(Circulation. 1996;93:1690-1701.)
© 1996 American Heart Association, Inc.
Articles |
Electrophysiological Mechanisms in Successful Radiofrequency Catheter Modification of Atrioventricular Junction for Patients With Medically Refractory Paroxysmal Atrial Fibrillation
From the Division of Cardiology, Department of Medicine, National Yang-Ming University; School of Medicine, Veterans General Hospital-Taipei; and Shin-Kong Memorial Hospital (S.-H.L.), Taiwan, ROC.
Correspondence to Shih-Ann Chen, MD, Director of Electrophysiology, Division of Cardiology, Department of Medicine, Veterans General Hospital-Taipei, 201 Sec 2, Shih-Pai Rd, Taipei, Taiwan, ROC.
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background Mechanisms and changes of electrophysiological (EP) characteristics in successful radiofrequency (RF) modification of right midseptal and posteroseptal areas for controlling rapid ventricular response to atrial fibrillation (Af) are not clear.
Methods and Results We studied 50 patients with medically
refractory paroxysmal Af. Group 1 consisted of 40 patients without dual
atrioventricular (AV) node physiology with modification
sites located in the mid/posteroseptal area. Of the 40
patients, 36 had successful modification (follow-up of 14±8
months), and 3 had AV block. Late follow-up
electrophysiological study (98±10 days)
showed pattern 1 (67%) with prolongation of AV node effective
refractory period (ERP, 
40 milliseconds) and Wenckebach block cycle
length (WBCL, 40 milliseconds); pattern 2 (22%) with prolongation of
AH interval (20 milliseconds), ERP, and WBCL; and pattern 3 (11%)
without any change in AV node conduction parameter. Change
in ventricular rate negatively correlated with change of
WBCL in patterns 1 (r=-.691, P=.019) and 2
(r=-.90, P=.01). Group 2 consisted of 10
patients with dual AV node pathway; elimination of slow pathway
property was performed. Late follow-up
electrophysiological study (92±7 days)
showed that change in ventricular rate negatively
correlated with change in AV node ERP (r=-.926,
P=.0001) and WBCL (r=-.969, P=.0001).
Four patients without significant modification effect had success after
RF energy was delivered to higher levels (follow-up, 15±7
months).
Conclusions RF modification of right mid/posteroseptal area is feasible in 92% of patients with paroxysmal Af. Mechanisms of successful modification might be elimination of posterior input and/or partial injury of the compact node. Furthermore, simple elimination of slow pathway might be inadequate for control of ventricular rate in patients with little difference in conduction properties between fast and slow pathways.
Key Words: atrioventricular node • fibrillation • atrium • mechanics • catheter ablation
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Pharmacological control of rapid ventricular response to paroxysmal atrial fibrillation may be difficult in some patients with normal or enhanced AV node conduction. Although class I and class III antiarrhythmic drugs might be effective in preventing and suppressing atrial fibrillation and AV node–blocking drugs might be effective in decreasing the ventricular response rate, they also may produce side effects and proarrhythmias.1 2 Alternative treatments include surgical maze procedure and ablation of AV junction with complete AV block to prevent rapid ventricular response during atrial fibrillation; however, the risk and morbidity associated with open heart surgery, the development of lifetime pacemaker dependency, and the loss of physiological AV activation sequence during sinus rhythm have been the major limitations of these procedures.3 4 5 6 7 8 9 10 11
Huang et al12 performed radiofrequency modification of AV junction in a canine model by an anterior approach, and Duckeck et al13 used the same method in a human study. Although the purpose of these two studies was to decrease ventricular rate during atrial pacing or atrial fibrillation, the results were disappointing because of a high incidence of immediate or late AV block and low clinical efficiency during the follow-up studies. Previous studies have demonstrated that radiofrequency modification of the right posteroseptal or midseptal area in patients with AV node reentrant tachycardia could eliminate slow pathway with cure of this tachycardia.14 15 16 17 Furthermore, follow-up electrophysiological study after elimination of slow pathway conduction showed that the fast pathway with its long Wenckebach block cycle length and effective refractory period was preserved.14 15 16 17 Previous studies demonstrated that deliverance of radiofrequency energy to the right posteroseptal and/or lower midseptal area could achieve control of ventricular response during atrial fibrillation by modification of the AV junction; authors suggested that the possible mechanism might result from elimination of slow pathway conduction with preservation of fast pathway conduction or from partial injury to the compact node.18 19 20 Almost all the patients in these studies had chronic atrial fibrillation, and evaluation of AV node electrophysiological properties after successful modification procedures was impossible.18 19 20
Mechanistic study of successful modification and changes of AV node conduction properties after modification is important in this era of interventional electrophysiology. Reports on radiofrequency modification of the AV junction for control of ventricular rate in patients with paroxysmal atrial fibrillation are limited, and the mechanisms in successful modification are not clear. The purposes of the present study were to develop a catheter modification technique to control the ventricular rate during atrial fibrillation in patients with or without dual AV node physiology and to investigate the electrophysiological mechanisms in successful modification of AV junction in patients with paroxysmal atrial fibrillation.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The study included 50 patients with medically refractory paroxysmal atrial fibrillation. All of the patients had frequent attacks of symptomatic paroxysmal atrial fibrillation with rapid ventricular response documented by ECG recordings. Patients were divided into two groups according to the absence (group 1) or presence (group 2) of dual AV node physiology, as documented by electrophysiological study. The frequency of symptomatic atrial fibrillation was estimated with the use of an event recorder (wrist recorder, Ralin Medical) during the week before radiofrequency modification procedures.
