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Catheter Ablation of
Supraventricular and
Ventricular Arrhythmias
Luz-Maria Rodriguez, Carl Timmermans, and
Hein J.J. Wellens
Historical Aspects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2139
Indications for Catheter Ablation of Tachycardias. . . . 2140
Key Points
• Catheter ablation has become the first truly curative
treatment for many supraventricular and some ventricular tachycardias.
• The success rate for anteroseptal and midseptal accessory
pathways ranges between 95% and 100%, but the risk of
creating a more complete atrioventricular (AV) block in
patients with midseptal accessory pathways is not negligible. The recurrence rate after ablation of accessory pathways is low, and if necessary, the patient can be reablated
with a high success rate. Patients should be followed for
at least 6 months after ablation.
• Catheter ablation in patients with AV nodal reentrant
tachycardia (AVNRT) has been very successful in curing
patients.
• The success rate for catheter ablation for common
atrial flutter ranges between 65% and 98%. There is a
risk of recurrence of ablated atrial flutter of 10% to
55%.
• In general, catheter ablation for atrial tachycardia is effective and safe.
• In ablation procedures to treat atrial fibrillation, ostial
pulmonary vein isolation is reported to result in a success
rate of 70% to 80%. Potential complications include
pulmonary vein stenosis and esophageal injury with or
without atrioesophageal fistula.
• Atrioventricular nodal ablation followed by pacemaker
implantation is limited to patents in whom catheter ablation cannot cure the supraventricular arrhythmia, such
as left atrial flutter, multifocal atrial tachycardia, and
some atrial fibrillation. It is an accepted modality in
patients with atrial fibrillation with a very rapid ventricular response that cannot be controlled with antiarrhythmic medication, external and internal cardioversion, and
perhaps the atrial implantable defibrillator.
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2158
• Catheter ablation of ventricular tachycardia (VT) is much
more modest in its success as compared to results in
patients with supraventricular tachycardias (SVTs). In
idiopathic VT, however, catheter ablation is a curative
technique and should be offered early in the treatment of
symptomatic patients.
• Primary idiopathic ventricular fibrillation is characterized by dominant triggers from the distal Purkinje system.
The triggers can be eliminated by focal energy delivery.
Historical Aspects
In 1967, programmed electrical stimulation of the heart was
introduced into clinical cardiology independently by Durrer
and coworkers1 in Amsterdam and by Coumel et al.2 in Paris.
Programmed electrical stimulation of the heart has revolutionized our methods of diagnosis and treatment of cardiac
arrhythmias.3 It resulted not only in the ability to localize
the site of origin of the arrhythmia but also in better understanding of arrhythmia mechanisms, better interpretation
of the arrhythmia electrocardiogram, and the development
of new treatment modalities like antitachycardia pacing4
and surgical5 or catheter ablation to cure or control cardiac
arrhythmias.6,7
In 1986, the first successful clinical arrhythmia ablation
using radiofrequency current was reported.8 Early experience
in ablation of supraventricular arrhythmias had variable
results. With evolving understanding of the anatomy of the
heart and the introduction of a new radiofrequency (RF) ablation catheter with a large (4 mm) distal electrode, the success
rate improved dramatically.9,10 To date, catheter ablation has
become the first truly curative treatment for many supraventricular and some ventricular tachycardias.11
The catheter ablation procedure should be preceded by a
careful analysis of the 12-lead arrhythmia electrocardiogram
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and an electrophysiologic study. The electrophysiologic study
should consist of a systematic analysis of the arrhythmia by
recording and measuring a variety of electrophysiologic
parameters during the basal state and by evaluating the
response to programmed electrical stimulation. Programmed
electrical stimulation of the heart not only gives important
information about the electrophysiologic properties of the
atrioventricular (AV) node, the His-Purkinje system, the
atria, and the ventricles, but also facilitates studying
the mechanism and localizing the site of origin or pathway
of an arrhythmia. How the electrophysiologic study and the
subsequent catheter ablative procedure should be conducted
will depend on the specific arrhythmia of the patient.
Indications for Catheter Ablation
of Tachycardias
The efficacy and the safety profile of catheter ablation have
resulted in the indications listed in Table 102.1.12 The
approaches to the different types of supraventricular and
ventricular tachycardias are discussed separately.
10 2
Catheter Ablation of Supraventricular
Tachycardias
Accessory Pathways
As also discussed in Chapter 93 on preexcitation, an accessory atrioventricular pathway is a connection between the
atrium and the ventricle crossing the AV groove on the left
or right side of the heart. Originally, accessory AV connections were divided into those located on the right or left free
wall, and the posteroseptal, anteroseptal, and midseptal
region. Use of catheter ablation requires a more precise localization of the accessory pathways in the AV groove (Fig.
102.1). Free wall accessory pathways are subdivided in a posterior, lateral, and anterior localization. Posteroseptal accessory pathways may also be found in the wall of the coronary
sinus and in some cases in the middle cardiac vein.13 Anteroseptal accessory pathways are those pathways located above
the His bundle, and the midseptal pathways are those located
in the midseptal area.14,15 The midseptum is the region
located superior to the ostium of the coronary sinus but
below the His bundle (Fig. 102.2). It is important to stress
that accessory pathways may be conducting in both direc-
TABLE 102.1. Indications for catheter ablation of supraventricular arrhythmias according to the American College of Cardiology (ACC)/
American Heart Association (AHA)/European Society of Cardiology (ESC) Guidelines12
Arrhythmia
Classification
Level of evidence
Accessory pathways
WPW syndrome (preexcitation symptomatic arrhythmias, well-tolerated
I
B
WPW syndrome (with AF and rapid-conduction or poorly tolerated AVRT)
I
B
AVRT, poorly tolerated (concealed accessory pathway)
I
B
Single or frequent AVRT episode(s) (concealed accessory pathway)
IIa
B
Preexcitation, asymptomatic
IIa
B
AV nodal reentry tachycardia (AVNRT)
Recurrent AVNRT
I
B
AVNRT with frequent episodes in patients who desired complete control of arrhythmias
I
B
Infrequent, well-tolerated AVNRT
I
B
Focal atrial tachycardia (AT)
Asymptomatic or symptomatic incessant AT(s)
I
B
Nonsustained and asymptomatic AT
III
B
Atrial flutter (AFL)
First episode and well-tolerated AFL
IIa
B
Recurrent and well-tolerated AFL
I
B
Poorly tolerated AFL
I
B
AFL appearing after use of class IC agents or amiodarone for the treatment of AF
I
B
Symptomatic non-CTI dependent AFL after failed antiarrhythmic drugs therapy
IIa
B
Supraventricular tachycardia after repaired congenital heart disease
Focal AT or scar macro reentry tachycardia
I
C
Classification
I: Evidence for/and/or general agreement that the procedure or treatment is useful and effective
II: There is confl icting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment
IIa: Weight of evidence is in favor of the procedure or treatment
III: There is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmful
Level A: (highest) derived from multiple randomized clinical studies
Level B: (intermediate) data are on the basis of a limited number of randomized trials, nonrandomized studies, or observational registries
Level C: (lowest): primary basis for the recommendation was expert consensus
AVRT, atrial ventricular reentry tachycardia; CTI, cavotricuspid isthmus; WPW, Wolff-Parkinson-White syndrome.
