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(Circulation. 1995;91:1086-1094.)
© 1995 American Heart Association, Inc.
Articles |
Characterization of Atrioventricular Nodal Behavior and Ventricular Response During Atrial Fibrillation Before and After a Selective Slow-Pathway Ablation
Presented in part at the 66th Scientific Sessions of the American Heart Association, Atlanta, Ga, November 8-11, 1993.
From the Electrophysiology Laboratory, Milwaukee Heart Institute of Sinai Samaritan Medical Center, University of Wisconsin, Milwaukee Clinical Campus.
Correspondence to Zalmen Blanck, MD, 2901 W KK River Pkwy, Suite 470, Milwaukee, WI 53215-3660.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background The presence of atrioventricular nodal dual-pathway physiology in patients with atrioventricular nodal reentrant tachycardia (AVNRT) provides an opportunity to characterize the effect of a selective slow-pathway ablation on the ventricular rate during atrial fibrillation (AF). This may have important clinical implications for the nonpharmacological management of AF with a rapid ventricular rate.
Methods and Results Selective radiofrequency catheter ablation of the atrioventricular nodal slow pathway was performed with a stepwise approach in patients with documented sustained AVNRT. The AV nodal conduction properties and refractoriness and the ventricular rate during induced AF were assessed at baseline and under autonomic blockade before and after a selective slow-pathway ablation in 18 patients (mean age, 34±8 years). Sustained AVNRT was induced with a mean cycle length of 339±58 ms. A slow-pathway ablation was successfully achieved with 5±4 applications of radiofrequency energy. The shortest cycle length of 1:1 AV conduction and the AV nodal effective refractory period significantly prolonged after ablation (367±53 versus 403±55 ms, P<.0001, and 258±55 versus 292±74 ms, P<.05, respectively). Selective slow-pathway ablation significantly prolonged the mean (526±93 versus 612±107 ms, P<.0001), the shortest (378±59 versus 423±73 ms, P<.0001), and the longest (826±150 versus 969±226 ms, P<.01) cycle lengths of the ventricular response to AF. Significant slowing of the ventricular rate during AF occurred in 13 patients (72%), including all eight patients in whom AV nodal dual-pathway physiology was abolished. Five patients did not have a significant change in the ventricular rate during AF; a persistent dual AV nodal pathway physiology was demonstrable in four of these patients. Loss of dual-pathway physiology after ablation had a sensitivity of 77%, specificity of 80%, and positive predictive value of 91% for slowing the ventricular rate during AF.
Conclusions In patients undergoing a slow-pathway ablation for control of AVNRT, selective slow-pathway ablation may cause a significant decrease in the ventricular rate during AF. These effects are primarily due to the prolongation of AV nodal conduction properties and refractory period of the residual AV nodal transmission system. These findings may have important therapeutic implications for the nonpharmacological treatment of AF, particularly in patients with underlying dual AV nodal physiology.
Key Words: catheter ablation • fibrillation • ventricles • autonomic agents
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Atrial fibrillation (AF) is the most common form of sustained tachyarrhythmia encountered in clinical practice. It has been estimated that 0.4% of the general population has AF.1 2 Ventricular rate control of AF is one of the major therapeutic objectives when sinus rhythm cannot be restored. Although AV nodal blocking agents are usually considered the first option, pharmacological therapy is ineffective in achieving optimal rate control in many patients with rapid ventricular response to AF. The application of radiofrequency energy to the AV junction has been shown to be a safe and effective modality for creating complete AV block when nonpharmacological management is considered for this arrhythmia.3 However, the most significant drawback of this therapeutic approach is a life-long pacemaker dependency.