Electrophysiological Study and
Radiofrequency Catheter Modification
Informed consent was obtained from all patients, and the study
protocol was approved by the Human Research Committee at our
institution.
Baseline Electrophysiological
Study
As described previously, the patients were studied in the
postabsorptive, nonsedated state.17 21 22 Antiarrhythmic
drugs were discontinued for at least five half-lives in all
patients. Three multipolar, tip-deflectable, closely spaced (2 mm)
electrode catheters (Mansfield, Boston Scientific) were positioned in
the right atrium, His bundle area, and right ventricle; two orthogonal
electrode catheters (Mansfield) were positioned in the coronary
sinus for recording and/or stimulation. Three surface leads (I,
II, and VI) were recorded simultaneously with
intracavitary electrograms with the use of a VR-13 and Midas 2500
recorder system (Electronics for Medicine) at a paper speed of 100
to 150 mm/s and filtered between 30 and 500 Hz. Electrical stimulation
was delivered by a programmable stimulator (DTU-215, Bloom Associates,
Ltd) with a pulse duration of 2 milliseconds (ms) at approximately
twice the diastolic threshold. Baseline
electrophysiological study consisted of
measurement of conduction intervals, followed by determination of
atrial, AV node, and ventricular refractory periods
(coupling intervals decreasing by 10-ms intervals). The definition of
dual AV node physiology was according to classic
criteria.23 Presence of dual AV node physiology was
established by a sudden prolongation of the AH interval of at least 50
ms for a 10-ms decrement during extrastimulus study (including single
and double atrial extrastimuli). Dual AV node physiology and effective
refractory periods of fast and slow pathways were assessed two or three
times to ensure reproducibility. Rapid right atrial stimulation (pacing
cycle length from 600 ms to 2:1 capture was noted) and right
atrial extrastimuli (single and/or double extrastimuli) were used for
induction of atrial fibrillation. Average ventricular rate
and the longest and shortest RR intervals were determined for each
patient. They were obtained from the 1-minute ECG recording
immediately before radiofrequency ablation, at the completion of the
ablation procedure, and during the follow-up study.
Autonomic Blockade Protocol
Autonomic blockade was intended to determine the effects of
radiofrequency modification independent of
innervation.24 25 26 Furthermore, use of autonomic blockade
could prevent possible fluctuation of autonomic tone that might affect
the electrophysiological properties during
the procedures. After the initial study was performed, autonomic
blockade was obtained by intravenous administration of 0.2
mg/kg propranolol and 0.04 mg/kg atropine. Atropine was
administered over a 2-minute period and was immediately followed by
propranolol administration at 1 mg/L per minute.
Electrophysiological study was repeated 10
minutes after administration of propranolol, and assessment
of AV node function was completed within 20 minutes. In this study,
comparisons of serial changes of
electrophysiological parameters
were performed after autonomic blockade.
Radiofrequency Catheter Modification
Different modification techniques and end points were used in
group 1 and group 2 patients. In general, radiofrequency modification
of AV junction was performed 2 days after baseline
electrophysiological studies. A 7-F,
quadripolar electrode catheter with a 4-mm distal electrode, 2- to 5-mm
spacing between electrodes, and a deflectable tip (Mansfield, Boston
Scientific) was used to deliver radiofrequency energy (Radionic-3C,
Radionics) through the distal electrode; a large electrosurgical paddle
(Valleylab) positioned on the posterior chest wall served as the
indifferent electrode. Ventricular rates were measured for
1 minute in the baseline state and after a steady state effect had been
reached during the infusion of different doses of isoproterenol (2 and
4 µg/min for 10 minutes, respectively).
The ostium of coronary sinus was defined with coronary
sinus venography.27 Locations of the His bundle catheter
and the coronary sinus orifice were identified and recorded
in the cinefilms before modification procedures. The right atrial
septum adjacent to the septal leaflet of the tricuspid valve and
extending from the ostium of the coronary sinus to the
recording site at the His bundle was divided into posterior,
medial, and anterior regions; then, each of these three regions was
further divided into three, two, and two subsections, respectively.
They were posterior-1 (P1), posterior-2 (P2), posterior-3 (P3) (around
the coronary sinus ostium), medial-1 (M1), medial-2 (M2),
anterior-1 (A1), and anterior-2 (A2) (Fig 1
). The
ablation sites were also analyzed in the similar phase of
cardiac cycle and respiratory cycle.
