Europace (2007) 9, 458–465
doi:10.1093/europace/eum067
Retrograde slow pathway conduction in patients
with atrioventricular nodal re-entrant tachycardia
Demosthenes G. Katritsis1*, Kenneth A. Ellenbogen2, Anton E. Becker3, and A. John Camm4
1
Department of Cardiology, Athens Euroclinic, 9 Athanassiadou St., Athens 11521, Greece; 2 Division of Cardiology, Medical
College of Virginia, Richmond, VA, USA; 3 Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;
and 4 Cardiac and Vascular Sciences, St George’s, University of London, London, UK
Received 22 February 2007; accepted after revision 21 March 2007; online publish-ahead-of-print 3 May 2007
KEYWORDS
Atrioventricular node;
Slow pathway;
Tachycardia;
Ablation
Aims To study retrograde slow pathway conduction by means of right- and left-sided septal mapping.
Methods and results Nineteen patients with slow–fast atrioventricular nodal re-entrant tachycardia
(AVNRT) were studied before and after slow pathway ablation. Simultaneous His bundle recordings
from right and left sides of the septum, using trans-aortic and trans-septal electrodes, were made
during right ventricular pacing. Pre-ablation, decremental retrograde ventriculo-atrial (VA) conduction
without jumps or discontinuities was recorded in eight patients (group 1). In six patients, retrograde
conduction jumps were demonstrated (group 2) and in the remaining four patients, there was
minimal prolongation of stimulus to atrium (St-A) intervals (group 3). The maximal difference (DSt-A)
between St-A intervals obtained with pacing at a constant cycle length of 500 ms and at the cycle
length with maximal retrograde VA prolongation was significantly longer measured from the right His
compared with the left His (122 + 25 vs. 110 + 33 ms, P ¼ 0.02, respectively) in group 1 and group 2
(140 + 23 vs. 110 + 35 ms, P ¼ 0.03), but not in group 3 (10+4 vs. 13 + 8 ms, P ¼ 0.35). Post-ablation,
DSt-A intervals were similar between right and left His recordings (77 + 37 vs. 76 + 33 ms, P ¼ 0.53,
respectively) in group 1, (100 + 24 vs. 103 + 21 ms, P ¼ 0.35) group 2, and (63 + 32 vs. 66 + 33 ms,
P ¼ 0.35) group 3.
Conclusion In patients with typical AVNRT, retrograde conduction through the slow pathway results in
earliest retrograde atrial activation on the left side of the septum and catheter ablation in the right
inferoparaseptal area abolishes this pattern. These findings are compatible with the concept of slow
pathway conduction by means of the inferior AV nodal extensions.
Introduction
Little data exist describing the physiology of retrograde
conduction over the slow pathway in patients with typical
(slow–fast) atrioventricular nodal re-entrant tachycardia
(AVNRT) before and after ablation. Initial studies have
demonstrated continuous ventriculo-atrial (VA) conduction
curves with either fixed or minimal prolongation of the VA
interval in patients with typical, slow–fast AVNRT.1–3 This
has traditionally been explained by attributing all retrograde conduction to the fast pathway.4 Decremental conduction or retrograde dual pathways, however, may also
occur,5–8 although retrograde dual pathway conduction is
demonstrated in only 4–23% of patients with slow–fast
AVNRT.7 The role, therefore, of retrograde slow pathway
conduction as the cause of decremental VA conduction is
unknown. Retrograde conduction through the slow
pathway is associated with a change in the retrograde
atrial activation sequence, with a switch from earliest
activation in the septal right atrium to earliest activation
recorded at the coronary sinus (CS) ostium.5,9 However,
although the atrioventricular (AV) node represents a true
septal structure, no detailed mapping of the left septum
has been performed during ventricular pacing.
We hypothesized that retrograde slow pathway conduction in patients with typical AVNRT can be mapped by analysis of the retrograde atrial activation pattern. We further
hypothesized that if the slow pathway represents a distinct
anatomical entity, ablation of the slow pathway in patients
with AVNRT should result in a change in the retrograde VA
conduction and the retrograde atrial activation sequence.
The purpose of this study was to perform detailed characterization of retrograde slow pathway conduction in patients
with AVNRT by means of right and left septal mapping
before and after slow pathway ablation.
Methods
Patients
* Corresponding author. Tel: þ30 210 6416600; fax: þ30 210 6819779/
6416661.
E-mail address: [email protected]
Nineteen patients with discontinuous AV nodal conduction curves
and inducible typical slow–fast AVNRT were studied before and
& The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: [email protected]
Retrograde slow pathway conduction
after successful completion of the ablation procedure.