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His bundle
1 anterior
2 perinodal
3 posterior
CS
AVN
FIGURE 102.1. The location of accessory pathways along the tricuspid and mitral annulus. AS, anteroseptal; CS, coronary sinus;
LA, left anterior; LL, left lateral; LP, left posterior; LPS, left posteroseptal; RA, right anterior; RL, right lateral; RP, right posterior; RPS,
right posteroseptal.
ostium
FIGURE 102.2. The location of the three types of midseptal accessory pathways (anterior, perinodal, posterior) in the space between
the ostium of the coronary sinus (CS) inferiorly, and the His bundle
superiorly. AVN, atrioventricular node.
tions (anterogradely and retrogradely), or only anterogradely,
or only retrogradely. The latter pathway is called a “concealed” pathway. Concealed pathways are of two types, the
rapidly and the slowly conducting one.
To perform an ablation procedure, catheters are inserted
through both femoral veins or the subclavian vein and positioned in the heart under fluoroscopy. A quadripolar catheter
is placed in the high right atrium, the His bundle, and the
right ventricular apex. A multipolar catheter is placed in the
coronary sinus. Finally, the ablation catheter is positioned at
the site of the accessory pathway as determined during the
electrophysiologic study. In general, two fluoroscopic views,
the left anterior oblique (LAO) and the right anterior oblique
(RAO) projection, are used to position the ablation catheter
in the accessory pathway region. In patients with a left-sided
accessory pathway, the usual approach is to insert the ablation catheter into the femoral artery, retrogradely advance
the catheter across the aortic valve, followed by positioning
under the mitral annulus (Fig. 102.3). Mapping of the left AV
groove to obtain specific electrograms, indicating the exact
localization of the accessory pathway, is performed before
attempting ablation. This requires a careful manipulation of
the ablation catheter under the mitral annulus and a good
understanding and interpretation of the recorded electrograms. This approach is used when the ventricular insertion
of the accessory pathway is the target of ablation. If the atrial
insertion of the accessory pathway needs to be ablated, the
ablation catheter should be positioned on the mitral annulus.
Some centers prefer a transseptal catheterization to ablate
left-sided accessory pathways, and in those patients, ablative
FIGURE 102.3. Figure illustrating the right anterior oblique (RAO)
projection (A) of catheters positioned in the coronary sinus (CS), the
high right atrium (HRA), the His bundle, and right ventricle (RV).
The tip of the radiofrequency (RF) ablation catheter is located under
the mitral valve in the left lateral region. The same catheters in the
left anterior oblique projection (LAO) (B).
Ablation Procedure
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energy is delivered at the atrial insertion of the accessory
pathway. The catheter inserted in the coronary sinus anatomically marks the AV groove and helps in mapping leftsided accessory pathways.
In patients with right-sided accessory pathways, the procedure is performed using either the femoral or subclavian
approach. The ablation catheter is carefully advanced most
of the time over and sometimes under the tricuspid annulus
to obtain the optimal electrograms indicating the exact location of the accessory pathway. Posteroseptal accessory pathways are located in the posteroseptal space (right and left)
just outside and below the coronary sinus ostium. Some
accessory pathways can also be located within the coronary
sinus or in one of its branches (e.g., middle cardiac vein).
Therefore, mapping of the posteroseptal space should also
include the first centimeters of the coronary sinus and its
posterior branches.13 Because of the vicinity of the conduction system (right bundle for anteroseptal accessory pathways; His bundle and AV node for midseptal accessory
pathways), mapping of these regions should carefully and
precisely be performed before delivering ablative energy. This
is to avoid complications such as right bundle branch block
or complete AV block, which may require permanent pacemaker implantation.
Optimal Ablation Site
Several electrophysiologic criteria are used to localize the
optimal site to deliver ablative energy.16–19 During preexcited
rhythms the following parameters are used to localize the
ventricular insertion of an accessory pathway: the local AV
interval, the earliest ventricular activation compared to the
delta wave, and the recording of an accessory pathway potential (Fig. 102.4). Certain morphologies of the unipolar electrogram and an early intrinsic deflection of the unipolar
A
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
HRA
HIS
AV
RF
RFU1
RFU2
B
95-2286
95-2286
A-V = –20 ms
99512
A V
AP
200 mm/sec
FIGURE 102.4. (A) Upper part: The 12-lead electrocardiogram
(ECG) in a patient with a left lateral accessory pathway. Lower part:
endocardial recordings recorded from the high right atrium (HRA),
His bundle, and the tip of the RF ablation catheter with the bipolar
(RF) and corresponding unipolar recordings (RFU1, RFU2). Note
that the bipolar electrogram of the RF catheter located at the successful ablation site shows an accessory pathway (AP) potential, and
an AV interval of −20 ms. Furthermore, the unipolar RFU1 shows a
PQS pattern. (B) After successful ablation preexcitation and the AP
potential have disappeared, the AV interval recorded from the tip of
the RF catheter ablation has lengthened to 100 ms.
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I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
97-0153
99518
RFd
RF1
RF2
25 mm/sec
start
FIGURE 102.5. The 12-lead ECG, the bipolar (RF) and the unipolar
(RFUI, RFU2) electrograms during RF ablation in a patient with
an anterogradely conducting left lateral accessory pathway. Note
the disappearance of preexcitation immediately after RF energy
application (*).
recording relative to the delta wave onset may also indicate
an optimal ablation site.18 The atrial insertion of an accessory pathway is usually localized by identifying the site of
the shortest ventriculoatrial (VA) interval during ventricular
pacing or during circus movement tachycardia or by recording an accessory pathway potential. In general, the following
criteria are considered to select the optimal site for delivering ablative energy in preexcited rhythms: the presence of an
accessory pathway potential, the onset of a local ventriculogram preceding the delta wave by 5 to 20 ms, a local AV
interval less than 40 ms, and a PQS morphology in the unipolar recordings.18,19 In patients with a concealed accessory
pathway, the ablation site of the atrial insertion is indicated
by the shortest VA interval.20 If the ablation catheter has good
tissue contact and the previously mentioned criteria are
present, the loss of preexcitation or retrograde conduction
should occur within seconds after delivering ablative energy.
