| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 1996;93:277-283.)
© 1996 American Heart Association, Inc.
Articles |
Effect of Slow Pathway Ablation on Ventricular Rate During Atrial Fibrillation
Dependence on Electrophysiological Properties of the Fast Pathway
From the Department of Cardiology, University of Vienna, Austria.
Correspondence to Gerhard Kreiner, MD, Klinik Innere Medizin II/Kardiologie, Allgemeines Krankenhaus/Universitätskliniken, Währinger Gürtel 18-20, A-1090 Vienna, Austria.
 |
Abstract |
|---|
 Top Abstract IntroductionMethods Results Discussion References |
|---|
Background Catheter ablation of the posteroseptal right atrium has been proposed for control of ventricular rate in patients with tachycardic atrial fibrillation (AF). However, the exact mechanism of rate control is unclear. Because the ablation site corresponds to the location of the slow pathway in patients with AV nodal reentry tachycardia (AVNRT), we investigated whether selective ablation of this posterior AV nodal input can provide a sufficient reduction in heart rate during AF.
Methods and Results In 30 patients with AVNRT, conduction properties of the AV nodal pathways were determined before and after slow pathway ablation. AF was induced by burst pacing at baseline and after ablation, and the mean ventricular cycle length was determined. After slow pathway ablation, the mean ventricular cycle length during AF increased (449±98 versus 515±129 milliseconds, P<.01). At baseline, the mean ventricular cycle length correlated with the Wenckebach cycle length of both the slow (r=.90) and fast (r=.86) pathways. After ablation, the mean ventricular cycle length was extremely well determined by the Wenckebach cycle length of the fast pathway (r=.94). However, the slope of the regression line was significantly steeper compared with baseline (1.50 versus 0.77, P<.0001), illustrating that the reduction in ventricular rate was not as evident if the fast pathway had a short Wenckebach cycle length.
Conclusions Selective elimination of the slow pathway reduces ventricular rate during AF. However, in patients with a short Wenckebach cycle length of the anterior AV nodal input that causes tachycardic AF, this effect may be insufficient to provide adequate control of ventricular rate.
Key Words: catheter ablation • tachyarrhythmias • heart rate • atrium • fibrillation
|
Introduction |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Under physiological conditions, AV conduction occurs through anatomically distinct AV nodal inputs and the AV node itself.1 Earlier attempts to slow the ventricular rate during tachycardic AF by catheter ablation essentially used titrated delivery of RF energy to impair fast conduction over the anteroseptal AV nodal input.2 However, because the site of ablation was rather close to the area where complete ablation of the AV junction can be accomplished, widespread use of this type of modification of AV conduction has been hampered by a high incidence of inadvertent complete AV block or insufficient rate control in other patients.2
A new catheter technique to modify AV conduction recently was proposed. RF energy was applied to the posteroseptal and midseptal area of the right atrium, ie, the sites typically targeted for ablation of the slow pathway in patients suffering from AVNRT.3 4 5 6 With this posterior approach, AV conduction could be modified successfully in the majority of patients with medically intractable tachycardic AF3 4 5 or atrial flutter.6 The exact mechanism of rate control, however, remains to be elucidated. It is certainly conceivable that ablation of the posterior AV nodal input can result in a slower ventricular rate, provided that it has a higher conduction capacity than the anterior input. However, it is unclear whether the observed decrease in heart rate can be explained solely on this basis.
Therefore, the goals of the present study were to determine the potential effect of selective slow pathway ablation on ventricular rate during AF and to delineate the electrophysiological determinants of ventricular rate during AF both before and after slow pathway ablation in a patient population with proven dual AV nodal pathways and AVNRT.
|
Methods |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
The study population consisted of 30 patients (age, 50±12 years; 23 women, 7 men) with dual AV node physiology who underwent RF catheter ablation of the slow pathway to eliminate AVNRT. None of them had documented episodes of spontaneous AF. Patients were included only if AVNRT could be induced without pharmacological challenge. Three patients had a history of syncope. Structural heart disease was present in 5 patients: cor pulmonale caused by chronic obstructive pulmonary disease (n=2), left ventricular hypertrophy in the presence of arterial hypertension (n=1), mitral valve prolapse (n=1), and a small atrial septal defect of the secundum type (n=1).
Electrophysiological Study
Protocol
The study was approved by an institutional review committee,
and
written informed consent was obtained from all patients. All
antiarrhythmic drugs had been discontinued at least five half-lives
before the study. No sedation was used. Under local
anesthesia with lidocaine, five multielectrode catheters
(Webster Laboratories) were inserted percutaneously
into the right subclavian vein and both femoral veins. A dodecapolar
orthogonal electrode catheter7 was placed in the
coronary sinus. Two quadripolar catheters were placed in the
high right atrium and the right ventricular outflow tract.
