(Circulation. 1995;91:84-90.)
© 1995 American Heart Association, Inc.
Articles |
Characterization of Junctional Rhythm After Atrioventricular Node Ablation
From the Department of Medicine (J.F.A., J.A.Y.L.W., C.R.K.), Division of Cardiology and Departments of Medicine and Statistics (M.S.), University of British Columbia, Vancouver, Canada.
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Abstract |
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Background Catheter ablation of the atrioventricular (AV) node with radiofrequency current (RFC) is associated with the short-term onset of a junctional escape rhythm (JER) in nearly all patients. However, the origin of the JER and short-term thermal effects of RFC on this junctional pacemaker activity are ill defined.
Methods and Results Short-term and noninvasive long-term follow-up studies were performed to examine the electrophysiological characteristics of the underlying JER in 45 patients who had undergone AV nodal ablation with RFC. Baseline characteristics and responses to overdrive ventricular pacing and intravenous atropine followed by an incremental isoproterenol infusion were determined. Short- and long-term responses were compared. HV intervals before and after ablation were 49±9 and 48±9 milliseconds, respectively (P=NS). Follow-up was 11±8.3 months. JER cycle length was 1526±298 milliseconds in the short-term setting and was present in 44 patients (98%) in the long-term setting, measuring 1426±223 milliseconds (P<.005). Junctional recovery times increased exponentially as overdrive pacing rates increased–there was no difference between short-term and long-term responses. Drug responses within each study were all significant when compared with baseline. However, there was no significant difference between short- and long-term responses, except at the highest dose of isoproterenol. Intravenous atropine (1 mg) caused an 8.6±9.3% decrease in JER cycle length in the short-term setting compared with a 7.6±7.3% decrease in the long-term setting. The decreases in JER cycle length with isoproterenol infusion (short-term versus long-term) were 10.1±9.6% versus 9.6±7.4% with 1 µg/min, 15.8±11.7% versus 17.4±8.5% with 2 µg/min, 17.9±11.2% versus 21.4±9.1% with 3 µg/min (all P=NS), and 20.6±12.1% versus 24.8±9.1% with 4 µg/min (P<.01).
Conclusions Radiofrequency ablation of the AV node is associated with development of a JER that is stable in the long-term setting. The lack of change in HV interval after ablation locates the junctional pacemaker proximal to the central fibrous body. The pattern of drug responses suggests an origin within the proximal His bundle at its junction with the AV node rather than the AV node itself. The overall similarity between short- and long-term characteristics of junctional pacemaker activity mitigates against any reversible thermal effects of RFC on this pacemaker focus.
Key Words: atrioventricular node • pacemakers • catheter ablation
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Introduction |
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Current concepts of atrioventricular junctional pacemaker location, physiology, and response to pharmacological modulation are derived mainly from animal studies.1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 Evaluation of junctional pacemaker function in the healthy human heart is difficult as this activity is nearly always suppressed.19 Studies in patients with complete atrioventricular (AV) block and stable junctional escape rhythms have been limited, and interpretation of the results must take into account the heterogeneity of underlying pathology and the demonstrated variability in location of pacemaker activity.6 20 21 22 23 The advent of catheter ablation of the AV node for treatment of supraventricular tachycardias has provided a new model of junctional pacemaker activity in humans.24 25
Ablation using direct current shocks produces relatively large irregular lesions,26 27 making accurate localization difficult. In contrast, radiofrequency energy produces small, well-circumscribed lesions that can be targeted very accurately.28 29 30 31 The lesions produced by radiofrequency energy are areas of coagulation necrosis resulting from resistive tissue heating in the region of electrode contact,32 33 and, as such, there may be a boundary zone in which the thermal effects of radiofrequency current may not be sufficient to cause tissue necrosis and therefore may be reversible. These reversible thermal effects could modify junctional pacemaker activity in the short-term setting.
The objectives of this study were twofold: first, to investigate in detail the electrophysiological characteristics of the junctional escape rhythm that develops after catheter ablation of the AV node using radiofrequency energy and to attempt to locate the origin of junctional pacemaker activity and, second, to determine any reversible thermal effects of radiofrequency energy by comparing short- and long-term junctional pacemaker responses to various pacing and pharmacological interventions.
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Methods |
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Patient Selection
All patients who had AV nodal ablation with radiofrequency current at University Hospital, University of British Columbia, were eligible for this study. The study protocol was approved by the Institutional Review Board of the University of British Columbia, and written informed consent was obtained.