A selective ablation of the AV nodal slow pathway in patients with AV nodal reentrant tachycardia (AVNRT) can effectively eliminate the tachycardia.4 5 6 7 8 Theoretically, a similar approach, by modifying the electrophysiological characteristics of the AV node, might lessen the ventricular rate of AF and yet, by maintaining the integrity of AV conduction, obviate the need for a permanent pacemaker. Based on this assumption, a recent case report9 in which radiofrequency pulses were applied to the posteroseptal region of the right atrium showed a significant decrease in the ventricular response to AF. Nonetheless, the impact of a selective slow-pathway ablation on the ventricular response to AF must be tested in patients whose electrophysiological properties of the AV node can be evaluated reliably before and after such an intervention. To this end, we systematically assessed the AV nodal conduction and refractoriness under autonomic blockade in patients undergoing AV nodal modification for control of AVNRT. Furthermore, the ventricular response to AF was analyzed before and after AV nodal modification. The main objective of this study was to characterize the impact of a selective slow-pathway ablation on the ventricular rate of induced AF in such a patient population.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patients undergoing radiofrequency catheter ablation of the AV nodal slow pathway for documented or suspected AVNRT were invited to participate in this investigational protocol if they met the following criteria: (1) age between 18 and 60 years, (2) inducible sustained AVNRT during electrophysiological studies, (3) no structural heart disease, (4) no contraindications for autonomic blockade, and (5) no prior attempt at fast- or slow-pathway catheter ablation. This protocol was approved by the Institutional Review Board of Sinai Samaritan Medical Center.
Electrophysiological Study
Each patient underwent a complete
electrophysiological
evaluation performed in a postabsorptive state. All antiarrhythmic
medications had been discontinued for at least five half-lives before
the study. Except for one patient who was sedated with intravenous
midazolam, all patients were anesthetized with intravenous propofol.
Electrode catheters were introduced percutaneously into femoral and
internal jugular veins and positioned under fluoroscopic guidance in
the right ventricular apex, high right atrium, and His bundle region. A
6F decapolar catheter was placed in the coronary sinus with the most
proximal pair of recordings positioned at the ostium. Surface ECG leads
(I, II, and V1), intracardiac electrograms, and time lines
were simultaneously displayed on a multichannel oscilloscope (EVR-180,
PPG Biomedical) and printed on a thermal recorder. Data were recorded
on optical disks (Biomedical Instrumentation Inc) for subsequent
reproduction. Electrical stimulation was performed with a programmable
digital stimulator (Bloom Associates). Atrial and ventricular
extrastimulation and incremental pacing were used to assess the
antegrade and retrograde AV nodal conduction and refractoriness. We
considered AV nodal dual-pathway physiology to be present when an
H1-H2 interval prolongation of 
50 ms (with or
without AVNRT initiation) in response to a 10-ms decrement in
A1-A2 interval was demonstrable. The induction
of AVNRT was attempted repeatedly to determine the most reliable and
reproducible method of tachycardia induction. When tachycardia could
not be initiated or sustained, isoproterenol was infused intravenously
and titrated to increase the sinus cycle length by a minimum of 20%,
and the stimulation protocol was repeated. Intravenous heparin was
administered as an initial dose of 2000 U followed by intermittent
boluses of 1000 U/h.
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 wall. The
ablation catheter was a 7F deflectable quadripolar catheter with a 4-mm
bulbous-tip electrode (Mansfield Scientific). The radiofrequency
generator was a LIZ-88 (American Cardiac Ablation Corp), which
generates radiofrequency energy at 540 kHz. This unit integrates the
power source and energy output monitoring circuitry into a single
package and gives direct readouts of the voltage and load
impedance.
A slow-pathway ablation was performed by the stepwise
approach, as
previously described.4 Briefly, the septal annulus of the
tricuspid valve, extending from the most posterior region adjacent to
the coronary sinus ostium (posterior) to the His bundle recording site
(anterior), was divided into posterior (P), medial (M), and anterior
(A) zones. Each zone was further divided into two sites. The ablating
catheter was initially positioned in the most posterior aspect of the
tricuspid septal site (P1), adjacent to the coronary sinus ostium. This
site was considered optimal for ablation if the local electrogram
showed an A/V ratio of 
0.5 or less. If the ablation attempt at this
site was unsuccessful, the ablation catheter was moved anteriorly while
an optimal A/V ratio was maintained to reach sites P2, M1, M2, and A1
if necessary. After the delivery of each pulse of radiofrequency
energy, pacing protocols were repeated to assess the inducibility of
AVNRT. Radiofrequency pulses were set at 60 to 80 V and delivered for
40 to 60 seconds. Whenever changes in the catheter tip position or
impedance rise were noted, the energy delivery was immediately
terminated. The end point of the ablative procedure was to render AVNRT
noninducible. The presence of a single AV nodal reentrant echo beat or
persistent AV nodal dual-pathway physiology was not considered a
procedural failure and did not necessitate further radiofrequency
applications.4
Study Protocol
After completion of the initial
electrophysiological evaluation,
incremental atrial and ventricular pacing, premature atrial
stimulation, and induction of AF were performed under autonomic
blockade. The same pacing protocol and AF induction were also repeated
under autonomic blockade 30 minutes after successful ablation.