A hexapolar catheter was positioned at the AV junction, and a
4-mm-tip catheter was used for mapping and ablation along the
tricuspid annulus. Digitized recordings (Bard
Electrophysiology) were stored in a dedicated computer system for
further analysis. Measurements were made from the computer
screen at a sweep speed of 200 mm/s. The stimulation protocol included
determination of the AV conduction curve by atrial extrastimulus
testing during sinus rhythm. Measurements of the AH interval were
obtained from the distal pair of electrodes of the His catheter. During
extrastimulus testing, a discontinuous AV conduction curve was defined
in the presence of a sudden prolongation of the
A1H1 interval by 
50 ms in response to a 10-ms
decrease in the paced atrial cycle.8 The ERP-fast was
defined as the longest AA1 interval that failed to conduct
through the fast pathway. The ERP-slow was defined as the longest
AA1 interval without propagation to the His-Purkinje
system. The functional refractory period of the atrium was determined
as the shortest AA1 interval attainable, regardless of the
paced coupling interval. Incremental atrial pacing was performed,
starting with a rate just below the spontaneous heart rate. Cycle
length was decreased by 10 ms after every fourth to fifth beat until
tachycardia was initiated or, if possible, until the
occurrence of a 2:1 block of AV conduction. Because patients with a
dual AV node generally exhibit an atypical Wenckebach periodicity with
a sudden increase in AH,9 10 WBCL-fast was estimated
to be
the longest A1A1 interval at which AV
conduction shifted to the slow pathway.11 12
WBCL-slow was
reached at the longest A1A1 interval resulting
in loss of 1:1 AV conduction. Subsequently, AF was induced by
high-rate atrial burst pacing. The first 10 RR intervals during AF
were measured to determine both the shortest and the longest
ventricular cycle lengths and to calculate the MVCL during
AF.
RF Catheter Ablation
After initiation of the tachycardia by
atrial pacing
and confirmation of the diagnosis of AVNRT, catheter ablation of the
slow pathway was
performed13 14 15 16 17
with a commercially
available RF generator (Radionics). The technique used was a
combination of the anatomic and electrogram mapping approaches. The
right posteroseptal area along the tricuspid annulus
extending from the coronary sinus ostium to the
recording site of the His bundle was divided into three
regions: posterior, medial, and anterior.14 15
Initially,
the most posterior region adjacent to the septal leaflet was mapped for
slow pathway potentials similar to those described by Jackman et
al.16 During the delivery of RF energy, the catheter
usually was moved slowly toward the limbus of the coronary
sinus ostium. If unsuccessful or if no satisfactory recordings
could be obtained, the mapping and ablation procedure was continued
with the catheter placed more anteriorly along the tricuspid annulus.
Whenever possible, ablation in this area also was guided by
recordings, as done by Jackman et al.16 However,
some electrograms obtained in this region resembled more closely those
described by Haissaguerre et al,17 which were also
believed to represent a marker for the slow pathway. In
instances in which no recordings considered to be
representative of slow pathway potentials of either
type could be obtained, ablation was performed according to the
approach using primarily anatomic landmarks.14 15
During
each energy application, the tracings were observed for the occurrence
of a junctional rhythm with intact retrograde fast pathway conduction.
RF pulses were delivered at 30 to 35 W, with a maximum duration of 120
seconds. The end point of the ablation procedure was defined as the
inability to induce AVNRT.16 18 This was achieved
either
by complete elimination of slow pathway conduction, as evaluated by
both extrastimulus testing and incremental pacing, or by impairment of
the slow pathway to the extent that it could not sustain 1:1 AV
conduction.16
Postablation Evaluation
Evaluation of AV conduction by atrial
extrastimulus testing,
incremental atrial pacing, and the induction and analysis of AF
was performed in analogy to the baseline study 20 minutes after the
last RF application. Finally, the success of the ablation procedure was
reevaluated by repetition of the stimulation protocols during an
infusion of orciprenaline.
Statistical Analysis
Data are presented as mean±SD
unless otherwise
specified. Comparisons between groups of data were performed with
two-tailed Student's t test for paired or unpaired data
as appropriate. Variables characterizing AV nodal conduction
properties were correlated with the parameters obtained
during AF. Comparisons of regression lines were performed with standard
methods.19 A value of P<.05 was considered
statistically significant.
|
Results |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Catheter Ablation
All patients had the common (slow-fast) form of AVNRT. Ablation of the slow pathway, rendering the tachycardia noninducible, was successful in all patients. The ablation site was in the posterior region in 15 patients. In 3 of these patients, energy also was delivered just inside the coronary sinus. In 15 patients, the ablation was successful at the medial third of the triangle of Koch. The number of RF pulses required was 3±2, with a duration of 85±27 seconds per pulse. The slow pathway was completely eliminated in 12 patients, whereas 18 patients still had some evidence of residual slow pathway conduction at extrastimulus testing or incremental atrial pacing (with no demonstrable 1:1 AV conduction). However, single AV nodal reentrant beats were inducible in only 5 of these patients. Control stimulation during the infusion of orciprenaline did not necessitate additional RF application in any patient. During a follow-up period of 5±3 months, no recurrence of tachycardia was observed.
