(Circulation. 1996;93:284-294.)
© 1996 American Heart Association, Inc.
Articles |
Electrophysiological Effects of Catheter Ablation of Inferior Vena Cava–Tricuspid Annulus Isthmus in Common Atrial Flutter
From the Cardiology Department, Lariboisière Hospital (B.C., O.T., P.C.), Paris, and Haut-Lévèque Hospital (M.H., B.F., J.C.), Bordeaux-Pessac, France.
Correspondence to Dr Bruno Cauchemez, Service de Cardiologie, Hôpital Lariboisière, 2 rue Ambroise Paré, 75475 Paris Cedex 10, France.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background The electrophysiological mechanisms for successful catheter ablation of atrial flutter (AFl) targeting the inferior vena cava–tricuspid annulus (IVC-TA) isthmus have not been determined.
Methods and Results Twenty patients with common AFl were studied. All had inducible common AFl, and 8 of them had both common and reverse AFl. Right atrial (RA) activation sequences were investigated during pacing from sites proximal (low lateral RA) and distal (proximal coronary sinus) to the IVC-TA isthmus both during entrainment of common or reverse AFl and during pacing in sinus rhythm. This was repeated after ablation. During pacing in sinus rhythm from the low lateral RA, the septum was activated by caudocranial and craniocaudal wave fronts. Similarly, during pacing from the proximal coronary sinus, the lateral RA was activated by two wave fronts. Catheter ablation of the IVC-TA isthmus induced dramatic changes in mapping due to the loss of caudocranial wave front in all but 1 patient. The septum and the lateral RA were activated by a single craniocaudal front as during entrainment of reverse or common AFl, respectively. After a follow-up of 8±2 months, common or reverse AFl occurred in 4 patients. Two had no or only unidirectional changes in the isthmus conduction induced by ablation. The other 2 had a late recovery of conduction.
Conclusions The present study provides evidence that the mechanism of successful AFl ablation targeting the IVC-TA isthmus is local bidirectional conduction block. This change can be used as a new and complementary electrophysiological end point for the procedure. AFl recurrences are associated with failure to achieve a permanent block.
Key Words: ablation • catheters • atrial flutter • electrophysiology • conduction
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Previous studies in animals and humans have shown that the mechanism of common AFl is a large reentrant circuit confined to the RA.1 2 3 4 5 6 7 8 The first attempts at AFl ablation were focused on the exit sites from the myocardial isthmus between the IVC and the TA. Initially, surgery was used,9 and then DC shocks.10 11 Later, ablation using RF energy was focused either on the middle of the IVC-TA isthmus or on the exit sites.12 13 14 15 16 The acute success rate was high with both techniques, yet there was a high recurrence rate, between 10% and 35%.12 13 14 15 16
In all these studies, the end point for the procedure was defined by tachycardia termination and inability to induce AFl.9 10 11 12 13 14 15 16 The use of the latter end point is questionable, since the inducibility of AFl is not systematically tested before ablation, and its reproducibility may be low.17 Furthermore, no study has determined the electrophysiological mechanism for successful ablation.
In this prospective study, we describe the modifications induced by catheter ablation of the IVC-TA isthmus in terms of both intra-atrial conduction time and RA activation sequence. This allows the definition of new electrophysiological criteria for the assessment of the AFl ablation procedure and provides new insight into the role of the isthmus in activation of the RA.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Patients
Twenty patients were prospectively included in this study. They were part of a cohort of 54 consecutive patients referred to both centers from April 1994 through December 1994 for RF catheter ablation of common AFl. Inclusion required (1) documented common AFl with an inverted P wave in leads II, III, and aVF giving a typical "sawtooth" pattern; (2) inducibility of sustained common AFl during electrophysiological study; and (3) electrophysiological criteria of AFl as described below (see electrophysiological definitions). Thirty-four patients were excluded because common AFl was not inducible (n=2); because sustained and recurrent atrial fibrillation was induced during pacing maneuvers, requiring repeated DC shocks or drug injection (n=30); or because the electrophysiological inclusion criteria were not fulfilled (n=2).
