(Circulation. 1995;91:1095-1100.)
© 1995 American Heart Association, Inc.
Articles |
Termination of Atrioventricular Nodal Reentrant Tachycardia by Premature Stimulation From Ablating Catheter
A Reliable Guide to Identify Site for Slow-Pathway Ablation
Presented at the 66th Scientific Sessions of the American Heart Association, Atlanta, Ga, November 8-11, 1993.
From the Electrophysiology Laboratory of the Milwaukee Heart Institute of Sinai Samaritan Medical Center and St Luke's Medical Center, University of Wisconsin, Milwaukee Clinical Campus.
Correspondence to Jasbir Sra, MD, 2901 W KK River Pkwy, Suite 470, Milwaukee, WI 53215-3660.
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Abstract |
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Background Slow-pathway ablation is currently used more frequently to control atrioventricular nodal reentrant tachycardia (AVNRT). However, in patients with the common type of AVNRT, successful ablation of the slow pathway can be difficult and time-consuming. We tested a simple method to predict a site for slow-pathway ablation in patients with AVNRT of the common variety.
Methods and Results Twenty patients with symptomatic common AVNRT (13 women and 7 men; mean age, 41±21 years) were included in the study. Once the AVNRT had a stable cycle length (±10 ms) for at least 20 cycles, single extrastimuli were delivered from the ablating catheter tip beginning with 20 ms less than the tachycardia cycle length and decrementing by 10 ms until tachycardia terminated or loss of capture occurred at the pacing site. The pacing protocol was performed systematically in a stepwise fashion at four adjacent sites starting from the posterior/inferior interatrial septum near the tricuspid annulus and moving progressively more anteriorly. The pacing protocol was then repeated in the same sequence, followed by delivery of radiofrequency current at each site to determine its effect at sites where AVNRT could not be terminated with a pacing protocol. AVNRT could be terminated in the anterograde direction from at least one site in 19 patients. Tachycardia could be terminated at two or more adjacent sites in 5 patients. The longest atrial coupling interval at the site of tachycardia termination was 67±27 ms (range, 30 to 130 ms) less than the AVNRT cycle length. Resetting of subsequent His bundle depolarization (H2), producing an H-H2 interval prolongation of 26±24 ms (range, 10 to 80 ms), occurred in 17 patients before termination of the tachycardia. In 18 of the 19 patients, the slow pathway was successfully ablated at the site at which AVNRT was terminated at the longest atrial coupling interval.
Conclusions Termination of tachycardia in the anterograde direction at the longest atrial coupling interval by extrastimuli delivered from the ablating catheter can be helpful for identification of an optimal site for slow-pathway ablation in patients with the common variety of AVNRT.
Key Words: atrioventricular node • catheter ablation • reentry • tachycardia
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Atrioventricular nodal reentrant tachycardia (AVNRT) is one of the most common paroxysmal forms of supraventricular tachycardia.1 2 3 Intracardiac electrogram recordings and programmed electrical stimulation have helped a great deal in improving our understanding of this arrhythmia. The evolution of this knowledge has led to the development of rational therapy, including transcatheter ablation using radiofrequency energy for control of AVNRT.4 5 6 7 8 9 10 11 12
To modify the AV node, slow-pathway ablation is currently performed more frequently as the initial approach.9 10 11 12 Identification of a specific ablation site is possible when retrograde conduction via the slow pathway can be demonstrated or slow-pathway potential is recorded.9 10 11 12 In patients with common AVNRT, however, retrograde slow-pathway conduction is seldom demonstrable, and recording of slow-pathway potential may be time-consuming. A stepwise approach seems more practical and therefore is frequently used, but it often necessitates several blind lesions; hence the need for a better method.10
In this study, we examined the role of slow intranodal pathway penetration of programmed atrial extrastimuli to guide the optimal site for slow-pathway ablation. The purpose of this report is to present our findings and suggest a potential therapeutic role of this relatively simple approach.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patient Population
Twenty patients with AVNRT of the common variety (slow-fast) were included in the study. The mean age (±SD) of these patients was 41±21 years (range, 18 to 81 years); 7 were men and 13 were women. All patients had a history of recurrent palpitations ranging in duration from 6 months to 50 years. One patient also had a history of recurrent syncope. One patient had coronary artery disease. None of these patients had coexistent AV accessory pathways. The inclusion criteria for patients with AVNRT in this study were (1) induction of sustained AVNRT of the common variety by programmed electrical stimulation and (2) a stable cycle length of tachycardia varying by no more than 10 ms over 20 consecutive beats. Patients who also had AVNRT of the uncommon variety in which the slow pathway could be mapped in the retrograde direction were excluded from the study.
