(Circulation. 1997;95:2541.)
© 1997 American Heart Association, Inc.
Articles |
Complex Electrophysiological Characteristics in Atrioventricular Nodal Reentrant Tachycardia With Continuous Atrioventricular Node Function Curves
From the Division of Cardiology (C.-T.T., S.-A.C., C.-E.C., Z.-C.W., C.-W.C., K.-C.U, Y.-J.C., W.-C.Y., M.-S.C.), Department of Medicine, School of Medicine, National Yang-Ming University, and the Veterans General Hospital-Taipei, Taipei, and Shin-Kong Memorial Hospital (S.-H.L.) and Veterans General Hospital-Taichung (J.-L.H.), Taiwan, ROC.
Correspondence to Shih-Ann Chen, MD, Division of Cardiology, Veterans General Hospital-Taipei, 201, Sec 2, Shih-Pai Rd, Taipei, Taiwan, ROC. E-mail sachen{at}vghtpe.gov.tw
Abstract
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.
Key Words: atrioventricular node • catheter ablation • tachycardia
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.
Methods
Patients
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.
Electrophysiological Study
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.
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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.
Definitions
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.
Statistical Analysis
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 
2 test with Yates’ correction or
Fisher’s exact test was used to compare the categorical data. A
probability value <.05 was considered significant.
Results
Baseline
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.
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Group 1
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.
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).
After critical AH delay, tachycardia was induced (
).
Ablation in the slow-pathway zone resulted in a decrease of
AHmax (
). B, Curve relating A2-H2 interval to
prematurity of atrial extrastimuli (A1-A2). Before ablation, a smooth
curve without evidence of dual AV nodal pathway was present
(
Group 2
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.
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Group 3
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.
Discussion
Major Findings
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.
Study Limitations
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
Conclusions
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
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Acknowledgments
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.
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