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Transcript
Diagnosis and ablation of atypical atrial tachycardia and flutter
complicating atrial fibrillation ablation
Fred Morady, MD, Hakan Oral, MD, Aman Chugh, MD
From the Division of Cardiovascular Medicine, University of Michigan Health System, Ann Arbor, Michigan.
Depending on the ablation strategy, up to 30% to 50% of patients
will develop an atrial tachycardia after undergoing radiofrequency
catheter ablation of atrial fibrillation. This review discusses the mechanisms, mapping techniques, and catheter ablation of atrial tachycardias that occur after radiofrequency ablation of atrial fibrillation.
KEYWORDS Atrial tachycardia; Entrainment mapping; Postpacing
interval
The incidence of atrial tachycardia after radiofrequency
catheter ablation of atrial fibrillation varies depending on
the extent of ablation in the left atrium. When the ablation
strategy is limited to ostial ablation to isolate the pulmonary
veins, atrial tachycardias are unusual, occurring in only 1%
to 2% of patients.1– 4 In contrast, when pulmonary vein isolation is achieved by a wide area ablation or when the left atrium
is targeted directly with ablation lines or by ablation of complex, fractionated atrial electrograms, left atrial tachycardias
are common, with a reported incidence ranging between 10%
and 30%.3– 6 Furthermore, when a concerted effort is made to
terminate persistent atrial fibrillation using an extensive stepwise approach of catheter ablation in the left and right atria,
atrial tachycardias are observed in ⬎50% of patients.7 Of note
is that the incidence of atrial tachycardia after radiofrequency
catheter ablation of atrial fibrillation can be lowered by creating a complete line of block in the mitral isthmus and across
the left atrial roof during the first catheter ablation procedure.8,9
Atrial tachycardias may occur acutely during an atrial
fibrillation ablation procedure and are often the arrhythmia
to which persistent atrial fibrillation converts during the
course of radiofrequency ablation.7 Atrial tachycardias also
commonly occur several days to weeks or months after
radiofrequency catheter ablation of atrial fibrillation. The
mechanism of the atrial tachycardia likely varies depending
on whether it is an acute or a late phenomenon after ablation
of atrial fibrillation. Recent evidence based on spectral analysis suggests that atrial tachycardias observed acutely during
radiofrequency ablation of atrial fibrillation often may be due
to preexisting drivers of atrial fibrillation that become manifest
after elimination of higher-frequency sources and fibrillatory
conduction (Yoshida et al, unpublished data). In contrast, atrial
tachycardias that occur late after radiofrequency ablation of
atrial fibrillation probably most often are a manifestation of
gap-related proarrhythmia.10
Atrial tachycardia may be macroreentrant, microreentrant, or focal. In reentrant atrial tachycardias, endocardial
activation spans all of diastole. The diameter of the reentrant
circuit is ⬎3 cm in macroreentry and ⬍3 cm in microreentry. Focal atrial tachycardias are caused by triggered activity
or abnormal automaticity, and endocardial activation is presystolic, generally limited to the second half of diastole. In
microreentrant and focal atrial tachycardias, there is centrifugal spread away from the site of origin of the arrhythmia.
Approximately 75% of atrial tachycardias that occur after
wide-area radiofrequency ablation to isolate the pulmonary
veins is caused by macroreentry.10 The other 25% is evenly
split between microreentry and focal atrial tachycardia.10 If a
sampling of local electrograms in the left and right atria demonstrates that the electrograms at all sites are limited to the
second half of diastole, a focal mechanism is likely. In contrast,
if the electrograms span all or most of diastole, this finding
indicates that the atrial tachycardia is due to reentry. If the atrial
tachycardia is paroxysmal as opposed to persistent, or if more
than 20 to 30 ms of variability is seen in the tachycardia cycle
length, then a focal mechanism is favored over reentry.
Atrial tachycardias can be mapped by endocardial activation mapping and/or entrainment mapping. With either
approach, use of a three-dimensional nonfluoroscopic mapping system is helpful in identifying and tagging appropriate
target sites and in creating contiguous ablation lesions when
an ablation line is needed to traverse a critical isthmus.
The majority of focal atrial tachycardias that occur after
radiofrequency catheter ablation of atrial fibrillation originate in a pulmonary vein or in the antrum of a pulmonary
vein.10 Therefore, mapping of a focal atrial tachycardia
should first be focused on these sites. A ring catheter is
helpful in identifying a focal pulmonary vein tachycardia
that may not be identified with a standard ablation catheter.
Pulmonary vein isolation usually is appropriate if there is
Drs Morady, Oral and Chugh have no conflicts of interest to report.
Address reprint requests and correspondence: Dr. Fred Morady, Cardiovascular Center, SPC 5853, 1500 East Medical Center Drive, Ann
Arbor, Michigan 48109-5853. E-mail address: [email protected].
(Heart Rhythm 2009;6:S29 –S32) © 2009 Heart Rhythm Society. All
rights reserved.