Disappearance of preexcitation within 10 seconds is a good
predictor for long-term success (Fig. 102.5). After the interruption of accessory pathway conduction and after a waiting
period of 30 minutes, the electrophysiologic study is repeated
under isoproterenol administration (1 to 3 μg/kg) to ensure
permanent interruption of the accessory pathway and
to exclude other possible supraventricular tachycardia
mechanisms.
Success Rate of Ablation of Accessory Pathways
The long-term success of catheter ablation depends on the
correct localization of the accessory pathway and the experience of the operator. The success rate for left free wall accessory pathways is currently as high as 95% to 99%.7 The
success rate for right free wall and posteroseptal accessory
pathways is less than for left free wall accessory pathways
and ranges between 90% and 93%. This is due to less good
catheter stability (right free wall accessory pathways) and to
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rate. Based on this information, patients should be followed
for 6 months after ablation.
the complexity of the posteroseptal space (posteroseptal
accessory pathways) where the accessory pathways may have
an anatomic epicardial insertion with widespread branching,
making complete ablation difficult. The success rate for
anteroseptal and midseptal accessory pathways ranges
between 95% and 100%, but the risk of creating complete
AV block in patients with midseptal accessory pathway is
not negligible. The success rate for a Mahaim-type accessory
pathway (a decrementally conducting pathway inserting into
the right ventricle) has also been reported as high as 90% to
100%.21 Recording of a Mahaim potential on the tricuspid
annulus is a good indicator for a successful ablation (Fig.
102.6). Finally, in patients with circus movement tachycardia, using a slowly conducting accessory pathway for ventriculoatrial conduction, the success rate is as high as 95%
to 100%.22
Complications of Accessory Pathway Ablation
The risk of radiofrequency catheter ablation is related to the
location of the accessory pathway. As previously mentioned,
ablation of a midseptal accessory pathway carries the risk of
complete AV block. In posteroseptal epicardially located
accessory pathways, where the ablation has to be performed
from the coronary sinus, there is a risk of damage to the
coronary artery or perforation of the venous system leading
to cardiac tamponade.13 A Multicentre European Survey25
reported on the complications of radiofrequency catheter
ablation in 2222 patients with accessory pathways. Fourteen
patients (0.63%) developed complete AV block, 16 patients
(0.72%) had a cardiac perforation with or without tamponade,
and 12 patients developed a clinically significant pericardial
effusion. In three patients, death was thought to be related
to the procedure. However, it is important to mention that
this study analyzed retrospective data from an early period
(1987–1992) of radiofrequency catheter ablation. Calkins et
al.26 in a prospective study found a similar incidence of the
same complications in the period 1992–1995. In children and
adolescents, the American Society of Pediatric Electrophysiology27 reported 3.2% of complications after radiofrequency
catheter ablation of supraventricular tachycardias in 4135
patients. The complications were complete AV block, cardiac
perforation, pericardial effusion, cerebral emboli, and pneumothorax. A multivariate analysis showed three independent factors for recognizing patients with a high probability
Recurrence of Conduction of Accessory Pathways
In our institution, the incidence of reappearance of conduction through an accessory pathway after catheter ablation is
around 8%. The time of recurrence of accessory pathway
conduction ranged from 3 hours to 3 months.23 These figures
are in agreement with other studies reporting a recurrence
rate of 8% to 12% after a time delay of 4 to 7 months.24
Several variables have been reported to be predictors for
recurrence of conduction over an accessory pathway: the
presence of multiple accessory pathways, a high number of
radiofrequency applications, young age,24 and a right-sided
location.23 In general, the overall recurrence rate is low, and
if necessary, the patient can be reablated with a high success
I
II
III
aVR
aVL
aVF
V1
V2
V3
HBEP
HBED
96-0419
V4
V5
V6
AF
PF
Mahaim
214 3
A
RB
M
A
M
RF
RB
RB
RB
HBED
HBEF
RVA
100 mm/sec
FIGURE 102.6. An electrophysiologic study in a patient with a
preexcited tachycardia with atrioventricular conduction over an
atriofascicular (Mahaim) fiber, and ventriculoatrial conduction over
the His-AV node pathway. Note the presence of a Mahaim potential
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(M) recorded with the tip of the RF catheter where successful ablation was performed. RB, right bundle; HBED, distal His bundle
electrogram; HBEF, proximal His bundle electrogram.
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tion. In the early days of catheter ablation, two approaches
were suggested: the anterior approach to interrupt the fast
pathway, and the posterior approach to block the slow
pathway. These approaches were named anterior and posterior based on the location of the fast and slow pathway in the
triangle of Koch. The fast pathway is located close to the His
bundle, in the anterior part of the triangle of Koch, and the
slow pathway is situated in the posterior part of this triangle
(Fig. 102.7). Currently, fast pathway ablation is seldom used
in view of the high risk of complete AV block (5% to 10%)
because of the proximity of the ablation site to the compact
AV node and proximal His bundle.31
Slow Pathway Ablation Procedure
FIGURE 102.7. The triangle of Koch, composed of the tendon of
Todaro (TT) superiorly and the tricuspid valve (TV) inferiorly. The
coronary sinus ostium forms the base and the His bundle the apical
part. The numbers in the triangle represent the three approaches to
perform RF ablation of AV nodal reentrant tachycardia: 1, anterior;
2, midseptal; and 3, posterior.
of developing a complication: the experience of the operator,
the presence of right-sided accessory pathways, and a body
weight of less than 15 kg. Also in this survey four deaths
(0.11%) were reported. In the early days of catheter ablation,
the fluoroscopy time was an important concern for eventual
complications. To date, with more experience, procedure and
fluoroscopy times have shortened, thereby reducing the risk
of complications due to radiation.
Atrioventricular Nodal Reentrant Tachycardia
Catheter ablation in patients suffering from AV nodal reentrant tachycardia (AVNRT) has been quite successful in
curing patients.28–33 It has become the treatment of choice
when the patient is symptomatic with this arrhythmia, not
responding to or not willing to take antiarrhythmic medica-
FIGURE 102.8. The catheter position used for ablation of AV nodal
reentrant tachycardia in two fluoroscopic views: (A) right anterior
oblique view; (B) left anterior oblique view. CS, coronary sinus; CSO,
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Two techniques have been used to ablate the slow pathway:
the anatomic technique 30,32 and the electrophysiologic technique.28,29 In the anatomic technique, fluoroscopic landmarks
are used to guide the positioning of the ablation catheter.