AV Nodal Ablation
The technique of AV nodal ablation used in
these patients has
been described in detail previously.31 A quadripolar
"reference" catheter with 5-mm interelectrode spacing was used to
localize the position of the earliest bipolar His-bundle electrogram
superiorly in the tricuspid ring in the region of the central fibrous
body. A quadripolar, deflectable ablation or "mapping" catheter
with a 4-mm tip electrode and 5-mm interelectrode spacing (Webster
Laboratories) was then manipulated so that the distal electrode was
located inferior and posterior to the reference position and the distal
bipolar electrogram showed a simultaneous or earlier His-bundle
potential. Radiofrequency current, at power outputs between 10 and 20
W, was delivered for up to 60 seconds between the distal electrode of
the mapping catheter and an indifferent patch electrode positioned over
the left scapula. If complete AV block was not produced, or was only
transient, mapping and delivery of radiofrequency current were repeated
as necessary. A permanent pacemaker was implanted within 24 hours of
successful ablation.
Short-term Junctional Pacemaker Activity
Immediately after
successful ablation, the presence or absence
of a stable escape rhythm was determined. Right ventricular pacing was
performed if no escape rhythm was present or if bradycardia was
associated with hemodynamic compromise. The persistence of complete AV
block was confirmed a minimum of 20 minutes after ablation.
In patients with persistent complete AV block and a stable junctional escape rhythm (as defined by regular ventricular electrograms preceded by His-bundle potentials but dissociated from atrial electrograms), one or more of the following parameters of junctional pacemaker activity were measured.
Baseline Junctional Cycle Length
Measurements were performed a minimum of 2 minutes after
cessation of ventricular pacing on recordings taken at a sweep speed of
100 mm/s.
HV Interval
Measurements were made on
recordings from the "reference"
catheter at the central fibrous body and compared with corresponding
measurements made immediately before ablation.
Junctional
Recovery Times
The response to ventricular overdrive pacing as
measured by
junctional recovery times following 60 seconds of pacing at incremental
rates of 55, 60, 65, 70, 75, 80, 90, and 100 pulses per minute (ppm).
If at any pacing rate the junctional recovery time was prolonged
sufficiently to produce presyncopal symptoms, further measurements were
ceased after the next higher pacing rate.
Results were normalized against spontaneous junctional cycle lengths so that both overdrive pacing cycle lengths and junctional recovery times were expressed as percentages of the junctional cycle length measured before each pacing run and are referred to as "pacing ratio" and "recovery time ratio," respectively.
Response
to Atropine and Isoproterenol
After the last measurement of junctional
recovery time, the
rhythm was monitored for 2 minutes before administration of 1 mg
atropine IV. The junctional cycle length was measured immediately
before atropine and at 1, 4, 8, and 12 minutes after atropine. At 12
minutes after atropine, an intravenous infusion of isoproterenol was
begun at 1.0 µg/min and increased every 3 minutes to 2.0, 3.0, and
4.0 µg/min or the maximum tolerated dose in this range. Cycle lengths
were measured before each increment in infusion rate and after 3
minutes at 4 µg/min.
Long-term Junctional Pacemaker Activity
Noninvasive follow-up
studies were performed on an outpatient
basis a minimum of 6 weeks after ablation with measurement of one or
more of the following.
Junctional Escape Rhythm
Patients' pacemakers were programmed to VVI mode at the minimum
rate necessary to allow an escape rhythm to emerge. The lowest rate
programmable was 30 ppm. If no escape rhythm was apparent at this rate,
brief periods of external pacemaker inhibition were used to unmask
escape rhythms with rates close to, but less than, 30 beats per
minute.
When an escape rhythm was established, a standard 12-lead ECG was recorded to confirm the presence of complete AV block and determine the QRS morphology. This ECG was compared with the ECG taken during junctional rhythm immediately after ablation. If the QRS morphology was unchanged, the escape rhythm was assumed to be junctional in origin.
The junctional cycle length was measured from a rhythm strip recorded at 100 mm/s.
Junctional Recovery Times
This was
possible only in patients with pacemakers capable of
unipolar sensing, allowing external inhibition of pacemaker output.
