Download Shortening of Fast Pathway Refractoriness After Slow Pathway

1103
Shortening of Fast Pathway Refractoriness After
Slow Pathway Ablation
Effects of Autonomic Blockade
Andrea Natale, MD; George Klein, MD; Raymond Yee, MD; Ranjan Thakur, MD
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Background Shortening of the anterograde effective refractory period (ERP) of the fast pathway has been reported after
radiofrequency ablation of the slow pathway. We hypothesized
that ERP shortening may be related to autonomic changes,
possibly catecholamine release, as a result of ablation.
Methods and Results To test this, 10 consecutive patients
with atrioventricular node reentry undergoing slow pathway
ablation were given autonomic blockade before the ablation
procedure. This was achieved by atropine 0.03 mg/kg and
propranolol 0.15 mg/kg IV supplemented by half the initial
dose after ablation and before the final study. A control group
of 10 patients underwent the protocol without autonomic
blockade. Before ablation, autonomic blockade did not alter
the ERP of either the fast pathway (295+±22 versus 298±26
milliseconds) or the slow pathway (264+36 versus 269±38
milliseconds). Autonomic blockade obscured dual pathway
physiology in 2 patients and brought it out in another 2 without
dual pathway physiology initially. Slow pathway ablation shortened the ERP of the fast pathway for the group as a whole
(331.5±54 versus 305.5±60 milliseconds, mean+SD, n=20,
P<.04). There was no difference in degree of ERP shortening
in control patients (23.5 +58 milliseconds) or autonomic blockade patients (25.5 +52 milliseconds).
Conclusions These data suggest that shortening of the ERP
of the fast pathway after slow pathway ablation is not mediated
by autonomic changes. (Circulation. 1994;89:1103-1108.)
Key Words * radiofrequency * autonomic agents physiology
Slow atrioventricular (AV) node pathway ablation
using radiofrequency energy is highly effective
for patients with AV node reentrant tachycardia.
Ablation can be guided either by recording "slow pathway" potentials1 or anatomically.2-4 Elimination of slow
pathway physiology has been accompanied by a shortening of the fast pathway effective refractory period.3'4
Decrease of the sinus cycle length after ablation led to
the suggestion3 that change in autonomic tone during
the procedure was responsible for this finding. To test
this hypothesis, we assessed the effects of slow pathway
ablation on AV node physiology in patients with and
without prior autonomic blockade.
Electrophysiological Study
Methods
The study population consisted of 20 consecutive patients
(15 women and 5 men) with a mean age of 37±14 years (range,
21 to 70 years) undergoing electrophysiological study and
radiofrequency catheter ablation of the slow pathway. Patients
were assigned to either the experimental or the control group
on the basis of laboratory schedule, taking into consideration
the length of the protocol in the autonomic blockade group.
Ten patients, mean age 36±+16 years (2 men, 8 women),
underwent our standard ablation protocol and were used as
control subjects. The other 10 patients, mean age 38±13 years
(3 men, 7 women) received autonomic blockade before the
ablation. All patients had symptomatic AV nodal tachycardia
of the common type and had previously been treated with
antiarrhythmic drugs without control of symptoms. No patient
had structural heart disease.
Received September 21, 1993; revision accepted November 6,
1993.
From the Department of Medicine, University of Western
Ontario, London, Ontario, Canada.
Correspondence to Dr George J. Klein, University Hospital, 339
Windermere Rd, London, Ontario, Canada N6A SA5.
Written and verbal consent was obtained from all patients.