Electrophysiology Studies
Before the catheter ablation and
after informed consent was
obtained, each patient underwent a complete electrophysiological
evaluation in a postabsorptive state. All antiarrhythmic medications
were discontinued for at least five half-lives before the study.
Patients were anesthetized with intravenous diprivan. Three quadripolar
electrode catheters were introduced percutaneously via femoral veins
and positioned under fluoroscopic guidance in the high right atrium,
the His bundle region, and the right ventricular apex. A fourth 6F
decapolar electrode catheter was inserted via a jugular vein and
positioned in the coronary sinus. Surface ECG leads (I, II, and
V1), intracardiac electrograms, and time lines were
displayed simultaneously on a multichannel oscilloscope (PPG Midas
system, Biomedical) and printed on a thermal recorder. Programmed
electrical stimulation was performed with a programmable digital
stimulator (Bloom Associates). The stimulation protocol consisted of
atrial and ventricular incremental pacing and extrastimulation. The
induction of AVNRT was attempted repeatedly to determine the most
reliable and reproducible method of tachycardia initiation. The
stimulation protocol was repeated after isoproterenol was infused and
titrated in patients in whom AVNRT could not be induced at baseline. In
patients requiring isoproterenol administration, all
electrophysiological parameters (before and after ablation) were
measured during isoproterenol infusion at the same infusion dose.
Intravenous heparin was administered as an initial dose of 3000 U and
subsequent boluses of 1000 U/h during the procedure. Each patient
underwent a follow-up study 1 day and 6 to 8 weeks after the ablative
procedure.
Pacing Protocol
Pacing was initiated from the radiofrequency
catheter tip at
twice diastolic threshold. Before initiation of the AVNRT, catheter
contact and pacing threshold were determined by pacing from the
catheter tip during sinus rhythm. After tachycardia initiation, single
extrastimuli were delivered with increasing prematurity, beginning with
a coupling interval 20 ms less than the tachycardia cycle length. The
coupling interval was then decreased by 10-ms decrements until one of
two outcomes occurred: tachycardia was terminated, or there was a loss
of capture at the pacing site due to atrial refractoriness.
The pacing
protocol used in this study followed a stepwise approach
used in our laboratory for ablation of the slow pathway.10
As shown in Fig 1
(right anterior oblique [30°]
radiographic view), the region extending from the most posterior
portion of tricuspid annulus adjacent to the coronary sinus ostium to
the His bundle recording site was divided into posterior (P), medial
(M), and anterior (A) sites. In each case, the following steps were
taken to position the ablation catheter. (1) The catheter was
positioned at the His bundle region to record the most distal His
bundle potential. (2) While the deflectable tip was fully bent, the
catheter was slowly withdrawn along the tricuspid septal annulus down
to the most posterior/inferior aspect of the interatrial septum
adjacent to the coronary sinus ostium (site P). This site was
considered optimal for testing if the bipolar recording obtained from
the distal electrode showed an A/V electrogram ratio of 0.1 to 0.5.
After initiation of tachycardia, the pacing protocol was performed
systematically in a stepwise fashion starting from the
posterior/inferior interatrial septum near the tricuspid annulus. Sites
more anterior to the M region (ie, sites A1 and
A2) were not tested. These posterior and medial sites were
chosen because of our cumulative experience showing successful outcome
of slow-pathway ablation at these sites without significant risk of AV
nodal block.10 12 To assess whether radiofrequency
pulses
delivered at the sites at which pacing failed to terminate the
tachycardia were able to eliminate the tachycardia, the ablating
catheter was repositioned at the posterior/inferior aspect of the
interatrial septum. The pacing protocol was repeated in the same order
as above (ie, P1, P2,
M1, and M2, in that order), and
irrespective of whether or not single extrastimuli delivered from the
ablating catheter tip terminated the tachycardia, this was followed by
delivery of radiofrequency current. Programmed stimulation was
performed after each delivery of radiofrequency current to assess
inducibility of AVNRT. If tachycardia was induced, the catheter tip was
advanced more anteriorly to the next adjacent site in a stepwise
fashion. The pacing protocol was repeated before delivery of each
radiofrequency current.