The 20 patients consisted of 16 men and 4 women with a mean age of 58±9 years. Symptoms had been present from 1 to 15 years. Patients were resistant to a mean of 3±1 antiarrhythmic drugs (range, 1 to 5), including amiodarone in 19 patients. Four patients also had episodes of documented paroxysmal atrial fibrillation, but AFl was their predominant clinical arrhythmia. One patient had a ventricular pacemaker for paroxysmal AV block. Structural heart disease was present in 6 patients (3 coronary artery disease, 2 dilated cardiomyopathy, and 1 aortic valve prosthesis) and chronic obstructive pulmonary disease in 3.
Electrophysiological
Study
The protocol was approved by the University Committee on Human
Research for both centers, and patients gave informed consent. The
patients were studied in the postabsorptive state under light sedation
with fentanyl and midazolam. Antiarrhythmic drugs were interrupted 5 or
more half-lives before the study, except for amiodarone,
which was interrupted 5±6 days before ablation in 19 patients. The
drug was taken for a mean of 7±10 and a median of 4 months (range, 0.3
to 36 months).
Four or five catheter electrodes were introduced through
both femoral
and left subclavian veins and positioned in the RA as shown in Fig
1
. One 6F decapolar catheter with a 2-mm interelectrode
distance and a 5-mm interbipole distance was positioned on the lateral
RA. Another multipolar catheter was positioned in the coronary
sinus, with its proximal bipole located at the ostium, as checked in
the 60° left anterior oblique view.18 One deflectable 7F
quadripolar catheter with a 2-mm interelectrode distance and a 4-mm tip
electrode was used for the mapping of the IVC orifice region and for
ablation. A quadripolar catheter was placed in the His bundle region.
In 9 patients, an additional "halo" catheter consisting of 10
bipoles (2-mm interelectrode distance, 5-mm interbipole distance;
Webster Laboratory) was positioned with one side on the lateral RA and
the other on the septal RA. The upper region of the RA was not studied.
Care was taken to keep the mapping catheters in the same stable
position throughout the study.
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Endocardial electrograms were filtered between 30 and 500 Hz and simultaneously recorded with surface leads I, II, III, and aVF on a 12-channel recorder (ES 2000, Gould Instrument, or Midas, PPG Biomedical) at a paper speed of 100 or 250 mm/s.
Atrial electrograms were recorded from three levels of the lateral RA (high, mid, and low) and from various levels on the septum: high, mid in the His bundle region, low at the coronary sinus ostium, and more inferior at the "lower septum" located between the IVC-TA isthmus and the coronary sinus ostium. The local atrial activation time was taken as the first sharp deflection of bipolar electrograms.
Pacing maneuvers were performed with a rectangular stimulus pulse of 1-ms duration at twice diastolic threshold amplitude (Savita VPA Medical). Two sites of pacing were used: the low lateral RA proximal to the IVC-TA isthmus and the PCS distal to it.