Atrioventricular nodal re-entrant tachycardia was diagnosed
according to standard criteria.10 Slow pathway ablation was accomplished by a combined anatomic and electrogram recording
approach from the right side in all patients.11,12 Patients were
studied in the post-absorptive state, under sedation with diazepam
and diamorphine, and after all antiarrhythmic agents had been discontinued more than 5 days. No patient had received amiodarone
for the preceding 3 months. The study received approval from our
institutional review board, and all patients signed written, informed
consent.
459
St-A measured from R His and proximal coronary sinus electrode
(pCS), were evaluated through the sign-rank test. This analysis
was repeated for St-Amax D and DSt-A. Intra-observer reproducibility
of activation patterns was evaluated using the Bland–Altman
method,16 which indicates the smallest detectable difference (i.e.
the amount of detectable change above the random measurement
error). The 95% confidence interval was estimated using the
Electrophysiological study
Electrodes were introduced into the right atrium, across the tricuspid valve to record a right-sided His bundle electrogram, the CS, the
right ventricular apex, and retrograde through the non-coronary
cusp of the aortic valve to record a left-sided His bundle electrogram (Figure 1A–C) as described elsewhere.13–15 As retrograde positioning of the left septal catheter through the non-coronary cusp
inevitably results in mapping of the anterior part of the septum, a
trans-septal approach that should allow additional mapping of the
left side of the septum was also attempted in 10 patients.
Deflectable decapolar catheters with 2/5/2 mm interelectrode distance with 2 mm interelectrode separation were positioned to
record the His bundle electrogram on both the right and left sides
of the septum. A deflectable decapolar catheter with 2/5/2 mm
interelectrode separation was used for mapping the CS with the
proximal pair of electrodes negotiating the ostium of the CS.
Ventricular pacing was performed at a constant cycle length of
500 ms and stepwise decremented by 10 ms until AV nodal refractoriness was reached. Stimuli of 1 ms duration were delivered at
twice the diastolic threshold. Care was taken to ensure catheter
stability during recordings by means of continuous verification
against stored fluoroscopic images and electrogram characteristics
(Figure 2A and B).
Bipolar electrograms were filtered at 30–500 Hz, amplified at
gains of 20–80 mm/mV, and displayed and acquired on a physiological recorder (Bard LabSystem Duo and Pro; Bard, Billerica, MA,
USA), together with surface electrocardiograms. All measurements
were accomplished at a speed of 200 mm/s using the on-line
automated caliper system. Measurements were analysed by two
different investigators at separate time intervals to assess
inter-observer reproducibility. To assess temporal reproducibility,
all measurements were made during repeated episodes of right
ventricular pacing.
Definitions
Stimulus to atrium (St-A) intervals at constant pacing cycle lengths
were measured from the stimulus artefact to the initial deflection of
the atrial electrogram on the His bundle recording. Stimulus to
atrium values obtained at retrograde VA maximal conduction decrement (St-Amax D) were also recorded. Ventriculo-atrial conduction
jumps or maximum decrement associated with change of retrograde
atrial activation sequence were considered to indicate conduction
via AV nodal inputs that engage fibres with slow pathway conduction
properties (Figure 3). Retrograde conduction jumps were diagnosed
using the criterion of an increase of at least 50 ms in the VA interval
for a 10 ms decrease in the ventricular coupling interval.10 For comparative purposes, the difference (DSt-A) between St-A and St-Amax
13
PostD was also used as a measure of slow pathway conduction.
ablation, St-A values obtained at constant pacing and at maximal
retrograde VA conduction decrement were measured.
Statistical analysis
Differences between St-A measured from the His bundle electrogram recorded from the right septum (R His) and the His bundle
electrogram recorded from the left septum (TA His), and between
Figure 1 (A–C) Positioning of recording electrodes on the right and
left septa through a trans-aortic and trans-septal approach, and the
coronary sinus at the anteroposterior (A), 308 left anterior oblique
(LAO) (B), and 308 right anterior oblique (RAO) (C) projections; R
His, right His bundle recording electrode; TA His, trans-aortic left
His bundle electrode; TS His, trans-septal left His bundle electrode.
460
D.G. Katritsis et al.