Using the posterior approach, the ablation catheter is positioned in the posterior third of Koch’s triangle (Fig. 102.8).
An atrial/ventricular (A/V) ratio of 0.5 or <1 in the electrogram recorded with the tip of the ablation catheter is required
prior to the delivery of energy. A successful radiofrequency
application is frequently associated with the appearance of a
short episode of an accelerated junctional rhythm. After each
application, conduction over the slow pathway and inducibility of AVNRT should be assessed. If this posterior
approach is unsuccessful, the catheter is carefully moved to
the midseptal region where ablative energy is again delivered. When using the electrophysiologic technique, ablation
is performed based on specific electrograms representing
slow pathway conduction.
Two distinct morphologies of slow pathway potentials
have been described. Jackman et al.28 described a sharp spikelike potential preceded by a lower frequency, lower amplitude atrial potential during sinus rhythm. The slow pathway
potential usually follows the atrial potential after 10 to
40 ms. The slow pathway potential is recorded in the vicinity
of the coronary sinus ostium, near the tricuspid annulus.
coronary sinus ostium; HRA, high right atrium; RF, radiofrequency
catheter; RV, right ventricle.
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Another type of slow pathway potential was described by
Haïssaguerre et al.29 This is a low-amplitude, low-frequency
signal, and it follows the atrial electrogram and is recorded
in the midseptal area. Acute success of AVNRT ablation
ranges from 90% to 100%.28,32 Few patients (1% in our laboratory) experience a recurrence of the arrhythmia and require
a second procedure. The risk of AV block using the posterior
approach is low (1%) compared to the anterior approach (5%
to 10%).26,33 Other complications, like venous thrombosis
and pericardial effusion, can occur but, in general, the risk
of the procedure is low because no arterial catheterization is
required.
Right Atrial Common Flutter
The most frequent form of atrial flutter, the so-called common
or typical atrial flutter, occurs in the right atrium and may
rotate in a counterclockwise (CCW) or clockwise (CW)
manner.34,35 Nonfluoroscopic mapping36 and the use of multiple endocardial electrograms37 have identified the circuit of
the right atrial common flutter. The CCW atrial flutter is a
broad band of peri-tricuspid activation that enters the isthmus
[the atrial tissue between the inferior vena cava (IVC) orifice
and the tricuspid annulus (TA)], slows in its medial part,
ascends the atrial septum, reaches the root of the superior
vena cava, usually crosses anteriorly and rarely, fuses around
it to descend the free wall. The CW atrial flutter, while
running in the opposite direction, shares the same circuit
with the same endocardial borders as the CCW atrial flutter.
On the 12-lead ECG, the common atrial flutter shows the
so-called sawtooth appearance.
Ablation Procedure
An atrial flutter ablation procedure usually requires the
insertion of the following catheters: a duodecapolar catheter
for detailed mapping of the lateral right atrial wall and the
IVC-TA isthmus, and multipolar catheters to record the activation of the coronary sinus ostium–TA isthmus, the His
bundle, and the coronary sinus. During the electrophysiologic study, the atrial flutter is induced and the type of isthmus
conduction evaluated.38 Thereafter, an ablation catheter is
positioned in the right atrial isthmus. The LAO and RAO
views are used to guide ablation, either using fluoroscopy or
a three-dimensional mapping system (Fig. 102.9).
Two approaches have been described to ablate common
atrial flutter: the anatomic approach39–42 and the electrophysiologic approach.43 The anatomic approach uses fluoroscopic
landmarks to localize the right atrial isthmus, and the electrophysiologic approach targets areas with critical isthmus
conduction determined on the basis of concealed entrainment or the presence of double potentials.43 Two isthmi have
been described 38: the posterior isthmus (IVC-TA), which
includes the space between the IVC and the TA (IVC-TA),
and the septal (TA-CS) isthmus, which is the space between
the TA (at the level of the posterior margin of the coronary
sinus ostium) to the posteroapical margin of the coronary
sinus ostium (CS) or to the eustachian ridge. In patients
without atrial conduction between the coronary sinus ostium
and the eustachian ridge, ablation of the septal isthmus produces complete conduction block from the TA to the coronary sinus ostium and to the IVC, eliminating both CCW
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and CW atrial flutter.38 A linear ablation is performed in one
of the previously mentioned isthmi, either by applying pointby-point radiofrequency energy or cryothermia, or by dragging the catheter during the radiofrequency application.
Regardless of the approach used, the end point for successful ablation is the noninducibility of atrial flutter after
completion of the ablation line and the demonstration of a
bidirectional isthmus conduction block and the presence of
double potentials in the cavotricuspid isthmus.41 Before ablation, pacing from the ostium of the coronary sinus results in
the propagation of the atrial impulse in a clockwise direction
to the IVC-TA isthmus and the lateral right atrium, and in a
counterclockwise direction to the septum and the high right
atrium. This pacing maneuver creates a collision of the atrial
wave fronts in the lateral right atrium (Fig. 102.10A). In contrast, during pacing from the right lateral wall, the atrial
impulse propagates in counterclockwise direction along the
ICV-TA isthmus and in a clockwise direction to the high
right atrium and septum (Fig. 102.10B). After completion of
the ablation during bidirectional isthmus block, pacing from
the coronary sinus ostium results in a single atrial wave
front descending along the lateral right atrium (Fig. 102.10C).
Pacing from the right lateral wall results in a single atrial
wave front ascending the high right atrium and descending
through the atrial septum (Fig. 102.10D). Finally, pacing is
repeated under isoproterenol perfusion44 to confirm the noninducibility of atrial flutter and bidirectional isthmus conduction block. Using this methodology, the acute success
rate of catheter ablation for common atrial flutter ranges
between 65% and 98%.38–43
In a number of patients with atrial fibrillation, the
arrhythmia may organize into atrial flutter while treating
these patients with class III45 or class IC46,47 antiarrhythmic
drugs. Catheter ablation of the right atrial isthmus may significantly reduce the incidence of atrial fibrillation in these
patients.45–47 After ablation, these patients should continue
to take the medication that changed atrial fibrillation into
atrial flutter.
Catheter ablation of the septal isthmus has a (small) risk
of complete AV block. Other complications are similar to
those reported for right-sided radiofrequency catheter ablation procedures.
Recurrences of Right Atrial Common Flutter
A high recurrence rate (10% to 55%) has been reported if
noninducibility of atrial flutter alone is used as a criterion
for successful ablation.40,48,49 The recurrence rate is lower (6%
to 9%) in patients with bidirectional isthmus conduction
block compared to patients with unidirectional isthmus conduction block or bidirectional isthmus conduction delay at
the end of the procedure.50 In our hospital, isoproterenol is
used to evaluate resumption of conduction after right atrial
isthmus ablation.44 In some patients, isoproterenol infusion
can unmask an apparent bidirectional isthmus conduction
block, necessitating a new ablative procedure in the isthmus
to create complete isthmus block.
