How to ablate typical atrial flutter

Europace (1999) 1, 151–155
‘HOW TO . . . ’ SERIES
How to ablate typical atrial flutter
A. Takahashi, D. C. Shah, P. Jaı̈s and M. Haı̈ssaguerre
Electrophysiologie Cardiaque, Hopital Cardiologique du Haut-Lévêque, Bordeaux-Pessac, France
Introduction
Typical atrial flutter, as referred to in this article,
includes both the counterclockwise and the clockwise
form of cavotricuspid isthmus-dependent right atrial
flutter. The counterclockwise form is the most common
and characterized by a stereotypical surface ECG
pattern showing negative sawtooth flutter waves in II,
III and aVF at a rate between 200–350 beats.min 1.
This surface ECG morphology of counterclockwise
typical flutter is remarkably consistent, allowing
assumptions about the circuit being entirely within the
right atrium and obligatory activation through the
cavotricuspid isthmus. However, in contrast, the surface
ECG morphology of clockwise flutter is more variable
and difficult to distinguish from non-isthmus-dependent
flutters. As a result, intracardiac activation mapping and
entrainment mapping is often necessary as confirmation.
Importantly, since both the clockwise and the counterclockwise forms share the same obligatory cavotricuspid
isthmus, a common strategy of ablation is clearly
applicable and has been shown to be effective.
Methodology
The aim of catheter ablation for typical atrial flutter is to
create a complete and stable bidirectional cavotricuspid
isthmus block, because flutter termination is not enough,
and recurrence is likely if isthmus conduction persists.
The procedure itself can be subdivided into (a) radiofrequency (RF) delivery and lesion creation (b) identification and ‘filling-in’ of residual conducting gaps (c)
assessment of isthmus conduction (Table 1).
RF delivery and lesion creation
In our laboratory, we use a standard 4-mm tip electrode
for temperature controlled sequential point-by-point RF
application, targeted at the isthmus between the inferior
vena cava (IVC) and the tricuspid annulus. RF delivery
Correspondence: Atsushi Takahashi, Electrophysiologie Cardiaque,
Hopital Cardiologique du Haut-Lévêque, Avenue de Magellan,
33604 Bordeaux-Pessac, France.
1099–5129/99/010151+05 r18·00/0
begins at the right ventricular (RV) annulus where a
large ventricular electrogram is recorded. To achieve a
complete block, as linear and as contiguous a series of
point applications as possible needs to be created. This
may be facilitated by fluoroscopic monitoring or by
non-fluoroscopic methods (e.g. using the Biosense system) of monitoring catheter positioning with or without
the use of long introducer sheaths for superior stability.
In addition to fluoroscopic monitoring, during counterclockwise flutter, RF is delivered point by point from the
tricuspid valve (TV) annulus on electrograms within the
isthmus region, coinciding with the centre of the surface
ECG flutter wave plateau, all the way from the TV
annulus to the IVC edge (Fig. 1). This ensures a lesion
perpendicular to the advancing wavefront and catheter
displacement to either side can be instantly and nonfluoroscopically recognized by the altered timing of the
site electrogram. For example, in case of lateral displacement, the site electrogram now coincides with the beginning of the surface ECG plateau (and with the end of the
plateau in case of medial displacement). Recognition of
seemingly minor changes in position is certainly facilitated by the naturally lower conduction velocities in
this region during flutter. During low lateral right
atrial pacing in sinus rhythm, sequential RF is similarly
delivered at electrogram sites in the isthmus region, with
a constant stimulus electrogram time from the TV
annulus to the IVC edge.
It is important to recognize, however, that the mere
fact of having delivered RF energy at a given point does
not ensure a transmural lesion; the efficacy of RF varies
according to contact, local blood flow, delivered power
and myocardial thickness. During unidirectional activation in atrial myocardium (as for example in the isthmus
during typical flutter or during pacing from the low
lateral right atrium or the ostium of the coronary sinus),
a local transmural RF lesion can be recognized by
double potentials separated by an isoelectric interval
(Fig. 2). Upon completion of the line of block in the
isthmus, however, during pacing from the low lateral
right atrium, activation passes around the TV annulus
instead of through it, to give rise to the second potential.
Thus widely separated double potentials can be recorded
all along the line.
RF delivery, therefore, should modify local electrograms, to result in double potentials during orthogonal
1999 The European Society of Cardiology
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A. Takahashi et al.