Electrophysiological
Definitions
Common AFl was defined as a reentrant
tachycardia with counterclockwise RA activation in an
anterior view. The mean cycle length of common AFl was 253±27 ms, with
a high-to-low lateral activation lasting 47±14 ms and a PCS to
His bundle region activation occurring in 35±22 ms. The presence of a
reentry was demonstrated by the criteria of entrainment described by
Waldo and colleagues.2 19 20 The fourth
criterion was
considered to be present if (1) a change in conduction time and
electrogram morphology occurred at a recording site with
decreasing pacing cycle lengths and (2) tachycardia
returned after pacing.20 21 22 During
common AFl, the fourth
criterion was observed in all patients during pacing of the low lateral
RA, which was orthodromically proximal to the IVC-TA isthmus and to the
area of slow conduction, whereas pacing from the PCS induced concealed
entrainment.7 21 22
In 8 patients, a reverse AFl with a mean cycle length of 256±21 ms was induced during pacing. This AFl used the same circuit as the common form but in the reverse direction. The low to high lateral RA activation time was 48±10 ms, and the His bundle region to PCS activation time was 43±16 ms. During reverse AFl, the fourth criterion of entrainment was observed during pacing of the PCS, whereas pacing from the low lateral RA induced concealed entrainment.23
With the medial part of the isthmus used as the pacing and recording site, the participation of the IVC-TA isthmus in the circuit was demonstrated by entrainment with exact resetting based on a first postpacing interval in the range of the tachycardia cycle length (no longer than 20 ms).14 24
Assessment of RA Activation Sequence and Conduction Times During
Pacing in AFl or Sinus Rhythm
During pacing of the low lateral RA,
"anterograde" intra-atrial conduction times were
assessed from the stimulation spike to the His bundle region, the lower
septum, and the PCS. During pacing of the PCS, "retrograde"
conduction times were measured to the high and low lateral RA. Pacing
was performed during common or reverse AFl (entrainment) or during
sinus rhythm, and conduction times were compared at identical cycle
lengths. Unless otherwise specified, pacing refers to pacing in sinus
rhythm, whereas entrainment refers to pacing in AFl.
During
entrainment, the conduction times were measured on the last
captured beat that was entrained but not fused (Fig
2).2 20 22 Furthermore,
measurements were
performed at the longest cycle length that captured the
tachycardia to minimize pacing-induced conduction delay
and any possible effect of a partially excitable
gap.25
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During sinus rhythm, stimulation included incremental pacing up to the rate of AFl entrainment and single extrastimuli delivered after a paced cycle length of 600 ms up to atrial refractoriness. Curves of intra-atrial conduction were constructed by plotting conduction times against the corresponding stimulus coupling interval. A jump in conduction time of more than 40 ms for a decrease in the corresponding coupling interval of 10 ms defined a discontinuity during either incremental pacing or extrastimulation.
Radiofrequency Ablation
Unmodulated 500-kHz RF current was
delivered in
unipolar fashion from a generator (HAT 200 or OSCOR Medical). RF energy
(20 to 30 W for 60 seconds) was applied during common AFl in the IVC-TA
isthmus as described by Cosio et al.13 Using a left
anterior oblique projection, we took care to deliver RF energy on
the same line of the medial part of the IVC-TA isthmus, thus avoiding
the more septal and lateral areas. In this location, sharp atrial
electrograms occurred in the medial part of the isoelectric portion
(plateau) of the surface flutter wave in inferior
leads.26 The end point for the procedure was both
interruption and inability to reinduce common AFl. The latter was
assessed regularly for 30 minutes after the last application to define
a successful ablation. The stimulation protocol for AFl induction
included burst (10 to 20 beats) and ramp (20 to 40 beats) pacing at
progressively shorter cycle lengths until 2:1 capture was noted.
Postablation assessment of RA activation sequences and conduction times was performed 30 minutes after the final RF application. An electrophysiological effect on conduction was not considered an end point for the procedure. Additional "intermediate" assessments were performed during the ablation process, after series of RF applications that terminated AFl (without premature beats) but were not successful in preventing its reinduction.
Follow-up
Patients were monitored for 48 hours after the
procedure. They were discharged without antiarrhythmic therapy and seen
every 3 months for ECG, Holter monitoring, and physical examination.
Additional evaluations were performed if symptoms recurred. A late
electrophysiological study was performed in
17 patients a mean of 16±11 weeks after ablation (range, 4 to 39
weeks) and a mean of 17±11 weeks after amiodarone interruption
in patients who took this drug. In one patient, induction of a
sustained atrial fibrillation prevented determination of
intra-atrial conduction. Three patients declined the study.
Statistical Analysis
Continuous variables are expressed as
mean±SD. The
significance of differences between
electrophysiological parameters
was assessed by Student's t test for paired data.
Fisher's
exact test was used for qualitative variables. A value of
P<.05 was considered statistically significant.