Left Atrial Flutter
At the present time, two different types of left atrial flutter
have been recognized. Spontaneous atrial flutter and atrial
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LAO
CS
Halo
His
Halo
CS
His
Cryo
Cryo
A
B
TV
SVC
His
Halo
IVC
Halo
CS
His
TV
PS
CS
IVC
SVC
C
flutters occurring after ablation of atrial fibrillation. Recently,
by mapping the spontaneous atrial flutter with the CARTOTM
Biosense system, electrical silent areas or zones of block in
the left atrium were demonstrated.51 Different types of reentrant circuits could be delineated: (1) single-loop reentrant
circuits, mainly rotating around the mitral annulus (Fig.
102.11); (2) multiple-loop circuits rotating around a silent area
or around a zone of block anchored in one of the pulmonary
veins; and (3) small reentry circuits localized in the left atrial
septum, fossa ovalis, or one of the pulmonary veins.51 Termination of the perimitral flutter circuits can be obtained by
deploying a line of ablation between the mitral annulus and
the superior right or left pulmonary veins, or by connecting
the mitral annulus and one of the silent zones. The peripulmonary vein circuits can be ablated by joining the pulmonary vein to the mitral annulus. Ablation of atrial flutters
with small reentry circuits should be performed at the area
of the slow conduction. The chronic success rate in this type
CAR102.indd 2146
FIGURE 102.9. The catheter positions for ablation of a common atrial
flutter in the right anterior (A), and
the left anterior oblique view (B). A
duodecapolar catheter (Halo) is positioned around the tricuspid annulus
in such a way that the proximal poles
(bipolar 20–19 and 18–17) are septally
located, and the distal part (bipolar
1–2 and 3–4) covers the posterior
isthmus region. The rest of the catheter covers the lateral wall of the
right atrium. The ablation catheter
(Cryo) is positioned in the posterior
isthmus. A quadripolar catheter is
located in the His bundle region, and
a decapolar catheter inserted in the
coronary sinus (CS) records left atrial
activation. (C) The delineation of the
cavotricuspidal isthmus for ablation
using the NavX system in the anteroposterior (AP) and bottom view in the
same patient. White spots with
numbers represent the number and
location of the ablation applications.
In this example, cryoablation was
used during the procedure.
of atrial flutter is around 75%. Atrial flutter after linear ablation for atrial fibrillation has been reported to be as high as
7% (Fig. 102.12).52 Recompletion of the previous ablation line
is necessary to treat this type of atrial flutter.
Catheter Ablation of “Incisional Tachycardia”
Atrial arrhythmias are a frequent clinical problem after surgical correction of congenital heart disease. Hemodynamic
impairment and pressure overload, together with the presence of surgical scars and prosthetic material, may result in
an arrhythmogenic combination of fi xed artificial obstacles
and electrophysiologic abnormalities that cause scar flutters
or macroreentrant incisional tachycardia.53 These tachycardias can occur after correction of atrial septal defects and
after corrective surgery for complex anomalies, such as the
Mustard, Senning, or Fontan procedures. They may also
occur following right or superior atrial incisions during
11/24/2006 10:52:51 AM
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I
III
HBEd
HBEp
H1920
H1718
H1516
H1314
H1112
H0910
H0708
H0506
H0304
H0102
CS78
CS56
CS34
CS12
CRYO
011425 A
B
C
D
E
200 mm/sec
200 mm/sec
lead III is shown. Intracardiac electrograms are recorded from the
FIGURE 102.10. (A,B) Atrial pacing during sinus rhythm before
His bundle area. H1.2 to H19.20 indicate 10 bipoles of the duodeablation. (A) Pacing at the coronary sinus ostium. (B) Pacing at the
capolar (Halo) catheter positioned around the tricuspid annulus, and
low lateral right atrium. Note a dual wave front of right atrial activaCS1.2 to CS7.8 represent four bipoles of a decapolar catheter placed
tion with bidirectional conduction, which collides in H.9.10. (C,D)
in the coronary sinus (CS). (E) Sinus rhythm with the presence also
Bidirectional conduction block with the presence of double potenof double potential.
tials in the cavotricuspid isthmus. (C) Pacing at the coronary sinus
ostium. (D) Pacing at the low lateral right atrium. The surface ECG
mitral valve surgery. The electrocardiogram (ECG) pattern of
these scar flutters or “incisional tachycardia” is variable; the
rate is often slightly below the lower limit usually accepted
for common atrial flutter. The localization and the size of
the scar may vary from patient to patient. Endocardial
mapping of the entire reentrant circuit is sometimes difficult
or impossible (especially after the Mustard and Senning procedures). Catheter ablation in these patients is targeted to
areas forming a critical part (isthmus) of the circuit, identified on the basis of electrogram timing, fragmentation,54 or
entrainment techniques.53 Using the entrainment technique,
Kalman et al.53 reported an acute success of 83%. Seventytwo percent of the patients had a long-term clinical improvement and 50% of these patients were asymptomatic and did
not require medical therapy after a mean follow-up period of
17 months. In some patients, the critical isthmus of conduction cannot be localized. In these cases, areas in proximity
to anatomic or surgical barriers showing concealed entrainment with local return intervals equal to the cycle length of
the tachycardia are targeted for ablation.55–58 In the study of
Kalman et al., reentry was more often found around the
atriotomy than around the septal patch of the atrial septal
defect repair. We and other authors have reported isthmusdependent common atrial flutter in most of these patients.57,59
With new mapping techniques, like the three-dimensional,
nonfluoroscopic mapping (CARTO) system, the scar can be
more precisely located and the ablation site can be better
directed and verified (Fig. 102.13).
397 ms
FIGURE 102.11. An example of a clockwise perimitral flutter (cycle length,
400 ms) bounded by an anterior silent
area (gray color) in the left anterior
oblique (LAO) (A) projection. The posteroanterior (PA) view (B) shows a zone
of block anchored in the left pulmonary
vein (LPV) and a posterior silent area
with bystander activation proceeding
superiorly and inferiorly, colliding on its
right lateral aspect. Radiofrequency
ablation was performed to connect the
mitral annulus to the anterior silent
area. Solid arrows, circuit loop(s); dotted
arrows, passive activation; double line,
zone of block; RPV, right pulmonary
vein.
