Complex Electrophysiological Characteristics in Atrioventricular Nodal Reentrant Tachycardia With Continuous Atrioventricular Node Function Curves
Background Although typical atrioventricular nodal reentrant tachycardia (AVNRT) with discontinuous AV node function curves has been well studied, there has been a lack of any significant information about AVNRT without evidence of dual AV nodal pathway physiology during atrial extrastimulus testing or atrial pacing.
Methods and Results Group 1 included 9 patients with continuous curves during atrial extrastimulus testing but without a jump (≥50 ms) of the atrial–His bundle (AH) interval during incremental atrial pacing. The maximal AH interval during atrial pacing (266±61 versus 168±27 ms, P=.007) or extrastimulus testing (290±60 versus 176±18 ms, P=.005) shortened significantly after ablation. Antegrade and retrograde AV node properties were similar before and after ablation. Group 2 included 14 patients with continuous curves and a jump of the AH interval during incremental atrial pacing. The atrial pacing cycle length with 1:1 AV conduction and effective refractory period (ERP) of the antegrade AV node increased significantly, whereas the maximal AH interval during atrial pacing (358±70 versus 203±28 ms, P=.001) or extrastimulus testing (338±75 versus 196±34 ms, P=.002) shortened significantly after ablation. Group 3 included 24 patients with discontinuous curves. The maximal AH interval during atrial pacing or extrastimulus testing and the ERP of the antegrade fast AV node shortened, whereas the ERP of the antegrade AV node increased significantly after ablation. The maximal AH interval before ablation, extent of decrease in maximal AH interval after ablation, ERP of the retrograde AV node before ablation, and tachycardia cycle length were significantly shorter in group 1 than groups 2 and 3.
Conclusions In AVNRT with continuous AV node function curves, dual AV nodal pathway physiology may or may not be demonstrated during atrial pacing. Significant shortening of the maximal AH interval during atrial pacing after radiofrequency ablation suggests successful elimination of AVNRT.
Typical AVNRT usually has dual AV nodal pathway physiology demonstrated by a discontinuous AV node function curve.1 However, others have shown2 the occurrence of typical AVNRT without this discontinuity when subjects have been tested at multiple cycle lengths, multiple atrial extrastimuli, and varying pacing sites. Although the ratio of the PR interval to the RR interval during rapid atrial pacing provides a method for demonstrating the slow AV nodal pathway conduction in some patients,3 there is a lack of any significant information in patients with AVNRT who do not have evidence of a discontinuous curve during atrial extrastimulus testing or atrial pacing. Furthermore, whether the successful ablation sites in these tachycardias with continuous AV node function curves are different from those with discontinuous curves remains unknown. Thus, the purposes of the present study were to investigate the complex electrophysiological characteristics and to explore the anatomic substrates by using RF catheter ablation in patients who had AVNRT along with continuous AV node function curves.
The study population consisted of three groups of patients. All patients were referred to receive electrophysiological study and RF catheter ablation at Veterans General Hospital-Taipei because of symptomatic AVNRT. Group 1 consisted of 9 patients with continuous AV node function curves and without a jump (≥50 ms) of the AH interval during incremental atrial pacing. Group 2 consisted of 14 patients with continuous AV node function curves and a jump of the AH interval during incremental atrial pacing. Group 3 consisted of 24 patients with discontinuous AV node function curves. No patients had retrograde dual AV nodal pathway physiology.