Atrial fibrillation was induced by rapid high right atrial or coronary sinus pacing. The shortest, mean, and longest ventricular cycle lengths were analyzed during the first 60 seconds of induced AF. In addition, the frequency distribution of ventricular cycle lengths during AF was tabulated by 20-ms intervals in each patient at baseline and during autonomic blockade before and after ablation. If spontaneous restoration of sinus rhythm did not occur within 5 to 10 minutes, DC electrical cardioversion was performed. Antiarrhythmic agents were not administered.
Autonomic Nervous System Blockade
Fluctuations in autonomic
tone during the procedure may
potentially impact on the ventricular rate during AF and may mask the
electrophysiological changes resulting from the ablation and preclude a
meaningful analysis. Therefore, autonomic blockade was used to
eliminate such an interference.
Autonomic blockade was achieved with a combination of esmolol and atropine in all patients before and after a slow-pathway ablation. Because administration of ß-adrenergic agents with long half-lives may prevent the inducibility of sustained AVNRT, intravenous esmolol, a nonselective ß-blocker with a short half-life (9.5 minutes),10 was used. A loading dose of 500 µg · kg-1 · min-1 was administered for 3 minutes and followed by a maintenance dose of 400 µg · kg-1 · min-1.11 The same dosage was used before and after ablation.
Parasympathetic nervous system blockade was achieved with intravenous atropine, which was administered at a dose of 0.04 mg/kg12 before ablation. A second dose of 0.01 to 0.02 mg/kg was given after ablation. Atropine was administered over 30 seconds approximately 5 minutes after the esmolol maintenance dose was infused. When isoproterenol was used, a period of at least 20 minutes was allowed for its washout before the study protocol was continued.
The atrial refractory period studies were performed at several drive cycle lengths, and only data obtained at identical cycle lengths before and after ablation were compared in each patient. Except for transient blurred vision and dry mouth resulting from the administration of atropine, no side effects or complications occurred from this investigational protocol or the ablative procedures.
Follow-up
All patients underwent a repeat
electrophysiological study with
and without isoproterenol 30 minutes after slow-pathway ablation and 24
to 48 hours later before hospital discharge.
Statistical Analysis
Data are expressed as mean value
±SD. Paired and unpaired
Student's t tests were used to compare continuous
variables. Two different statistical methods were used to compare
changes in the ventricular cycle length during AF in all patients as a
group and in each patient individually. The changes in the mean,
shortest, and longest ventricular cycle lengths were analyzed with a
paired two-tailed Student's t test. The two-sided
Kolmogorov-Smirnov nonparametric statistical analysis was used to
assess the change in the frequency distribution curve of ventricular
cycle lengths tabulated at 20-ms intervals. This method was used
because the frequency distribution curve of the ventricular cycle
lengths during AF did not follow a normal distribution in all patients.
We considered a change in the ventricular cycle length during AF
significant in each patient only if both statistical methods showed a
P<.05.
The presence of a correlation between electrophysiological parameters and the change in ventricular cycle length during AF was examined by linear regression analysis.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Between March 1992 and August 1993, 20 patients agreed to participate in this study. Two patients were excluded from the subsequent analysis because of the inducibility of AVNRT 24 hours after ablation in 1 patient and inability to induce sustained AF after ablation in the other. The remaining 18 patients form the basis of this study. There were 11 women and 7 men, with a mean age of 34±8 years. None of the patients had a history of heart disease or any structural heart disease demonstrable by two-dimensional echocardiography. Tachycardias induced in the laboratory were sustained AVNRT of the common (16 patients) or uncommon (1 patient) variety. The remaining patient had both common and uncommon (slow-slow) forms of AVNRT. Isoproterenol was required in 8 patients for inducing or maintaining AVNRT. The mean cycle length of the AVNRT was 339±58 ms.
Ablation Results
The induction of AVNRT was successfully
abolished by a selective
slow-pathway ablation in all patients. The patients received a mean of
5±4 (range, 1 to 17; Table 1
) radiofrequency
applications,
the last of which (ie, successful pulse) had a mean voltage, power, and
duration of 70±8 V, 49±10 W, and 38±12 seconds,
respectively.
