© 2004 by European Society of Cardiology
Copyright © 2004, European Society of Cardiology
Atrioventricular nodal fast pathway modification: mechanism for lack of ventricular rate slowing in atrial fibrillation
aDepartments of Cardiovascular Medicine and Molecular Cardiology, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Research Building FF1-02, Cleveland, OH 44195, USA
bMaurice Lev Congenital Heart and Conduction System Center, The Heart Institute for Children, Hope Children's Hospital, Oak Lawn, IL, USA
* Corresponding author. Tel.: +1-216-445-6637; fax: +1-216-445-4168. mazgalt{at}ccf.org
Received 18 September 2003; revised 24 October 2003; accepted 27 October 2003
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Abstract |
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 Top Abstract 1. Introduction2. Methods3. Results4. DiscussionReferences |
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Objectives: Atrioventricular node (AVN) modification is one of the alternatives for ventricular rate control in patients with drug refractory atrial fibrillation (AF). However, the underlying mechanisms, and in particular the role of the dual pathway electrophysiology is not clear. By using a novel index, His electrogram (HE) alternans, we have previously demonstrated in rabbits that both the slow (SP) and the fast pathways (FP) are involved in AVN conduction during AF. This electrophysiological–morphological study was designed to address the role of selective FP ablation on AVN conduction during AF. Methods and Results: In 12 rabbit AVN preparations dual pathway conduction was confirmed by HE alternans during A1A2 pacing protocol, as well as during AF. On average 48% of the conducted beats during AF utilized the FP. Selective FP ablation (n = 12) guided by HE alternans resulted in only-SP conduction, with longer AVN conduction time at basic beats, but without change of AVN effective refractory period (ERP). Interestingly, despite elimination of all FP-conducted beats during AF, the selective FP ablation allowed previously concealed SP beats to be conducted, resulting in little net effect on the ventricular rate (average His–His interval 199±10 ms before versus 201±13 ms after FP ablation, p>0.05). Morphological evidence indicated that FP ablation created lesions within the transitional cells of the superior approaches at the junction between the central fibrous body and the AVN. However, extension of FP ablation lesion into the compact AVN domain resulted in non-selective AVN modification and slowing of ventricular rate during AF. Conclusions: Despite its longer ERP, FP is responsible for a substantial number of ventricular beats during AF. However, selective FP ablation has a minor effect on ventricular rate. The most likely mechanism for this phenomenon is that FP ablation allows previously concealed SP beats to be conducted. On the other hand, ventricular rate slowdown could be achieved if FP ablations caused collateral damage in the compact node. This study highlights the usefulness of HE alternans as a novel tool to monitor dual pathway conduction during AF and to guide AVN modification.
KEYWORDS Atrial fibrillation; Ablation; Arrhythmia (mechanisms); AV-node; Conduction system; Supraventricular arrhythmia; Rabbit; Dual pathway electrophysiology
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1. Introduction |
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TopAbstract1. Introduction2. Methods3. Results4. DiscussionReferences |
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Atrioventricular node (AVN) modification (i.e. partial impairment of conduction by ablation) has emerged as one of the alternatives for ventricular rate control in patients with drug-refractory atrial fibrillation (AF). Although it is being used clinically, the mechanisms underlying AVN modification are not clear [1–4].
Since AVN modification for rate control during AF targets similar anatomical sites as the ablations of the fast pathway (FP) and slow pathway (SP) in patients with AVN reentrant tachycardia (AVNRT), it has been speculated that the modification procedures involve the dual pathway electrophysiology [1–3,5]. Clinical practice has indicated that the anterior septal (i.e. the FP) approach for AVN modification has lower success rate and higher incidence of AVN block compared with the posterior (i.e. the SP) approach, leading to empirical recommendation that AVN modification should target the SP rather than the FP [1–3,5]. The mechanistic basis for such conclusion remains unclear.
The simplest reasoning as to why FP-ablation is less effective would be that propagation via FP might not be functioning at all during AF due to its long effective refractory period (ERP). If so, FP-targeted modification should be considered vain a-priori. Such a preposition, however, contradicts clinical reports that in about one third of patients FP-ablation did result in ventricular rate slowing during AF [5]. The difficulty to solve these uncertainties is due in large to the fact that there is no available index to monitor dual pathway electrophysiology during AF. In addition, both experimental and clinical modifications of the FP during AF are guided by anatomical landmarks and are performed without objective quantification of the degree and selectivity of the procedure. Moreover, it has never been shown conclusively whether the procedure indeed modified the FP, or inflicted collateral damage on the AVN itself.