Table 1
RF delivery and lesion creation
Essential catheters
Identification and
ablation of residual gap
4 mm ablation catheter
8 mm ablation catheter
Essential recording (1) Atrial
electrograms coinciding with the centre
of the surface ECG flutter wave plateau
during CCW flutter or coinciding with
the initial downslope of the positive
flutter wave during CW flutter
(2) Atrial electrogram with a constant
stimulus electrogram time from the TV
annulus to the IVC
Assessment of isthmus conduction
(1) Pacing catheter placed at low lateral RA or CS
(2) Recording catheters (quadripolar or
multielectrode) placed at ablation line, lateral RA,
His region and CS
Single or fractionated atrial
electrogram centered on or spanning
the isoelectric interval of adjacent
double potentials
(1) Only clockwise atrial activation sequence
during low lateral RA pacing and only
counterclockwise atrial activation sequence during
CS pacing
(2) Parallel double potentials with isoelectric
interval all along the ablation line during low
lateral RA and CS pacing
Optional catheter Irrigated tip ablation catheter for a resistant conducting gap
CW=clockwise; CCW=counterclockwise; RA=right atrium; CS=coronary sinus; TV=tricuspid valve; IVC=inferior vena cava.
unidirectional activation, and to this end, power output
and/or target temperature need to be manipulated. At
one extreme, when power delivery is obviously limited
by local temperature (as a result of insufficient perielectrode local blood flow) the use of irrigated or cooled
tip catheters, allowing the dissociation of delivered
power from the endocardial surface temperatures while
avoiding impedance rise, may be helpful[1]. Larger
lesions with each application may also shorten the
procedure: to this end, 8 mm electrodes, multielectrode catheters, and irrigated tip catheters may be
useful (Fig. 3).
Figure 1 An electrophysiological strategy to create a
complete linear block in the cavotricuspid isthmus during
counterclockwise typical flutter. This illustration depicts
the technique of mapping and targeting the isthmus so as
to create a series of contiguous point lesions. A series of
closely spaced point lesions are created by sequentially
withdrawing the catheter along a corridor defined by atrial
electrograms, coinciding with the centre of the surface
ECG flutter wave plateau (top tracing, lead II shown)
from the RV (bottom, with a large ventricular electrogram) to the IVC edge (middle tracing, miniscule ventricular electrogram). This ensures that the created lesion is
perpendicular to the advancing unidirectional wavefront in
the isthmus. As the isochrones indicate during flutter, the
wavefront enters the lateral isthmus at 120 ms, the centre
of the plateau is at 150 ms and activation at the coronary
sinus ostium occurs at 220 ms, with intervening slow
conduction — depicted by the closely spaced isochrones.
As a result of both unidirectional activation and slow
conduction in the isthmus, slight displacement of the
catheter on either side of the central corridor is easily
evident from the concordant change in activation timing
of the atrial electrogram (stippled electrograms). CS=
coronary sinus; IVC=inferior vena cava; TV=tricuspid
valve annulus; V=ventricular electrogram; EC=
Eustachian crest. (Reproduced with permission[5].)
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Atrial flutter ablation
153
Identification and ablation of residual gaps
Because of variations in isthmus anatomy and in the
ability of current catheter technology to create consistent transmural lesions, isthmus conduction frequently
persists despite apparently sufficient ablation. Locating
and ablating residual gaps in the ablation line is therefore necessary. During typical atrial flutter, such residual
gaps can be identified by local electrograms with a single
or a fractionated potential centred on, or spanning, the
isoelectric interval of adjacent double potentials. This
has allowed efficient ablation of flutter recurrence after
previous ablation[2]. The same approach has been utilized during pacing from either side of the isthmus,
targeting single or fractionated potentials adjacent to
double potentials and centred on their isoelectric intervals; the aim is to establish a continuous corridor of
double potentials with isoelectric intervals across the full
width of the isthmus.
Assessment of isthmus conduction
Figure 2 An electrophysiological strategy of creating a
complete linear block in the cavotricuspid isthmus during
counterclockwise typical flutter. Completion of a line of
block during flutter. A partial line of block is depicted as
a filled in black area in the centre, at the 150 ms isochrone
beginning from the right ventricular edge of the isthmus.
Activation passes through the remaining conducting part
of the isthmus (the gap) and curves around antidromically
to activate the downstream flank of the lesion after a
delay. This results in low amplitude double potentials
being recorded on the lesion, characteristically widest at
the edge furthest from the gap (in this case, the RV edge).
Thus the double potentials narrow towards the ‘gap’ and a
single electrogram at 150 ms coinciding with the surface
ECG plateau centre is recorded from this remaining
conducting tissue. Transmural ablation at this unique
site could complete the line of block. CS=coronary
sinus; IVC=inferior vena cava; TV=tricuspid valve
annulus; V=ventricular electrogram; EC Eustachian
crest. (Reproduced with permission[5].)