Successful ablation sites were P1 and P2 in 12 patients and M1 and M2
in 6 patients.4
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Electrophysiological Parameters Before and After Ablation
Electrophysiological parameters, including the atrial-His (AH)
interval, the shortest cycle length of 1:1 antegrade and retrograde
conduction, the AV nodal functional and effective refractory periods,
and the presence of AV nodal dual-pathway physiology, were determined
in each patient (Table 2).
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After autonomic blockade and before ablation, the shortest cycle length of 1:1 AV conduction lengthened from 348±72 to 367±53 ms (P<.05), and antegrade AV nodal dual-pathway physiology was present in 14 patients (versus 13 at baseline). Four patients (patients 2, 9, 10, and 16) demonstrated two or more "jumps" in their discontinuous AV nodal conduction curves during atrial extrastimulation, suggesting the presence of more than one slow pathway. AVNRT remained inducible with a mean cycle length of 390±51 ms in 10 patients.
The electrophysiological parameters measured under
autonomic blockade
before and after a slow-pathway ablation are listed in Tables 2
and 3. After ablation, there was a significant lengthening in
the shortest cycle length of 1:1 AV conduction (403±55 versus
367±53,
P<.0001) and in the AV nodal effective refractory period
(292±74 versus 258±55, P<.05). There was no
significant
difference in preablation versus postablation values of the AH
interval, the functional refractory period of the AV node, or the
shortest cycle length maintaining 1:1 retrograde ventriculoatrial
conduction (Table 3).
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Atrioventricular nodal
dual-pathway physiology was abolished after a
slow-pathway ablation in 8 of 14 patients (57%) (Table 2). In
these 14
patients, the fast-pathway effective refractory period remained
unchanged in 8 patients, prlonged (20 ms) in 4, and shortened (20
ms) in 2 patients after a slow-pathway ablation (Table 2).
Of the remaining 4 patients with a continuous AV nodal conduction curve under autonomic blockade before ablation, 1 developed the dual-pathway physiology after ablation. It should be pointed out that in 3 of these patients (patients 12, 13, and 17), the AV nodal dual-pathway physiology was demonstrable at baseline (ie, before autonomic blockade).
Data on isoproterenol administered intravenously at 1 to 5 µg/min (mean, 2±1 µg/min) were compared in 8 patients before and after ablation. There was no significant difference in the shortest cycle length of 1:1 AV conduction (291±36 versus 289±44 ms, P=NS) or the AV nodal effective refractory period (209±11 versus 214±12 ms, P=NS) after ablation in any of these 8 patients.
Ventricular Response During Atrial Fibrillation Before and After
Slow-Pathway Ablation
The mean, shortest, and longest ventricular (RR)
cycle lengths
during AF at baseline and after autonomic blockade (before the
ablation) were compared. There was a significant lengthening in the
mean (526±93 versus 476±78 ms, P=.004) and the
shortest
(378±59 versus 344±57 ms, P=.004) RR cycle
lengths after
autonomic blockade. The mean and shortest RR cycle lengths during AF
had a better correlation with the shortest cycle length of 1:1 AV
conduction (r=.88 and r=.91, with
P<.0001 for both) than with the AV nodal effective
refractory period (r=.73 and r=.68, with
corresponding values of P=.0005 and P=.001,
respectively) or functional refractory period (r=.60 and
r=.66, with P<.007 and P<.002,
respectively). No correlation was found between the AH interval and the
RR cycle lengths during AF.
After ablation, there was a statistically
significant lengthening of
the mean (612±107 versus 526±93 ms, P<.0001), the
shortest (423±73 versus 378±59 ms, P<.0001), and the
longest (969±226 versus 826±150 ms, P<.004)
ventricular
cycle lengths during AF (Table 3). In addition, the frequency
distribution curve of the ventricular cycle lengths during AF shifted
to the right after the ablation (P<.0001, Fig 1).
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When the ventricular response during AF before and after ablation was
compared in each patient, 13 patients (72%) had significant RR cycle
length prolongation after ablation (Table 2, patients 1 through
13).
This included all 8 patients in whom AV nodal dual-pathway physiology
was abolished after the ablation (Fig 2), 3 patients
with persistent AV nodal dual-pathway physiology, and 2 patients in
whom this finding was not demonstrable before or after the
ablation.