CAR102.indd 2147
y+
7 ms
LPV
RPV
SA
RFC
Mitral
SA
Left anterior oblique
Posteroanterior
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35 ms
10 2
I
V1
II
V2
RUPV
LUPV
–210 ms
aVR
V4
aVL
V5
aVF
A
FIGURE 102.12. (A) Left atrial electroanatomic map of a patient
with a “gap-related” left atrial flutter recorded during the tachycardia in the LAO projection. Color bars indicate the local activation
time relative to the reference catheter. Gray color represents the
scars caused by prior RF ablation. The arrhythmia revealed a circle
(arrows) traveling around the left pulmonary veins, traveling up left
*
V3
III
LLPV
*
*
*
V6
B
before the left pulmonary veins and down the posterior left atrial
wall, passing a gap with slow conduction in the ablation line encircling the left pulmonary veins. The red points show the gap in the
ablation line. (B) The 12-lead during tachycardia showing positive
flutter waves in the inferior leads and V1 (stars).
Right atrium: activation maps
y+
A
012219
I
II
III
B
H1718
H1516
aVR
x+
H1314
H1112
H0910
aVL
aVF
L
V2
213 ms
Left posterior oblique view
y+
H0102
CS910
CS78
CS56
V3
V4
V5
V6
25 mm/sec
AFL (240 ms)
R
CS
H0708
H0506
H0304
V1
D
x+
1.63 cm
0 ms
z+
CS34
CS12
RF
CS
200 mm/sec
Conventional mapping (170 ms)
FIGURE 102.13. An example of an atrial arrhythmia in a patient
with patch closure of an atrial septal defect after excision of a left
atrial myxoma. (A) Atrial flutter with positive flutter waves in lead
II and negative in lead III. (B) Counterclockwise atrial activation
along the tricuspid annulus (TA). The bipolar CS 9–10 is not activated in tandem with the halo catheter, and double potentials, as a
CAR102.indd 2148
C
I 012219
III
HBEd
HBEp
H1920
TA
Left anterior oblique-caudal view
result of a previous ablation attempt, were recorded on the cavotricuspid isthmus (bipolar RF). These fi ndings suggest a bystander
counterclockwise activation along the TA. (C) Confi rms reentry
around the septal scar. (D) Bystander activation around the TA via
two wave fronts. These two wave fronts collide in the posterior
isthmus which was previously successfully ablated.
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Atrial Tachycardia
As shown in Chapter 91 on supraventricular tachycardias, the P wave axis and width can be very helpful in localizing the likely site of origin of atrial tachycardia.
Atrial tachycardia can be classified according to its mechanism into automatic, triggered activity and reentry. As
pointed out in Chapter 91, supraventricular tachycardias
may be paroxysmal or incessant. Results from a metaanalysis study show that the clinical and electrophysiologic
characteristics of atrial tachycardia may vary between different age groups.60 This study demonstrated that pediatric
patients have more often automatic and incessant forms,
whereas the adult patients present more often the nonautomatic forms with a paroxysmal pattern.60 Furthermore,
right-sided atrial tachycardia and multifocal atrial tachycardia were more common in adults. It is important to know
that in patients with incessant atrial tachycardia the inability to control the ventricular rate may result in a dilated
(tachycardia-induced) cardiomyopathy. In these patients,
catheter ablation of the site of abnormal impulse formation
leads to cure of the arrhythmia and regression of pump
failure.61,62 Atrial tachycardia can originate in the right or in
the left atrium. The localization in the right atrium includes
the crista terminalis, the right atrial appendage, the intraatrial
septum (Fig. 102.14) around the tricuspid valve, and the coronary sinus ostium. In a few patients, the site of origin of the
atrial tachycardia can be localized in the sinus node area
(sinoatrial node reentrant). Atrial tachycardia originating
from the left atrium is more commonly located in the ostia
of the pulmonary veins and less frequently located in the free
wall and the atrial appendage. Rarely, atrial tachycardia may
be found in the Marshall ligament and may be the trigger of
atrial fibrillation (Fig. 102.15).63
A
B
A BLATION PROCEDURE
Currently, two techniques are used to localize the site of
origin of atrial tachycardia: the technique using multielectrode catheters and the three-dimensional, nonfluoroscopic
mapping (CARTO, EnSiteTM) system; or a combination of
both techniques (Figs. 102.14 and 102.15). The left atrial
tachycardia is approached by the transseptal technique. The
electrophysiologic criteria used to localize the site of origin
are the earliest atrial activation time preceding the surface
ECG P wave, an optimal pace map, and concealed entrainment. Catheter ablation of focal atrial tachycardia has a high
success (99%) and low recurrence rate (4%).64 Chen et al.64
found that the presence of a right-sided atrial tachycardia was
the only independent predictor of successful catheter ablation. Although the left atrium is easily accessed using the
transseptal technique, left-sided mapping may be more difficult than right-sided mapping. In general, catheter ablation
for atrial tachycardia is effective and safe. No procedurerelated complications have been reported.
Atrial Fibrillation
To date, catheter ablation of atrial fibrillation has been shown
to be most effective in patients with symptomatic paroxysmal atrial fibrillation resistant to antiarrhythmic drugs.
Strategies aimed at treating atrial fibrillation are trigger
elimination and substrate modification.
C
D
RA septum
02.2397
I
II
III
aVR
aVL
02.2397
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
aVF
HISD
V1
HISP
LA septum
02.2397
y+
45 ms
–77 ms
z+
CS910
V2
LA
RA
x+
His
CS78
V3
CS34
V5
CS12
V6
CARTO
10 mm/mV 25 mm/s
1.50 cm
–5
10 mm/mV 200 mm/s
FIGURE 102.14. The 12-lead ECG (A) of a patient with a focal atrial
tachycardia. Mapping of the right (RA) and left atrium (LA) showed
the earliest activation in the inferior part of the left side of the
atrial septum (B,C). The electroanatomic mapping during atrial
tachycardia confi rmed this location (D). Color bars indicate the
CAR102.indd 2149
CS
TV
CS56
V4
MV
–20
200 mm/s
local activation time relative to the reference catheter. Ablation
from the left septum stopped the tachycardia. CS, coronary sinus;
HISD, HISP, His bundle electrograms distal and proximal; TV, tricuspid valve.
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chapter
A
10 2
B
y+
y+
LSVP
–125 ms
–125 ms
LSPV
LMPV
x
+
LA
R
z+
His
LIPV
MV
L
LIPV
x+
TV
RA
CS
2.00 cm
2.00 cm
C
I
010892
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
25 mm/sec
D
I
010892
III
HBEd
HBEp
H1920
H1718
H1516
H1314
H1112
H0910
H0708
H0506
H0304
H0102
CSd
CSm
CSp
RF *
200 mm/sec
510 ms
*
FIGURE 102.15. Left (LA) and right atrium (RA) electroanatomic
map during atrial tachycardia in the posterior-anterior (A) and LAO
(B) views. Color bars indicate the local activation time relative to
the reference catheter. Earliest activation (red color) occurs in the
posterolateral region close to the atrioventricular groove with activation spreading gradually from that region over the entire LA.