Characteristics of AV Conduction
During the procedure, the
sinus cycle length decreased slightly
but significantly (750±135 ms before versus 697±108 ms after
ablation; P<.01). Table 1
shows the
characteristics of AV conduction and refractoriness at baseline and
after slow pathway ablation. The AH interval remained unchanged. At
baseline, discontinuous conduction curves were demonstrable by
extrastimulus testing in 20 patients, whereas in 10 patients the
ERP-fast was shorter than the functional refractory period of the
atrium, precluding an exact determination. After ablation, the ERP-fast
could be measured in 25 patients. Statistical analysis
comparing the ERP-fast before and after ablation was performed in those
20 patients in whom data were available both before and after ablation,
revealing a significant shortening after slow pathway ablation. At the
baseline study, the ERP-slow could generally not be determined, either
because of initiation of the tachycardia or because it was
less than the functional refractory period of the atrium; thus, it was
not used in further analysis. Because all patients displayed at
baseline an atypical Wenckebach periodicity during incremental atrial
pacing, the WBCL-fast could be estimated in all cases both before and
after slow pathway ablation. At baseline, the median of the sudden
increase in AH observed during incremental atrial pacing was 75 ms
(range, 45 to 190 ms). Table 1 shows that there was a
statistically
insignificant trend toward a shorter WBCL-fast after the procedure. The
WBCL-slow at baseline could be determined in 20 patients in whom
incremental pacing could be continued until the occurrence of 2:1 AV
block without initiation of the tachycardia. The WBCL-fast
and WBCL-slow correlated closely (r=.93). According to the
definition of a successful end point of slow pathway ablation, the
WBCL-slow after ablation either did not apply (if slow pathway
conduction was not present during incremental pacing at all) or was
virtually identical to the WBCL-fast (inability to sustain 1:1 AV
conduction through the slow pathway).
|
Ventricular Rate During AF
The durations of the induced
episodes of AF were not different
before (median, 12 seconds; range, 5 to 720 seconds) and after (median,
12 seconds; range, 5 to 300 seconds) slow pathway ablation. Seventeen
episodes of AF lasted for >1 minute (before ablation in 7 patients,
after ablation in 4 patients, and both before and after ablation in 3
patients). In these patients, the MVCL calculated over the first 10 RR
intervals was correlated with the MVCL determined over 1 minute of AF.
Fig 1 shows that there was an excellent correlation with
a slope of the regression line close to 1 and an intercept around
0.
|
Table 2 shows the effects of catheter ablation on
ventricular cycle lengths during AF. Catheter ablation of
the slow pathway significantly slowed the heart rate during AF, as
reflected by a significant prolongation of all the variables
evaluated (ie, MVCL and minimal and maximal ventricular
cycle lengths). A subgroup analysis with patients stratified
according to either complete (n=12) or incomplete (n=18)
elimination of
slow pathway conduction revealed a significant increase in MVCL during
AF for both groups (410±43 ms before versus 496±84 ms after
ablation,
P<.01; 475±115 ms before versus 528±153 ms after
ablation, P<.05). Furthermore, the postablation MVCL was
not significantly different between the two groups, indicating that
ablation of the slow pathway to the point where 1:1 AV conduction
cannot be maintained has the same effect as complete elimination of the
slow pathway.
|
The anatomic location of successful slow pathway ablation had no impact on the degree of slowing of the ventricular rate during AF. In patients ablated in the posterior region (n=15), MVCL increased from 451±84 to 518±128 ms (P<.01). In patients in whom AVNRT was eliminated by ablation within the medial region (n=15), MVCL increased from 446±113 to 512±136 ms (P<.05). Furthermore, there was no correlation between the total amount of energy delivered and the increase in MVCL (r=-.35, P=NS).