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In group 1 (absence of dual AV node physiology), radiofrequency energy
was delivered during atrial fibrillation under continuous infusion of
isoproterenol (4 mg/min) to assess the immediate effect of
modification. Ventricular rate during atrial fibrillation,
obtained after administration of isoproterenol or atropine, might
simulate the maximal rate of clinical atrial
fibrillation.19 20 The ablation catheter was initially
positioned against the posterior septum, at the level of or lower than
the coronary sinus ostium, to record a stable electrogram
for at least 10 seconds with a maximal
atrial-to-ventricular electrographic ratio of 0.5
or less. Radiofrequency energy was delivered for 20 seconds with power
of 30 W. If there was no change in the ventricular rate or
no accelerating junctional rhythm within 20 seconds, higher energy
(step-up 5 W for 20 seconds, up to 40 W) was delivered to the
original site. Whenever there was an abrupt lengthening of the RR
interval or appearance of the accelerating junctional rhythm, the
application of energy was immediately discontinued. If the
ventricular rate was still higher than the end point
ventricular rate, higher energy was delivered to the
effective site or the ablation site was changed. In each subsection
level, radiofrequency energy was delivered to three close sites before
the ablation catheter was repositioned progressively upward (more
superior and anterior positions) along the tricuspid annulus.
Radiofrequency energy was never delivered at the upper third atrial
septum, where a His bundle potential was visible. The end point of the
procedure was an average ventricular rate of 
120 to 130
beats per minute (bpm) or an average ventricular rate of
70% to 75% of the ventricular rate during infusion of
isoproterenol (4 µg/min). If the end point ventricular
rate could not be achieved after delivering energy to the posterior
(P1, P2, P3) and medial (M1, M2) areas, the patient would choose
medication or complete ablation of AV node.
In group 2 (presence of dual AV node physiology), radiofrequency energy was delivered during sinus rhythm to eliminate slow AV node pathway. The presumed ablation sites were according to the subsection levels and electrogram patterns as the technique used in patients with AV node reentrant tachycardia.17 Energy was delivered at a power setting of 30 to 40 W for 20 to 60 seconds, and it was terminated immediately in the event of an increase in impedance, dislocation of the catheter, or occurrence of AV block.17 Because this study protocol for group 2 patients was designed to assess the role of the slow pathway in ventricular rate during atrial fibrillation, the end point was complete elimination of slow AV node pathway regardless of the change of ventricular rate during atrial fibrillation. If the ventricular rate measured after successful ablation of slow AV node pathway was higher than the optimal value (the same as group 1), the patients were encouraged to participate in follow-up at the clinic and receive late follow-up electrophysiological study to evaluate the change of AV node conduction properties and ventricular rate during atrial fibrillation. The patients who still had symptomatic atrial fibrillation after ablation of slow pathway would receive a second modification session with the technique used in group 1 patients.
For all group 1 and 2 patients, the ventricular rate was
determined again 30 minutes after the modification procedures.
Follow-up Study
After the modification procedures, the patients were observed in
the intensive care unit for 24 to 48 hours. If the patients had
transient AV block during the modification procedure, they were
observed in the intensive care unit for 4 days until the continuous
monitoring showed stable AV conduction. All patients had regular
follow-up, and patients with successful modification received no
antiarrhythmic drug. They were seen in the outpatient clinic at 1 week,
1 month, and then every 3 months; a history of recent symptoms was
taken. Physical examination, 12-lead ECG, 24-hour Holter monitoring,
and wrist recorder for cardiac events were performed. All patients
were encouraged to receive a late follow-up
electrophysiological study to evaluate the
change of AV node conduction properties.
Statistical Analysis
All continuous variables are expressed as mean±SD. The
differences before and after radiofrequency ablation were performed by
using Student's t test or ANOVA with repeated measures.
Regression analysis was used to correlate the
ventricular rate and AV node conduction properties. A value
of P<.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Characteristics
There were 41 male and 9 female patients with a mean age of 66±9 years (range, 43 to 80 years) who agreed to enter the study. All patients had frequent attacks of paroxysmal atrial fibrillation, with a mean history of 5±2 years (range, 1 to 8 years); they were all refractory to or intolerant of 4±1 antiarrhythmic drugs (including propranolol, digoxin, diltiazem, verapamil, quinidine, procainamide, disopyramide, propafenone, and amiodarone) for controlling paroxysmal atrial fibrillation or decreasing ventricular rate during atrial fibrillation. The estimated frequency of symptomatic atrial fibrillation during the week before modification procedure was 3±2 times a day (range, 1 to 12 times a day). Thirty patients (60%) had associated diseases, including hypertensive cardiovascular disease in 20, ischemic heart disease in 4, rheumatic valvular disease in 2, and chronic obstructive pulmonary disease in 4 patients. The symptoms during attacks of atrial fibrillation included blurred vision, dizziness, shortness of breath, chest pain, and syncope. Baseline echocardiographic examination before ablation showed that the mean left atrial diameter was 38±6 mm (range, 32 to 46 mm), left ventricular end-diastolic diameter was 47±10 mm (range, 37 to 60 mm), and the left ventricular end-systolic diameter was 34±5 mm (range, 30 to 41 mm). The mean right and left ventricular ejection fractions by radionuclide examination were 42±6% and 48±4%, respectively.
Baseline Electrophysiological
Characteristics
Baseline electrophysiological study
showed that the AH interval during sinus rhythm was 72±11 ms, the
effective refractory period of the AV node was 294±37 ms, and the
minimal atrial pacing cycle length with 1:1 AV nodal conduction
was 323±35 ms. Ten patients (20%) had dual AV node physiology. The
baseline average ventricular rate during atrial
fibrillation was 139±16 bpm. Atrial fibrillation was induced by atrial
extrastimuli (35 patients) or atrial burst pacing (15 patients). After
autonomic blockade, the
electrophysiological properties of AV node
conduction did not show significant change (Table 1).