Figure 2 (A and B) Verification of catheter position. Following the last ventricular extra-stimulus at 220 ms, there are both retrograde and
anterograde (seen on sinus beat as well as following drive train) His bundle potentials on the right and left His catheters through the aorta. (A)
No His can be seen on the trans-septal catheter. (B) No retrograde His is recorded, but anterograde His bundle potentials are seen in
the following sinus beat on all three His-recording catheters. Recordings are at 100 mm/s. I, lead I of the surface ECG; II, lead II of the
surface ECG; R His, right His bundle recording electrode; TA His, trans-aortic left His bundle recording; TS His, trans-septal left His bundle
recording; CS, coronary sinus.
method described by Shrout and Fleiss.17 Concordance between
observers was assessed using the kappa coefficient. All reported
P-values are based on two-sided tests and compared with a significant level of 5%. SPSS version 11.0 (SPSS Inc., USA) software was
used for all statistical calculations.
Results
Electrophysiological study and ablation
Nineteen patients (11 men) with a median age of 41 years
(range: 32–51) were studied before and after successful
completion of the ablation procedure. All patients had
normal left ventricular function, without evidence of
underlying structural heart disease. Atrioventricular nodal
conduction jumps and typical slow–fast AVNRT were
reproducibly induced by atrial pacing in all patients.
Ventricular pacing induced tachycardia in only two patients.
Recording of a reproducible His bundle electrode from the
trans-aortic approach was feasible in 18 patients.
Recording of the His bundle electrogram from the transseptal catheter was possible in only three out of the 10
patients in whom the technique was applied, despite prolonged mapping efforts. Comparisons between right and
left His recordings, therefore, were mainly made by considering the left His recorded from the trans-aortic electrode.
Slow pathway ablation was successfully accomplished in all
patients, with elimination of inducibility of tachycardia
and prevention of induction of echo beats. Continuous VA
nodal conduction curves were documented in all patients
after successful ablation.
Retrograde slow pathway conduction
461
Figure 3 Shift of the earliest retrograde atrial activation sequence at retrograde conduction jump. During constant ventricular pacing, atrial
activation on the right His precedes that recorded at other His catheters. At decremental retrograde conduction (S1–S2 ¼ 280 ms), the left
(trans-aortic) atrial activation slightly precedes that of the right (216 compared with 218 ms) (left panel). At retrograde conduction jump
(S1–S2 ¼ 270 ms), the earliest atrial activation is recorded on the left septum by the trans-aortic electrode and precedes that of the right
His by 12 ms (259–247 ms) (right panel). At maximum conduction decrement (S1–S2 ¼ 240 ms), this difference became 19 ms, as indicated
in Figure 5. Recordings are at 200 mm/s. Abbreviations are as in Figure 2.
Figure 4 Example of decremental retrograde conduction. Following the last ventricular extra-stimulus at 220 ms, there is a shift of retrograde atrial activation from the right to the left side of the septum, and DSt-A on the right His is 232–112 ¼ 120 ms, whereas in the left His
becomes 211–108 ¼ 103 ms. Recordings are at 200 mm/s. Abbreviations are as in Figure 2.
Slow pathway retrograde conduction
Pre-ablation
Pre-ablation, three patterns of retrograde conduction were
noted. In eight patients (group 1), decremental retrograde
VA conduction without jumps or discontinuities was recorded
(Figure 4). In six patients (group 2), typical retrograde conduction jumps with a discontinuous conduction curve were
demonstrated (Figure 5). In the remaining four patients
(group 3), there was minimal prolongation of St-A times
(Figure 6). Induction of tachycardia with ventricular pacing
was possible in two patients from group 3. Stimulus to
atrium and St-Amax D intervals with ventricular extrastimulation are presented in Tables 1–3. Considering DSt-A
times, there were significantly longer DSt-A intervals on
the right His compared with the left His (122 + 25 vs.
110 + 33 ms, P ¼ 0.02, respectively) in group 1 and group 2
(140 + 23 vs. 110 + 35 ms, P ¼ 0.03), but not in group 3
(10 + 4 vs. 13 + 8 ms, P ¼ 0.35). No statistically significant
differences were seen in DSt-A intervals on the right His
462
D.G. Katritsis et al.
Figure 5 Example of discontinuous retrograde conduction. Following the last ventricular extra-stimulus at 240 ms, there is a shift of the
earliest retrograde atrial activation from the right to the left side of the septum, and DSt-A is 152 ms (278–126) on the right and 129 ms
(259–130) on the left His. Recordings are at 200 mm/s. Abbreviations are as in Figure 2.
Figure 6 Example of non-decremental retrograde conduction. Following the last ventricular extra-stimulus, there is no shift of retrograde
atrial activation sequence, and DSt-A is 8 ms on the right and 11 ms on the left His. Recordings are at 200 mm/s. Abbreviations are as in
Figure 2.
compared with those on the pCS in group 1 (122 + 25 vs.