Electrophysiological Determinants of
Ventricular Rate During AF
At baseline, the ventricular response
during AF was
determined by the electrophysiological
properties of the fast and slow AV nodal pathways. Linear regression
analysis revealed a good correlation between ERP-fast (n=20)
and both the mean and the minimal ventricular cycle lengths
during AF (r=.78 with MVCL; r=.75 with minimal
ventricular cycle length). Similarly, WBCL-fast correlated
closely with MVCL (r=.86) and minimal
ventricular cycle length (r=.80). WBCL-slow
(n=20) also was a good predictor of ventricular rate during
AF because it correlated well with MVCL (r=.90) and minimal
ventricular cycle length (r=.87). Moreover, as
Fig 2 shows, the slope of the regression line
determining the relation between WBCL-slow and MVCL during AF was
significantly steeper compared with the slope of the corresponding
regression line using WBCL-fast.
|
After ablation of the slow pathway,
the ventricular rate
during AF was extremely well predicted by the
electrophysiological properties of the fast
pathway. ERP-fast (n=25) correlated with both the mean
(r=.86) and minimal (r=.82)
ventricular cycle lengths. The strongest determinant of the
ventricular response during AF was WBCL-fast
(r=.94 with MVCL; r=.93 with minimal
ventricular cycle length). Fig 3 illustrates
how elimination of the slow pathway affected the relation between the
fast pathway and ventricular rate during AF. The slope of
the regression line after slow pathway ablation was significantly
steeper; in fact, it was even steeper compared with the slope of the
regression line characterizing the relation between WBCL-slow and MVCL
before ablation (P<.001). Therefore, slow pathway ablation
altered the relation between the conduction properties of the fast
pathway and the mean heart rate during AF in a way that suggests that
the reduction in ventricular rate that can be expected
after ablation depends strongly on the characteristics of the fast
pathway. It is more pronounced in the presence of a fast pathway with a
relatively long WBCL, whereas significant overlap in
ventricular rates before and after slow pathway ablation
exists if the fast pathway has a high conduction capacity. To further
examine the degree of slowing of ventricular rate during AF
as a function of the conduction properties of the fast pathway, a
subgroup analysis was performed. Group A (n=14) included only
patients who had WBCL-fast 
350 ms both before and after slow pathway
ablation; group B (n=8) comprised patients who had WBCL-fast >350 ms
both before and after slow pathway ablation. The sinus cycle lengths
did not change significantly within these groups (group A, 681±91 ms
before versus 657±85 ms after ablation; group B, 892±140 ms
before
versus 776±106 ms after ablation). Table 3 shows that
the MVCL in group A was significantly shorter compared with group B
both before and after slow pathway ablation. Although slow pathway
ablation resulted in a significant increase in MVCL in both groups, the
increase was significantly greater in group B. Moreover, the MVCL in
group A after slow pathway ablation (corresponding to a mean heart rate
of 138 beats per minute) was significantly shorter than in group B at
baseline.
|
|
Finally, we evaluated whether the increase in MVCL after slow
pathway
ablation might be explained simply by the overall increase in the WBCL
of the AV node. In 3 of the 20 patients in whom we could obtain
WBCL-slow at baseline, the WBCL-fast after ablation was actually
shorter than the WBCL-slow before ablation. In the remaining 17
patients, the 
WBCL of the AV node after versus before ablation (ie,
postablation WBCL-fast minus preablation WBCL-slow) was calculated and
correlated with MVCL during AF in these patients. The corresponding
values are 45±28 ms for WBCL of the AV node and 71±70 ms
for
MVCL, respectively. As Fig 4 shows, there was some
degree of correlation between these two variables. However, the
flat slope of the regression line suggests that the changes in MVCL
during AF cannot be explained solely by the overall increase in the
WBCL of the AV node caused by selective slow pathway ablation.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
Effect of Slow Pathway Ablation on Ventricular Rate During AF
The present study shows that before ablation of the slow pathway the ventricular response during AF depends on the conduction properties of both AV nodal pathways, whereas after ablation of the slow pathway, there is a very strong relation between the conduction properties of the fast pathway and the ventricular cycle length. Despite the observed shortening of the ERP-fast and a trend toward a shorter WBCL-fast, which is in agreement with several previous studies,13 16 20 elimination of the slow pathway results in a significant increase in ventricular cycle length during AF. Similarly, a recently published report by Blanck et al,21 who investigated the effects of slow pathway ablation on the ventricular response during AF in a cohort of 18 patients with AVNRT under autonomic blockade, demonstrated a significant prolongation of ventricular cycle lengths during AF after elimination of the slow pathway.