In a similar fashion to short-term measurements, ventricular pacing at rates between 55 and 100 ppm was performed with the implanted pacemaker for durations of 60 seconds. Pacing output was abruptly inhibited at the end of each pacing run by a train of external stimuli from a temporary pacemaker connected to skin electrodes on the anterior chest wall. The interval between the onset of the last paced ventricular complex and the first escape beat was measured. This interval was called the junctional recovery time if the escape beat displayed the same QRS morphology as the baseline junctional escape rhythm. Escape complexes showing altered QRS morphology, suggestive of a ventricular origin, were excluded from analysis, and recovery times were repeated at the same pacing cycle length to obtain a junctional escape beat.
Drug Responses
Atropine and isoproterenol
were administered, and measurements
were taken according to the same protocol used in the short-term
setting.
Statistical Analysis
All results are expressed as
mean±SD unless otherwise stated.
Regression of analysis was used to describe the relationship
between pacing ratio and recovery time ratio. Drug responses were
subjected to repeated measures ANOVA. Differences between matched
short-term and long-term responses for corresponding times and dosages
of drug administration were analyzed using paired t tests.
Holm's adjustment for multiple comparisons34 was included
to assess differences between sequential postatropine measurements and
isoproterenol dose increments.
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Results |
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Patient Characteristics
Fifty-five patients had undergone AV nodal ablation. Four patients declined participation in the study. Of the remaining 51 patients, 45 have returned for long-term follow-up and had data available from both short- and long-term studies. There were 26 men and 19 women (age, 62±11 years). AV nodal ablation was achieved with 2.9±2.3 (median, 2) radiofrequency applications delivering 19.9±4.4 W for 34±13.5 seconds. Thirty-seven patients had atrial fibrillation, which was paroxysmal in 23. Four patients had ectopic atrial tachycardia, and 4 patients had AV nodal reentry. In those patients with AV nodal reentry, 2 patients had AV nodal ablation performed at a time before we routinely attempted AV nodal modification for this arrhythmia. The other 2 patients had failed attempted AV nodal modification—one patient elected to proceed to complete ablation, and the other patient developed complete AV block as a complication of the attempted modification.
Short-term Findings
All 45 patients had stable junctional
escape rhythms (cycle
length, 1526±298 milliseconds) after ablation. HV intervals on
recordings from the "reference" catheter at the central fibrous
body were 49±9 milliseconds before ablation and 48±9
milliseconds
after ablation (difference not significant) (Table 1
).
No "split" His potentials were found in any patient. The QRS
morphology on surface ECGs recorded during junctional rhythm was
unchanged in 44 patients. One patient had a new right bundle-branch
block.
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Junctional recovery times were assessed in 18 patients in the
short-term setting, providing 109 data points (Fig 1).
Incremental overdrive pacing resulted in an exponential rise in
junctional recovery time according to the following equation:
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where y is recovery time ratio and x is pacing ratio. In all 18 patients, the recovery interval was always terminated by a junctional escape beat confirmed by intracardiac recordings and surface ECG morphology.
In 31 patients who received
atropine, there was a small but significant
decrease in junctional cycle length. The peak effect occurred at 4
minutes after atropine with junctional cycle length decreasing from
1526±298 to 1398±248 milliseconds (P<.001). The
percentage decrease in junctional cycle length from baseline was
8.6±9.3% (Table
).
The response to isoproterenol
was analyzed in a similar fashion
to atropine (Table). There was a decrease in cycle length from
1420±280 milliseconds at baseline (12 minutes after atropine) to
1271±268 milliseconds with an infusion rate of 1.0 µg/min,
1140±244
milliseconds with 2.0 µg/min, 1098±207 milliseconds with 3.0
µg/min, and 1083±254 milliseconds with 4.0 µg/min. Percentage
decrements from baseline were 10.1±9.6%, 15.8±11.7%,
17.9±11.2%,
and 20.6±12.1%, respectively. The decrease in junctional cycle length
was significant (P<.0001) at each dose when compared with
baseline. Also, the difference between dose increments was significant
(P<.01) for the 1.0- to 2.0-µg/min and 2.0- to
3.0-µg/min increments.
Long-term Findings
At 11±8.3 months after ablation, 44
of 45 patients had stable
junctional escape rhythms. The long-term junctional cycle length of
1426±223 milliseconds was significantly shorter than the junctional
cycle length measured in the short-term setting (P=.005)
(Table). One patient remained in paced rhythm at 30 ppm, and
the escape
rhythm could not be determined because external inhibition of the
permanent pacemaker was not possible. This patient's cycle length
immediately after ablation was 1850 milliseconds.