The 10 patients with dual AV node physiology still had this property
after autonomic blockade.
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Effects of Radiofrequency Catheter Modification in Group 1
Patients
Immediate and Early Outcomes
The immediate results showed that 34 of 40 patients had marked
decrease in ventricular rate, fulfilling the end point of
the study protocol; 4 patients had unsuccessful modification with
ventricular rate still higher than the end point; and 2
patients had complete AV block immediately after modification
procedures. The average ventricular rates of the 34
patients with successful modification during baseline and 2 and 4
µg/min isoproterenol infusion before modification were 133±18,
161±12, and 179±16 bpm, respectively; they decreased significantly to
89±15, 116±23, and 125±22 bpm after successful modification
(P<.001) (Figs 2 and 3A). The 4 patients
with unsuccessful modification refused AV node ablation, instead
choosing to receive medication and hoping to have delayed effects from
radiofrequency energy on AV conduction. The average
ventricular rate obtained from the 4 patients during
baseline and 2 and 4 µg/min isoproterenol infusion before
modification was 135±19, 169±7, and 186±16 bpm, respectively;
ventricular rate changed to 112±27 (P=.015),
160±11 (P=.182), and 167±15 (P=.036) bpm
immediately after modification, respectively. Of the 8 patients with
transient AV block (mean duration, 9±6 seconds; range, 4 to 20
seconds) immediately after discontinuation of application of
radiofrequency energy, the sudden appearance of second-degree (1
patient; 16 hours later) or complete (4 patients; 1, 6, 12, or 14 hours
later) AV block occurred in 5 patients within 24 hours after
modification procedures. AV node conduction did not recover in the
patient with second-degree AV block but did recover in the 4
patients with complete AV block on the fourth, fifth, sixth, and
seventh day after ablation, respectively. Thus, the short-term
success rate was achieved in 33 of 40 patients (82.5%): 4 patients had
partial effects, 1 patient had 2:1 AV block, and 2 patients had
complete AV block. The 3 patients with AV block received
implantation of a physiological model
pacemaker.
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%) in
ventricular rate (bpm) and AV Wenckebach block cycle length
(AVWB) after successful modification in group 1 patients with pattern 1
change. b indicates quantitative slope.The mean number of radiofrequency pulses required for successful modification was 12±4 (range, 2 to 19 pulses). During successful radiofrequency pulse, the mean delivery time was 14±5 seconds (range, 8 to 26 seconds) and the mean power was 35±4 W (range, 30 to 40 W). The total procedure time was 2.6±1.4 hours (range, 1.5 to 4.1 hours), and radiation exposure time was 38±12 minutes (range, 20 to 62 minutes).
Late Results
Of the 34 patients with initial success, 1 patient had recurrent
palpitation with maximum ventricular rate up to 150 bpm
during atrial fibrillation at 2 weeks after ablation. This patient
underwent a second procedure without late recurrence. Nine
patients had occurrence of asymptomatic paroxysmal
atrial fibrillation detected with 24-hour Holter recordings
during the follow-up period, and the average
ventricular rate during atrial fibrillation was
significantly less than that before modification (81±9 versus 139±14
bpm, P<.01). The average ventricular rate
during atrial fibrillation obtained in the late follow-up study was
similar to that obtained immediately after modification (Fig 3A
).
The 4 patients without good response to AV node modification received
propranolol (120 mg/d) and/or verapamil (160 or
240 mg/d) to suppress AV node conduction and were free of symptoms
related to rapid ventricular rate. Three-month
follow-up electrophysiological study
showed that 3 of the 4 patients had significant decreases in
ventricular rate with isoproterenol (4 µg/min) (189±18
versus 131±10 bpm, P<.001) (group 1, pattern 1, patients
3, 6, and 7; Table 2) (Fig 3B). The 3 patients with
delayed modification effects on AV conduction discontinued medication
without any late recurrence of symptomatic atrial
fibrillation. The other patient (group 1, pattern 1, patient 4; Table 2) did not have a significant decrease in ventricular rate;
this patient refused to receive any further intervention and became
asymptomatic with oral propranolol (120 mg)
and verapamil (120 mg).
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After discharge, late AV block or symptomatic bradycardia was not observed in any of the patients with successful modification or in the patients with delayed success. Thus, total success was achieved in 36 patients (90%) who were asymptomatic without any antiarrhythmic drug during a follow-up period of 14±8 months (range, 3 to 22 months). Occurrence of symptomatic atrial fibrillation was not found. Early or late complication (including stroke or thromboembolism related to atrial fibrillation) did not occur in any patient.
Changes in Electrophysiological
Characteristics After Modification
Twenty-seven of the 37 patients (73%) without persistent AV
block received late follow-up
electrophysiological study (mean, 98±10
days; range, 80 to 110 days after modification). The
electrophysiological properties of the AV
node obtained after autonomic blockade were used for comparison between
the serial electrophysiological studies.
The electrophysiological
parameters obtained after autonomic blockade did not show
significant change (Table 1). The changes in
electrophysiological parameters
of AV node conduction were divided into three patterns (Table 2).