Each patient was studied in the fasting state under sedation
achieved with intravenous midazolam and fentanyl. Under 2%
local anesthesia, three quadripolar catheters were introduced
percutaneously into the right femoral vein and advanced to the
high right atrium, His bundle recording position, and right
ventricular apex, respectively. An octapolar catheter was
placed in the coronary sinus via the left subclavian vein. A
baseline study was performed in all patients to confirm the
diagnosis of AV node reentrant tachycardia5 and to measure
antegrade and retrograde conduction parameters. Briefly, the
study consisted of atrial and ventricular incremental pacing to
block and extrastimulus testing with at least two drive cycle
lengths. Presence of dual AV node physiology was established
by a sudden prolongation of the atrio-His (AH) interval of at
least 50 milliseconds for a 10-millisecond decrement during
extrastimulus testing. The stimulation sequence that most
clearly demonstrated dual physiology was identified and was
used as a quick reference for assessing ablation of the slow
pathway. In addition, the latter sequency of pacing was repeated three or four times to assess reproducibility of dual AV
node physiology and variability of fast and slow pathway
effective refractory period.
Autonomic Blockade Protocol
After the initial study was performed, autonomic blockade
was obtained by administration of 0.03 mg/kg atropine and
0.15 mg/kg propranolol.6-9 Atropine was given over a 2-minute
period and immediately followed by propranolol administered
over a 5-minute period. Electrophysiological study was repeated beginning 10 minutes later.
Radiofrequency Ablation
A 7F quadripolar deflectable catheter (Mansfield-Webster,
Watertown, Mass) with a large-tip electrode was used for
ablation. Radiofrequency energy was delivered by a device
that operates at 350 kHz and provides continuous monitoring
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Circulation Vol 89, No 3 March 1994
of current, impedance, and energy (RFG-3C, Radionics, Burlington, Mass). A power setting of 30 W was used for each
ablation attempt. Current was applied for 40 seconds if
junctional tachycardia was observed during the ablation. Application of energy was interrupted if junctional tachycardia
did not occur within 10 seconds or if impedance rose. The
approach used in our laboratory to achieve ablation of the
slow pathway was described recently.4 It consists of a series of
anatomically guided lesions directed to the region between the
orifice of the coronary sinus and tricuspid annulus. The left
anterior oblique view was used to confirm the position of the
catheter in the area of interest. The end point was elimination
of the slow pathway as evaluated by atrial extrastimulus
testing. In the absence of dual AV node physiology, elimination of all echo beats served as the marker of successful
ablation.
Evaluation After Ablation
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Thirty to 45 minutes after the last radiofrequency ablation,
the presence of slow pathway conduction was assessed by
programmed atrial stimulation. If antegrade slow pathway
conduction was eliminated, electrophysiological evaluation
was repeated according to the same protocol as previously. In
the patients subjected to autonomic blockade, half of the
initial dose of atropine and propranolol was provided as a
supplement, followed by electrophysiological study performed
10 minutes later. All patients were monitored continuously for
24 hours after the procedure. Patients were discharged without
antiarrhythmic medication and were reevaluated at 3 months
in the clinic. Follow-up electrophysiological testing was not
performed unless the patient developed evidence of recurrence of tachycardia.
Additional Measurements
The interval from atrial activation at the His bundle recording to atrial deflection at the proximal coronary sinus (AhAcs) was measured during AV node reentrant tachycardia and
ventricular pacing to assess whether shorter values, which may
reflect closer slow and fast pathways,2 predict fast pathway
effective refractory period shortening after ablation.
The longest AH interval with 1:1 atrioventricular conduction during incremental pacing was obtained in the autonomic
blockade group before and after ablation to assess whether
this parameter provides useful information to distinguish
successful slow pathway ablation even in the absence of dual
AV node physiology.
Statistical Analysis
Statistical analysis of electrophysiological data before and
after ablation and before and after autonomic blockade was
performed by use of the two-tailed paired Student's t test with
correction for multiple comparisons. Student's t test for independent samples was also used when appropriate. Data were
expressed as mean±SD. A probability value <.05 was considered statistically significant.