Right atrial activation occurs through a superior connection (Bachmann’s bundle) activating the left septum and the rest of the RA
from superior to inferior. This activation is blocked in a bidirectional manner in the cavotricuspidal isthmus, as a result of a previous RF ablation. Red dots indicate radiofrequency applications. CS,
coronary sinus; LIPV, left inferior pulmonary vein; LMPV, left intermediate pulmonary vein; LSPV, left superior pulmonary vein; MV,
mitral valve; TV, tricuspid valve. (C) The 12-lead ECG shows isoelectric p waves in lead I and aVL and positive in the inferior and
precordial leads with 2 : 1 atrioventricular conduction. (D) Endocardial recordings during atrial tachycardia of the RA and LA. The
cycle length of the tachycardia is 320 ms. Note the Marshall potential (*) preceding the atrial electrograms recorded with mapping/
ablation RF catheter, positioned between the LSPV and the CS. From
top to bottom, ECG leads I and III; bipolar intracardiac recordings
from distal (HBEd) and proximal (HBEp) His bundle; high septal (H
1920), lateral (H1516), and low (H0102) RA obtained from a duodecapolar catheter positioned around the tricuspid annulus; distal
(CSd), medial (CSm), and proximal (CSp).
T RIGGER ELIMINATION
As demonstrated by Haïssaguerre et al.,65 the majority of
the triggers for atrial fibrillation originate from the pulmonary veins, but they may also be found in other areas, for
example, the left atrium, Marshall ligament,65 coronary
sinus, and superior vena cava.66 In the first 45 patients
studied by Haïssaguerre et al., a single focus of atrial ectopy
was identified in 29 patients, two foci were identified in
nine patients, and three or four foci were identified in seven
patients. Focal ablation, inside the pulmonary vein(s), was
performed in this population. This approach has been abandoned due to the high recurrence rate67 and the occurrence
of pulmonary vein stenosis with or without pulmonary
hypertension.68 Therefore, other approaches were developed,
for example, ostial isolation of the arrhythmogenic pulmonary vein(s) 67 or empirical isolation of all four pulmonary
veins69 (one by one pulmonary vein isolation or encircling
two by two pulmonary veins). Ostial pulmonary vein
CAR102.indd 2150
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2151
C
I
RSPV
Lasso
LSPV
Lasso
03.1945
17
18
II
V1
220
HRA D
His
CS
200
RSPV12
RSPV34
A
200
140 110 140 90 100
RSPV56
RSPV78
Cryo
RSPV910
LSPV LSPV12
Lasso
310
220
200
200
310
220
200
200
Lipv LSPV34
LSPV56
CS
B
LSPV78
LSPV910
100 mm/s
FIGURE 102.16. This is an example of mapping of the pulmonary
veins (PVs) using circular catheters (Lasso) in a patient with paroxysmal atrial fibrillation who underwent PV isolation with cryothermia. (A) Fluoroscopy view in anterior-posterior projection showing
two Lasso catheters in the right superior (RSPV) and left superior
PV (LSPV), the coronary sinus (CS) and the His bundle catheters.
(B) Lasso catheter and the cryoablation catheter in the LSPV; a
isolation can be performed either by recording the pulmonary vein potential electrograms using circular mapping
catheters with fluoroscopy guidance (Fig. 102.16) or, empirically, using a three-dimensional mapping system (Fig.
102.17).69,70 The chronic outcome using these two approaches
is reported to range between 70% and 80%. The procedure
end points, when pulmonary vein potentials are used to
guide ablation, are shown in Figures 102.18 and 102.19.
Although the incidence of pulmonary vein stenosis has
decreased when a more ostial ablation is performed, the
development of new complications has emerged, for example,
esophageal injury with or without an atrioesophageal
fistula.71 Therefore, other ablative energies for ablation of
atrial fibrillation (see New Ablative Energy Sources, below)
need to be considered.
SUBSTRATE MODIFICATION
In patients with chronic atrial fibrillation (persistent and
permanent), the substrate (all conditions responsible for the
continuation of the arrhythmia, e.g., areas of fragmentation,
wave front curvature, sink-source relationship, etc.) is essential for the maintenance of the arrhythmia. At the present
time, two techniques are used to modify the substrate. One
technique encircles the right and left pulmonary veins two
by two and connects the two superior pulmonary veins with
a posterior line (Fig. 102.20).70 A second technique consists
of delivering focal applications at the sites of fragmented
electrograms in both atria during atrial fibrillation (Fig.
102.21).72 However, complications may occur with the first
technique, such as pulmonary vein stenosis and atrioesophageal fistula.71 The latter is due to the vicinity of the esophagus to the left pulmonary veins and to the thickness of the
CAR102.indd 2151
decapolar catheter is inserted in the LIPV (recording/pacing). (C)
Initiation of a paroxysm of atrial fibrillation by a PV extrasystole
(arrow). Note the earliest rapid and irregular activation in the RSPV
in comparison to the LSPV or in the right atrium (HRA D). From
top to bottom: leads I, II, V1, high right atrium (HRA D), circular
mapping of the ostium (from 12 to 910) of the RSPV and LSPV.
posterior wall of the left atrium (3 mm). A longer follow-up
is needed to evaluate the impact of substrate modification on
the arrhythmia burden in patients with chronic atrial
fibrillation.
FIGURE 102.17. This figure shows an example of an isochronal
activation map during coronary sinus pacing after anatomically
isolation of all four pulmonary veins. Color coding represents activation times. The earliest activation is located at the pacing site (red
color). Note the abrupt color change from shades of yellow or green
to purple (latest activation). The latest activation is around the PVs.
Red dots represent RF applications. LA, left atrium; LLUP, left lower
PV; LUPV, left upper PV; RLPV, right lower PV; RUPV, right upper
PV.
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04.0268
19
20
21
10 2
22
I
II
V1
HBED
CS34
LSPV12
LSPV34
LSPV56
FIGURE 102.18. An example of entrance block between
the left atrium and the left superior pulmonary vein
(LSPV) after isolation with cryoablation. During coronary sinus (CS) pacing the left atrium and the PV potentials are dissociated (arrows). From top to bottom: leads
I, II, and V1, HBED, His bundle electrogram distal, circumferential mapping from the ostium of the LSPV
(LSPV12 to LSPV910). Cryo, cryocatheter.