118 + 20 ms, P ¼ 0.10), group 2 (140 + 23 vs. 115 + 47 ms,
P ¼ 0.21), and group 3 (10+4 vs. 10 + 4 ms, P ¼ 0.72).
Post-ablation
Post-ablation, all patients demonstrated decremental
VA conduction without conduction jumps (Tables 1–3 and
Figure 7). Considering DSt-A times, no significant differences between the right and left His were noted (77 + 37
vs. 76 + 33 ms, P ¼ 0.53, respectively) in group 1,
(100 + 24 vs. 103 + 21 ms, P ¼ 0.35) group 2, and
(63 + 32 vs. 66 + 33 ms, P ¼ 0.35) group 3. Similarly, no significant differences were found between DSt-A times
obtained from the right His and pCS (77 + 37 vs.
Retrograde slow pathway conduction
463
Table 1 Group 1. Decremental retrograde conduction
Pre-ablation
R His
TA His
pCS
Post-ablation
St-A
St-Amax D
S1–S2
124 + 12
121 + 9
150 + 10
246 + 31
231 + 38
268 + 28
226 + 10
226 + 10
226 + 10
R His
TA His
pCS
St-A
St-Amax D
S1–S2
124 + 14
124 + 13
155 + 9
202 + 42
200 + 38
235 + 38
220 + 36
220 + 36
220 + 36
St-A intervals at constant pacing and at ventriculo-atrial conduction decrement (St-Amax D) during ventricular pacing; S1–S2 is the pacing interval at which
maximum ventriculo-atrial conduction decrement was obtained. R His, His bundle electrogram recorded from the right septum; TA His, His bundle electrogram recorded from the trans-aortic catheter on the left septum; pCS, proximal coronary sinus. Values are expressed in ms as mean + SD.
P . 0.05 for the comparison between R His and TA His.
P , 0.05 for the comparison between R His and TA His.
P , 0.05 for the comparison between R His and pCS.
Table 2 Group 2. Discontinuous retrograde conduction (ventriculo-atrial jumps)
Pre-ablation
R His
TA His
pCS
Post-ablation
St-A
St-Amax
129 + 7
128 + 8
155 + 12
269 + 27
238 + 41
270 + 45
D
S1–S2
230 + 15
230 + 15
230 + 15
R His
TA His
pCS
St-A
St-Amax D
S1–S2
149 + 16
151 + 23
161 + 5
249 + 16
255 + 20
269 + 17
228 + 18
228 + 18
228 + 18
St-A intervals at constant pacing and at ventriculo-atrial conduction jump (St-A jump) during ventricular pacing. S1–S2 is the pacing interval at which
maximum ventriculo-atrial conduction decrement was obtained. Abbreviations are as in Table 1.
P . 0.05 for the comparison between R His and TA His.
P , 0.05 for the comparison between R His and TA His.
P , 0.05 for the comparison between R His and pCS.
P . 0.05 for the comparison between R His and pCS.
Table 3 Group 3. Non-decremental retrograde conduction
Pre-ablation
R His
TA His
pCS
Post-ablation
St-A
St-Amax D
S1–S2
127 + 12
116 + 15
136 + 26
136 + 9
129 + 7
146 + 26
302 + 12
302 + 12
302 + 12
R His
TA His
pCS
St-A
St-Amax D
S1–S2
116 + 19
108 + 22
132 + 26
179 + 13
174 + 11
190 + 24
235 + 34
235 + 34
235 + 34
St-A intervals at constant pacing and at ventriculo-atrial conduction decrement (St-Amax D) during ventricular pacing. S1–S2 is the pacing interval at which
maximum ventriculo-atrial conduction decrement was obtained. Abbreviations are as in Table 1.
P . 0.05 for the comparison between R His and pCS.
P . 0.05 for the comparison between R His and pCS.
80 + 38 ms, P ¼ 0.26) in group 1, (100 + 24 vs. 107 +
18 ms, P ¼ 0.25) group 2, and (63 + 32 vs. 58 + 40 ms,
P ¼ 0.35) group 3.
Reproducibility of activation patterns
The sequence of atrial activation was reproducible during
ventricular pacing, with no change in the retrograde atrial
activation sequence when analysed at separate time intervals and by two different observers. Using the 95% limits
of agreement that provided from the Bland and Altman
method, we observed that 88% of the values were within
the interval of agreement. High concordance was also
found between the two observers (kappa statistic ¼ 0.84,
P , 0.01).