To analyze the changes in AV conduction during AF
after slow
pathway ablation, three principal factors need to be taken into
account: AV nodal refractoriness, concealed AV nodal conduction, and
summation of the atrial impulses entering the AV node. The
ventricular response in AF is presumably the result of a
complex interplay of these variables.22 It was shown
previously that the ventricular rate during AF is strongly
correlated with the ERP of the AV
node21 23 24 and the
shortest paced atrial cycle length resulting in 1:1 AV
conduction.21 23 It is therefore not surprising that
in a
patient population with proven dual AV nodal pathways, elimination of
the pathway exhibiting the shorter refractory period and the shorter
WBCL results in slowing of the ventricular response during
AF. However, theoretically this effect might be counteracted if one
assumes that during AF the slow pathway contributes significantly to
concealed conduction into the AV node. The present data do not
prove or disprove the role of concealed conduction. Nevertheless, the
observed increase in ventricular cycle length after slow
pathway ablation may provide some indirect evidence that a reduction of
concealed conduction resulting from elimination of an AV nodal input
does not play a principal role. This is in agreement with a study of
Brugada et al10 that demonstrated that concealed
conduction from one AV nodal pathway to another does not play a role in
determining the ventricular response during AF in patients
with dual AV node physiology. Although an overall increase in the WBCL
of the AV node and an increase in AV nodal refractoriness after
elimination of the slow pathway may be factors contributing to the
slowing of the ventricular rate, the findings of the
present study cannot be explained solely on this basis. This is
illustrated, for example, by the rather weak correlation between the
WBCL of the AV node and MVCL during AF. In particular, the flat
slope of the regression line indicates that the actual increase in MVCL
during AF is more pronounced than one might expect from the increase in
WBCL of the AV node. Furthermore, the overall increase in AV nodal
refractoriness cannot account for the observed impact of slow pathway
ablation on the relation between WBCL-fast and the
ventricular cycle length during AF, ie, the significant
increase in the slope of the regression line. The most likely
explanation for these two findings is a reduction in summation of
atrial impulses reaching the AV node after elimination of one AV nodal
input. Hashida et al25 developed a model of AV nodal
conduction that showed that summation of excitatory stimuli needs to
occur during AF until a threshold value that leads to conduction of the
impulse is reached. Elimination of the posteroseptal
approach to the AV node presumably reduces the likelihood of summation,
which results in a greater reduction in ventricular rate
than can be accounted for by the overall increase in WBCL of the AV
node. Furthermore, Zipes et al26 demonstrated that a
premature stimulus that is blocked if it approaches the AV node through
a single pathway can elicit an impulse propagation if it enters the AV
node with the same prematurity through two pathways. Considering that
this phenomenon is of significance only if the tissue encountered by
the impulse is still refractory, it is conceivable that this concept
might explain why the reduction in ventricular rate is more
pronounced in the presence of a fast pathway with a longer WBCL. If the
remaining anteroseptal AV nodal input blocks antegrade conduction at
lower rates, it might depend on summation to conduct to the ventricle
more than a fast pathway with an immanent short refractoriness.
Elimination of the posteroseptal AV nodal input would
therefore lead to an increase in the slope of the regression line
between WBCL-fast and ventricular cycle length during AF,
as observed in the present study.
Clinical Implications
Olsson et al27 found a
typical bimodal distribution
of RR intervals in patients with chronic AF and concluded that this was
evidence of dual AV nodal pathways being a ubiquitous phenomenon. In
fact, a posterior atrionodal input, corresponding to the location of
the slow pathway, has been established as one of the
physiological approaches to the AV
node.1 28 29 It has been suggested that
the functional
defect in humans with AVNRT may be an abnormally long refractory period
of the fast pathway rather than the presence of an abnormal slow
pathway.30 It is conceivable that the posterior AV nodal
input also may play a role in determining the ventricular
response during AF in patients not exhibiting distinct differences in
refractoriness between the anterior and posterior AV nodal pathways.
Therefore, attempting to slow the ventricular rate during
AF by ablation of this posterior approach to the AV node may seem
promising. In fact, several recent publications reported adequate
control of heart rate during AF3 4 5 or
atrial
flutter6 in the majority of patients after RF ablation of
the posteroseptal or midseptal right atrium. However,
because most of the patients studied by Williamson et al4
and Feld at al5 were in chronic AF, the effect of this
ablation on AV nodal conduction and refractoriness could not be
evaluated to clarify the exact mechanism of rate control. Based on the
present data, the effect of selective elimination of the posterior
AV nodal input alone, even if it is known to exhibit a shorter
refractory period than the anterior approach to the AV node, may not be
sufficient to provide adequate control of ventricular rate
in all cases. In fact, it seems particularly insufficient in the
presence of tachycardic AF owing to a fast pathway with a short WBCL.