Each patient underwent a baseline electrophysiological study in a fasting, unsedated state at least five half-lives after discontinuation of antiarrhythmic drugs.4 5 Informed consent for the study and ablation was obtained from each patient. Four multipolar, closely spaced (interelectrode space, 2 mm) electrode catheters (Mansfield Division of Boston Scientific Inc) were introduced from the right and left femoral veins and placed in the high right atrium, His bundle area, posteroseptal aspect of the tricuspid annulus, and right ventricle for programmed electrical stimulation and recording. One orthogonal electrode catheter with the distal 3 cm free of electrodes (Mansfield Division of Boston Scientific Inc) was introduced from the right internal jugular vein and placed in the coronary sinus to record the electrical activity around the posteroseptal and proximal coronary sinus areas. Intracardiac electrograms were displayed simultaneously with ECG leads I, II, and V1 on a multichannel oscilloscopic recorder (model VR-13, PPG Biomedical Systems, Cardiovascular Division) and were recorded on paper at a speed of 100 to 150 mm/s. The filter was set from 30 to 500 Hz. A programmed digital stimulator (DTU-210 or 215, Bloom Associates Ltd) was used to deliver 2.0-ms electrical impulses at approximately twice the diastolic threshold. The standard protocol consisted of right atrial and right ventricular incremental pacing to block and single extrastimulus testing with at least two drive cycle lengths. If dual AV nodal pathways could not be demonstrated, double atrial extrastimuli were tested. All electrophysiological data were collected with the patients in an unsedated state and without the presence of isoproterenol or atropine. In all patients premature ventricular extrastimuli were delivered when the His bundle was refractory during tachycardia. If tachycardia was not induced under the baseline state, isoproterenol (at graded doses from 1 to 4 μg/min IV) or atropine (0.01 to 0.02 mg/kg IV) was infused to facilitate its induction. AVNRT was diagnosed according to standard criteria.6
Mapping and Ablation
To define the possible anatomic sites of the slow pathways, the stepwise upward method was used for mapping and ablation. The right atrial septum adjacent to the septal leaflet of the tricuspid valve, extending from the ostium of the coronary sinus to the recording site at the His bundle area, was divided into posterior, medial, and anterior regions (Fig 1⇓). These regions were further divided into three, two, and two subsections, respectively: posterior-1 (P1), posterior-2 (P2), and posterior-3 (P3) (around the coronary sinus ostium), medial-1 (M1) and medial-2 (M2), and anterior-1 (A1) and anterior-2 (A2).5 The ostium of the coronary sinus was demarcated by coronary sinus venography.
A multipolar, closely spaced (2 mm), deflectable, large-tip (4 mm) electrode catheter (Mansfield Scientific) was used for mapping and ablation. To determine the possible anatomic sites of the slow pathway, the mapping and ablation catheter tip was initially positioned in the posterior area, then the medial, and finally in the anterior areas, if necessary. The presumed ablation site was considered optimal if bipolar electrograms obtained from the distal electrodes showed an AV ratio of 0.1 to 0.5 or a possible slow pathway potential.7 8 An RF generator (Radionic-3C, Radionics, Inc) was used to deliver energy at 30 to 40 W for 20 to 60 seconds. Energy was terminated if a junctional rhythm was not present during 10 seconds of the application, and another ablation site was selected. Energy was also terminated immediately in the event of an increase in impedance, dislocation of the catheter, prolongation of the PR interval, or occurrence of AV block. An attempt to induce AVNRT with evaluation of AV nodal conduction properties was conducted immediately after each application of the RF energy. The end point of the procedure was modification or ablation of the slow pathway with noninducibility of AVNRT with isoproterenol (2 to 4 μg/min IV).
Evaluation After Ablation
An electrophysiological study was performed 30 minutes after the ablation procedure. After hospital discharge, all patients were followed up closely and returned to the outpatient clinic in the second week, the first month, and the second month after ablation, and then every 3 months. Long-term efficacy was assessed clinically on the basis of the resting surface ECG, 24-hour Holter monitoring, and clinical symptoms.