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Ablative Procedure
Radiofrequency current was delivered
between the distal
electrode of the ablating catheter and an external adhesive patch
electrode (Scotchplate 1149C, 3M Co) placed on the chest. The
radiofrequency ablation unit was a Radionics RFG-3C lesion generator.
The ablation catheter was a 7F deflectable quadripolar catheter with a
4-mm bulbous-tip electrode (Webster). In each site, one pulse of
radiofrequency energy (30 to 35 W for 20 to 50 seconds) was delivered
before the catheter was placed in a new site.
Follow-up
Programmed stimulation was repeated at 30 minutes
and 1 day
after a successful ablation. Complete electrophysiological studies were
performed 6 to 8 weeks after the procedure in patients with successful
results. Isoproterenol infusion was routinely used when baseline study
could not initiate AVNRT. All patients underwent two-dimensional
echocardiography/Doppler studies 1 day after the procedure to look for
any complications.
Definition of Terms
All intervals were measured from the
onset of local
electrograms. At least two H-H intervals were measured before and after
the pacing stimulus. All tachycardia cycles are labeled Ae
and H for atrial and corresponding His deflection. The atrial and His
deflections in response to the extrastimulus (S2) are
designated A2 and H2, respectively. The
criteria used to verify AVNRT (common variety) have been discussed in
detail before and were used for the purpose of this study as
well.10 The H-to-H2 interval change was
considered to have occurred if H-H2 minus H-H was at least
10 ms different. The relation between Ae-A2
(prematurity) and corresponding H-H2 throughout the
coupling zone was also measured at each pacing site.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Sustained AVNRT of the common variety (cycle length, 325±42 ms) was induced in all patients (Table
) either during
baseline study (15 patients) or after isoproterenol infusion (5
patients). Dual-pathway physiology was demonstrated in 16 patients
during the electrophysiology study.
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Termination of AVNRT by Premature Extrastimuli
In 19
patients, AVNRT terminated in the anterograde direction by
premature extrastimuli delivered from the tip of the ablating catheter
(Figs 2 through 4). In 14
patients, AVNRT was terminated at only one of the four sites tested by
the atrial extrastimuli. In 5 patients (patients 1 through 5),
tachycardia was terminated at two adjacent sites. In 1 patient (patient
12), the tachycardia was terminated at three adjacent sites. AVNRT
cycle length, the longest atrial coupling interval
(Ae-A2) at which the tachycardia was terminated
by the atrial extrastimuli, and the sites are given in the
Table
. The
longest atrial coupling intervals (Ae-A2) that
resulted in tachycardia termination measured 67±27 ms (range, 30 to
130 ms) less than the tachycardia cycle length. In the 5 patients
(patients 1 through 5) in whom termination was noted from two adjacent
sites, the longest atrial coupling interval causing tachycardia
termination from the two sites differed by 62±19 ms (range, 40 to 60
ms). In the only patient (patient 12) in whom the tachycardia was
terminated from three sites, the longest atrial coupling intervals from
the three sites were 270, 240, and 210 ms, respectively. In the
remaining patient (patient 8) with AVNRT cycle length of 250 ms, the
tachycardia was not terminated by the extrastimuli at any of the four
sites.
