the same atrionodal input. However, the propagation of the wavefronts in the other two cases could not spread directly toward the apex of Koch's triangle during atrial pacing with shorter CLs, but instead appeared to approach the AV nodal region via the posterior “slow” pathway input. This particular phenomenon may be caused by: 1) previous ablation lesions, 2) local fibrosis due to the older age or, 3) local functional block due to a negative balance of the source and sink [12,13,16].
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3.2.2. Retrograde AV nodal conduction This study demonstrated that the sites of the earliest retrograde atrial activation were conspicuously located at different sites among our patients with slow–fast, slow– intermediate and fast–intermediate forms of AVNRT. McGuire et al. had demonstrated the retrograde conduction with high-resolution mapping by using sixty electrodes during open-heart surgery [17]. However, another previous study by Anselme et al. showed that retrograde atrial activation over the fast pathway was heterogeneous within Koch's triangle and the coronary sinus during different modes of activation [18]. They emphasized that some challenging cases with complete heart block during the energy delivery may be caused by the anatomic heterogeneity and potentially dynamic properties of retrograde AV nodal conduction. To the best of knowledge, the present study is the first study to investigate the retrograde conduction by using high-resolution noncontact mapping in different types of AVNRT. Furthermore, the sites of the earliest retrograde atrial activation gradually shifted from the fast pathway region to the slow pathway region during shortened pacing CLs, rather than a sudden shift in the patients with retrograde dual AV nodal pathways. This phenomenon may imply that 1) the VA interval prolongation during shortened pacing CLs may be caused by a conduction delay inside the AV node or by a change in the location of the exit sites from the AV node; and 2) anisotropic conduction and the distributed cell layers inside Koch's triangle may contribute to the VA conduction delay. Previous studies demonstrated that functionally fast AV nodal pathways may be located in the posteroseptal right atrium, where slow pathway modification is performed [19]. In case No. 7 in the present study, the earliest retrograde atrial activation of the fast pathway was unusually low (adjacent to the coronary sinus ostium) while the antegrade slow pathway was oppositely situated at the top of Koch's triangle. Failure to recognize the presence of posterior fast AV node pathways may account for sporadic occurrences of AV block, complicating the ablation in patients with AVNRT. Coronary sinus venography demonstrated a large coronary sinus ostium and a persistent left superior vena cava. A large coronary sinus may have contributed to the complicated atrionodal input in that case. 3.2.3. Koch's triangle and the electrogram voltage Simultaneous intracellular and extracellular electrograms showed that the downstroke of the unipolar electrogram indicated the local activation [20]. Furthermore, the sections of the unipolar electrogram occurring before or after the downstroke of the deflection are caused by activation fronts distant from the recording sites [21], and the fundamental advantage of applying the unipolar electrograms also demonstrates that the voltages of the unipolar recording do not vary with the direction of the electrode axis as those of the bipolar recordings. Previous studies also indicated that the peak-to-peak voltages of the unipolar electrogram are
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determined primarily by the distant excitation waves instead of the local activation [22,23]. Previous studies demonstrated at least two distinct groups of atrionodal connections that may result from different cell types and anisotropic conduction [2,17,24,25]. McGuire et al. used a high-density plaque electrode, introduced during openheart surgery, to simultaneously acquire a large number of signals from a defined region. They demonstrated double potentials and fragmented potentials inside Koch's triangle [2,25]. Thus, the electrogram characteristics inside Koch's triangle would be expected to display a relatively lower range of voltages. In the present study, we demonstrated a similar result in the isopotential maps and virtual electrograms that were exported and analyzed from the noncontact mapping system. Koch's triangle did reveal a lower range of voltages as compared to outside Koch's triangle during sinus rhythm and atrial pacing, possibly due to the transitional cell distribution including multiple layers and anisotropic conduction. Furthermore, the lower one-third of Koch's triangle demonstrated the lowest voltage zone in our patients. In previous studies, this region was composed of a posterior