Long-term junctional
recovery times were measured in 26 patients
providing 168 data points (Fig 2). All recovery beats
had QRS morphology unchanged from the baseline junctional escape
rhythm. As in the short-term setting, there was an exponential rise in
recovery times with incremental pacing rate. The slope of the
regression curve was not as steep as that for the short-term
results-this difference was of borderline significance. However, only
12 of these 26 patients had measurements of junctional recovery times
performed both in the short-term setting after ablation and at
long-term follow-up (Fig 3). When the paired data were
compared in this subgroup, there was close concordance between short-
and long-term responses with no significant difference between the
regression curves (Fig 3c).
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In 35 patients, junctional
cycle length decreased from 1426±223 to
1353±186 milliseconds 4 minutes after atropine (P<.001).
When percentage changes in junctional cycle length after atropine were
compared with corresponding short-term responses in the 21 patients
having paired data, there was no significant difference
(Table).
The long-term isoproterenol response was also
similar to short-term
findings (Fig 4). Junctional cycle length decreased from
1370±204 to 1245±203, 1132±175, 1085±159, and
1036±145
milliseconds with 1.0, 2.0, 3.0, and 4.0 µg/min, respectively.
Comparisons of short- and long-term percentage changes in those
patients with paired data revealed no significant differences at 1.0-
(n=16), 2.0- (n=13), and 3.0-µg/min (n=8) doses.
However, at the
4.0-µg/min dose (n=8), the difference was significant
(P<.01) (Table).
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Discussion |
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The patients in the present study provide a model of junctional pacemaker activity in humans that has not been extensively studied previously. The method of AV nodal ablation used in these patients involved a small number of radiofrequency energy applications to a region inferior and posterior to the central fibrous body in the triangle of Koch.31 The site of the lesion producing complete AV block was most likely proximal to the penetrating His-bundle.35 36 Therefore, the origin of the escape rhythm could have been either the distal or "compact" portion of the AV node or the most proximal portion of the His-bundle at its junction with the AV node. The evidence supporting this localization is both direct and indirect.
There was no significant change in HV intervals measured at the central fibrous body. The His-bundle potentials recorded at this site had a 1:1 association with succeeding ventricular electrograms, confirming that the electrical impulse recorded was propagated without any added delay to the ventricles. There was no evidence of "split" His-bundle potentials, which would suggest a lesion in the His-bundle itself with the possibility of an escape rhythm originating distally.37 38 39 40 41 Indirect evidence supporting a distal AV nodal or an AV node/His-bundle junction origin for the escape rhythm comes from the drug responses. The AV junction is richly innervated by both parasympathetic and sympathetic nerve fibers,8 9 42 and modulation of autonomic tone can have profound effects on both AV node conduction and automaticity.4 6 8 17 However, it has been shown that the response to autonomic modulation of AV junctional automaticity is different than that observed for AV conduction.13 14 15 16 In contrast to AV conduction, in which the accentuated antagonism between sympathetic-parasympathetic interactions shows sympathetic predominance, AV junctional automaticity is predominantly under vagal control.9 12 17 Acetylcholine depresses AV nodal automaticity, and it has been suggested that the proximal AV node is more sensitive to acetylcholine and more responsive to atropine than the distal or compact AV node and His-bundle,4 5 38 41 43 44 although depression of automaticity of the proximal His-bundle by acetylcholine has been demonstrated.45 A recently reported immunohistochemical analysis of innervation of the human cardiac conduction system42 has shown that acetyl cholinesterase (AChE)-positive nerve fibers (ie, vagal inhibitory nerves) are more numerous in the transitional region of the AV node than in the compact node. Also, compared with the AV node itself, the penetrating His-bundle and bundle branches showed only isolated and sparse AChE positive nerve fibers. In our patients, there was an 8.6% decrease in junctional cycle length after intravenous atropine in the short-term setting and a 7.6% decrease at follow-up. These changes were highly significant statistically, although the physiological significance may be less marked.