Therefore, in patients in whom adequate control of heart rate could be
achieved,3 4 5 6 some degree
of preexisting impairment of AV
conduction caused by the underlying heart disease might have
contributed to the success of the procedure. For example, Feld et
al5 reported successful modification of the AV conduction
in 7 of 10 patients studied. Of note, 2 of these had permanent
pacemakers previously implanted for sick sinus syndrome that were
programmed to VVI at a low rate.5 However, as suspected by
Williamson et al,4 in some patients additional injury to
the compact node may have contributed to the reduction in
ventricular rate. This would also explain why transient or
permanent complete AV block occurred in 6 of 19 patients studied
despite application of RF energy in an interrupted, conservative
fashion. This incidence of complete AV block usually is not seen in
patients undergoing selective ablation of the slow pathway for control
of AVNRT. Della Bella et al6 studied a cohort of 14
patients suffering from AF or atrial flutter. Complete AV block
occurred in 2 patients.6 In contrast to the previously
mentioned studies,3 4 5 several patients
were studied during
sinus rhythm.6 It is of note that in 4 of 8 patients in
whom the AH interval was available after the ablation procedure, AH was
100 ms, although it was unchanged from baseline values.6
This prolongation of the AH interval lends further support to the
hypothesis that there might have been some preexisting impairment of AV
conduction contributing to the success of the procedure. In 6 patients
studied during sinus rhythm, the WBCL of the AV node increased from
346±33 to 458±75 ms.6 This postablation value is
certainly not considered to be within the normal range. Furthermore, as
Della Bella et al pointed out, the AV nodal WBCL is far beyond that
reported in patients undergoing selective ablation of the slow pathway
for elimination of AVNRT, which is a population known to have a higher
conduction capacity through the posteroseptal AV nodal
input than through the anteroseptal input. In the study of Della Bella
et al,6 no patients in whom it could be tested had
evidence of dual AV node physiology. Similarly, in the present
study, the overall increase in the WBCL of the AV node was much
smaller. Therefore, the reduction in ventricular rate
achieved in these patients6 may not have been due solely
to selective elimination of a distinct posteroseptal AV
nodal input in all cases.
Limitations
Because the episodes of induced AF were generally
short, lasting
from a few seconds to <1 minute in most cases, we focused on the
analysis of the first 10 RR intervals, which could be obtained
in all patients. This may not necessarily be predictive of the events
during longer episodes or in chronic AF. However, the findings
regarding the relation between AV conduction and refractoriness and the
ventricular response during AF may be more valid when only
the first few beats are analyzed because
hemodynamic alterations secondary to longer AF episodes
may be more likely to change the autonomic tone, which influences the
conduction properties of the AV node.31 Furthermore, the
comparison between the MVCL determined over the first 10 RR intervals
with the MVCL during 1 minute of AF demonstrated a rather close
relation.
Because the study was not performed under autonomic blockade,
as was
that of Blanck et al,21 it is possible that the observed
small decline in the resting sinus cycle length, which is in agreement
with previously published data,13 might indicate a slight
increase in sympathetic tone during the procedure. However, it was
shown recently that the decrease in refractoriness of the fast pathway
is not related to changes of the autonomic tone.20
Nevertheless, we cannot entirely rule out that a small increase in
sympathetic tone might have led to slight underestimation of the
increase in MVCL during AF in some patients. However, we do not believe
that this could have significantly altered the findings of this study.
In particular, in the subgroup of patients in whom the procedure seemed
least effective, ie, those patients who had a WBCL-fast 350 ms
before and after ablation, the sinus cycle length remained virtually
unchanged.
Conclusions
Selective ablation of the slow pathway in
patients with AVNRT
significantly reduces ventricular rate during AF. However,
this effect is more pronounced if the remaining fast pathway has a
relatively long WBCL, leading to lower heart rates to begin with.
Selective elimination of this posterior AV nodal input alone may not be
sufficient to achieve adequate control of the ventricular
rate in patients with tachycardic AF who have a short WBCL of the
anteroseptal AV nodal input.
|
Selected Abbreviations and Acronyms |
|---|
|
Received January 23, 1995; revision received June 27, 1995; accepted August 29, 1995.
|
References |
|---|
|
TopAbstractIntroductionMethods Results Discussion References |
|---|
1. Racker DK. Transmission and reentrant activity in the sinoventricular conducting system and in the circumferential lamina of the tricuspid valve. J Cardiovasc Electrophysiol. 1993;4:513-525. [Medline] [Order article via Infotrieve]
2. Duckeck W, Engelstein ED, Kuck KH. Radiofrequency current therapy in atrial tachyarrhythmias: modulation versus ablation of atrioventricular nodal conduction. Pacing Clin Electrophysiol. 1993;16:629-636. [Medline] [Order article via Infotrieve]
3. Fleck RP, Chen PS, Boyce K, Ross R, Dittrich HC, Feld GK. Radiofrequency modification of atrioventricular conduction by selective ablation of the low posterior septal right atrium in a patient with atrial fibrillation and a rapid ventricular response. Pacing Clin Electrophysiol. 1993;16:377-381. [Medline] [Order article via Infotrieve]
4.
Williamson BD, Man KC, Daoud E, Niebauer M,
Strickberger SA, Morady F. Radiofrequency catheter modification
of atrioventricular conduction to control the
ventricular rate during atrial fibrillation.