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In the remaining 5 patients (Table 2, patients
14 through 18), only one
of the statistical methods showed a significant slowing of the
ventricular rate during AF (P<.05), and they were
considered to have only a trend toward significant slowing of the
ventricular rate during AF. Interestingly, 4 (80%) of these 5 patients
had AV nodal dual-pathway physiology after ablation (Fig 3),
including the patient whose AV nodal dual-pathway
physiology was unmasked after a slow-pathway ablation. This was in
marked contrast to the 23% incidence of persistent AV nodal
dual-pathway physiology among 13 patients with significant RR
prolongation (P<.02). In these two subgroups of patients
(patients 1 through 13 versus 14 through 18), comparison of the
magnitude of change in the shortest cycle length of 1:1 AV conduction
and the mean RR cycle length during AF before and after the ablation
showed a significant statistical difference (P<.05).
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Linear regression analysis demonstrated that the change in the mean RR cycle length during AF before and after ablation had a modest correlation with the change in the AV nodal effective refractory period (r=.67, P=.002). The correlation between the change in mean RR cycle length and the change in the shortest cycle length of 1:1 AV conduction did not reach statistical significance.
The loss of AV nodal dual-pathway physiology after ablation had a sensitivity of 77% and a specificity of 80%, with positive and negative predictive values of 91% and 57%, respectively, for slowing of the ventricular response during AF.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Major Findings
This study demonstrated that a selective ablation of the AV nodal slow pathway in the majority of patients with AVNRT led to a significant slowing of the ventricular rate during induced AF. Among several electrophysiological parameters, the elimination of AV nodal dual-pathway physiology and prolongation of AV nodal effective refractory period were associated with a marked reduction in the ventricular response to AF. These data may have important therapeutic implications for patients suffering from AF with rapid ventricular rate, and they might also provide further insight into the physiological behavior of the AV node in such a prevalent arrhythmia.
Electrophysiological Properties of the AV Node After
Modification
A selective slow-pathway ablation not only eliminates
AVNRT but
also can modify the electrophysiological properties of the residual AV
nodal conduction
system.4 5 6 7 8
Previous studies have shown
that the shortest cycle length of 1:1 AV conduction and the effective
refractory period of the AV node are both prolonged after a
slow-pathway ablation.13 Interestingly, however, in
patients with a demonstrable dual-pathway physiology at baseline,
prolongation of these two parameters is of a greater magnitude when the
AV nodal dual-pathway physiology is completely
abolished.13 The present study, by reaffirming these
findings under autonomic blockade, indicates that changes in the AV
nodal conduction characteristics and refractory periods observed after
a slow-pathway ablation are independent of autonomic influences.
Shortening of the fast-pathway effective refractory period has been previously reported after a selective slow-pathway ablation in patients with AVNRT.5 A recent study14 demonstrated such a phenomenon occurring in 70% of patients with AVNRT undergoing a slow-pathway ablation. The shortening of the fast-pathway effective refractory period in the latter study was demonstrable with and without autonomic blockade. It has been shown in a computer model of dual-pathway physiology that the antegrade activation of the slow pathway may electrotonically delay fast-pathway depolarization.15 Based on this observation, therefore, shortening of the fast-pathway effective refractory period after slow-pathway ablation has been attributed to the elimination of such an electrotonic influence that the slow pathway might exert on the fast pathway.15 This hypothetical interaction may be accountable for shortening of the fast-pathway effective refractory period occurring in the clinical setting. However, in our series of 14 patients with demonstrable dual-pathway physiology at baseline, shortening of the fast-pathway refractoriness after ablation was encountered in only 2 patients (28%) despite a complete loss of the AV nodal dual-pathway physiology in 8 patients (57%). Nonetheless, it should be pointed out that although the initiation and maintenance of AVNRT require the existence of two anatomically and functionally distinct pathways known as fast and slow pathways, the AV nodal structure is probably more complex in patients with AVNRT than can be portrayed as a structure with a single fast and slow pathway. In fact, multiple AV nodal pathways may be demonstrable in as many as one third of patients.13 Therefore, in such a complex structure with possible reciprocal electrotonic interactions between different pathways, it might be difficult at times to assess the effect of a slow-pathway ablation on its faster counterpart and vice versa.