Antegrade AV node conduction curves were drawn from the results of programmed atrial extrastimulus testing. Dual-pathway physiology was characterized by a jump (≥50 ms) in H1-H2 or H2-H3 at a critical range of A1-A2 or A2-A3 coupling intervals (10-ms decrease) that resulted in a discontinuity between the portion of the curve to the right of the jump in H1-H2 or H2-H3 (fast pathway conduction) and the portion of the curve to the left of the jump (slow pathway conduction). Comparable discontinuous A1-A2 versus A2-H2 or A2-A3 versus A3-H3 curves were also demonstrated. Continuous AV node conduction curves were defined as those without a jump of H2-H3 or A3-H3 at all ranges of A2-A3 coupling intervals. A jump of the AH interval during atrial pacing was defined as the difference of any consecutive AH intervals ≥50 ms during incremental atrial pacing, which might be a manifestation of dual AV nodal pathways.2
AHmax was defined as the longest AH interval measured during atrial pacing and extrastimulus testing; it was determined before and after ablation. The ERP of the AV node was defined as the longest A1-A2 or A2-A3 interval measured at the His bundle site that failed to generate a nodal response to a premature atrial extrastimulus. In patients with dual AV nodal pathway physiology, the ERP of the AV node was the ERP of the slow pathway.
All data are expressed as mean±SD. The paired t test was used to compare the continuous data before and after ablation. The ANOVA test was used to compare the continuous data among different groups. The χ2 test with Yates’ correction or Fisher’s exact test was used to compare the categorical data. A probability value <.05 was considered significant.
Group 1 included 6 women and 3 men (mean age, 53±23 years); group 2, 9 women and 5 men (mean age, 54±20 years); and group 3, 14 women and 10 men (mean age, 53±15 years). Age, sex, AH interval, HV interval, and tachycardia cycle length were similar among the three groups. The Table⇓ summarizes the electrophysiological characteristics of the AV node before and after RF ablation in the three groups. Details of each patient are shown in Fig 2⇓.
Sustained typical AVNRT was induced during incremental atrial pacing and/or atrial extrastimulus testing in all patients before ablation. No evidence of dual AV nodal pathway physiology was found during atrial pacing or extrastimulus testing (Fig 3⇓). AHmax during atrial pacing at WCL (266±61 versus 168±27 ms, P=.007) and atrial extrastimulus testing (290±60 versus 176±18 ms, P=.005) shortened significantly after ablation. The AH interval (76±14 versus 78±15 ms) during sinus rhythm, 1:1 antegrade AV nodal conduction (308±28 versus 337±50 ms), ERP of the antegrade AV node (276±31 versus 279±37 ms), 1:1 retrograde AV nodal conduction (308±45 versus 326±41 ms), and ERP of the retrograde AV node (258±32 versus 251±22 ms) were similar before and after RF ablation. All patients had successful elimination of the slow pathway without tachycardia or residual echoes. The mean number of RF energy applications was 2±1. The successful ablation site was located at the posterior zone in 7 (78%) and medial zone in 2 (22%) patients. During the follow-up period of 18±11 months (range, 6 to 45), no patient had a recurrence of tachycardia.
Sustained typical AVNRT was induced during incremental atrial pacing and/or atrial extrastimulus testing in all patients before ablation. No dual AV nodal pathway physiology was present during one and double atrial extrastimulus testing, but an AH “jump” occurred during incremental atrial pacing (Fig 4⇓). The atrial pacing cycle length with 1:1 AV conduction (338±63 versus 380±71 ms, P=.001) and ERP of the antegrade AV node (263±28 versus 320±71 ms, P=.003) increased significantly, whereas AHmax during atrial pacing at WCL (358±70 versus 203±28 ms, P=.001) or atrial extrastimulus testing (338±75 versus 196±34 ms, P=.002) shortened significantly after ablation. The AH interval (75±19 versus 78±18 ms) during sinus rhythm, 1:1 retrograde AV nodal conduction (333±42 versus 344±47 ms), and ERP of the retrograde AV node (285±42 versus 266±52 ms) remained unchanged after ablation. All patients had successful elimination of the slow pathway without tachycardia or residual AH jump or echoes during incremental atrial pacing. The mean number of RF energy applications was 2±1. The successful ablation sites were located at the posterior zone in 11 (79%) and medial zone in 3 (21%) patients. During the follow-up period of 23±13 months (range, 6 to 45), no patient had a recurrence of tachycardia.
