Mark D O’Neill MB BCH DPhil, Pierre Jaïs MD, Anders Jönsson
MD, Yoshihide Takahashi MD, Frédéric Sacher MD,
Mélèze Hocini MD, Prashanthan Sanders MB BS PhD, Thomas
Rostock MD, Martin Rotter MD, Jacques Clémenty & Michel
Haïssaguerre MD.
Hôpital Cardiologique du Haut Lévêque &
Université Victor Segalen Bordeaux II, 33604 Bordeaux, Pessac,
France.
Address for
correspondence: Mark D O’Neill MB BCH DPhil, Hôpital
Cardiologique du Haut Lévêque, & Université
Victor Segalen Bordeaux II, 33604 Bordeaux, Pessac, France. Email:
mdconeill@btinternet.com
Abstract
Much of our
understanding of the mechanisms of macro re-entrant atrial tachycardia
comes from study of cavotricuspid isthmus (CTI) dependent atrial
flutter. In the majority of cases, the diagnosis can be made from
simple analysis of the surface ECG. Endocardial mapping during
tachycardia allows confirmation of the macro re-entrant circuit
within the right atrium while, at the same time, permitting curative
catheter ablation targeting the critical isthmus of tissue located
between the tricuspid annulus and the inferior vena cava. The
procedure is short, safe and by demonstration of an
electrophysiological endpoint - bidirectional conduction block across
the CTI - is associated with an excellent outcome following
ablation. It is now fair to say that catheter ablation should be
considered as a first line therapy for patients with documented
CTI-dependent atrial flutter.
Key Words: Atrial flutter;
cavotricuspid isthmus; ablation
Introduction
Since the first description of atrial flutter in humans almost a
century ago, electrophysiological techniques have evolved to facilitate
a comprehensive understanding of the arrhythmia mechanism which in
turn, has led to a highly effective therapeutic strategy. This
review is confined to cavotricuspid isthmus-dependent flutter and
details the development of the understanding, diagnosis and therapy of
this common arrhythmia. Specifically, the approach used for the
catheter ablation of atrial flutter at our institution is described in
detail.
Insights from electrocardiography
Early
recognition of the difference between atrial flutter (AFL) and atrial
fibrillation (AF) was made by Jolly and Ritchie with the demonstration
of regular atrial activity in the inferior leads of the surface
electrocardiogram. Lewis and colleagues demonstrated in animal
studies that constant and ordered activation of at least part of the
atrium was responsible for the flutter waves on the surface ECG and
remarkably deduced that atrial flutter was likely due to intra-atrial
circus movement around the venae cavae (for historical review, see Lee
1).
Cavotricuspid
isthmus-dependent counterclockwise flutter is the archetypal atrial
macro-re-entrant arrhythmia, the anatomical circuit of which has now
been well described with both conventional and newer mapping modalities
2-5. The route of
the re-entrant circuit is bordered anteriorly by the tricuspid annulus
and posteriorly by the venae cavae orifices, the crista terminalis and
the Eustachian ridge
6.
The so-called cavotricuspid isthmus (CTI) serves as the critical zone
of slowed conduction which facilitates perpetuation of the re-entrant
circuit and also serves as an ideal target for its physical
interruption by radiofrequency ablation
4,7.
Flutter waves
are atrial complexes of constant morphology, polarity and cycle length
in a rate range from 240 to 340 per minute
6
(
Figure 1). The presence
of flutter waves in the inferior limb leads and in V1 is specific for
cavotricuspid isthmus-dependent flutter
6:
negative flutter waves in the inferior leads and a positive wave in V1
with transition of morphology across the anterior leads is consistent
with a counterclockwise atrial circuit with lateral-to-medial
activation of the cavotricuspid isthmus (CTI) while activation in the
reverse direction (clockwise) is suggested by positive flutter waves in
the inferior leads and a negative deflection in V1, which accounts for
5-10% of all CTI-dependent flutter. There are rare forms of tachycardia
with similar P wave morphology, for example atrial tachycardia
originating from the ostium of the coronary sinus. Endocardial
mapping in this case will demonstrate caudo-cranial activation of both
the RA septum and lateral wall, which is not in keeping with
counter-clockwise rotation around the previously described flutter
circuit.