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Results |
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Conduction Times During Transient Entrainment of AFl
During entrainment of common AFl from the low lateral RA, conduction time to the PCS was 123±24 ms, and during entrainment from the PCS, conduction time to the low lateral RA was 190±25 ms. During entrainment of reverse AFl from the low lateral RA, conduction time to the PCS was 186±32 ms, and during entrainment from the PCS, conduction time to the low lateral RA was 131±12 ms (Table 1
).
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RA Activation Sequence and Conduction Time During Pacing in Sinus
Rhythm: Comparison With Data During Entrainment
Conduction during
low lateral RA stimulation. In all patients,
pacing the low lateral RA produced two caudocranial wave fronts: one
clockwise in the lateral wall, the other counterclockwise in the septum
activating the lower septum and then the PCS. However, there was a
craniocaudal activation of the high septum and His bundle region, with
the collision between wave fronts occurring near the PCS (Fig
3, left). Activation of the His bundle region occurred
only 6±18 ms after the PCS.
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Conduction times to the lower septum
and PCS during pacing were
identical to those during common AFl entrainment (96±23 and
98±24 ms,
respectively, to the lower septum, P=.10; 124±26 and
123±24 ms to the PCS, P=.53). They were shorter to the
His
bundle region during pacing than during common AFl entrainment (130±25
and 159±30 ms, respectively, P<.001) owing to the earlier
capture of the His bundle region by the craniocaudal wave front during
pacing (Table 1
).
No discontinuity was observed in the
conduction curves. The conduction
times during pacing at a basic cycle length of 600 ms are listed in
Table 2.
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Conduction during PCS stimulation. In
all patients, pacing the
PCS produced two caudocranial wave fronts: one counterclockwise in the
septum, the other clockwise in the lateral RA activating the low
lateral and then the mid lateral RA. However, there was a
craniocaudal activation of the high lateral RA, with the collision
between wave fronts occurring near the mid lateral RA (Fig 3,
right).
The high lateral RA was activated 22±21 ms after the low.
Conduction times to the low lateral RA during pacing were similar to those during reverse AFl entrainment (122±25 and 131±12 ms, respectively, P=.3). Times were shorter to the high lateral RA during pacing than during reverse AFl entrainment (144±26 and 179±15 ms, respectively, P<.001) owing to the craniocaudal wave front during pacing.
In 8 patients, a discontinuity
in the conduction times from the
PCS to the low lateral RA was observed during incremental stimulation,
and in 6 of the 8, this resulted in initiation of common AFl (Fig
4). A jump of 69±29 ms in the conduction time to the
low lateral RA occurred for a corresponding coupling interval of
204±26 ms with a dramatic change in the lateral RA activation. The
high lateral RA became activated 51±12 ms before the low
lateral RA, and a change in electrogram morphology of the low lateral
RA occurred. This discontinuity suggested retrograde block in the
IVC-TA isthmus, with all the lateral RA becoming activated by a
craniocaudal wave front. No discontinuity in the conduction curve was
observed when extrastimulation was used. Conduction times during pacing
at basic cycle lengths are listed in Table 2.
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RA Activation Sequence and Conduction Times After
Ablation
In all patients, common AFl was terminated and rendered
noninducible after a mean of 15±8 and a median of 14 (range, 3 to 40)
RF applications in the IVC-TA isthmus. Dramatic changes in RA
activation sequences and conduction times (Table 1) were
observed after
ablation.
Conduction during low lateral RA stimulation. In 17
patients,
pacing the low lateral RA after ablation of the isthmus resulted in
delayed activation of the lower septum and PCS compared with before
ablation; the lower septum and PCS were now activated after the
His bundle region (Tables 1 and 2). Conduction
times to the His
bundle region were not modified, so that all the septum was
activated craniocaudally via a single clockwise front (as
during reverse AFl) (Fig 5, left). This suggested an
anterograde conduction block in the IVC-TA isthmus without an
alternative conduction pathway in the posterior RA. The postablation
conduction times were not significantly different (although slightly
shorter) from those observed during entrainment of reverse AFl (182±26
and 186±32 ms, respectively, to the PCS, P=.4) (Fig
6). In 2 patients, ablation increased the conduction
times to the PCS without change to the lower septum. In one patient
(patient 18), ablation failed to induce any significant
modification.