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Slow-Pathway Ablation
AVNRT could not be induced in 18
patients after delivery of
radiofrequency current at the site at which termination of AVNRT was
accomplished at the longest atrial coupling interval. Only 2 of these
patients had single AV nodal reentrant echo beat inducible after
ablation despite isoproterenol infusion; hence, no further lesions were
given. The mean power of the pulse that abolished the tachycardia was
32±8 W for 35±10 seconds. The total number of pulses given was
3±1
(range, 1 to 5). The mean procedure time was 131±35 minutes (range, 81
to 209 minutes). In 4 of the 5 patients with termination of tachycardia
at two adjacent sites, radiofrequency current delivered at the sites of
termination with shorter atrial coupling intervals (which were
posterior to the sites of termination with longer coupling intervals)
did not abolish the tachycardia. In 1 patient, tachycardia was not
inducible after ablation at the site of termination with a shorter
coupling interval, 40 ms shorter and posterior to the site of
termination with the longest coupling interval; hence, the effect of
radiofrequency current at the site of termination with the longer
coupling interval could not be evaluated. In the remaining patient
whose tachycardia was not terminated, a stepwise approach was used and
the slow pathway was ablated after four radiofrequency pulses. Thus,
overall, at 18 sites at which pacing terminated the tachycardia, a
single radiofrequency pulse was successful in eliminating the
tachycardia. On the contrary, at 26 other sites at which radiofrequency
pulses were given in this study and pacing either did not terminate the
tachycardia or the tachycardia was terminated at shorter coupling
intervals as well, the radiofrequency pulses were ineffective in
eliminating the tachycardia. The shortest cycle length of 1:1 AV
conduction prolonged from 293±30 to 367±48 ms
(P<.001)
after slow-pathway ablation. AV nodal effective refractory period also
prolonged, from 245±30 to 298±53 (P<.01) ms. The AH
interval and shortest cycle length of 1:1 ventriculoatrial (VA)
conduction remained unchanged.
H-H2 Response to Ae-A2
While
the H-H2 interval was 10 ms shorter (compared
with H-H) in 2 patients before termination of the tachycardia,
H-H2 interval prolongation (mean, 26±24 ms; range, 10 to
80 ms) occurred in 17 patients at the site of termination with the
longest coupling interval (Table). Figs 2 through
4 show examples of
various types of resetting responses in patients 9, 10, and 17. Fig
5 shows H-H2 response to
Ae-A2 at the four sites tested in patients 9
and 10. In these two patients, an H-H2 interval
prolongation was observed at the site of successful slow-pathway
ablation. At other sites, there was minimal H-H2 interval
prolongation or no change, or H2 occurred earlier than
expected. Of the 17 patients with H-H2 interval increase
before termination of the tachycardia, no H-H2 interval
change was observed in 13 patients at longer atrial coupling intervals.
In four patients, H2 activation occurred earlier by 10 ms
at longer coupling intervals, followed by an H-H2 interval
increase at shorter coupling intervals. Fig 4 is a graphic
demonstration of such a response in patient 17.
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Follow-up
None of the patients had inducible AVNRT at 1-day
and 6- to 8-week
follow-up electrophysiology study. During a mean follow-up of 6±3
months, no patient had clinical evidence of tachycardia.
Echocardiography done 1 day after the ablation showed no evidence of
any complications.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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In this study, the termination of AVNRT at the longest coupling interval by premature stimulation from the ablating catheter tip identified the site for successful slow-pathway ablation. It was indeed the slow pathway that was ablated in all of these patients, because after ablation, (1) AVNRT could not be induced; (2) PR and AH intervals remained unchanged; and (3) the shortest cycle length of 1:1 AV conduction and (4) AV nodal effective refractory period were significantly prolonged in all patients.
Previous reports have suggested that the slow pathway can be successfully ablated by either identification of slow-pathway potentials or use of a stepwise approach.9 10 Alternatively, when retrograde slow-pathway conduction can be demonstrated, mapping of the earliest atrial activation can also lead to a successful outcome. This latter approach, although ideal in patients with uncommon (fast-slow) AVNRT, is seldom an option in patients with common AVNRT, because retrograde fast-pathway conduction does not permit evaluation of retrograde slow-pathway propagation even if present. However, in many patients, retrograde atrial activation via the slow pathway may not be demonstrable, even if retrograde fast-athway block was achieved. This indeed was the case in 77% of the patients who underwent retrograde fast-pathway ablation during our earlier experience.10 In the absence of demonstrable retrograde slow-pathway conduction to the atria or identifiable slow-pathway potentials, the anatomic approach remains the only practical method for slow-pathway ablation.