extension to the AV node which included AV junctional cells and muscle fibers parallel to the tricuspid valve annulus [24,26]. The AV junctional cells in the posterior extension appear to participate in the slow pathway conduction and resemble nodal cells in their cellular electrophysiology, response to adenosine, and lack of connexin-43 [24]. In addition, the non-uniform distribution of the muscle fibers contributed to the slow conduction and low voltage. The specific electrophysiologic characteristics in the lower one-third of Koch's triangle could provide supplementary information to identify the slow pathway region and to guide the RF ablation of AVNRT. According to the previously published literature from this laboratory, there is a high correlation between the contact and noncontact electrograms when the distance from the mapping sites to the balloon center is less than 38 mm [27]. In our study group, the average distance from the balloon center to Koch's triangle for each patient was 27.4 ± 9.1 mm. 3.2.4. Catheter ablation Treatment of patients with AVNRT by ablation of the slow AV nodal pathway typically has a high success rate and a low complication rate, but inadvertent AV block may sometimes occur. Previous studies demonstrated that functionally fast AV nodal pathways might be located in the posteroseptal right atrium, where slow pathway modification is performed conventionally [19]. In those studies, RF ablation of the retrograde fast pathway affected the antegrade fast pathway, and the location of the antegrade and retrograde fast pathways may be anatomically similar [28,29]. In this study, we additionally characterized the sequential nature of the retrograde atrial activation route and thereby avoided the occurrence of AV block. Recognition of the activation route of retrograde conduction and acquisition of a precise 3D geometry may help avoid inadvertent AV block in certain difficult cases undergoing RF catheter ablation of AVNRT. In the present study, two patients failed the ablation in the previous ablation
sessions because of repeated episodes of AV block during the RF energy applications, however, they did not have highdegree AV block in the present study. In the conventional ablation treatment approach using only fluoroscopy, the successful ablation site of the slow pathway is usually located in the bottom one-third of Koch's triangle (near the coronary sinus ostium) and far from the usual AV node. However, in some particular cases, inadvertent AV block may occur when the region of the slow pathway is located in the middle or even the top onethird of Koch's triangle. The atrionodal input in those cases was remarkably different from that in the typical cases, possibly due to a peculiar distribution of the AV nodal cells and coronary sinus structure. Therefore, detailed localization of the retrograde fast pathway exit site and angiographic imaging of the coronary sinus anatomy may be necessary in some difficult cases before the catheter ablation of AVNRT. 4. Limitations Because this study group only included the difficult AVNRT cases, more studies need to characterize in more detail the atrial conduction into and out of Koch's triangle and to more fully assess the clinical relevance. The AV node proper may present signals as low voltage potentials that are even smaller and may be below the sensitivity of the noncontact recording, however, the feasibility of recording these potentials has not yet been evaluated. 5. Conclusion Noncontact three-dimensional mapping can identify the atrionodal inputs of the antegrade and retrograde conduction, demonstrate the geometry of Koch's triangle, and assess the electrophysiologic characteristics inside and outside of Koch's triangle. The precise geometry acquired by the noncontact mapping system may help avoid inadvertent AV block in some difficult cases undergoing catheter ablation of AVNRT. References [1] Jackman WM, Beckman KJ, McClelland JH, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med 1992;327:313–8. [2] Tai CT, Chen SA, Chiang CE, et al. Multiple antegrade atrioventricular node pathways in patients with atrioventricular node reentrant tachycardia. J Am Coll Cardiol 1996;28(3):725–31. [3] Tai CT, Chen SA, Chiang CE, et al. Complex electrophysiological characteristics in atrioventricular nodal reentrant tachycardia with continuous atrioventricular node function curves. Circulation 1997;95 (11):2541–7. [4] Tai CT, Huang JL, Lin YK, et al. Noncontact three-dimensional mapping and ablation of upper loop reentry originating in the right atrium. J Am Coll Cardiol 2002;40(4):746–53. [5] Schilling RJ, Peters NS, Davies DW. Simultaneous endocardial mapping in the human left ventricle using a non-contact mapping catheter: comparison of contact and reconstructed electrograms during sinus rhythm. Circulation 1998;98:887–98.
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