The standard discontinuous conduction curve remains a major index to reveal dual pathway electrophysiology in patients with AVNRT [6]. Clinical studies in such patients demonstrated that after successful SP-ablation and induction of AF, the ventricular rate was slower [7,8]. It is obvious, however, that the causal relationship between this outcome and the SP-ablation remains circumstantial since the direct involvement of either the SP or FP during AF could not be objectively determined. The situation is even more difficult in patients with permanent AF, where the AVN conduction curve cannot be obtained.
Recently, we have demonstrated that a novel index, His electrogram (HE) alternans, can be used to determine the AVN conduction through FP or SP on a beat-by-beat basis [9]. Specifically, at long coupling intervals the FP-wavefront first reaches the superior domain of the His-bundle, resulting in an earlier, high-amplitude superior HE (SHE) and a later, low-amplitude inferior HE (IHE). In contrast, at short prematurities the SP-wavefront first reaches the inferior domain of the His-bundle, producing an opposite phenomenon with earlier, high-amplitude IHE and a later, low-amplitude SHE. By using the HE alternans we have demonstrated for the first time in rabbits that both FP and SP were involved in AVN conduction during AF [10].
We have observed that a significant portion of the conducted beats during AF in the rabbit heart utilize the FP. In fact, after selective SP-ablation all conducted beats propagated exclusively via the FP [10]. Therefore, our simplest working hypothesis was that selective FP-ablation, without inflicting damage to the compact node, should be able to slow the ventricular rate during AF. In order to help resolve the contradictions between such hypothesis and the available clinical observations, we performed the present electrophysiological–morphological study while utilizing the index of HE alternans and addressed the following questions: (1) What is the contribution of the FP to the AVN conduction during AF? (2) Is it possible to selectively ablate the FP without inflicting damage to the compact node? (3) What is the impact of such successful selective FP-ablation on the AVN conduction and ventricular rate during AF? (4) What is the plausible mechanism for the observed outcome?
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2. Methods |
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TopAbstract1. Introduction2. Methods3. Results4. DiscussionReferences |
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This study was approved by the Institutional Animal Research Committee and is in compliance with the "Guide for the Care and Use of Laboratory Animals" published by the National Institutes of Health (Publication #85-23, revised 1996).
2.1 Rabbit AVN preparations
The experiments were performed on 12 New Zealand white rabbit atrial-AVN preparations that were instrumented as previously described [9,10]. Briefly, after sodium pentobarbital (50 mg/kg) anesthesia, the heart was removed, placed in a glass chamber, and superfused with oxygenated Tyrode's solution (in mmol/l: NaCl 128.5, KCl 4.7, CaCl2 1.3, MgCl2 1.05, NaHCO3 25, NaH2PO4 1.19, and glucose 11.1; pH 7.3–7.4 at 36 °C; saturated with 95%O2/5%CO2; flow rate 35 ml/min). After trimming, the final preparation contained the triangle of Koch and the surrounding right atrial and ventricular tissues [9,10] (photographs of AVN preparations are shown in Figs. 5 and 6
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2.2 Electrical stimulation and recordings
Bipolar leads (0.2 mm spacing) were custom-made from 125-µm Ag-AgCl Teflon-isolated wire and used to record atrial electrograms at the crista terminalis and interatrial septum. Roving bipolar electrodes were used to obtain HE as previously described [9,10]. Although the HE alternans is present in both the SHE and IHE recordings in a complementary (opposite) fashion and both can be used to monitor the His-bundle activation pattern, [9,10] we will use only the IHE for simplicity of presentation. Bipolar, platinum–iridium leads of similar design were used for atrial pacing (2 ms duration, twice the diastolic threshold). All electrodes were positioned with micromanipulators (WPI, M330). An 8-channel, programmable stimulator (AMPI, Master-8) was used for pacing. The recorded signals were amplified and filtered at 50–3000 Hz (Axon Instruments, CyberAmp 380), saved on tape (Vetter Digital, 4000A), and later analyzed by AxoScope (Axon Instruments) at 200 µs per sample per channel.