Sustained typical AVNRT was induced during incremental atrial pacing and atrial extrastimulus testing in all patients before ablation. Dual AV nodal pathway physiology with a discontinuous curve was demonstrated in all patients. AHmax during atrial pacing at WCL (353±66 versus 162±37 ms, P=.001) or atrial extrastimulus testing (352±54 versus 163±39 ms, P=.001) and ERP of the antegrade fast AV node (311±40 versus 288±36 ms, P=.002) shortened, whereas ERP of the antegrade AV node conduction (267±40 versus 288±36 ms, P=.001) increased significantly after ablation. The AH interval (69±15 versus 68±15 ms) during sinus rhythm, the atrial (326±43 versus 342±45 ms) and ventricular (329±72 versus 336±65 ms) pacing cycle lengths with 1:1 antegrade and retrograde AV nodal conduction, and ERP of the retrograde AV node (272±33 versus 271±44 ms) remained unchanged after ablation. All patients had successful elimination of the slow pathway without tachycardia or residual evidence of dual AV nodal pathway physiology. The mean number of RF energy applications was 2±1. The successful ablation sites were located at the posterior zone in 18 (75%) and medial zone in 6 (25%) patients. During the follow-up period of 28±10 months (range, 6 to 43), no patient had a recurrence of tachycardia.
Comparisons Among Groups 1, 2, and 3
AHmax during atrial pacing (266±61 versus 358±70 versus 353±66 ms, P<.05) or extrastimulus testing (290±60 versus 338±75 versus 352±54 ms, P<.05) before ablation and the extent of decrease in AHmax after ablation during atrial pacing (35±14% versus 42±12% versus 53±14%, P<.05) or extrastimulus testing (36±15% versus 42±18% versus 53±13%, P<.05) were significantly shorter in group 1 than groups 2 and 3. The ERP (258±32 versus 285±42 versus 282±33 ms, P<.05) of the retrograde AV node before ablation and tachycardia cycle length (317±34 versus 369±35 versus 370±50 ms, P<.05) were also significantly shorter in group 1 than groups 2 and 3. The other parameters of AV node function and the successful ablation sites were similar among the three groups.
In patients (group 1) with AVNRT but without manifestation of dual AV nodal pathways during atrial pacing and extrastimulus testing, AHmax, ERP of the retrograde AV node, and tachycardia cycle length were significantly shorter than those in patients (groups 2 and 3) with dual AV nodal pathway physiology during either atrial pacing or atrial extrastimulus testing. After successful ablation, AHmax significantly shortened in all three groups, whereas the ERP of the AV node remained unchanged in group 1, although it increased significantly in groups 2 and 3.
Mechanisms of Failure to Demonstrate Dual AV Nodal Pathway Physiology
There are several possible mechanisms to explain the continuous AV node function curves in AVNRT. The functional refractory period of the atrium limits the prematurity with which atrial premature depolarization will encounter the ERP of the AV node, which produces an inability to dissociate the fast and slow AV nodal pathways.2 In the present study, two driven cycle lengths and two atrial extrastimuli were tested in group 1 and 2 patients; thus, the possibility that this mechanism produced continuous AV node function curves is small. The refractory periods of the fast and slow pathways may be similar; thus, more rapid atrial pacing rates, introduction of multiple atrial extrastimuli, or drugs such as propranolol, verapamil, or digoxin may be required to dissociate them.9 10 11 In group 2 patients with continuous AV node function curves, the presence of a sudden AH jump during incremental atrial pacing suggested that dual AV nodal pathways were present with similar refractory periods. Finally, as a demonstration of discontinuity is dependent on a difference between the maximal conduction time of the fast pathway and the minimal conduction time of the slow pathway, an AH jump may not be present during either atrial pacing or extrastimulus testing if this difference in the conduction times of the two pathways is too small.12 13 Thus, the lack of a demonstration of dual AV nodal pathways in group 1 patients may be due to similar refractory periods or conduction times in the dual pathways.