Figure
1. Twelve lead electrocardiogram of counterclockwise
cavotricuspid isthmus dependent atrial flutter with a variable
ventricular response rate. Note the presence of the negative “saw
tooth” flutter waves in leads II, III and aVF in addition to the
positive flutter wave in V1 with a transition of morphology across the
anterior precordial leads.
An important
subgroup of patients to consider are those presenting with atrial
flutter following catheter ablation of the left atrium for treatment of
atrial fibrillation. It has recently been shown that over 50% of
patients with electrophysiologically confirmed counterclockwise
CTI-dependent flutter as the arrhythmia of recurrence following LA
ablation for AF show upright flutter waves in the inferior leads, a
finding which is most likely due to the left atrial debulking and
resultant voltage abatement among this group
8.
Therefore, while the presence of negative flutter waves in the inferior
leads is highly suggestive of CTI dependent flutter, their absence does
not exclude the diagnosis, most notably in the context of structural
heart disease or prior left atrial ablation .
Electrophysiological evaluation of CTI-dependent flutter
Coronary sinus activation sequence
Following
a thorough evaluation of the surface ECG, a quadripolar deflectable
diagnostic catheter (Xtrem, ELA Medical) and mapping/ablation catheter
are advanced from the right femoral vein to the coronary sinus (CS) and
right atrium respectively. The distal pole of the CS catheter is
positioned at 4 to 6 o’clock in the LAO position. If the
patient is in AFL at the time of the study, the coronary sinus
activation sequence should be from proximal to distal (
Figure 2), although equally this
could be the case for any tachycardia mechanism originating in the
right atrium, and may also be seen in some left atrial flutters, for
example counterclockwise perimitral flutter. Conversely, flutter
localized to the superior right atrium may activate the distal CS
earlier than the proximal CS, via Bachmann’s bundle. Together
with the typical ECG findings, a proximal-to-distal CS activation
sequence is not diagnostic for, but rather is highly suggestive of
CTI-dependent flutter as the underlying tachycardia mechanism.
Figure
2. The upper aspect of the figure shows leads I, II, III
and V1 of the 12 lead electrocardiogram. The middle two tracings
are the endocardial signals recorded at the distal (RF D) and proximal
(RF P) bipoles of the ablation catheter. The lower pair of
tracings shows the bipolar electrograms recorded via a quadripolar
catheter positioned with CS 3-4 at the ostium of the coronary sinus
(CS). Note the coincidence of the atrial electrogram on RF D with
the centre of the plateau of the flutter wave, indicating a medial
position of the ablation catheter on the cavotricuspid isthmus
(CTI). The activation sequence in the CS is from proximal to
distal as expected for counterclockwise CTI-dependent flutter.
Endocardial mapping
Once
the diagnosis of CTI-dependent flutter is suspected from the surface
ECG and the CS activation sequence, more detailed intra-atrial mapping
is performed. Using the CS as a stable reference, up to eight
points are sequentially mapped within the right atrium, including
approximately four points around the tricuspid annulus, and their
timing relative to flutter wave onset and the clearest CS signal
determined, to evaluate the direction of impulse propagation during
tachycardia. For the majority of patients with CTI-dependent
counterclockwise flutter, the atrial electrogram recorded on the
mid-isthmus lies within the plateau phase of the flutter wave, between
50 and 90ms prior to the onset of the pronounced negative deflection
associated with the septal ascent of the depolarisation
wavefront. Demonstration of a right atrial activation time
which is significantly shorter than the tachycardia cycle length or the
identification of colliding activation fronts in the right atrium are
features which are highly suggestive of a left atrial flutter origin
5.