Results
Radiofrequency ablation was successful in eliminating slow pathway conduction in all 20 patients. None of
the patients included in the study developed transient or
persistent AH prolongation with delivery of radiofrequency energy. The two groups did not differ with
respect to age, sex, and sinus cycle length at baseline
(control, 825±+ 197 milliseconds versus study group,
817±229 milliseconds). In addition, the most common
site of successful slow pathway ablation was similar in
the two groups, being the midseptal region in 80% of
the cases. The mean number of radiofrequency applications required for slow pathway ablation (control,
TABLE 1. Electrophysiological Effects of Slow Pathway
Ablation in the Control Group (Group 1)
SCL
AH
1:1 Ant
1:1 Ret
Preablation
825+197
66+20
Postablation
857+177
66+18
423±75
401±90
338±50
401 --55
396-+-74
361±57
ERPFP
283±48
...
ERPsp
Ret ERPAVN
268±65
348±121*
SCL indicates sinus cycle length; AH, atrio-His interval; 1:1
ANT, 1:1 Ret, minimum cycle length maintaining one-to-one
conduction over the atrioventricular (AV) node anterogradely
and retrogradely, respectively; ERPFP, effective refractory period
of the fast pathway; ERPsp, effective refractory period of the slow
pathway; and Ret ERPAVN, retrograde effective refractory period
of the AV node.
*P<.05.
17±9 versus study group, 16±8) and the total fluoroscopy time, including the diagnostic study (control,
30±12 minutes versus study group, 28±16 minutes),
were not different.
Effects of Slow Pathway Ablation in the
Control Group
Sustained slow-fast AV node reentrant tachycardia
was induced in 9 of 10 patients before ablation. In the
remaining patient, nonsustained tachycardia was induced. Clear evidence of dual AV node physiology was
present in all patients before ablation. Sinus cycle
length prolonged slightly after ablation (825 ± 197 versus
857±+177 milliseconds, P=NS). This reflected a decrease of heart rate in 6 patients and increase in 3. The
effects of ablation on the refractory and conduction
properties of the AV node are shown in Table 1. There
was no change in the AH interval. The anterograde
Wenckebach cycle length increased slightly (401±55
versus 423±75 milliseconds, P=NS). The antegrade
effective refractory period of the AV node prolonged
(283±48 versus 338±50 milliseconds, P<.01), whereas
the effective refractory period of the remaining fast
pathway shortened (361+57 versus 338±50 milliseconds, P=.09). The average decrease of the fast pathway
effective refractory period was -23.5±58 milliseconds
(range, +60 to -120 milliseconds).
One patient had no retrograde ventriculoatrial conduction before ablation as opposed to two after ablation. The patient who apparently lost retrograde conduction had a preablation retrograde Wenckebach cycle
length equal to the postablation sinus node cycle length.
Retrograde Wenckebach cycle length did not change
after ablation (396±74 versus 401±90 milliseconds,
P=NS), but there was an increase in the retrograde
refractory period of the AV node (268±65 versus
348±121 milliseconds, P=.02). Increase of the retrograde AV node effective refractory period was usually
associated with prolongation of the sinus node cycle
length after ablation.
Effects of Autonomic Blockade
Before autonomic blockade, sustained AV node reentrant tachycardia was induced in 8 of 10 patients.
Natale et al Autonomic Blockade After Slow Pathway Ablation
1105
HL266212
4001
300'
* .
0
S
300'
Cl
Cl
Cl
N9
200
OS.
S
00
100
100
*
o
1 50
n
200
300
400
A1A2
500
600
FIG 1. Curve relating atrio-His (AH) interval to prematurity of
atrial extrastimuli in a patient. Before autonomic blockade, dual
atrioventricular node pathway physiology is present (o). After
autonomic blockade (e), conduction over the slow pathway is
eliminated. A1A2 indicates interval between atrial deflection of
the last drive cycle and the extrastimulus (at the His bundle
catheter); A2H2, AH interval at the His bundle catheter after the
extrastimulus.
Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017
After autonomic blockade, tachycardia was still inducible in only two of these patients. A discontinuous AV
node function curve was present in 8 subjects at the
baseline study. Autonomic blockade brought out dual
AV node physiology in 2 patients (patients 3 and 6) but
obscured it in 2 others (patients 2 and 9). In patient 2,
slow pathway conduction was abolished after autonomic
blockade (Fig 1). In patient 9, the AV node function
curve became continuous after autonomic blockade
because of slower conduction of the fast pathway. This
resulted in a more progressive AH interval prolongation. However, tachycardia was consistently induced
with the same coupling interval that was associated with
30-millisecond prolongation of the AH interval. This
was considered to be the fast pathway effective refractory period (Fig 2).
When autonomic blockade revealed dual AV node
physiology, this reflected a shift to the left of the slow
pathway curve, which was favored by a reduction in the
atrial functional refractory period in patient 3. In
addition, the degree of overlap between the fast and
slow pathway components of the AV node curve diminPD 504938
400
OS&
300
Cl
Cl4
200
Cl4
0
200
0
0000
100
ot
1 50
250
350
450
550
A1 A2
FIG 2. Curve relating atrio-His (AH) interval to prematurity of
atrial extrastimuli in a patient. Discontinuous curve (o) became
continuous (5) because of predominant 3-blocking effect on the
fast pathway, which resulted in a more progressive AH prolongation and transition from fast to slow pathway. A1A2 indicates
interval between atrial deflection of the last drive cycle and the
extrastimulus (at the His bundle catheter); A2H2, AH interval at
the His bundle catheter after the extrastimulus.
250
350
450
550
A1A2
FIG 3. Atrioventricular (AV) node function curve before (o) and
after (o) autonomic blockade in a patient. Autonomic blockade
disclosed dual AV node physiology, possibly by shortening slow
pathway refractoriness. In addition, shortening of the functional
refractory period of the atrium allowed shorter A1A2 to be
achieved. A1A2 indicates interval between atrial deflection of the
last drive cycle and the extrastimulus (at the His bundle catheter); A2H2, AH interval at the His bundle catheter after the
extrastimulus.
ished because of a rightward shift of the fast pathway
effective refractory period in patients 3 (Fig 3) and 6.
Sinus node cycle length was significantly shortened
after autonomic blockade (817+229 versus 624± 72 milliseconds, P=.02). Unlike the control group, ablation
did not cause any heart rate change in this group
(624±72 versus 629±82 milliseconds, P=NS).
Effects of Autonomic Blockade on
Electrophysiological Properties of the AV Node
Autonomic blockade did not produce any change in AH
interval (70±15 versus 71±16 milliseconds, P=NS) or
minimum cycle length maintaining 1:1 antegrade (365 +69
versus 347+43 milliseconds, P=NS) and retrograde conduction (313±68 versus 306±51 milliseconds, P=NS).
Similarly, fast and slow pathway effective refractory periods (295±22 versus 298±26 milliseconds, P=NS and
264±36 versus 269±38 milliseconds, P=NS, respectively)
as well as the retrograde AV node effective refractory
period (258±50 versus 257±37 milliseconds, P=NS) were
not altered. Despite autonomic blockade, the fast pathway
effective refractory period shortened after ablation of the
slow pathway (298±26 versus 273±50 milliseconds,
P=.08). The mean shortening of the effective refractory
period was -25.5±51 milliseconds, and it ranged from
+50 to -90 milliseconds (Fig 4).
Effects of Ablation on the Electrical
Properties of the AV Node in the
Presence of Autonomic Blockade
No change in antegrade and retrograde AV node
refractoriness and Wenckebach cycle was documented
in the group with autonomic blockade. Unlike the
control group, the retrograde effective refractory period
of the AV node did not prolong (257±37 versus 266+57
milliseconds, P=NS) (Tables 2 and 3).
Additional Measurements
The Ah-Acs interval was measured during AV node
reentrant tachycardia as a poterntial reflection of the
distance between the fast (anterior) and slow (posterior) pathways. There was no difference in this interval
between patients with shortening of the fast pathway
1106
Circulation Vol 89, No 3 March 1994
RE 134283
400-
300
0
Ce
200
100-
o
1 50
250
350
450
550
650
A1 A2
FIG 4. Atrioventricular node function curve before (o) and after
(V) ablation in a patient undergoing autonomic blockade. After
elimination of the slow pathway, shortening of the fast pathway
refractoriness is observed despite autonomic blockade. A1A2
indicates interval between atrial deflection of the last drive cycle
and the extrastimulus (at the His bundle catheter); A2H2, AH
interval at the His bundle catheter after the extrastimulus.