2.3 Pacing protocol and definition of electrophysiological terms
All preparations were first paced at a basic cycle length (A1A1 interval) of 300 ms. The AVN conduction curve was generated by interposing a premature stimulus A2 after every 20th basic beat A1, and by progressively shortening the A1A2 coupling interval in 5 ms steps until the occurrence of AVN block. The resultant atrial-His conduction times A2H2 were plotted versus A1A2 prematurities. AVN ERP was defined as the longest A1A2 coupling interval at which the A2 beat did not conduct to the His-bundle. AVN functional refractory period (FRP) was determined as the shortest observed His–His (H–H) interval.
AF was simulated by high-rate atrial pacing with random coupling intervals (range 75–125 ms). The custom software permitted the same sequence of pacing intervals to be generated repeatedly. During simulated AF, 2000 H–H intervals were collected and measured to determine the shortest, longest, and average values. The above observations were made in control and repeated after FP-targeted modifications.
Low and high amplitude IHE were defined as the two distinct signal levels of HE recorded from the inferior domain of the His-bundle. Thus, a low-IHE indicates a beat conducted by FP and a high-IHE indicates a beat conducted by SP [9,10].
2.4 FP-targeted modification of the AVN conduction
In the absence of clear criteria for identification of FP location [11–13], we used miniature (<2 mm2) thermoelectric probes to explore by localized cooling the tissue in the superior AVN approaches [9,10]. Multiple positions could be tested since the effect of cooling was prompt and fully reversible. There were no effects on AVN conduction when the cooling was delivered to the tissue above the Eustachian ridge (see Figs. 5 and 6
). Clear effects were noted when cooling was delivered about 1–2 mm below the Eustachian ridge and 1–2 mm proximal to the apex of the triangle of Koch. The probe's position was considered within the FP-domain when moderate cooling (
25 °C) resulted in prolongation of the conduction time of basic beats, but without a significant change in the AVN ERP or the maximal observed AVN delay [11]. Proper positioning was further confirmed by the loss of all low-IHE (i.e. the FP-conduction signature) at any coupling interval and during simulated AF. After these explorations the cooling probe was removed and replaced by an ablation unipolar electrode made of 125-µm Teflon-isolated platinum–iridium wire and mounted on micromanipulator.
Small, point-size permanent lesions were created by delivering constant current pulse (30 mA, 0.5–1 s). We attempted to achieve complete elimination of the FP-signature (i.e. the low-IHE), and such permanent functional block of the FP-conduction was achieved in all 12 preparations with 2.7±0.9 ablations. This was confirmed by repeating the pacing protocol with generation of conduction curves and by recordings during simulated AF. In both cases only high-IHE were present. In addition, the modified conduction curve was shifted upward only in the range of long A1A2 prematurities, while the ERP and the maximum AVN conduction times remained unchanged.
2.5 Extension of FP lesions into the compact node domain
This procedure was performed in order to test the hypothesis that lesions intended to ablate selectively the FP may result in ventricular rate slowing due to inadvertent damage to the compact node. In two of the 12 preparations, after an initial selective FP-ablation was performed as explained above, we moved the ablation electrode 1–1.5 mm inferiorly toward the compact nodal domain. Ablation in this position retained the SP-pattern of conduction established after the initial FP-ablation, but in addition slowed the ventricular rate.
2.6 Morphological examination
After completion of the electrophysiological observations and ablations, the AV conduction system was studied by serial sectioning. The sections were made perpendicular to the endocardial surface and oriented, in general, parallel to the AV conduction axis. As described previously [14] sections were cut at 7-µm steps and each 10th section was retained. Alternate sections were stained by hematoxylin–eosin or Weigert–van Gieson stains. In this manner, the consecutive sections permitted examination of all major components of the conduction system, including the inferior approaches, the AVN, the superior approaches and the penetrating His-bundle. During the examination of multiple sections, a special attention was paid on determining the sites where the ablation procedures had created lesions.
2.7 Statistical analysis
All data are expressed as mean±S.D. where appropriate. Comparisons before and after FP-ablation were performed using paired Student's t-test. A value of P<0.05 was required for statistical significance.
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3. Results |
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TopAbstract1. Introduction2. Methods3. Results4. DiscussionReferences |
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3.1 Use of localized cooling to guide the FP-targeted modification
As explained in Section 2, the probe was positioned sequentially in several (typically 3–4) spots and progressive cooling was applied. At the proper position, a graded elimination of FP-conduction was achieved by cooling the tip moderately in the range 35–25 °C. Fig. 1 illustrates the observations in one heart during simulated AF. Note that in control at 36 °C (A) the FP-conduction was present, in this heart, in 60% of the beats (low-IHE, *). Cooling to 31 °C (B) eliminated most of the low-IHE so that only 25% of all beats were conducted via the FP (low-IHE, *). At 26 °C the FP signature was completely eliminated and the conduction utilized exclusively the SP (C, high-IHE). However, this progressive cooling did not slow the heart rate. Note that the total number of conducted beats in IHE trace did not change for the same time interval, suggesting that elimination of low-IHE was compensated by the appearance of "new", previously not seen high-IHE. After exploration with the cooling probe, ablation lesion was created at the same spot to produce permanent FP-ablation, as explained below.