1547-5271/$ -see front matter © 2009 Heart Rhythm Society. All rights reserved.
doi:10.1016/j.hrthm.2009.02.011
S30
Heart Rhythm, Vol 6, No 8S, August Supplement 2009
demonstrates an unusual site of origin, such as the anterior
wall of the left atrium. Once the site of origin has been
accurately identified, focal atrial tachycardias usually are
successfully ablated with a single application of radiofrequency energy.
In a series of 116 macroreentrant atrial tachycardias that
started several days to weeks after circumferential pulmonary vein ablation for paroxysmal or persistent atrial fibrillation, the most common type was a perimitral tachycardia
traversing the mitral isthmus.10 This type of tachycardia
accounted for approximately 40% of macroreentrant tachycardias. The next most common type of macroreentrant
tachycardia, which accounted for approximately 20% of
macroreentrant atrial tachycardias, had a wavefront traversing the left atrial roof. Less common sites of macroreentry
were the left atrial septum, cavotricuspid isthmus, base of
the left atrial appendage, and right atrial septum.10
Macroreentrant tachycardias are ablated by linear ablation across the critical isthmus. The critical isthmus may lie
between two anatomic landmarks, such as the mitral annulus and the left inferior pulmonary vein, or it may be a
relatively narrow channel bounded by sites of scar or double
potentials. Whenever feasible, the endpoint of ablation
should be not only the termination of tachycardia but also
complete conduction block across the ablation line. In the
case of an ablation line across the mitral isthmus, block in
the counterclockwise direction is demonstrated by differential pacing in the coronary sinus. If pacing from a distal site
in the coronary sinus results in a longer stimulus–atrial
interval anterior to the ablation line than when pacing from
a more proximal site, this finding indicates that the wavefront is traveling around the mitral annulus in only the
clockwise direction (Figure 1A). Furthermore, pacing in the
Figure 1 A: Counterclockwise block across an ablation line in the mitral
isthmus. The ablation catheter is positioned in the left atrial appendage.
Pacing was performed in the coronary sinus, and as the pacing site was
switched from the distal electrodes (CS1-2) to a more proximal pair of
electrodes (CS3-4), the interval between the pacing stimulus and the
ablation catheter shortened from 230 to 210 ms. B: Clockwise block at the
mitral isthmus. Note that atrial activation progresses from the proximal
(CS9-10) to distal (CS1-2) electrodes during pacing with the ablation
catheter in the left atrial appendage. Abld and Ablp ⫽ distal and proximal
bipolar recordings from the ablation catheter, respectively; Stim ⫽ stimulus.
evidence of pulmonary vein conduction, even if the focal
atrial tachycardia is not arising in the pulmonary vein, to
minimize the possibility of recurrent atrial fibrillation.
If the pulmonary veins are ruled out as the site of origin
of a focal atrial tachycardia, mapping then should focus on
the other most likely sites of origin, namely, the posterior
left atrium, mitral annulus, coronary sinus, superior vena
cava, and crista terminalis. Sometimes activation mapping
Figure 2
Block across a roof line. During left atrial appendage (LAA)
pacing, the interval between the stimulus and the electrogram recorded by
the ablation catheter was 140 ms at an inferior posterior left atrial site (top
left panel) and 160 ms at a more superior site (bottom left panel). This
finding indicates an ascending wavefront on the posterior wall of the left
atrium, consistent with block at the roof. In the absence of roof block, there
would be a descending wavefront on the posterior left atrium during LAA
pacing. Right: Posterior views of electroanatomic left atrial maps with the
ablation catheter icon at the two positions on the posterior wall. Abbreviations as in Figure 1.
Morady et al
Atrial Tachycardias
S31
left atrial appendage or anterior to the ablation line will
result in proximal-to-distal atrial activation within the coronary sinus if there is block in the clockwise direction
(Figure 1B).
Conduction block across the left atrial roof also can be
assessed by pacing from within the left atrial appendage. If
there is an ascending wavefront on the posterior wall of the
left atrium, this finding indicates block across the roof line
(Figure 2).
In other regions of the left atrium, the definitive demonstration of complete conduction block may be more difficult. At a minimum, widely split double potentials should be
demonstrated along the entire ablation line (Figure 3).
Multiple macroreentrant atrial tachycardias commonly
are encountered after radiofrequency catheter ablation of
atrial fibrillation. A given tachycardia may have multiple
loops, or a different tachycardia may immediately take the
place of a tachycardia that has been successfully ablated. In
multiloop tachycardias, each loop of the tachycardia must
Figure 3 A: Termination of an atrial tachycardia by an ablation line
across the left atrial septum. The final application of radiofrequency energy
(arrow) resulted in conversion to sinus rhythm. Red tags on the electroanatomic map indicate the sites at which radiofrequency energy was
applied. B: Widely split double potential (180 ms) was present along the
entire ablation line, consistent with complete block across the line. CSd ⫽
distal pair of electrodes of the coronary sinus catheter; CSp ⫽ proximal pair
of electrodes of the coronary sinus catheter. Other abbreviations as in
previous figures.