This study, therefore, highlights a rather simple and reliable method of identifying the site for successful slow-pathway ablation in patients with AVNRT of the common variety. At the site of termination of AVNRT with the longest coupling interval, a successful ablation of the slow pathway was achieved in 18 of the 19 patients.
Significance of Resetting by Extrastimuli
Introduction of
premature stimuli during AVNRT may reset the
tachycardia if the premature impulse penetrates the reentrant
circuit.13 14 15 By definition, the
resetting phenomenon is
considered to have occurred if the H-H2 interval is
different from the AVNRT cycle length. Once the A2 impulse
penetrates the AVNRT and resets the tachycardia, A2 is
likely to terminate the tachycardia on further shortening of the
coupling intervals (Ae-A2), unless loss of
atrial capture is encountered. However, the ability to reset and/or
terminate tachycardia depends on the tachycardia cycle length, size of
the excitable gap, and distance and conduction time from the site of
stimulation to the tachycardia
circuit.16 17 18 Single
extrastimuli delivered from high atrial sites rarely terminate AVNRT,
particularly when the tachycardia is rapid. Uniform resetting and
termination of tachycardia with atrial extrastimuli and subsequent
successful slow-pathway ablation suggest proximity of the ablating
catheter tip to the reentrant circuit at those sites. From these
posterior and midseptal sites, intranodal penetration of A2
was possible in all except 1 patient with relatively rapid tachycardia
(cycle length, 250 ms).
All of the resetting responses observed in this study can be explained on the basis of excitable gap and recovery properties of the tissue encountered by A2. A progressive increase in the A2-H2 and consequently H-H2 intervals at progressively shorter Ae-A2 intervals suggests incomplete recovery of the slow pathway during propagation of A2 in the orthodromic direction. Its block in the orthodromic direction will result in tachycardia termination. In the presence of a larger excitable gap, more complete recovery of the slow pathway from prior impulse and A2 penetration farther downstream could conceivably result in A2-H2 (and H-H2) shortening, as observed in some patients. In all of the above scenarios, the A2 impulse in all likelihood also propagated in the antidromic direction to a variable degree along the slow pathway, resulting in either block or collision with oncoming reentrant impulse.
Limitations of the Study
The reason for the difference in
successful site among various
patients remains unexplained. The location of slow pathways, or atrial
approaches to the slow pathways, may vary among different individuals.
Furthermore, this study also cannot address the precise location or
exact relation of the ablating electrodes to the slow pathway. The
catheter positions were determined fluoroscopically, and the original
pacing sites and the subsequent ablation sites might therefore not be
exactly the same, although fluoroscopically these were in similar
regions. One can also argue as to whether ablation from sites other
than those chosen on the basis of resetting responses might have been
equally successful. This is unlikely, however, because other
radiofrequency lesions were applied along the posterior and midseptal
area and were not successful in abolishing AVNRT. Lesions outside the
zone selected here are seldom effective for ablation of the slow
pathway. It is conceivable that in some patients, multiple atrial
inputs into the slow pathway may exist, in which case ablation of
single or several adjacent sites is unlikely to abolish AVNRT.
Notwithstanding the above criticisms, the slow-pathway ablation
approach guided by the ease of A2 penetration of the AV
node as detailed here seems logical and is successful. This
represents an improvement over the existing anatomic approaches
to slow-pathway ablation.
Summary and Clinical Implications
This study highlights a
simple and reliable approach to localizing
the site for successful slow-pathway ablation by use of the response to
extrastimuli from the ablating catheter tip. If the tachycardia can be
terminated at a given site, tachycardia termination from other sites
should be attempted. The site at which the AVNRT termination occurs
with the longest atrial coupling interval is where initial
radiofrequency current should be applied. This approach should minimize
the number of radiofrequency pulses by identifying the site for
successful slow-pathway ablation in patients with common AVNRT. A
randomized study comparing this method with previously published
methods such as a purely anatomic approach, mapping of slow-pathway
potentials, and "inferior" or "midseptal" approach may
be
useful to compare the number of radiofrequency pulses, procedure time,
and complications in patients undergoing slow-pathway ablation in
patients with AVNRT.
Received July 21, 1994; revision received September 19, 1994; accepted October 2, 1994.
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