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3.2 FP-ablation effects on His-electrogram alternans and AVN conduction curve
Fig. 2 shows one example of the effects of selective FP-ablation on the AVN conduction curve and the IHE corresponding to each A1A2 prematurity. In control (panel A, and panel C-filled circles) the IHE indicated that the transition between the FP and SP occurred at A1A2=175 ms. The FP-ablation (panel B, and panel C-open circles) eliminated HE alternans seen in control, so that only high-IHE were recorded after the ablation (B) indicating that only the SP was now operative at all prematurities. The conduction curve (C-open circles) showed an upward shift (prolonged AVN conduction times) at basic beats and long prematurities, while the maximum achievable conduction time and the AVN ERP were not altered, suggesting an uninterrupted SP-conduction [11].
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We were able to achieve selective FP-ablation in all 12 preparations. Table 1 summarizes the average results. Note that FP-ablation prolonged the basic AVN conduction times, but did not change AVN ERP, AVN FRP, as well as maximal AVN conduction times.
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3.3 Selective FP-ablation and ventricular rate during simulated AF
Fig. 3 shows one example of the effects of FP-ablation on dual pathway conduction and ventricular rate during simulated AF. Before ablation (panel A), both wavefronts were participating in AVN conduction as evident from the presence of high and low (stars) amplitude IHE. After successful FP-ablation (panel B), only high-IHE was seen, suggesting that functionally only SP-conduction remained. Although the ablation eliminated HE alternans, it did not prolong the average H–H intervals. As during the cooling experiments (see above), the reduction in the number of beats with FP-signature was compensated by the appearance of new beats with SP-signature. Table 2 summarizes the shortest, the average and the longest H–H intervals, and the percentage of low- and high-IHE in 12 preparations before and after FP-ablation. The FP-ablation resulted in an exclusive SP-conduction during simulated AF, but it did not change the shortest and the average H–H intervals (all P>0.05), although the longest H–H interval was slightly increased.
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It is usually assumed that the shortest H–H intervals observed during AF are an estimation of the FRP of the node [15]. Since the shortest H–H intervals remained unchanged after selective FP-ablation, we concluded that this functional characteristic of the AVN should be related to conduction via the SP. Fig. 4 provides supportive evidence from one experiment, and similar findings were obtained in other experiments as well. In this case 1069 H–H intervals (out of a total of 2000 consecutive beats) were designated as SP-related since they terminated with a high-IHE. The remaining H–H intervals were termed FP-related. Note that in control (panel A) the shortest H–H were indeed SP-related, while intervals terminating with a low-IHE were longer. After selective FP-ablation (panel B) all 2000 intervals were SP-related. The shortest H–H (i.e. the AVN FRP) did not change (157 ms in A, 157 ms in B). The average H–H interval (which is directly linked to the ventricular rate) also did not change (arrows, 208 ms in A, 209 ms in B) since the FP-related intervals were replaced, on average, by comparable in length SP-related intervals.
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3.4 Morphological findings after FP-ablation
Serial sections revealed that successful FP-ablation created a lesion within the superior transitional cells at the "bottle neck" between the central fibrous body and AVN (Fig. 5). No substantial morphological damage was evident in the compact node. This suggested that carefully placed lesions in the anterior AVN approaches could selectively eliminate the FP signature in the HE.
As previously explained in Section 2, in two preparations after successful selective FP-ablation an additional lesion was created approximately 1–1.5 mm inferiorly toward the compact node domain. In the preparation illustrated in Fig. 6 (left) the selective FP-ablation was first achieved with lesions 1 and 2. (Lesion 2 was needed to eliminate few residual low-IHE observed after lesion 1). Morphological examination confirmed that these two initial ablations were limited to the superior approaches, similar to the observations made in Fig. 5. The additional inferior lesion (point 3), however, inflicted partial damage within the AVN compact region (Fig. 6, right). The electrophysiological consequences of these morphological alterations are illustrated in Figs. 7 and 8.