As indicated earlier, termination of flutter during RF
delivery is not a sufficient end-point because it does not
result in stable isthmus block[3,4]. Mechanical ectopic
induced termination, and/or transient block or conduction slowing within the isthmus are enough to terminate
flutter, without, however, eliminating or affecting the
substrate. During pacing from one side of the ablation
lesion, time to activation on the opposite side and an
activation sequence within the right atrium demonstrating a 180 change in direction of activation on the other
side, have been used to demonstrate isthmus block. This
activation sequence has been documented both sequentially by using mapping and simultaneously with a
duodecapolar electrode catheter during low lateral atrial
or coronary sinus (CS) pacing. More recently, the
achievement of a complete corridor of double potentials,
with isoelectric intervals in a parallel configuration from
the tricuspid annulus to the inferior vena cava edge, has
been effectively used as a more sensitive marker of block
in the cavotricuspid isthmus than the indirect indicators
described above.
Follow up
Recurrence rates of flutter have declined (from 44% to
9%) with the use of objective end-points based on
assessment of isthmus conduction. In most cases, recurrence represents recovery of isthmus conduction after
complete block; thus verification of the stability of
achieved block is important. Recurrence is frequently
noted within 3 months of the initial procedure and
almost always represents the original flutter, though
there may be variations in cycle length due to the effects
of ablation on conduction or that of drugs. Ablation
targeting residual gaps is effective and economical in
terms of time in the above situations.
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A. Takahashi et al.
Figure 3 An example of a single discrete gap in the previous ablation line. 1–6 depict
electrograms during withdrawal mapping in typical atrial flutter in the IVC-TV
isthmus from the RV edge[1] to the IVC edge[6]. Note the widely separated double
potentials (straddling the surface ECG flutter wave plateau) with an isoelectric
interval of 95 ms in 1 and the gradual narrowing with progressive withdrawal (2–6)
until the triple/fractionated potential in 5, followed by reappearance of narrower
double potentials in 6 (interspike interval, 65 ms) at the IVC edge. A single RF
application at site 5 (*) was successful in terminating flutter and producing bidirectional isthmus block. (Reproduced with permission[2].)
Complications
The procedure, as described above, is very well tolerated; a few patients require intravenous sedation and or
analgesics for pain relief during RF delivery. Few side
effects have been reported; and mostly minor ones relate
to femoral venous catheterization. One exception is the
small but significant risk of atrioventricular block when
ablating in the so-called ‘septal isthmus’, falling to
zero as a more lateral target is selected. In general,
the embolic risk, in cases of atrial flutter, has been
considered minimal; however, transoesophageal studies
Europace, Vol. 1, July 1999
have shown a small incidence of atrial thrombi, and
some investigators have reported systemic emboli from
left atrial thrombi. Ordinarily, of course, the pulmonary
circulation filters out thrombi either dislodged or produced during ablation in the right atrium. This may not
occur in the presence of a right to left intracardiac shunt.
Indications
Since the present day ablation procedure is well
tolerated, indications have expanded. While non-
Atrial flutter ablation
pharmacological therapy was earlier limited to refractory and incapacitated patients with haemodynamic
consequences, RF catheter ablation is now offered to
more and more patients with symptomatic and at least
single drug refractory atrial flutter. It may even legitimately now be considered as alternative first line therapy
for all those with symptomatic sustained typical atrial
flutter.
References
155
[2] Shah DC, Haı̈ssaguerre M, Jaı̈s P et al. Simplified electrophysiologically directed catheter ablation of recurrent common
atrial flutter. Circulation 1997; 96: 2505.
[3] Cauchemez B, Haı̈ssaguerre M. Fischer B, Thomas O,
Clémenty J, Coumel P. Electrophysiological effects of catheter
ablation of inferior vena cava-tricuspid annulus isthmus in
common atrial flutter. Circulation 1996; 93: 284.
[4] Poty H, Saoudi N, Aziz AA, Nair M, Letac B. Radiofrequency
catheter ablation of type I atrial flutter. Prediction of late
success by electrophysiological criteria. Circulation 1995; 92:
1389.
[5] Shah DC, Haissaguerre M, Jais P, Clementy J. Atrial flutter:
contemporary electrophysiology and catheter ablation. PACE
1999; 22: 344–59.
[1] Jaı̈s P, Haı̈ssaguerre M, Shah DC. Successful irrigated-tip
catheter ablation of atrial flutter resistant to conventional
radiofrequency ablation. Circulation 1998; 98: 835–8.
Europace, Vol. 1, July 1999