Downloaded from http://circ.ahajournals.org/ by guest on June 17, 2017
effective refractory period and those without (13.8±10
versus 9.1±7 milliseconds, P=NS).
The longest AH interval during incremental pacing
with 1:1 AV conduction appeared to be a useful indicator of persistence of the slow pathway regardless of
the presence of dual AV node physiology during extrastimulus testing. After successful ablation of the slow
pathway, the longest AH interval achievable systematically decreased (291±82 versus 118±26 milliseconds,
P=.00005).
Discussion
Shortening of the fast pathway effective refractory
period has been reported3,4 immediately after ablation
of the slow pathway. This observation seems to depend
on complete elimination of slow pathway conduction.
Indeed, this finding has not been described in other
series with higher percentages of residual slow pathway
conduction after ablation.1,2 Kay et al3 suggested either
increased sympathetic tone or selective destruction of
TABLE 2. Electrophysiological Effects of Slow Pathway
Ablation After Autonomic Blockade (Group 2)
Postablation,
Preablation,
Autonomic
Autonomic
Blockade
Preablation
Blockade
624±72*
629±82.7
817±229
SCL
68±16
AH
71+15
70+15
1:1 Ant
347±43
367±61
365+69
1:1 Ret
311+48
313+68
306±51
298±26
273±50
295+22
ERPFP
264±36
...
269±38
ERPsp
257+37
Ret ERPAVN
258±50
266±57
SCL indicates sinus cycle length; AH, atrio-His interval; 1:1
ANT, 1:1 Ret, minimum cycle length maintaining one-to-one
conduction over the atrioventricular (AV) node anterogradely
and retrogradely, respectively; ERPFP, effective refractory period
of the fast pathway; ERPsp, effective refractory period of the slow
pathway; and Ret ERPAVN, retrograde effective refractory period
of the AV node.
*P<.05, preablation autonomic blockade compared with preablation.
parasympathetic innervation to explain the tendency of
the fast pathway effective refractory period to shorten.
Supporting their hypothesis was the faster heart rate
after ablation. Our study demonstrates that ablation of
the slow pathway induced shortening of the fast pathway effective refractory period and that the extent of
this change was not affected by autonomic blockade.
Recently, Lesh et aD10 proposed that an electrotonic
interaction between fast and slow pathway may produce
such changes. Electrotonus simply defined is a voltage
change attributable to the flow of current through a
structure.1" In the case of an excitable membrane, it is
the change of potential produced by current flows that
occur whenever a voltage difference exists between two
sites within the syncytium. Cranefield and Hoffman12
first reported that the subthreshold depolarizing pulses,
such as electrotonic current, applied during repolarization prolong the action potential duration of papillary
muscle. Subsequently, others have demonstrated the
influence of electrotonic interaction on the action potential recorded from different regions of the myocardium.13-18 It appears that myocardial refractoriness and
action potential duration are dependent on the pattern
and the timing of activation. Therefore, the sequence of
excitation and different speed of propagation affect
local recovery properties through electrotonic interaction that operates during the excitation process. Electrotonic influence reflects the existence of anisotropy
and nonuniform activation in the myocardium. In the
case of the AV node tissue and surrounding myocardium, when the entire region has been excited, current
from the last area to be activated, namely the slow
pathway, may retard repolarization of areas excited
earlier in the activation sequence such as the fast
pathway. Loss of this interaction after ablation might
then shorten refractoriness in the fast pathway. However, if this were the case, the shortening of the effective
refractory period of the fast pathway should be expected in all patients, whereas it is evident in approximately 60% of them. We tried to distinguish patients
susceptible to shortening of the effective refractory
period of the fast pathway by analyzing the interval
between the atrial activation at the His bundle region
and the coronary sinus during reentrant tachycardia. A
shorter Ah-Acs interval may identify a more closely
spaced fast and slow pathway,2 heralding higher probability of electrical interaction. In our population, the
Ah-Acs interval did not predict the effect of slow
pathway ablation on fast pathway effective refractory
period. However, patients in whom ablation was followed by prolongation of the fast pathway effective
refractory period had a shorter Ah-Acs interval. It
seems conceivable that fast pathway effective refractory
period prolongation may reflect less "selective" damage
to the slow pathway.