Pattern 1 had significant prolongation of AV node effective refractory
period (40 ms) and AV node Wenckebach block cycle length (40 ms);
pattern 2 had significant prolongation of AH interval (20 ms),
effective refractory period, and Wenckebach block cycle length; and
pattern 3 did not show significant change in AV node conduction
property. Comparisons among patterns 1, 2, and 3 showed (1) changes in
effective refractory period (28.3±27.3% versus 33.5±33.7%,
P>.05) and Wenckebach block cycle length (29.6±25.8%
versus 26.8±32.6%, P>.05) were similar between patterns 1
and 2 and (2) changes in baseline ventricular rate during
atrial fibrillation were similar among the three patterns
(-32.8±11.1%, -38.3±9.3%, and -27.7±7.8%;
P>.05).
Correlation between ventricular rate and
electrophysiological parameters
of AV node conduction showed different findings among patterns 1, 2,
and 3. Pattern 1 showed a change in average ventricular
rate that correlated negatively with a change in Wenckebach block cycle
length (r=-.691, P=.019, slope=-0.42) (Fig 3C)
but did not correlate with a change in AV node effective refractory
period (r=-.442, P=.0664, slope=-0.18). Pattern
2 showed (1) a change in ventricular rate correlated
negatively with a change in AH interval (r=-.90,
P=.01, slope=-0.49), AV node effective refractory period
(r=-.91, P=.01, slope=-0.25), and Wenckebach
block cycle length (r=-.93, P=.006,
slope=-0.27) and (2) of the 8 patients who developed transient AV
block in this study, 5 belonged to pattern 2, as did the 3 who had
delayed AV block with subsequent recovery of conduction. Pattern 3
showed that a decrease in ventricular rate did not
correlate with any of the AV node
electrophysiological parameters
because these parameters did not change after the
modification procedure.
Location of Effective Ablation Sites
Of the 36 patients who had successful modification, radiofrequency
energy was delivered to one site (16 patients, 44%), multiple close
sites within one subsection level (8 patients, 23%), or multiple close
sites on more than one subsection level (12 patients, 33%).
Comparisons among patterns 1, 2, and 3 showed that 4 of 18 (22.2%)
pattern 1 (patients 4, 14, 15, and 18), 1 of 6 (16.7%) pattern 2
(patient 6), and 1 of 3 (33.3%) pattern 3 (patient 3) patients had
effective modification sites confined to the P1, P2, and P3 levels
(P>.05); 9 of 18 (50%) pattern 1, 4 of 6 (66.7%) pattern
2, and 2 of 3 (66.7%) pattern 3 patients had the final effective
modification sites on the M2 level (P>.05). Of the 8
patients with transient AV block, the ablation sites with transient AV
block were one in P2 and seven in M2 levels. Of the 2 patients with
immediate complete AV block, the ablation sites were in M2 levels
(Table 2).
Effects of Radiofrequency Catheter Modification in Group 2
Patients
Immediate and Early Outcomes
Of the 10 patients with dual AV node physiology, the slow pathway
was eliminated completely. The mean number of radiofrequency pulses
required to eliminate the slow pathway was 4±2 (range, 2 to 9). During
successful radiofrequency pulse, the mean delivery time was 40±9
seconds (range, 30 to 60 seconds) and the mean power was 37±2 W
(range, 30 to 40 W). The total procedure time was 2.0±0.4 hours
(range, 1.5 to 2.6 hours), and radiation exposure time was 27±8
minutes (range, 20 to 39 minutes).
The immediate results showed that only 6 patients (pattern 1) had a
significant decrease in ventricular rate (-29±3%,
P<.001; range, -24% to -33%); the other 4 patients
(pattern 2) had no change in ventricular rate (-4±2%,
P>.05; range, -1% to -6%) (Table 3). The
average ventricular rate obtained from the 6 patients with
significant effects was 144±8, 169±10, and 186±11 bpm during
baseline, and 2 and 4 µg/min isoproterenol infusion before
modification; these ventricular rates decreased
significantly to 103±8, 120±9, and 135±11 bpm after successful
modification (Fig 4A). The 4 patients with partial
modification effects continued to receive medication and hoped to have
delayed effects from radiofrequency energy on AV conduction. The
average ventricular rate obtained from the 4 patients was
142±7, 170±10, and 188±11 bpm during baseline, and 2 and 4 µg/min
isoproterenol infusion, respectively, before modification; it showed no
significant change after modification (136±7, 160±9, and 178±9,
respectively; P>.05) (Fig 4B).
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Late Results
In patients with pattern 1 and pattern 2 changes, the average
ventricular rate during atrial fibrillation obtained in the
late study was similar to that obtained immediately after modification
(Fig 4A and 4B). The 6 patients with significant modification effects
continued to be asymptomatic without an antiarrhythmic
drug; 4 patients had occurrence of asymptomatic
paroxysmal atrial fibrillation during follow-up 24-hour Holter
recordings, and the average ventricular rate during
atrial fibrillation was significantly less than the
ventricular rate before modification (147±7 versus
98±8 bpm, P<.0001). The 4 patients without
significant modification effect continued to have symptoms related to
rapid ventricular rate during atrial fibrillation. These
patients agreed to receive radiofrequency modification using the same
protocol and technique as in group 1 patients. There was no occurrence
of transient or delayed AV block. All patients had significant decrease
of ventricular rate (-26.6±6.8%, P<.01) in
follow-up study (Fig 4B). The 4 patients continued to be
asymptomatic after successful modification without an
antiarrhythmic drug during the follow-up period. Thus, all group 2
patients were asymptomatic without an antiarrhythmic
drug after elimination of slow pathway or further modification of the
AV junction during a follow-up period of 15±7 months (range, 3 to
24 months). None of the patients had an occurrence of
symptomatic atrial fibrillation or complication (stroke or
thromboembolism related to atrial fibrillation).