N Engl J Med. 1994;331:910-917.
5.
Feld GK, Fleck RP, Fujimura O, Prothro DL, Bahnson TD,
Ibarra M. Control of rapid ventricular response by
radiofrequency catheter modification of the
atrioventricular node in patients with medically
refractory atrial fibrillation.
Circulation. 1994;90:2299-2307.
6. Della Bella P, Carbucicchio C, Tondo C, Riva S. Modulation of atrioventricular conduction by ablation of the `slow' atrioventricular node pathway in patients with drug-refractory atrial fibrillation or flutter. J Am Coll Cardiol. 1995;25:39-46. [Abstract]
7.
Jackman WM, Friday KJ, Yeung-Lai-Wah JA, Fitzgerald
DM, Beck B, Bowman AJ, Stelzer P, Harrison L, Lazzara R. New
catheter technique for recording left free-wall accessory
atrioventricular pathway activation: identification of
pathway fiber orientation. Circulation. 1988;78:598-610.
8. Josephson ME. Supraventricular tachycardias. In: Josephson ME, ed. Clinical Cardiac Electrophysiology: Techniques and Interpretations. 2nd ed. Philadelphia, Pa: Lea & Febiger; 1993:191.
9. Rosen KM, Denes P, Wu D, Dhingra RC. Electrophysiological diagnosis and manifestation of dual A-V nodal pathways. In: Wellens HJJ, Lie KI, Janse MJ, eds. The Conduction System of the Heart. Leiden, Netherlands: HE Stenfert Kroese BV; 1976:453-466.
10. Brugada P, Roy D, Weiss J, Dassen WRM, Wellens HJJ. Dual atrio-ventricular nodal pathways and atrial fibrillation. Pacing Clin Electrophysiol. 1984;7:240-247. [Medline] [Order article via Infotrieve]
11. Sung RJ, Huycke EC, Keung EC, Tseng CD, Lai WT. Atrioventricular node reentry: evidence of reentry and functional properties of fast and slow pathways. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology: From Cell to Bedside. Philadelphia, Pa: WB Saunders; 1990:514.
12. Zhang X, Fisher JD, Kim SG, Matos JA, Waspe LE, Johnson C. Comparison of ramp and stepwise incremental pacing in assessment of antegrade and retrograde conduction. Pacing Clin Electrophysiol. 1986;9:42-52. [Medline] [Order article via Infotrieve]
13.
Kay GN, Epstein AE, Dailey SM, Plumb VJ.
Selective radiofrequency ablation of the slow pathway for the treatment
of atrioventricular nodal reentrant
tachycardia: evidence for involvement of perinodal
myocardium within the reentrant circuit.
Circulation. 1992;85:1675-1688.
14.
Jazayeri MR, Hempe SL, Sra JS, Dhala AA, Blanck Z,
Deshpande SS, Avitall B, Krum DP, Gilbert CJ, Akhtar M.
Selective transcatheter ablation of the fast and slow
pathways using radiofrequency energy in patients with
atrioventricular nodal reentrant
tachycardia. Circulation. 1992;85:1318-1328.
15. Kalbfleisch SJ, Strickberger SA, Williamson B, Vorperian VR, Man C, Hummel JD, Langberg JJ, Morady F. Randomized comparison of anatomic and electrogram mapping approaches to ablation of the slow pathway of atrioventricular node reentrant tachycardia. J Am Coll Cardiol. 1994;23:716-723. [Abstract]
16. Jackman WM, Beckman KJ, McClelland JH, Wang X, Friday KJ, Roman CA, Moulton KP, Twidale N, Hazlitt HA, Prior MI, Oren J, Overholt ED, Lazzara R. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofrequency catheter ablation of slow-pathway conduction. N Engl J Med. 1992;327:313-318. [Abstract]
17.
Haissaguerre M, Gaita F, Fischer B, Commenges D,
Montserrat P, d'Ivernois C, Lemetayer P, Warin JF. Elimination
of atrioventricular nodal reentrant
tachycardia using discrete slow potentials to guide
application of radiofrequency energy.
Circulation. 1992;85:2162-2175.
18. Lindsay BD, Chung MK, Gamache MC, Luke RA, Schechtman KB, Osborn JL, Cain ME. Therapeutic end points for the treatment of atrioventricular node reentrant tachycardia by catheter-guided radiofrequency current. J Am Coll Cardiol. 1993;22:733-740. [Abstract]
19. Sokal RR, Rohlf FJ. Comparison of regression lines. In: Sokal RR, Rohlf FJ, eds. Biometry. 2nd ed. New York, NY: Freeman & Co; 1981:499-509.
20.