Ventricular Response During Atrial Fibrillation
The
ventricular response during AF is typically characterized by
irregular RR intervals. Although the exact reason for these
irregularities is not well understood, two possible mechanisms have
been offered. First, the concept of "concealed conduction"
introduced by Langendorf16 17 and supported by
several animal
studies18 19 20 21 suggested
that the degree of
concealment in the AV node during rapid and irregular transmission of
the fibrillatory atrial impulses was the main determinant of the
ventricular rate during AF. On the basis of this hypothesis, therefore,
the AV node behaves primarily as an electrical conduit that, depending
on its refractoriness and excitability, randomly allows a complete
transmission of the atrial impulses. In addition to the phenomenon of
concealed conduction occurring in the AV node, the rate and
irregularity of the atrial impulses22 and summation or
inhibition of the wave fronts approaching the AV node from different
inputs20 23 may contribute to the ventricular rate of
AF.
The second hypothesis suggests that the AV node functions solely as a
pacemaker and that its rate or timing of depolarization is
electrotonically altered by the atrial
impulses.24 25 26
Although the results of the present study cannot prove or disprove the validity of either of the two theories, prolongation of the RR cycles during AF after a selective slow-pathway ablation strongly suggests that the AV nodal conduction plays some role in the ventricular response to AF. Therefore, even if the concept of the electrotonic modulation is valid, our data support the notion that the atrial impulses must propagate through some portion of the AV node before they can modulate the AV nodal pacemaker.21
AV Nodal Modification for Control of Ventricular Response in Atrial
Fibrillation
Previous studies have shown that the mean ventricular
response
during AF correlates with the AV nodal conduction and effective
refractory period.27 28 Thus, it seems conceivable to
anticipate an increase in the RR cycle length during AF after the AV
nodal properties are modified. In this series of patients with AV nodal
reentry, we were able to demonstrate a significant reduction of the
ventricular rate during AF by ablating the critical slow pathway. These
results suggest that before the AV node was modified, the ventricular
response of AF was determined predominantly by the electrophysiological
properties of the slow pathway. Interestingly, a marked reduction of
the ventricular rate during AF was demonstrated in all 8 patients
(100%) in whom the AV nodal dual-pathway physiology was completely
eliminated, as opposed to only 3 (43%) of 7 patients who had
demonstrable dual-pathway physiology after ablation. Therefore, a
residual slow pathway after ablation, although unable to maintain
sustained AVNRT, was still capable of contributing to a relatively
rapid ventricular response during AF in most patients exhibiting
dual-pathway physiology. Conversely, among 4 patients without any
demonstrable dual-pathway physiology before the ablation, a
slow-pathway ablation resulted in a significant decrease of the
ventricular rate during AF in 2 patients without any marked
prolongation of the AV nodal conduction properties or refractoriness
after ablation. One might speculate that although the AV nodal
dual-pathway physiology could not be demonstrated in this subset of
patients, the slow pathway was probably the predominant pathway
determining the ventricular rate during AF before the AV nodal
modification.
Although we did not specifically address the effect of a fast-pathway ablation on the ventricular rate during AF, the possibility of achieving rate control seems unlikely, for two reasons. First, several studies have shown that a selective fast-pathway ablation does not alter the shortest cycle length of 1:1 AV conduction or the AV nodal effective refractory period.4 13 29 Second, the result of the present study has clearly shown that complete abolition of slow-pathway conduction leads to a significant slowing of the ventricular response during AF despite intact fast-pathway conduction, suggesting that, at least in this series, the slow pathway was the primary determinant of the ventricular rate in AF before ablation. In fact, one might argue that conduction of the atrial impulses across the fast pathway, by blocking retrogradely in the slow pathway, may ordinarily contribute to its concealment and, therefore, ablation of the fast pathway may potentially enhance the ventricular rate during AF. Obviously, further studies are needed to address this issue.
Prior Studies
Radiofrequency energy has been used to modify
the AV nodal
properties for control of the ventricular rate during atrial
tachyarrhythmias. Both the anterior/superior aspect of the interatrial
septum and the posterior/inferior aspect of the septal annulus of the
tricuspid valve have been targeted for achieving such a rate
control.30 31 32 The anterior/superior
approach was shown to
be initially effective in only 35% of patients with atrial
tachyarrhythmias, including AF.30 However, in a long-term
follow-up in patients with an initial successful AV nodal modification,
a rate control persisted in only one third of patients, and the
remaining patients either developed a complete AV block (54%) or had a
recurrence of their original symptoms.