Changes in Electrophysiological
Characteristics After Modification
Larger differences in baseline fast and slow pathway effective
refractory periods were found in the 6 patients with significant
modification effects (362±30 versus 285±21 ms, P<.001).
Late follow-up electrophysiological
study (mean, 92±7 days; range, 80 to 104 days) did not detect dual AV
node physiology in any of the group 2 patients, and the other
parameters were similar to those found immediately after
the ablation procedure (Table 3). The ventricular rate
negatively correlated with change in AV node effective refractory
period (r=-.926, P=.0001, slope=-31.3) and
Wenckebach block cycle length (r=-.969, P=.0001,
slope=-41.7) (Fig 5). The 6 patients with significant
modification effects showed a significant increase in AV node effective
refractory period (25±7%, P<.001; range, 18% to 38%)
and Wenckebach block cycle length (21±5%, P<.001; range,
16% to 31%); the other 4 patients without significant modification
effect did not show significant change in
electrophysiological characteristics (Table 3). The change in AV node effective refractory period was the
difference between the fast pathway effective refractory period after
slow pathway ablation and the slow pathway effective refractory period
before ablation.
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The 4 patients without significant modification effect in the first
modification session continued to receive further modification
procedures. The late follow-up study after the second modification
session showed significant prolongation in AV node effective refractory
period (25.7±11.4%, P<.001) and Wenckebach block cycle
length (25.6±8.2%, P<.001); furthermore, only 1 patient
had prolongation of AH interval after successful modification (Table 3).
Location of Effective Ablation Sites
The sites with successful elimination of slow pathway were three
in P1, five in P2, and two in M1 areas. However, the 4 patients with
successful results after the second modification session had effective
ablation sites in the higher subsection levels (Table 3).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Major Findings
This study has demonstrated that with the use of radiofrequency catheter modification of the posterior and/or midatrial septum, 92% of the patients with paroxysmal atrial fibrillation and uncontrolled ventricular rates refractory to antiarrhythmic drugs could achieve adequate slowing of the ventricular rate and be free of symptoms without any antiarrhythmic drug or the need for a permanent pacemaker. Follow-up electrophysiological study demonstrated different patterns of AV node conduction after modification. However, elimination of slow AV node pathway alone could not achieve the optimal ventricular rate in some patients. Elimination of posterior input and/or injury to the compact node were the possible mechanisms in successful modification.
Comparisons With Complete Ablation and Modification of
Anterior/Superior AV Nodal Area
The conventional target sites for complete ablation or
modification of the AV junction were located anteriorly and superiorly
on the tricuspid annulus.4 5 6 7 8 9 10 11 12 13 The most significant
drawback found in complete ablation of the AV junction is a lifelong
pacemaker dependency.4 5 6 7 8 9 10 11 Several investigators used an
anterior/superior approach to modify AV conduction, and most of the
patients with initial success had delayed recurrence of rapid
ventricular rate during atrial
tachyarrhythmias.12 13 Recent
studies19 20 have shown that the target sites for
modification of AV conduction with the posterior/inferior
approach were located in the posterior and/or midatrial septum. The
benefit of this approach is lower risk of complete AV block, and most
of the patients had preservation of AV node conduction. However, a
randomized study would be necessary to compare the morbidity,
mortality, and long-term effects in complete ablation or
modification of AV junction.
Possible Mechanisms in Successful Modification of AV Node
Conduction
The determinants of ventricular rate during atrial
fibrillation were controversial. In vitro studies28 29 30 31 32 33 34 35 36 37 38
have shown that asynchronous conduction, concealed conduction,
summation, cancellation of wave fronts, rate and irregularities of
atrial impulses, local reentry, pacemaker activity of the nodal cells,
electrotonic modulation, and the
electrophysiological parameters
of AV node function may all contribute. Studies in
humans39 40 showed that the mean ventricular
rate during atrial fibrillation correlated significantly with AV node
conduction properties. Thus far, no model has incorporated all of these
elements to account for the ventricular response rate in
atrial fibrillation.
Several investigators19 20 41 have speculated that the possible mechanisms in successful modification of AV junction for treatment of atrial fibrillation might include elimination of slow AV node pathway or partial injury to the compact node with decrease of ventricular rate during atrial fibrillation. However, none of these studies had electrophysiological parameters to support the hypothesis. In the present study, serial electrophysiological studies were performed in patients with or without dual AV node pathway physiology. Because there was no pathological finding and most of the patients with successful modification had the cumulative effects from multiple lesions, the specific mechanism was difficult to define.