Entrainment manoeuvres and post
pacing interval
In
addition to this activation mapping, entrainment manoeuvres can be
employed in the right atrium and coronary sinus, to confirm and exclude
the right and left atria as the chamber of arrhythmia origin
respectively. Entrainment involves pacing from multiple, separate
sites within the right atrium at cycle lengths of 10-20ms faster than
the tachycardia cycle length, observing its effect on flutter wave
morphology
9 and estimating
proximity of pacing site to tachycardia circuit by analysis of the post
pacing interval. The pacing site is considered to lie within the
tachycardia circuit when the post pacing interval is within 30ms of the
tachycardia cycle length. Entrainment from sites which are
outside the flutter circuit will demonstrate manifest fusion on the
surface ECG and the PPI will exceed the flutter cycle length by more
than 30ms. Pacing performed from within the circuit but outside a
protected isthmus demonstrates manifest entrainment, characterized by
surface ECG fusion, progressive fusion at faster pacing rates and all
sites which are orthodromically activated having a PPI equal to the
flutter cycle length. Transient entrainment performed from within the
protected CTI isthmus demonstrates a long stimulus-to-p wave interval,
in keeping with its role as an area of slow conduction in which
unidirectional block of the antidromic wave front probably
occurs. Mapping of the septal aspect of the CTI demonstrates the
earliest atrial electrogram relative to the onset of the flutter wave
on the surface ECG, and entrainment from this position demonstrates a
short stimulus-to-p wave interval with concealed fusion, confirming
this as the likely exit site from the zone of slow conduction critical
to maintenance of the tachycardia. This manoeuvre is
repeated for a minimum of two right atrial sites, usually incorporating
the RA septum and lateral wall at the very least.
Many patients
with a history of atrial flutter who been referred for ablation therapy
are in sinus rhythm at the time of their procedure. If the 12
lead electrocardiogram recorded during the clinical arrhythmia is
consistent with CTI-dependent flutter, and the medical history gives no
cause to suspect a left atrial origin, it is our practice to proceed
directly to radiofrequency ablation of the CTI rather than to attempt
induction.
Catheter ablation of CTI-dependent flutter
Electrophysiological study and ablation is performed in the post
absorptive state and under light sedation (midazolam 2-5mg and/or
analgesia (nalbuphine 10 to 20mg). All antiarrhythmic medication, with
the exception of amiodarone, is discontinued at least five half lives
prior to the procedure. For patients already receiving oral
anticoagulation, this is discontinued 48 hours prior to the procedure
and continued for one month after the procedure. Otherwise,
patients do not routinely receive anticoagulation medication before,
during or after an elective CTI ablation.
All surface
ECG leads are recorded continuously throughout the procedure to
facilitate rapid review however only leads I, II, III and V1 are
displayed in real time. Bipolar intracardiac electrograms are
recorded in the coronary sinus using a quadripolar deflectable catheter
and from the atrial endocardium using a conventional quadripolar
thermocouple D curve 8mm tip catheter (Biosense Webster). All
electrograms are sampled at 1KHz, filtered from 30 to 500Hz, amplified
at 0.1mV/cm and displayed at a sweep speed of 100ms using a
Windows-based digital amplifier/recording system for offline analysis
(Bard Electrophysiology).
Ablation of
the CTI is performed in the patient’s presenting rhythm, be it flutter
or sinus rhythm. In the case of the latter, pacing is performed
from the proximal pole of the CS (cycle length 600ms) as this location
is more stable than a pacing catheter positioned in the inferolateral
right atrium.
The anatomical target
It is
now well established that the anatomical target for interruption of the
macro re-entrant circuit comprising typical atrial flutter is the
cavo-tricuspid isthmus
4,5.
Using an 8mm tip ablation catheter, the linear lesion is made by a
continuous application of RF energy beginning at the ventricular end of
the CTI (A:V electrogram amplitude ratio of ~1:2) and dragging the
catheter towards the atrial aspect of the CTI with a 60-90s delay at
successive ablation points before moving the catheter.