Patients with congenital complete AV block may have a twofold or greater increase in junctional rate with exercise.20 This level of response, secondary to alterations in both parasympathetic and sympathetic tone that occurs during exercise, reflects an AV nodal origin. In the present study, response of junctional rhythm to exercise was not determined. The combination of 1 mg atropine followed by isoproterenol infused at the maximum rate of 4 µg/min produced 21% decrease in junctional cycle length in the short-term setting and 25% decrease at long-term follow-up. This response to catecholamine stimulation is in agreement with previous studies in animals that have shown a marked acceleration of junctional pacemaker automaticity after selective administration of norepinephrine via the AV node artery.4 13 In the study by Crick et al,42 nerves staining positive for neuropeptide Y and tyrosine hydroxylase (presumptive sympathetic innervation) were present in similar proportion to AChE-positive nerves in the compact AV node and were the predominant innervation of the penetrating His-bundle and bundle branches. Previous studies of heart rate responses to isoproterenol in humans have not clearly defined a dose-response curve for junctional pacemaker activity.46 47 48
The responses to pharmacological interventions noted above suggest that the focus of junctional pacemaker activity in this group of patients is a structure that is under minimal vagal control, yet retains responsiveness to sympathetic stimulation–the distal AV node/proximal His-bundle.
Overdrive suppression is a characteristic property of cardiac tissues that manifest intrinsic automaticity through spontaneous diastolic depolarization.19 However, the response to overdrive suppression of junctional pacemakers is different than that of the sinus node.49 50 Sinus node recovery times tend to follow a bell-shaped distribution with paradoxical shortening at higher pacing rates most likely due to entrance block into the sinus node. In the present study, the recovery times of junctional pacemakers showed an exponential response to incremental overdrive pacing as demonstrated by other investigators.51
Comparison of short- and long-term junctional recovery times in the subgroup of patients with paired data revealed a close agreement between short-term and long-term responses.
Haines and coworkers32 33 developed a thermodynamic model of myocardial tissue heating produced by radiofrequency energy. This model allows prediction of lesion size through measurement of electrode tip temperature and also states that lesion radius and depth are directly proportional to the electrode radius.33 Tissue temperature varies inversely with distance from the electrode tip, and the temperature at the border between viable and nonviable tissue was determined to be approximately 48°C. According to the thermodynamic model, tissue heating of some degree may extend as far as 10 mm from a radiofrequency electrode with a diameter of 1.6 mm and a constant tip temperature of 80°C.32 In this model, the zone of irreversible thermal damage would be surrounded by a rim of tissue at least 1 mm thick that is heated to more than 44°C and an additional 0.5 mm heated above 43°C. The effects of these temperatures on cellular automaticity is unclear as is the length of time required for any altered function to return to normal. The actual cooling of tissue has been shown to follow a monoexponential function with a half-time of temperature decay equal to 19 seconds.32 Therefore, if reversible thermal effects do occur, it is likely that a lower limit for the time to reversal could be less than 1 minute. Effects of this short duration would not be detected in our study. However, effects lasting 1 hour or more (the approximate time to completion of the short-term study protocol) might be detected.
In our group of patients, the difference between short- and long-term baseline junctional cycle lengths was statistically significant but, again, the physiological significance is less certain. In absolute values, this was approximately 100 milliseconds and equal to a difference in heart rates of approximately 3 beats per minute. Factors other than thermal effects of radiofrequency energy that may have been responsible for this difference include changes in autonomic tone and the presence of antiarrhythmic drugs in the immediate postablation setting. Antiarrhythmic drugs were discontinued after ablation. The similarities between short- and long-term junctional recovery times and drug responses (except at the highest dose of isoproterenol) argue against a prolonged thermal effect on short-term junctional pacemaker activity.
To summarize, the present study shows that radiofrequency ablation of the AV node is associated with development of a junctional escape rhythm that is stable in the long term. The origin of the junctional pacemaker could be in a region that includes the distal or compact AV node and the proximal portion of the His-bundle at its junction with the AV node. The pattern of response to atropine and isoproterenol is more consistent with proximal His-bundle than AV nodal origin. Reversible thermal effects of radiofrequency energy on junctional pacemaker activity lasting more than 1 hour were not detected, although short-term effects could not be excluded.
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Acknowledgments |
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Dr Yeung-Lai-Wah was supported by the British Columbia Health Care Research Foundation and the Heart and Stroke Foundation of British Columbia and Yukon.
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Footnotes |
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Reprint requests to John A.Yeung-Lai-Wah, MBChB, FRCPC, FACC, Vancouver Hospital (University of British Columbia), Department of Medicine, Rm S-124, 2211 Wesbrook Mall, Vancouver, BC, Canada, V6T 2B5.
Results of this study have been presented in part by Dr Alison in the Young Investigator Awards Competition during the 13th Annual Scientific Session of the North American Society of Pacing and Electrophysiology.
Received July 25, 1994; accepted July 31, 1994.
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