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Conduction during PCS stimulation. In 19
patients, pacing the
PCS after ablation of the isthmus resulted in delayed activation of the
low lateral RA compared with before ablation; the low lateral RA was
now activated after the high lateral RA (Tables 1 and
2).
Conduction times to the high lateral RA were not modified, so that all
the lateral RA was activated craniocaudally via a single
counterclockwise front (as during common AFl) (Fig 5, right).
This
indicated a retrograde conduction block in the IVC-TA isthmus and the
absence of an alternative pathway in the posterior RA. Postablation
conduction times were not significantly different (although slightly
shorter) from those observed during transient entrainment of common AFl
(182±27 and 190±25 ms, respectively, to the low lateral RA,
P=.14; 41±11 and 46±14 ms for high to low
lateral RA
interval, P=.16) (Fig 7). In 1 patient
(patient 18), no modification in conduction occurred.
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Heterogeneous
conduction changes. In 13 patients,
the changes in RA activation were present in both
anterograde and retrograde directions at each pacing cycle
length without discontinuity in the conduction curve ("apparent
complete" block) (Fig 8). In 6 patients, the changes
occurred at a critical cycle length ("rate-dependent" block)
or could be unidirectional, always in anterograde direction.
For 2 of these patients (patients 9 and 17), a nonclinical reverse AFl
was induced (Fig 9).
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Progressive Conduction Changes During the Ablation
Process
In 15 patients, initial RF applications terminated
tachycardia without preventing common AFl induction (35
terminations). In 25 terminations, repeated evaluation of conduction
times showed various data: (1) no change in anterograde and
retrograde conduction times (n=6); (2) a transient conduction block in
the IVC-TA isthmus that disappeared within 14 to 30 minutes (n=4); (3)
unidirectional changes that became bidirectional with subsequent RF
applications (n=12); (4) a progressive prolongation in conduction times
(n=12) with a concomitant increase in the induced AFl cycle length (Fig
10, left, first termination); (5) a discontinuity
occurring at longer cycle lengths than initially, facilitating AFl
induction (n=5), either the reverse form during pacing from the low
lateral RA or the common form during pacing from the PCS (Fig
10,
right, second termination); and (6) in one patient, common AFl still
inducible, despite a reversal in RA activation sequence suggesting
conduction block in the isthmus. The conduction time from the low
lateral RA to the PCS was longer during AFl entrainment than during
pacing at the same cycle length, suggesting, for this patient,
anterograde concealed conduction in the IVC-TA isthmus, ie, a
major slowing of the counterclockwise front through the isthmus with
longer conduction times than the clockwise wave front outside the
isthmus.
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Follow-up
During a mean follow-up period of 8±2 months
(range, 5
to 13 months), common AFl recurred in 3 patients 2 weeks to 2 months
after ablation, and it did not recur in the 17 others. A reverse AFl
occurred in patient 9. There was a trend for a better outcome in
patients with an initial "apparent complete" block in the isthmus
compared with patients with "rate-dependent" block or
unchanged isthmus conduction (one AFl recurrence in 13 patients
[8%] and three AFl recurrences or occurrence in 7 patients
[43%], respectively, P=.10).