Recording of slow pathway potential (high/low- or low/high-frequency potential) during clinical electrophysiological study and detailed endocardial mapping of the AV junction with multiple electrodes during cardiac surgery demonstrated that the fast pathway was located anterior and the slow pathway was located posterior to the compact AV node.14 15 42 43 44 45 Thus, the P level and lower part of the M level might be the posterior input area, whereas the upper part of the M level might be the compact node area.
Possible Elimination of Posterior Input
During atrial pacing from a single site, the impulses penetrate
the AV node from the same direction, through either the anterior or
posterior AV nodal input. During atrial fibrillation, both inputs may
be used randomly.32 In the isolated AV junctional
preparation of the rabbit heart, Janse32 compared the
functional properties of both inputs and found that AV conduction
through the anterior input was blocked at lower atrial pacing rates
than when the posterior input was used. Mazgalev et al34
obtained similar results during premature atrial stimulation. They also
demonstrated that during atrial fibrillation, AV conduction could be
modulated by "summation" or "inhibition" of atrial impulses
entering the AV junction from different inputs. In contrast to the
experiments of Janse and Mazgalev et al, Chorro et al37
did not find significant differences in ventricular
response rate during incremental atrial pacing from either site. A
possible explanation for this difference might be that in isolated
superfused AV junctional preparations, when subjected to high pacing
rates the interstitial fluid in the center of the AV node
is not adequately refreshed. A change in electrolyte composition in the
extracellular space might affect the conduction properties of the AV
node during high atrial rates.37
Previous studies14 15 16 17 have demonstrated that radiofrequency modification of the right posteroseptal or midseptal area in patients with AV node reentrant tachycardia could eliminate the slow pathway with cure of this tachycardia. Furthermore, the follow-up electrophysiological study after elimination of slow pathway conduction showed that the fast pathway was preserved with its long Wenckebach block cycle length and effective refractory period.14 15 16 17 Thus, the ventricular rate would be controlled by the ablation of some or all of these posterior atrionodal inputs if conduction were poorer through the anterior atrionodal inputs than through the posterior inputs.19 20 40 41 However, if the properties of the anterior and posterior atrionodal inputs were similar, the decrease in ventricular rate would be smaller after ablation of the posterior input. Results of the present study (group 2 patients with dual pathway physiology) showed that more marked decrease of ventricular rate occurred in patients with larger changes of the effective refractory period and Wenckebach block cycle length (larger difference between the electrophysiological properties of fast and slow pathways). Blanck et al40 also demonstrated that the mechanism of decrease in ventricular response to pacing-induced atrial fibrillation after ablation of the slow pathway in patients with AV node reentrant tachycardia could be mostly explained by elimination of posterior input.
In the patients without dual AV node physiology, the possible presence of posterior input could not be excluded. Because some patients might have better conduction properties of anterior input than posterior input (shorter refractory period of anterior input, without AH jump) and the AH interval, AV node effective refractory period and Wenckebach block cycle length would not change after elimination of posterior input.16 17 Decrease in ventricular rate after modification might result from destruction of the summation effects from both the posterior and anterior inputs.31 Furthermore, some patients might have a little overlapping of conduction properties between the anterior and posterior inputs (shorter refractory period of posterior input, without AH jump), and the AV node effective refractory period and Wenckebach block cycle length would increase after elimination of posterior input (without change in AH interval).16 17 These mechanisms are possible in group 1 patients. The present study demonstrated that the change in ventricular rate had a closer relation to change in AV Wenckebach block cycle length than to change in AV node effective refractory period (group 1 patterns 1 and 2 and group 2), and the relation between change in AV Wenckebach block cycle length and AV node effective refractory period is not 1:1; thus, these findings may support an argument for additional effects of radiofrequency ablation of slow pathway or AV nodal input, such as reduction in summation rather than simple prolongation of overall AV nodal effective refractory period, as a mechanism for ventricular rate control.
Possible Injury to the Compact Node
Several investigators have demonstrated that successful ablation
of the slow AV node pathway with a posterior approach might be
accompanied with inadvertent ablation of the fast AV node
pathway. Jackman et al14 reported injury to the fast
pathway in 1 patient after deliverance of radiofrequency energy at the
coronary sinus ostium. Langberg et al46 reported
that 14% of patients had unintended injury of the fast pathway during
slow pathway ablation with a posterior approach. Williamson et
al20 reported that transient or permanent third-degree
AV block occurred in 6 of the 19 patients who received radiofrequency
modification of AV junction, and the authors suggested that target
sites near the orifice of the coronary sinus may be
sufficiently close to the compact node to injure that structure. The
present study also showed that sites with successful outcome were
in the same locations as sites with transient AV block. It may be that
the rate was controlled, at least in some patients, by partial injury
to the compact node.
Microelectrophysiological studies47 48 have shown that the compact nodal cells are responsible for most of the increment of conduction time and block during Wenckebach periods. Because the accurate anatomic sites of compact AV node and transitional cells are unknown from the six subsection levels, possible injury of transitional cells in group 1 patients with different patterns was not clear.
In group 2 patients with pattern 1 change, simple elimination of slow pathway could significantly decrease ventricular rate; however, in group 2 patients with pattern 2 change, a significant decrease in ventricular rate was achieved after further modification of the AV junction in multiple sites of higher subsection levels. Thus, pathological lesions in the group 2 patients with pattern 2 change might include injury to the compact node in addition to the slow pathway (posterior input). The present study also suggested that some patients with dual AV node physiology must receive further modification after elimination of the slow pathway to fulfill the optimal end point.