Radiofrequency energy (550Hz unmodulated sine-wave output) is delivered
through a Cordis Stockert generator in temperature control mode with
the temperature limited to 60
oC and the power to 60W.
Ablation is not
routinely performed at the septal aspect of the CTI or inside the
ostium of the CS in order to minimize the risk of circumflex artery
injury, atrioventricular block or cardiac perforation. Nevertheless,
lateral or septal positions are occasionally used when linear block
cannot be achieved by ablation in the medial isthmus.
At our
institution, an irrigated 3.5 mm tip catheter is used in all patients
undergoing pulmonary vein isolation and left atrial ablation for atrial
fibrillation. Unless there is evidence of persisting
bidirectional conduction block across the CTI from a previous catheter
intervention, it is our practice to ablate the CTI routinely in these
patients following completion of the left atrial procedure. In
those patients admitted electively for conventional CTI ablation for
typical flutter, a non-irrigated 8mm tip catheter is used (Cordis
Webster D curve).
The length,
depth and anatomical complexity of the cavotricuspid isthmus can vary
considerably between patients with a resultant impact on the success of
radiofrequency ablation
10,11.
To facilitate effective ablation at the ventricular aspect of a “long”
CTI, a long sheath can be used. Similarly, where there is
difficulty in completing the IVC end of the line because of a prominent
Eustachian ridge preventing a smooth drag back across the isthmus, the
catheter may be looped and apposed to the isthmus from the atrial side
and advanced from the IVC towards the Eustachian ridge. In
patients where conduction block across the isthmus cannot be achieved
with a conventional catheter, the use of an irrigated tip catheter has
been shown to facilitate achievement of bidirectional CTI conduction
block
12. Interestingly,
there is a significant correlation between the surface atrial ECG
amplitude and the amount of RF energy required to achieve complete
isthmus block, a finding which may be of use in the preprocedural
choice of ablation catheter for typical atrial flutter
13. Paradoxically, higher voltages
recorded at the CTI using an electroanatomic approach do not correlate
with reduced ability to achieve bidirectional conduction block when
ablation is performed with a conventional 8mm tip RF catheter
14.
The electrophysiological target
The
flutter wave morphology in counterclockwise CTI dependent flutter is
characteristic, consisting of a downsloping “plateau” phase, followed
by a short, sharp negative deflection, then a sharp positive deflection
with a positive ‘overshoot’ which in turn leads to the next
plateau. The anatomical location of the medial part of the CTI
has been shown to correlate well with the timing of the atrial
electrogram relative to the plateau of the flutter wave and ablation
targets the atrial electrogram occurring simultaneously with the middle
of the plateau phase of the flutter wave in lead II (
Figures 2 & 3). When ablation is
performed during flutter, careful attention to this relationship
ensures radiofrequency energy is delivered perpendicular to the
advancing wavefront and allows immediate recognition of displacement of
the catheter medially or laterally, based on delay or advancement of
the atrial electrogram respectively, relative to the plateau
15. When performed during proximal
coronary sinus pacing, RF energy is sequentially delivered at
electrogram sites in the isthmus region with a constant
stimulus-to-atrial electrogram time across the length of the isthmus.
Figure
3. Cartoon depiction of the anatomical-to-electrophysiological
relationship at the cavotricuspid isthmus (CTI) during CTI-dependent
counterclockwise flutter. Shown are Lead II of the surface ECG,
bipolar electrograms recorded at the distal pole of the ablation
catheter (RFd) and the proximal pole of the coronary sinus catheter
(CSp) positioned in close proximity to the CS os. Note the
mid-plateau position of the ablation signal and the end-plateau
position of the CSp signal, corresponding to the anatomical position of
the mid and septal aspects of the CTI respectively.