Lessons From RF Ablation
In typical AVNRT with dual AV nodal pathways, successful modification or elimination of the slow pathway with no induction of tachycardia is the usual end point of RF catheter ablation.7 8 14 15 16 17 After ablation, AHmax shortened significantly, whereas the ERP of the AV node prolonged significantly, as shown by the data from group 3.
In group 2 patients with continuous curves and demonstration of dual AV nodal pathways during incremental atrial pacing, the changes of AHmax and ERP of the AV node after successful ablation were similar to those in group 3 patients. Furthermore, successful ablation in the slow-pathway area in these patients resulted in loss of the “tail” of the conduction curve representing the slow pathway.18 These findings were similar to those of Sheahan et al18 and suggested that the smooth AV node function curve in group 2 patients in fact consisted of two distinct components representing both fast and slow AV nodal pathways even when the typical discontinuity was absent. However, Sheahan et al18 did not analyze the change of the AH interval during incremental atrial pacing. In their patients, AH interval jump might be present during incremental atrial pacing. Furthermore, loss of this jump after ablation suggested elimination of the slow AV nodal pathway. The findings in the present study were also similar to the report by Baker et al3 that a PR/RR interval ratio >1.0 during atrial pacing at the maximal rate with stable 1:1 AV conduction is a good indicator of antegrade slow pathway conduction; after slow pathway ablation, the maximal PR/RR ratio became <1.0.
AHmax shortened significantly in group 1 patients without manifestation of dual AV nodal pathways during atrial pacing and extrastimulus testing, but other electrophysiological data remained unchanged after successful ablation. Furthermore, the extent of the decrease in AHmax after successful ablation was the smallest in group 1 patients. These findings suggest that group 1 patients still have slow and fast AV nodal pathways that may have similar refractory periods and conduction times. McGuire et al13 have shown that in 10 dogs with continuous AV node function curves and AV nodal reentrant echo, the WCL of AV conduction and the refractory period of the AV node were not altered after dissection of the posterior atrionodal connections. They considered that the mechanism of cure in AVNRT is damage to the putative atrial segment of the reentrant circuit located in the posterior approaches to the AV node between the coronary sinus orifice and the tricuspid annulus.13 However, further studies are required to determine whether the results from the animal model can be extrapolated to humans.
Stimulating from different sites in the atrium or using pharmacological intervention may have elicited some evidence of dual AV nodal pathway physiology in group 1 patients, but these procedures were not done in this study because they would have affected the electrophysiological data for comparison. An exhaustive attempt using more extrastimuli to demonstrate discontinuities in the AV node function curve was not made because of our reluctance to inadvertently produce atrial fibrillation. The protocol in this study did not include autonomic blockade. Several studies have demonstrated that unstable autonomic tone does not really affect AV node functional properties.19 20
In typical AVNRT with continuous AV node function curves, dual AV nodal pathway physiology may or may not be present during atrial pacing. Nonetheless, significant shortening of AHmax during atrial pacing after RF ablation suggests successful elimination of AVNRT.
Selected Abbreviations and Acronyms
|AHmax||=||maximal atrial–His bundle interval|
|AVNRT||=||atrioventricular nodal reentrant tachycardia|
|ERP||=||effective refractory period|
|H1||=||His bundle potential of the last paced beat|
|H2||=||His bundle potential of the first coupled beat|
|H3||=||His bundle potential of the second coupled beat|
|WCL||=||Wenckebach block cycle length|
This work was supported in part by grants from the National Science Council (NSC 85-2331-B-010-047, 85-2331-B-010-048, and 85-2331-075-071), Taipei, Taiwan, ROC.
- Received August 26, 1996.
- Revision received December 2, 1996.
- Accepted December 16, 1996.
- Copyright © 1997 by American Heart Association
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