Discussion
Our results indicate that in patients with typical AVNRT, retrograde VA activation patterns compatible with both fast
and slow pathway retrograde conduction can be observed
during ventricular pacing, depending on the retrogradeeffective refractory periods of the two pathways. The fact
that initiation of tachycardia by ventricular pacing was possible in only two of our patients who demonstrated retrograde conduction decrement or dual pathways suggests
that the retrograde refractory period of the slow pathway
is usually shorter than that of the fast pathway. In 12–30%
of patients with AVNRT, tachycardia can be initiated by ventricular extra-stimuli.4,7 This mode of tachycardia initiation
requires that the slow pathway has a retrograde refractory
464
D.G. Katritsis et al.
Figure 7 Effect of catheter ablation. Same recording as in Figure 5. Following the last ventricular extra-stimulus at 220 ms, there is no shift
of the earliest retrograde atrial activation, and DSt-A is 110 ms on the right and 108 ms on the left His. Recordings are at 200 mm/s.
Abbreviations are as in Figure 2.
period longer than that of the fast pathway. Consequently,
the ventricular extra-stimulus blocks in the slow pathway
and is conducted over the fast one, thus preventing the
demonstration of any retrograde jump or significant
decrement.
When a retrograde conduction jump or maximum decrement occurs, there is a shift of retrograde activation with
significantly shorter Stim-A intervals on the left septum,
thus indicating that fibres from the slow pathway are primarily responsible for retrograde conduction. In this
respect, our findings are compatible with the observation
that the leftward inferior extension is shorter in length
than the rightward inferior extension18 and support our
earlier reports that the inferior nodal extensions may play
a role in slow pathway conduction.13–15 Damage to this
area through radiofrequency ablation resulted in abolition
of these differences. Catheter ablation in the right inferoparaseptal area has been shown to affect the right inferior
atrial extension.19 In a previous case report, histopathological examination of the septum following slow pathway ablation showed a white endocardial patch at the site of ablation
in the apex of Koch’s triangle, a remnant of the inferior
extension beyond the scar, and also distinct endocardial
thickening on the left ventricular septal surface.19 Thus,
ablation targeting the slow pathway from the right side of
the septum may well affect the left nodal extension as
well. These observations provide a rationale for the welldocumented observation that a successful ablation procedure may not result in complete slow pathway
elimination.20–22
Our data provide further evidence in support of the initial
hypothesis of Becker and co-workers13–15,18 supporting the
role of the inferior AV nodal extensions as the anatomic substrate of the slow pathway in human.
Study limitations
First, our patient numbers are small to allow detailed comparisons between the three groups. Perhaps unavoidably,
the nature of this study had made recruitment extremely
difficult. Secondly, our findings depend on conventional
catheter mapping techniques, and we cannot exclude
subtle catheter movements affecting our results.
Nevertheless, retrograde activation patterns were shown
to be consistent and reproducible. Thirdly, while performing
right ventricular pacing, it may be difficult to obtain recordings of the retrograde His bundle potential. In the literature,
retrograde conduction properties of the fast and slow
pathways have been derived indirectly by analysing the
conduction curves (V1–V2/A1–A2). Thus, in cases of discontinuous retrograde curves, the longest V1–V2 interval in
which conduction fails in the fast pathway is assumed to
be the retrograde-effective refractory period of the fast
pathway, and the shortest attainable A1–A2 interval on the
fast pathway conduction curves is assumed to be its functional refractory period. Similarly, analysis of curves left
of the discontinuity, which represent slow pathway conduction, provides the refractory periods of the slow pathway.4
This method assumes that no other causes of discontinuities
in VA conduction, such as intraventricular conduction
delays, exist. Of course, retrograde refractoriness of the
His-Purkinje system may also be an important factor with
respect to VA conduction patterns. Anatomic slow pathway
ablation, however, does not affect conduction in the His
bundle.
In summary, our study has shown that in patients with
typical AVNRT, VA activation patterns compatible with both
fast and slow pathway retrograde conduction can be
obtained. Retrograde conduction through the slow
Retrograde slow pathway conduction
pathway results in the earliest retrograde atrial activation
on the left side of the septum, and catheter ablation in
the right inferoparaseptal area results in abolition of this
pattern. These findings are compatible with the concept of
slow pathway conduction by means of the inferior AV
nodal extensions.
Acknowledgements
We are grateful to D. Panagiotakos, PhD, and G. Kurlaba, BSc, for
their help with statistical analysis.
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