The end point
Completion
of the linear lesion by radiofrequency energy requires subsequent
quantitative demonstration of bidirectional conduction block across the
CTI in order to achieve the best outcomes for catheter ablation of
atrial flutter. Complete bidirectional conduction block across
the CTI may be defined as: a descending wave front on the lateral
atrial wall up to the line of block during proximal CS pacing
representative of a reversed atrial depolarization sequence; a greater
activation delay measured to the second double potential recorded on
the line of block when compared with the delay measured to the atrial
electrogram further lateral to the line during proximal CS pacing (
Figure 4); a decreasing activation
delay measured medial to the line when pacing from immediately lateral
to the line and from further lateral to the line
16. Other electrophysiological
features consistent with conduction block across the CTI include a
reversal in bipolar electrogram polarity immediately lateral to the
line during proximal CS pacing, signifying reversal of the vector of
activation
17 (
Figure 4); change in morphology of
the unipolar electrogram (from QS, rS or RS to R or Rs) recorded
immediately lateral to the line of block during proximal CS pacing
18; mapping of a corridor of double
potentials with an intervening isoelectric interval along the line of
ablation
19,20;
demonstration of a reversal in the direction of atrial depolarization
during proximal CS pacing either by sequential right atrial mapping
with the ablation catheter or the use of a multipolar diagnostic
catheter positioned along the lateral aspect of the tricuspid
annulus. In practice, a craniocaudal activation of the septum
(PCS activated after His bundle region) during pacing of the low
lateral RA indicates an counterclockwise block in the isthmus, whereas
a craniocaudal activation (low after high RA) of the lateral RA during
pacing of the PCS indicates a clockwise block, and is reflected by
increased positivity of the terminal component of the P wave in lead II
(
Figure 5). When taken together
with an abrupt increase in the degree of separation of atrial bipolar
electrograms recorded on the line of block, and the highly unlikely
situation of ablation resulting in unidirectional clockwise conduction
block
21, it is usually
sufficient to document the atrial electrogram separation and confirm
maximum conduction delay immediately medial to the line during low
lateral right atrial pacing.
Figure
4. Verification of conduction block in a clockwise direction
across the CTI. Pacing is performed at the proximal coronary
sinus. In the left panel, the mapping/ablation catheter (RF) is
placed medial to the line of block confirming a short delay (36ms) from
the pacing site. In the middle panel, the RF catheter is placed
on the ablated CTI, documenting a delay from the pacing site of
154ms. By moving the RF catheter immediately lateral to the line
of block, the delay shortens to 148ms, consistent with cranio-caudal
activation of the lateral right atrium and at least unidirectional
block of the CTI. Note also the reverse polarity of the
electrograms recorded at RFd when moving from the CTI to a more lateral
position.
Figure
5. The left panel shows a 12 lead electrocardiogram following
termination of the atrial flutter described in figures 1 and 2 but
prior to achievement of bidirectional conduction block. The right
panel shows a 12 lead electrocardiogram following completion of
bidirectional conduction block. The stimulus artifact represents
proximal coronary sinus pacing in both cases. The important
feature to note is the increased positivity of the terminal component
of the P wave in lead II in the right panel relative to the left.
This represents cranio-caudal activation of the lateral right atrium
which is now activated late relative to the septal RA and LA following
achievement of conduction block across the isthmus.
Complications
Although
uncommon, complications have been reported for ablation confined to the
CTI. Injury to the right coronary artery has been described
22. The atrioventricular (AV) node
may be adversely affected by modification of local vagal afferent input
related to RF stimulation or by a global vagal response to pain during
energy delivery
23. Of
course, direct thermal injury to the node or its critical inputs may
also result in transient or even permanent AV block.
Conclusion
Radiofrequency ablation has been shown to be more effective than
anti-arrhythmic medication in preventing recurrences of and reducing
hospitalizations for CTI-dependent atrial flutter
24. Catheter ablation
is safe, cost-effective and should be considered as the first line
treatment of choice for the majority of patients
25.
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