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As seen from the conduction curve in Fig. 7, after the initial FP-ablations (points 1, 2 in Fig. 6) the conduction times prolonged at longer prematurities (open circles), but there was no change of either the longest A2H2 intervals or the ERP of the AVN. After the lesion at point 3 (Fig. 6), however, the ERP prolonged from 95 to 165 ms and all conduction times also significantly prolonged (Fig. 7, triangles). This suggested that, following selective FP-ablation, the additional modification of the AVN inflicted partial damage to the remaining functional SP.
This was further confirmed by the observations during simulated AF (Fig. 8). Note that in control (panel A) one could easily identify in the IHE trace the signatures of both the FP (low-IHE, stars) and the SP (high-IHE). After the ablations in points 1 and 2 (Fig. 6), the IHE trace contained only high amplitude electrograms (Fig. 8, panel B), indicating that the conduction to the bundle of His was now utilizing only the SP. As previously discussed, the ventricular rate remained virtually unchanged (average H–H=234 ms in panel A, vs. 231 ms in panel B). After lesion 3 (Fig. 6) the IHE trace still contained only the SP-signature (Fig. 8, panel C, high-IHE), but now the ventricular rate was significantly slowed (average H–H=334 ms).
Thus lesions placed in close proximity and inferiorly to the sites of successful selective FP-ablation could inflict collateral damage to parts of the compact node, and therefore, slow the ventricular rate as a result of an overall nonselective FP plus SP modification.
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4. Discussion |
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4.1 Major findings
This study confirmed the concept that FP- and SP-wavefronts are functional entities that coexist during the propagation of each conducted beat. At long prematurities the FP-wavefront is leading, while the posterior SP-wavefront remains concealed until FP is blocked (or delayed) at shorter prematurities. During AF, the propagated beats utilize either the SP or the FP. Selective FP-ablation has no significant effect on H–H intervals, since newly manifest SP beats maintain the ventricular rate unchanged. This confirms that SP is a major determinant of ventricular rate during AF, and explains why its ablation produces consistent rate slowing [1,2,4,10]. The present study has further demonstrated that HE alternans provide an essential tool to monitor dual pathway conduction and guide AVN modification during AF.
4.2 HE alternans versus conduction curve in evaluation of dual pathway conduction
Based on the changes in the AVN conduction curve after SP or FP modifications, the concept that FP-conduction has relatively short AV delays and blocks easier due to longer ERP is well accepted [10,11,16,17]. However, especially in the absence of conduction discontinuity ("jump"), [6,18] one cannot determine with certainty at which prematurity the transition from FP to SP takes place, and whether a lesion results in full or partial ablation of the affected conduction pathway.
The HE alternans permitted to determine precisely the prematurity at which transition from FP to SP occurred (Fig. 2) and to confirm that, once the FP was successfully eliminated, the SP became manifest and sustained AVN conduction at both long and short prematurities. Such was the case illustrated in Fig. 6. In that preparation judging only by the conduction curve lesion 1 would be deemed successful. In fact successful elimination of the FP-wavefront was achieved only after lesion 2 and the established SP-conduction was documented by high-IHE during both basic and premature beats, and simulated AF (Fig. 8B). In this regard, HE alternans were more sensitive tool than the conduction curve to reveal the transition between the two wavefronts.
4.3 FP-targeted modification of AVN conduction during AF
Based on the HE alternans this study clearly demonstrated that dual pathway conduction was present during simulated AF (Figs. 1, 3, 8). This confirmed previous observations [10]. Since a large portion of beats was conducted by FP during AF, it was logical to speculate that selective FP-ablation might have significant effect on ventricular rate. The present results, however, did not support this expectation.
During simulated AF, successful FP-ablation resulted in elimination of all low-IHE (Figs. 3, 8). However, there was no significant change in either the average or the shortest H–H intervals (Table 2). While the average H–H interval is a direct measure of the ventricular rate, the shortest H–H interval is thought to represent the FRP of the AVN during AF [15].
The fact that the removal of the FP-conduction had such negligible effects during AF may initially appear unexpected, in view of the fact that before ablation 48% of the conducted beats were with FP-signature (i.e. low-IHE). This apparent discrepancy can be explained if one assumes that SP was actually present during every conducted beat. However, successful conduction via the FP produced a concealment of the delayed SP-wavefront, [19] which did not reach the His-bundle. This was obvious during the generation of the conduction curves (Fig. 2) when the FP-ablation replaced all low-IHE with high-amplitude spikes (i.e. SP-conduction). Similarly, during AF, the FP-ablation simply revealed the presence of the previously concealed SP-wavefront while the average rate of successful His-bundle penetrations remained unchanged.