Figure 4
A: Perfect postpacing interval of 260 ms at the cavotricuspid
isthmus, indicating that this atrial tachycardia was cavotricuspid isthmus dependent. B: After ablation across the cavotricuspid isthmus, there was no
change in atrial cycle length or P-wave morphology, but double potentials
(circled) were present along the cavotricuspid isthmus, suggesting that the
cavotricuspid isthmus was blocked. C: Postpacing interval just lateral to the
ablation line in the cavotricuspid isthmus was found to be 60 ms longer than
the tachycardia cycle length, indicating that the tachycardia no longer was
using the cavotricuspid isthmus. A site with a perfect postpacing interval was
found at the upper right atrial septum. Abbreviations as in previous figures.
be addressed. A change in atrial activation sequence or
P-wave morphology, or a sudden change in a cycle length,
indicates that the tachycardia that was being ablated has
S32
changed to a different loop or to a different tachycardia.
However, the transition to a different loop of a tachycardia
or to a different tachycardia may occur with no discernable
change in the activation sequence among the atrial electrograms that are being recorded, P-wave morphology, or cycle
length. It is important to keep this in mind when ablation
across an isthmus appears to not be affecting the tachycardia
(Figure 4A). The isthmus already may have been blocked
and may no longer be participating in the tachycardia. This
should be suspected if double potentials are present along
the ablation line and is easily confirmed by determining the
postpacing interval near the ablation line (Figure 4B). If a
previously perfect postpacing interval now is ⬎30 ms
longer than the tachycardia cycle length, this finding indicates that the tachycardia circuit has changed (Figure 4C).
In a series of 21 microreentrant atrial tachycardias that
occurred after circumferential pulmonary vein ablation, the
most common sites of origin were the coronary sinus, the
antrum of a pulmonary vein, and the anterior wall of the left
atrium or base of the left atrial appendage.10 Entrainment
mapping usually is the most efficient method for localizing
an effective target site for ablation. A single application of
radiofrequency energy often is sufficient for eliminating an
atrial tachycardia caused by microreentry.
Two situations may necessitate radiofrequency ablation
within the coronary sinus. The first is a perimitral flutter that
has persisted despite thorough endocardial ablation at the mitral isthmus such that double potentials are present along the
line. In approximately 70% of cases, epicardial fibers continue
to conduct despite extensive endocardial ablation and can be
ablated only from within the coronary sinus. The second situation that necessitates ablation within the coronary sinus is a
microreentrant or macroreentrant tachycardia involving the
coronary sinus, independent of the mitral isthmus.11
When radiofrequency catheter ablation is performed in
the coronary sinus, the catheter of choice is an irrigated-tip
catheter. Power should be limited to 20 to 25 W, and the
application of energy should be discontinued if there is a
rapid rise or fall in impedance or a rapid rise in temperature.
Sometimes a power setting of 30 to 35 W is required for
successful ablation. A higher power setting should be considered when a tachycardia fails to respond to ablation with
20 to 25 W and when entrainment mapping or activation
mapping indicates that the coronary sinus is still an appropriate target site.
In a series of 78 patients who underwent radiofrequency
catheter ablation of 155 atrial tachycardias that occurred
Heart Rhythm, Vol 6, No 8S, August Supplement 2009
after circumferential pulmonary vein ablation, 86% of the
tachycardias were successfully ablated and became noninducible, and the ablation procedure was deemed successful
in 85% of the patients.10 When the pulmonary veins that
demonstrated recovery of conduction were reisolated during
the same ablation session, only a small proportion of patients had recurrent atrial fibrillation or atrial tachycardia
during long-term follow-up.
Because atrial tachycardias that occur after radiofrequency ablation of atrial fibrillation often are persistent, are
difficult to suppress with rhythm control medications, and
often are associated with rapid ventricular rates, these arrhythmias may cause more severe symptoms than the atrial
fibrillation for which the patient originally underwent catheter ablation. However, although catheter ablation of atrial
tachycardias that occur after radiofrequency ablation of
atrial fibrillation may be a time-consuming process that
requires mental and physical fortitude, the tachycardias usually can be successfully eliminated.
References
1. Oral H, Knight BP, Tada H, et al. Pulmonary vein isolation for paroxysmal and
persistent atrial fibrillation. Circulation 2002;105:1077–1081.
2. Oral H, Knight BP, Morady F. Left atrial flutter after segmental ostial radiofrequency catheter ablation for pulmonary vein isolation. Pacing Clin Electrophysiol 2003;26:1417–1419.
3. Karch MR, Zrenner B, Deisenhofer I, et al. Freedom from atrial tachyarrhythmias after catheter ablation of atrial fibrillation: a randomized comparison
between 2 current ablation strategies. Circulation 2005;111:2875–2880.
4. Oral H, Ozaydin M, Tada H, et al. Mechanistic significance of intermittent
pulmonary vein tachycardia in patients with atrial fibrillation. J Cardiovasc
Electrophysiol 2002;13:645– 650.
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2612.
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