Finally, acute effects of radiofrequency delivery in the
relatively small triangle of Koch may also be implicated
as a potential mechanism for the shortening of the fast
pathway effective refractory period. In this case, transmission of heat from the site of ablation to the surrounding tissue might have influenced the conduction
properties of the fast pathway fibers. In fact, increase of
temperature below the values required to permanently
injure the myocardial tissue has been shown to increase
conduction velocity and shorten the refractory period.19
Natale et al Autonomic Blockade After Slow Pathway Ablation
1107
TABLE 3. Electrophysiological Effects of Slow Pathway Ablation in the Control and Autonomic Blockade Groups
Retr
Retr
SCL
1:1 Ant 1:1 Ant 1:1 Ret 1:1 Ret FPERP FPERP AVNERP
SCL
AVNERP AVNERP
Patient pre Abl post Abl pre Abl post Abl pre Abl post Abl pre Abl post Abl pre Abl AFPERP pre Abl post Abl
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Control group
1
950
550
450
400
960
400
500
500
395
265
+55
500
2
940
1020
450
400
450
500
360
310
300
-50
250
450
820
1020
500
3
550
360
340
410
400
340
-10
290
350
4
...
1280
870
420
...
450
330
...
400
...
380
-120
730
5
420
...
360
530
380
500
330
260
-30
...
...
640
710
345
340
420
350
310
265
-40
245
6
425
290
7
340
330
270
600
880
340
300
300
230
-60
190
180
320
8
770
1070
380
420
355
500
290
250
+30
265
500
340
320
9
700
880
360
360
360
260
230
+60
220
230
10
810
640
460
450
320
290
410
340
310
-70
300
280
Autonomic blockade group
1
680
730
380
450
330
320
290
320
260
+30
240
240
2
750
800
400
360
380
320
360
300
360
-60
300
310
3
670
270
670
380
440
300
290
330
240
+40
300
300
4
680
610
340
340
320
300
285
260
270
-25
220
190
340
5
610
600
250
320
230
300
210
270
-90
240
240
...
6
620
330
340
...
...
620
320
270
300
-50
...
7
580
550
360
320
270
280
230
300
220
-80
240
190
8
540
320
280
510
360
340
270
210
230
-60
300
300
9
...
600
610
380
460
...
400
300
350
240
+50
360
10
540
560
330
360
260
270
280
260
245
-10
210
270
SCL indicates sinus cycle length; pre Abl, before ablation; post Abl, after ablation; 1:1 Ant, 1:1 Ret, minimum cycle length maintaining
one-to-one conduction over the atrioventricular (AV) node anterogradely and retrogradely, respectively; FPERP, effective refractory
period of the fast pathway; AVNERP, effective refractory period of the slow pathway; AFPERP, absolute change of the fast pathway
refractory period after ablation; and Retr AVNERP, retrograde effective refractory period of the AV node.
However, other unknown effects of radiofrequency energy on the adjacent tissues cannot be excluded. Regardless of the mechanism, any such effect of radiofrequency delivery should be transient and should
disappear with time. Although we did not obtain electrophysiological data at long-term follow-up, results
from others20 support this explanation, with a tendency
of the fast pathway effective refractory period to prolong with time.20
Effects of Autonomic Blockade on Cardiac
Electrical Properties
Kay and colleagues3 have shown that slow pathway
ablation in the absence of autonomic blockade may be
accompanied by a reduction of the sinus cycle length.