Anatomically the lesions that produced selective FP-ablation were limited to quite a small area near the apex of the triangle of Koch. Therefore, it is conceivable that inadvertent damage to the compact AVN region could be inflicted during the procedure. Partial injury of the compact node would slow the ventricular rate [7]. We have done this deliberately and confirmed that such morphological damage of the SP results in slower ventricular rate during AF (Figs. 6–8). These results not only provide explanation for the clinical observations that ablations using the AVN superior septal approach for control of ventricular rate in AF have minimal effect in most patients, but also provide explanation that collateral damage of the compact node might be responsible for rate slowing observed in a small portion of patients [3,5].
4.4 Substrate of FP and functional model of dual pathway electrophysiology during AF
The morphological evidence indicated that selective FP-ablation created a lesion within the superior transitional cells between the central fibrous body and the AVN. However, the compact AVN remained intact (Fig. 5). These results are consistent anatomically with a model of dual pathway electrophysiology according to which the FP utilizes the "bottle neck" formed by the superior transitional cells between the central fibrous body and the compact AVN that reach the superior domain of the His-bundle [9].
According to such model, three basic scenarios could be encountered during AF depending on the prematurity and/or the organization of the atrial-AVN engagement (Fig. 9, panels A–C). In Fig. 9A (for beats with longer coupling intervals), the FP-wavefront (green) propagates through transitional cells' region ahead of the SP-wavefront (orange), invades the superior domain of the His-bundle, and transversely activates the inferior domain generating low-IHE. At that time, the delayed SP still transverses the posterior nodal extensions, encounters the refractory tail of the FP, and remains concealed. Panel 9B illustrates the alternative situation (e.g. during shorter coupling intervals) when a beat is propagated via the SP-wavefront (blue). Note the reversed sequence of engagement of the His-bundle, with the inferior domain depolarized longitudinally, resulting in a high-IHE signal. Panel 9C illustrates a beat with excessive prematurity for which the FP blocks due to its longer ERP, while the SP is still capable of conduction and generates again high-IHE. Panels A–C thus show how random engagement during AF of the superior and inferior His domains by the FP and SP, respectively, produces the characteristic alternating HE (alternans) seen in Figs. 1, 3 and 8. Finally, panel 9D shows the end-result of successful selective FP-ablation. Note that now all beats are being conducted in the SP-domain with high-IHE. The beats conducted by the FP before the ablation (panel A, green) have been carried via the SP after the ablation (panel D, orange).
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The proposed model, although only intended for conceptualization purposes, indicates that anatomical and functional asymmetry of the atrial-nodal-His connection can support dual pathway electrophysiology without requiring the presence of specific isolated cable-like structures [19]. Recent experimental mapping studies support this view [20,21].
4.5 Study implications and limitations
In addition to providing a deeper understanding of the dual pathway AVN electrophysiology, our results may have important implications with respect to the AVN modification during AF. FP-ablation had minute effect in slowing ventricular rate during AF. The most likely mechanism for this phenomenon is that FP-ablation allows previously concealed SP beats to be conducted. Slower rate could be achieved only if ablations also caused collateral damage in the compact nodal region (Figs. 6–8). The latter procedure is obviously very risky, since inadvertent complete AVN block can be easily produced. Therefore, the safer site for application of the SP modification should be the posterior/inferior approaches. We have previously demonstrated that SP-ablation in this manner invariably resulted in slowing of ventricular rate during AF while preserving the compact nodal region intact [10].
It should be noted that while FP-ablation procedures in this study were deemed successful based on the observed functional responses, we could not be sure if the propagation in the FP-domain was fully interrupted. It could be inferred from the model (Fig. 9) that elimination of the FP signature in the His-recording would also be observed if the wavefront were just sufficiently delayed relative to the SP.
This as well as our previous studies, [9,10] reiterate that dual pathway electrophysiology is a normal, inherent property of the AVN in rabbits. As we acknowledged before, [10] although HE alternans have been demonstrated in rabbits as well as in canines, [22] and most likely exist in humans as well, [23,24] further clinical evidence is needed in order to establish the existence of this novel index and its usefulness in patients.
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Acknowledgements |
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This study was supported in part by grant from NIH (NHLBI RO1 HL60833).
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Notes |
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Time for primary review 29 days
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