Preliminary reports of the posterior/inferior approach have demonstrated a significant slowing of the ventricular response to AF in 70% of patients with chronic AF who were refractory to medical therapy.31 32 The remaining 30% of these patients either did not respond to this intervention or developed a complete AV block during application of radiofrequency energy. It should be pointed out that none of the studies mentioned above have assessed the presence of a dual-pathway transmission system in the study patients before the transcatheter ablation. Therefore, it remains unclear which patient populations will respond to these approaches and whether or not the rate control achieved by a posterior/inferior approach is solely due to a selective AV nodal slow-pathway ablation.
Clinical Implications
The results of this study clearly
demonstrate that in patients
with AV nodal reentry, a selective slow-pathway ablation can reduce the
ventricular rate during induced AF, particularly when AV nodal
dual-pathway physiology is completely abolished or the AV nodal
effective refractory period is lengthened after ablation. These data
lend support to the hypothesis that a rate control in patients with AF
undergoing a posterior/inferior approach is due to a selective
slow-pathway ablation.31 32 Furthermore, on the basis
of
these observations, it seems reasonable to anticipate that patients
with an underlying dual-pathway physiology might be more suitable
candidates for such a therapeutic modality than those without this
phenomenon.
One may argue that the reported success rate of AV nodal modification for rate control in patients with AF31 32 seems exceedingly higher than the incidence of dual-pathway physiology in patients without AVNRT. Although this argument cannot be dismissed entirely, several possibilities may be considered. First, even though the exact incidence of dual-pathway physiology in the general population is unknown, it is not uncommon to find this phenomenon fortuitously in individuals without any documented cardiac arrhythmia who undergo electrophysiological studies.33 Second, patients with a rapid ventricular rate during AF who do not respond adequately to the AV nodal blocking agents should be considered a subgroup of patients with unusual AV nodal electrophysiological properties. Therefore, the incidence of dual-pathway physiology in this patient population who were the subject of previous reports31 32 may be much higher than that in the general population. Third, although patients without dual-pathway physiology may also demonstrate a reduction of the ventricular rate during AF after a slow-pathway ablation, the magnitude of rate reduction may be far more significant in those with dual-pathway physiology.
Knowledge of the presence of dual-pathway physiology may be important in some patients undergoing a posterior/inferior ablation for rate control of AF. A complete abolition of this phenomenon may be used as a therapeutic end point, particularly when AF is paroxysmal and not present at the time of the ablative procedure. Once the AV nodal modification is verified by the loss of dual-pathway physiology, its impact on the ventricular rate of the induced AF can be determined.
Potential Limitations
Several points in the observations made
in this study deserve
further comment. First, none of the study patients had documented
clinical AF. Therefore, it remains unclear whether the results of the
present study can be extended to patients with clinical AF. Second,
the impact of a slow-pathway ablation on the ventricular response to AF
was assessed during autonomic blockade. Thus, in the absence of
autonomic blockade, and especially when the adrenergic tone is
enhanced, it remains unknown whether or not the AV nodal modification
will lead to any significant reduction of the RR cycle length. Third,
we did not specifically attempt to eliminate the AV nodal slow pathway
completely, as evidenced by the presence of residual dual-pathway
physiology after ablation in 7 patients (39%). It is possible,
therefore, that further attempts at a complete abolition of the AV
nodal slow pathways would have resulted in a rate control of AF in a
higher number of patients. Finally, the vast majority of our patients
had a common variety of AVNRT. The impact of a slow-pathway ablation on
the ventricular response to AF in patients with an underlying uncommon
AVNRT remains to be explored.
Summary and Conclusions
Successful slow-pathway ablation in
patients with AVNRT
significantly decreased the ventricular rate during induced AF as a
result of modifying AV nodal conduction and refractoriness. Notably,
ablation of the AV nodal dual-pathway physiology predicted a
significant reduction in the ventricular rate during AF. These findings
support the potential role of selective slow-pathway ablation as a
therapeutic modality for rate control in patients with clinical
AF.
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Acknowledgments |
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We would like to thank Chris Martin, Inga Hawkins, David Krum, MS, Brian Miller, and Brian Schurrer for their help in the preparation of this manuscript.
Received July 5, 1994; revision received September 19, 1994; accepted October 5, 1994.
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References |
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TopAbstractIntroductionMethods Results Discussion References |
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