This is consistent with either increased sympathetic tone
or selective destruction of parasympathetic innervation.
In the present study, both increase and decrease of the
heart rate were noted in individuals in the control group
after ablation. This may be related to variable degrees
of sedation in individuals. This was clearly autonomically mediated, being completely obscured by autonomic blockade. However, autonomic blockade was
unable to modulate the shortening of fast pathway
effective refractory period after slow pathway ablation.
Although incomplete sympathetic blockade at the AV
node level may be theorized, this is unlikely, considering
that autonomic blockade achieved in our study completely blunted the postablation sinus node response.
Since the sinus node and the AV node have similar
sensitivity and response to autonomic blockade,2' it is
probable that the same degree of autonomic inhibition
was achieved at the AV node level.
In most patients, administration of propranolol and
atropine before ablation reduced the sinus cycle length,
suggesting a predominant effect of the parasympathetic
system on this region.22-24 In contrast, autonomic blockade did not result in significant change in fast and slow
pathway properties, implying a balanced innervation to
the AV node. After autonomic blockade, however,
sustained reentrant tachycardia was inducible in only
two patients. It is possible that sympathetic activation
during tachycardia is important in the maintenance of
the arrhythmia.
Interestingly, autonomic blockade obscured dual
pathway physiology (ie, the discontinuous curve) in
some patients and made it manifest in others. Discontinuous curves became continuous after autonomic
blockade in two patients. In one of them, this reflected
a reduction of conduction velocity over the fast pathway, which allowed a more progressive AH prolongation with a smoother transition from the fast to the slow
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Circulation Vol 89, No 3 March 1994
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pathway. This behavior supports a predominant
13-blocking effect. In another patient, a continuous
curve after autonomic inhibition was the result of
complete abolition of slow pathway conduction, which
suggests that the sympathetic component of the autonomic system or the ,3-blocking effects prevailed on the
slow conducting pathway. In two patients, dual physiology became manifest only after autonomic blockade. In
one of them, the fast pathway curve shifted to the right
and the slow to the left after autonomic blockade. This
suggested a more pronounced 1-blocking effect on the
fast pathway and a predominant vagolytic effect on the
slow pathway (Fig 3). In the second patient, both fast
and slow pathway curves shifted to the left after autonomic blockade, suggesting vagolytic modulation on
both pathways. Shortening of slow pathway effective
refractory periods was more pronounced, reducing the
degree of overlap of the two function curves. A different
response of fast and slow pathways to autonomic blockade, suggesting unbalanced autonomic innervation to
different portions of the AV node region, is consistent
with previous reports after selective inhibition of one of
the two autonomic limbs.25-27
An unexpected observation was the tendency of
ablation to prolong retrograde AV node refractoriness
in the control group. This was not evident after autonomic blockade, suggesting that the latter effect is
autonomically mediated.
Conclusions
In summary, radiofrequency ablation of the slow
pathway is frequently followed by changes in sinus rate
and shortening of the fast pathway effective refractory
period. After autonomic blockade, the former was eliminated, whereas the latter persisted. The fast pathway
effective refractory period shortening documented in
our study and by other investigators reflected mechanisms other than autonomic modulation. It is possible
that loss of electrotonic interaction between fast and
slow pathway after ablation contributes to this effect.
Alternatively, a direct and acute effect of radiofrequency ablation on the fast pathway cannot be ruled
out. The absence of repeat, long-term electrophysiological testing constitutes a limitation of this study.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
Acknowledgments
This study was supported by the Heart and Stroke Foundation of Ontario, Toronto, Canada. Dr Klein is a Distinguished
Research Professor of the Heart and Stroke Foundation.
22.
23.
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Roman CA, Moulton KP, Twidale N, Hazlitt HA, Prior MI, Oren
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A Natale, G Klein, R Yee and R Thakur
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Circulation. 1994;89:1103-1108
doi: 10.1161/01.CIR.89.3.1103
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