A complete
electrophysiological study was
done in 16 patients (Fig 11). The three patients with
AFl recurrence had intact conduction in the IVC-TA isthmus in
both the anterograde and retrograde directions. In 1 patient
(patient 18), this was already observed immediately after ablation, and
in the two others, this was due to a late recovery of conduction. The
tachycardia was inducible in 2 of them and not inducible in
1, even during isoproterenol infusion. In patient 9, there was
unidirectional retrograde conduction in the isthmus and reverse AFl was
inducible, as it was at the time of ablation. The remaining 13 patients
had no inducible AFl. An "apparent complete" and bidirectional
block was observed in 6 patients and a "rate-dependent" or
unidirectional (anterograde) block in the 7 others. Fig 11
shows the various changes observed between early and follow-up
electrophysiological studies. The 4
patients with no electrophysiological data
had no AFl recurrence.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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By analyzing RA activation sequences and conduction times during pacing in sinus rhythm before and after application of RF energy at the IVC-TA isthmus, the present study specifies the electrophysiological mechanisms for acute successful AFl ablation and provides new insight into the mechanisms of AFl recurrences. Furthermore, the reversal in the RA activation sequence induced by ablation provides new insight into the role of the isthmus in activation patterns of the RA during sinus rhythm.
Mechanism of Successful Ablation of Common AFl
The
applications of RF energy at the IVC-TA isthmus produced
in all patients an elimination of common AFl, confirming previous
studies.13 14 16 In most patients, the
mechanism of
success is the creation of a persistent bidirectional conduction block
in the IVC-TA isthmus. This is demonstrated by dramatic changes in RA
activation sequence and conduction times during pacing from sites
proximal (low lateral RA) or distal (PCS) to the isthmus. Initially,
the septal or lateral end of the isthmus was directly activated
within 125 ms from the other end by a caudal input generating a
caudocranial RA activation. After ablation, there was an increase of 60
ms in the conduction times in both directions due to a loss of caudal
input, each end of the isthmus being activated
craniocaudally.
In most patients, an "apparent complete" block was present after ablation, while in the others, the block occurred beyond a critical cycle length, with a possible discrepancy in anterograde and retrograde properties. Only one patient had no significant change. Two patients had a prolongation of conduction time from the low lateral RA to the PCS without any change in the lower septum. This may be due to a longitudinal dissociation in the atrial fibers of the isthmus going to the septum or due to a peculiar activation from the posterior RA.
A tight link between conduction block in the isthmus and AFl elimination is further highlighted by intermediate evaluations and follow-up electrophysiological studies. As long as AFl is inducible during the ablation process, only various degrees of conduction slowing and unidirectional block are observed. Transient AFl noninducibility is due to transient block in the isthmus. Finally, AFl becomes not inducible after completion of isthmus ablation. In some patients, incomplete ablation of the isthmus can be proarrhythmic by increasing the isthmus "refractory period," thus facilitating the induction of tachycardia in either the common or reverse direction.
It is important to note that a total conduction block cannot be differentiated from a major conduction slowing in the isthmus. This concealed conduction in the IVC-TA isthmus was observed in only one patient, as demonstrated by a common AFl still inducible despite a reversal in RA activation sequence. The use of isoproterenol may have been helpful to confirm the presence of conduction block rather than markedly delayed conduction. Because of these limitations, assessment of conduction block cannot be the sole end point for determining successful AFl ablation, and noninducibility of AFl must still be considered as well.
The assessment of conduction times and RA activation sequences is used in patients in sinus rhythm and is particularly useful in patients without inducible AFl or with easily inducible atrial fibrillation. Practically, a craniocaudal activation of the septum (PCS activated after His bundle region) during pacing of the low lateral RA indicates an anterograde block in the isthmus, whereas a craniocaudal activation (low after high RA) of the lateral RA during pacing of the PCS indicates a retrograde block. The nonachievement of these patterns is the proof of persistent conduction in the isthmus, and we think it requires the continuation of the ablation procedure on the basis of the follow-up data.