Natale A, Klein G, Yee R, Thakur R. Shortening
of fast pathway refractoriness after slow pathway ablation: effects of
autonomic blockade. Circulation. 1994;89:1103-1108.
21.
Blanck Z, Dhala AA, Sra J, Deshpande SS, Anderson AJ,
Akhtar M, Jazayeri MR. Characterization of
atrioventricular nodal behavior and
ventricular response during atrial fibrillation before and
after a selective slow-pathway ablation.
Circulation. 1995;91:1086-1094.
22. Watanabe Y, Watanabe M. Impulse formation and conduction of excitation in the atrioventricular node. J Cardiovasc Electrophysiol. 1994;5:517-531. [Medline] [Order article via Infotrieve]
23. Toivonen L, Kadish A, Kou W, Morady F. Determinants of the ventricular rate during atrial fibrillation. J Am Coll Cardiol. 1990;16:1194-1200. [Abstract]
24. Fujiki A, Tani M, Mizumaki K, Yoshida S, Sasayama S. Quantification of human concealed atrioventricular nodal conduction: relation to ventricular response during atrial fibrillation. Am Heart J. 1990;120:598-603. [Medline] [Order article via Infotrieve]
25. Hashida E, Yoshitani N, Tasaki T. A study on the irregularity of the sequence of R-R intervals in chronic atrial fibrillation in man based on the time series analysis and the information theory. Jpn Heart J. 1978;19:839-851. [Medline] [Order article via Infotrieve]
26.
Zipes DP, Mendez C, Moe GK. Evidence for
summation and voltage dependency in rabbit
atrioventricular nodal fibers.
Circ Res. 1973;32:170-177.
27.
Olsson SB, Cai N, Dohnal M, Talwar KK.
Noninvasive support for and characterization of multiple intranodal
pathways in patients with mitral valve disease and atrial
fibrillation. Eur Heart J. 1986;7:320-333.
28. Janse MJ, Anderson RH, McGuire MA, Yen Ho S. `AV nodal' reentry, I: `AV nodal' reentry revisited. J Cardiovasc Electrophysiol. 1993;4:561-572. [Medline] [Order article via Infotrieve]
29. Sung RJ, Lauer MR, Chun H. Atrioventricular node reentry: current concepts and new perspectives. Pacing Clin Electrophysiol. 1994;17:1413-1430. [Medline] [Order article via Infotrieve]
30.
McGuire MA, de Bakker JMT, Vermeulen JT, Opthof T,
Becker AE, Janse MJ. Origin and significance of double
potentials near the atrioventricular node: correlation
of extracellular potentials, intracellular potentials, and
histology. Circulation. 1994;89:2351-2360.
31. Waxman MB, Wald RW, Cameron D. Interactions between the autonomic nervous system and tachycardias in man. Cardiol Clin. 1983;1:143-185.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  Y. Zhang, S. Bharati, K. A. Mowrey, and T. N. Mazgalev His Electrogram Alternans Reveal Dual Atrioventricular Nodal Pathway Conduction During Atrial Fibrillation: The Role of Slow-Pathway Modification Circulation, February 25, 2003; 107(7): 1059 - 1065. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Rokas, S. Gaitanidou, S. Chatzidou, C. Pamboucas, D. Achtipis, and S. Stamatelopoulos Atrioventricular Node Modification in Patients With Chronic Atrial Fibrillation : Role of Morphology of RR Interval Variation Circulation, June 19, 2001; 103(24): 2942 - 2948. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K.-C. Ueng, S.-H. Lee, D.-J. Wu, C.-S. Lin, M.-S. Chang, and S.-A. Chen Radiofrequency Catheter Modification of Atrioventricular Junction in Patients With COPD and Medically Refractory Multifocal Atrial Tachycardia* Chest, January 1, 2000; 117(1): 52 - 59. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Garrigue, K. A. Mowrey, G. Fahy, P. J. Tchou, and T. N. Mazgalev Atrioventricular Nodal Conduction During Atrial Fibrillation : Role of Atrial Input Modification Circulation, May 4, 1999; 99(17): 2323 - 2333. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. D. Krahn, G. J. Klein, R. Yee, M. N. Basta, and J. K. Lee Progressive Anterior Ablation in the Coronary Sinus Region : Evidence to Support the Presence of a `Slow Pathway' Input in Normal Patients? Circulation, November 18, 1997; 96(10): 3477 - 3483. [Abstract] [Full Text]
|
|
|
|
|
|
S. M. Markowitz, K. M. Stein, and B. B. Lerman Mechanism of Ventricular Rate Control After Radiofrequency Modification of Atrioventricular Conduction in Patients With Atrial Fibrillation Circulation, December 1, 1996; 94(11): 2856 - 2864. [Abstract] [Full Text]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||