Other Possible Mechanisms
Change in electronic modulation or concealment within the AV
junction due to radiofrequency energy, possible anatomic differences of
AV node, or different sensitivity of AV node to thermal effects of
radiofrequency energy must be considered.28 29 30 35 36 38
The effects of autonomic changes on AV conduction would be minimal
because autonomic blockade was used in the serial studies. Injury to
the His bundle is an unlikely explanation for control of the
ventricular rate because His bundle depolarization was not
visible in the target-site electrograms and the location of
transient or permanent AV block was always away from the His
bundle.18 19 20
Consideration of AV Block in Modification Procedures
Despite the absence of a His bundle depolarization in the
electrograms at the target sites and the posterior position of the
target sites relative to the AV node, the delivery of radiofrequency
energy at times resulted in transient or permanent AV block. In an
attempt to avoid AV block, radiofrequency energy was used as a
step-up method, discontinuing application of the energy whenever
there was a sudden slowing in the ventricular rate or
appearance of accelerating junctional tachyarrhythmia.
However, inadvertent AV block occurred in 3 patients.
Williamson et al20 reported that approximately two thirds
of the patients with transient AV block had delayed onset of persistent
AV block 36 to 72 hours after the procedure. In the present
study, 5 of the 8 patients with transient AV block had delayed
occurrence of AV block within 16 hours after the procedure, and 4
patients had recovery of AV conduction. It is possible that transient
thermal injury to the AV conduction system results in an inflammatory
reaction that is responsible for the delayed occurrence of AV block.
Although this study showed that the 4 patients had recovery of AV
conduction, long-term follow-up was necessary. The present
study also showed that most of the ablation sites with transient or
persistent AV block were in the M2 level; thus, care should be taken
when radiofrequency energy is delivered in a higher level. Furthermore,
if transient AV block occurs during an attempt to modify AV conduction,
continuous ECG monitoring on an inpatient basis is appropriate for a
period of 3 to 4 days to watch for a delayed recurrence of AV
block.
Accidental AV block with lifetime pacemaker dependency and loss of physiological AV activation sequence during sinus rhythm were the major limitations for the modification or complete ablation of AV junction.4 5 6 7 8 9 10 11 In consideration of the transient and delayed AV block and the possibility of late sudden death in patients receiving the modification procedure, more efforts would be necessary to decrease the radiofrequency pulse number and pathological area to decrease the possibility of late complications. In addition, this procedure should be reserved for patients with atrial fibrillation who are sufficiently symptomatic to justify ablation of the AV junction and implantation of a permanent pacemaker.
Late Outcome
Although the average ventricular rates during atrial
fibrillation decreased significantly immediately after the modification
procedure, the ventricular rate obtained from baseline
condition and isoproterenol infusion increased slightly during late
follow-up study. The ventricular rate increased during
the late follow-up study compared with the immediate result and may
reflect partial recovery of AV conduction from the immediate effects of
radiofrequency energy. Nevertheless, the average
ventricular rate during high-dose isoproterenol in the
late follow-up study was still 25% lower than at baseline
level, a degree of attenuation adequate to result in the persistent
resolution of symptoms. This change was similar to reports about
modification of AV junction for patients with chronic atrial
fibrillation.19 20 Furthermore, the late follow-up
ventricular rate did not differ significantly from the data
obtained immediately after the modification procedure. Thus, these
results demonstrated that immediate success could predict the late
effects in most of the patients.
Study Limitations
Several limitations should be considered. (1) Possible mechanisms
of successful modification were decided from the serial changes of AV
node electrophysiological properties and
modification sites; none of these changes could be proved by
pathological findings. (2) For the patients with effective modification
sites in multiple levels, complex mechanisms including elimination of
posterior input and injury of compact node were possible. (3) The other
10 patients without late follow-up
electrophysiological study might have other
patterns of change in electrophysiological
parameters. (4) Although detailed division of the anatomic
zones in the AV junction was used to guide the ablation site in this
study, there is still some difficulty in identifying these zones in
patients with shorter length of Koch triangle, and the catheter
position may change slightly with heartbeats and respiration. (5) Among
the group 1 patients, presence of dual AV nodal physiology could not be
excluded in 2 patients because atrial fibrillation was induced during
atrial double extrastimuli; however, the 2 patients did not have
evidence of slow pathway conduction during atrial single extrastimulus
and rapid atrial pacing. (6) The true incidence of atrial fibrillation
after successful modification procedure was not clear because
asymptomatic atrial fibrillation cannot be easily
detected.
Conclusions
Results of the present study suggest that it may be
appropriate to attempt first to modify AV conduction in patients with
medication-refractory paroxysmal atrial fibrillation and rapid
ventricular rates who are appropriate candidates for
ablation of the AV junction. The mechanisms of successful modification
might be elimination of posterior input and/or partial injury of the
compact node. Furthermore, simple elimination of slow pathway might be
inadequate for control of ventricular rate in patients with
smaller difference of conduction properties between fast and slow
pathways.
Received September 5, 1995; revision received October 26, 1995; accepted November 5, 1995.
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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