In one patient discharged despite no change in isthmus conduction, AFl recurred within 2 weeks. Furthermore, the appearance of reverse AFl not previously documented in a patient discharged with persistent "retrograde" isthmus conduction suggests the need to complete isthmus ablation until bidirectional block. The other mechanism for AFl recurrence is a late complete recovery of conduction in the IVC-TA isthmus that we observed only in the patients with AFl recurrence. Regarding the number of recurrences, the present study does not allow determination of the optimal degree of conduction block that must be achieved during the procedure to minimize the risk of late recurrence. It suggests a better outcome for "apparent complete" block, but this point needs further study. Furthermore, the use of amiodarone may have interfered in the mechanism of conduction recurrence. In addition to the electrophysiological end point, more appropriate modes of RF energy application, using larger tips or irrigated electrodes, may also prevent these recurrences by creating larger and deeper atrial lesions with fewer applications.14 27 28 29
Indirect Evidence for Slow Transverse Conduction in the Posterior
RA: RA Activation as a Dual-Component Process
The disruption induced
by ablation in the RA activation
sequence is an impressive finding. Whereas initial RA activation was
fusion of different wave fronts, ablation of the isthmus eliminates a
caudocranial wave front, with the result that RA activation appears to
be dependent on a single craniocaudal wave front. The finding is also
confirmed by the comparison at similar cycle lengths of conduction
times during pacing with those obtained during AFl entrainment. During
entrainment, the conduction times measured on the last paced beat offer
a reference point for purely unidirectional conduction times during
either counterclockwise (common AFl) or clockwise (reverse AFl) RA
activation.2 20 22 30 Nearly
identical conduction times in
both directions indicate that the impulse travels through the same area
at the same velocity in both modes of stimulation. This strongly
suggests that in most patients there is no transverse activation going
through the posterior intercaval RA wall (or that the latter has a very
long conduction time) and that this area of block is present not
only during AFl5 6 31 but also during
pacing in sinus
rhythm. We do not know whether this condition is truly
physiological or whether it is peculiar to patients
presenting with atrial arrhythmias. In a recent study, the
borders of the area of block were the crista terminalis and the
eustachian ridge.32
Results of the present study have other implications: (1) The absence of an alternative pathway to the caudal activation front in the low RA strongly supports the rationale for using the IVC-TA isthmus as a target for RF ablation in AFl.13 (2) Because the RA activation behaves like a dual wave front model, the initiation of AFl requires conduction block in one component, as demonstrated by discontinuity in conduction curve in the present study.33 34 35 This was observed mainly during preablation pacing from the PCS that produced a retrograde block in the isthmus region and induced common AFl. Far less frequent was induction of anterograde block with initiation of reverse AFl using lateral RA pacing, which was observed only after energy applications. A different arrangement of longitudinal and transverse myocardial fibers could explain these differences in anterograde and retrograde directions.35 36 37 38 (3) While slow conduction in the IVC-TA isthmus is well accepted during AFl, it is controversial during pacing in sinus rhythm.7 The results of the preablation study, showing similar conduction times to the PCS both during common AFl entrainment and pacing at similar cycle lengths, suggest that there is no additional conduction delay along the isthmus during AFl compared with pacing in sinus rhythm. In a previous report from Olshansky et al,7 the slow conduction was not observed during pacing in sinus rhythm. The differences between the two studies may be due to a different location of the pacing site inducing different wave fronts with different collision sites.39 40 41 42 43 44
Conclusions
The present study provides evidence that the
mechanism of
successful AFl ablation targeted to the IVC-TA isthmus is local
bidirectional conduction block leading to dramatic changes in the RA
activation sequence. These changes can be used as new and complementary
electrophysiological end points for the
procedure.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This work was supported in part by grant P 940906 from the Délégation à la Recherche Clinique de l'Assistance Publique and the Fédération Française de Cardiologie. We wish to thank Dr James Coromilas for his helpful suggestions in the elaboration of this manuscript. We wish to acknowledge Dominique Belly, Dr Janine Bizot, Dr Xavier Copy, Dr Isabelle Denjoy, Agnes Dutrey, and Dr Frank Halimi for their contributions and Annie Gouverneur for assistance with drawings.
Received June 1, 1995; revision received August 21, 1995; accepted September 10, 1995.
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References |
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TopAbstractIntroductionMethods Results Discussion References |
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G. F. Van Hare and A. L. Waldo The Atrial Flutter Reentrant Circuit: Additional Pieces of the Puzzle Circulation, August 1, 1996; 94(3): 244 - 246. [Full Text]
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