LSPV78
LSPV910
Cryo
50 mm/s
Catheter Ablation of the
Atrioventricular Junction
Currently, AV junctional ablation followed by pacemaker
implantation is limited to patients in whom catheter ablation cannot cure the supraventricular arrhythmia (such as in
left atrial flutter, multifocal atrial tachycardia, and atrial
fibrillation). It is an accepted treatment for symptomatic
patients with atrial fibrillation in whom the arrhythmia and
the ventricular response cannot be controlled by the currently existing treatment modalities, like antiarrhythmic
drugs, external or internal cardioversion, and the implantable atrial defibrillator.73 Atrioventricular junctional ablation results in complete heart block and requires chronic
pacing. For successful ablation, the catheter is positioned
across the tricuspid valve to record a high atrial, small His
bundle and small ventricular deflection. The success rate of
this technique is close to 100%. On rare occasions, interruption of conduction over the AV node–His-Purkinje system
cannot be achieved from the right side, and a left-sided
approach is necessary. Modification or partial, instead of
complete, AV nodal conduction74 has a moderate long-term
success rate; therefore, complete interruption of the AV junction and pacemaker implantation is preferred in patients
with rapid, uncontrollable ventricular rates. The best site for
ventricular pacing in these patients is currently being studied,
following reports of detrimental effects of right ventricular
apical pacing.
RUPV
LAA
LUPV
I
III
020147
L910
LLPV
RLPV
L78
L56
L34
R
L12
CS78
MA
CS56
CS34
Cryo
50 mm/sec
FIGURE 102.19. This figure demonstrates the loss of PV potential
of the left superior pulmonary vein (L) during coronary sinus pacing
(CS) during cryoapplication. From top to bottom: leads I and III,
circumferential recordings of the ostium of the left superior PV (L12
to L910), left atrial electrograms recording from several sites from
the CS (CS78 to CS34).
CAR102.indd 2152
FIGURE 102.20. Posterior-anterior view of an electroanatomic
reconstruction of the left atrium, including the pulmonary veins
(PV). Dark red dots represent ablation lines. A circumferential lesion
was placed around the left and right PVs >5 mm from the orifices.
In addition, two linear lesions were placed, one connecting the circular lesions in the posterior wall and one connecting the left circular lesion with the mitral valve (MV) (so-called left atrial
isthmus).
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2.45 mV
Bipolar
1-Map > 21 Tip
0.12 mV
L
R
ABL ABL
V4
420
410
420
410
370
400
CS d
CS 3–4
FIGURE 102.21. A biatrial map (mesh
presentation) in the anterior-posterior
view. The arrow points to the electrogram recorded from the inferolateral (Inf
lat) aspect of the right atrium. Note the
short cycle length and fragmented atrial
electrogram in this area (90 ms). RF
application at this site terminated atrial
fibrillation.
CS 5–6
220
200
210
190
210
190
200
190
220
190
200
CS 7–8
CS P
90
Inf lat 1-2
Inf lat 3-4
Catheter Ablation of Ventricular Tachycardia
Sustained monomorphic ventricular tachycardia (VT) is in
75% of cases associated with ischemic heart disease. In the
remaining patients, cardiomyopathy (dilated or hypertrophied), valvular heart disease, and arrhythmogenic right ventricular dysplasia/cardiomyopathy are among the underlying
cardiac causes. Sustained monomorphic VT may also occur
in the absence of any other cardiac abnormality and is then
called idiopathic. As discussed in Chapter 96, the 12-lead
ECG during VT may be of help in identifying the etiology
and the site of origin of the arrhythmia. Therefore, an effort
should always be made to obtain a 12-lead ECG during VT.75
An electrophysiologic study is performed to analyze the
number of VTs, their morphology, their site of origin, using
mapping and entrainment techniques, and (in ischemic VT)
the critical zone of slow conduction in the reentry circuit.
In comparison to the outcome of catheter ablation in the
patients with supraventricular tachycardias, the success rate
in patients with VT is more modest.
Catheter Ablation of Idiopathic
Ventricular Tachycardia
Idiopathic VT usually originates from the right ventricular
outflow tract, and is in or close to the specific conduction
system of the left ventricle. In a small series of patients,
idiopathic VT has been found to originate in the root of the
aorta and pulmonary artery. In the left ventricle, most idiopathic VTs are localized in the inferoposterior aspect of the
septum in or close to the left posterior fascicle.76 Rarely, VTs
are localized in or close to the anterior fascicle.77 The ECG
characteristics of left ventricular idiopathic VT are discussed
in Chapter 96.
Ventricular tachycardias originating in the right ventricular outflow tract typically have a left bundle branch blocklike configuration with an intermediate or vertical QRS axis
CAR102.indd 2153
210
200
in the extremity leads (Fig. 102.22). The mechanism of this
VT is considered to be triggered activity. These VTs are frequently exercise related and catecholamine sensitive, and
can be terminated by intravenous adenosine or beta-blocker
A
I
B
92364
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
92102
400 ms
FIGURE 102.22. A typical example of an idiopathic right ventricular outflow tract tachycardia. (A) Note the vertical axis and the left
bundle branch block-like shape of the QRS complex. (B) An optimal
match between the clinically recorded 12-lead ECG and the ECG
recorded during pacing on the septal site of the right ventricular
outflow tract.
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chapter
administration. Recently, we reported that in patients with
idiopathic left bundle branch block–shaped VT, the origin of
the arrhythmia may be in the root of the pulmonary artery.78
The QRS shape of these VTs did not much differ from those
originated in the right ventricular outflow tract (RVOT). The
VTs arising in the inferoposterior aspect of the septum of the
left ventricle have a right bundle branch block-like configuration and a left or northwest QRS axis (Fig. 102.23). These
VTs can frequently be initiated by programmed electrical
stimulation and terminated by intravenous verapamil.76 The
mechanism of these VTs is probably microreentry in the left
posterior fascicle.
Mapping of these VTs consists of localizing the earliest
ventricular endocardial activation during VT. Additionally,
an optimal pace map (with the 12-lead ECG showing an
identical QRS morphology during ventricular pacing as the
QRS during spontaneous VT) (Fig. 102.22B) is required. Furthermore, recording of a fascicular potential can be useful in
selecting successful sites in idiopathic VT originating from
the inferoposterior aspect of the left ventricle79 (Fig. 102.24).
In our experience,80 catheter ablation of the right ventricular
outflow tract VT successfully eliminated the arrhythmia in
29 out of 35 patients (83%) and in 12 out of 13 VT (92%) from
the left ventricle. After a mean follow-up period of 30 months,
A
B
I
I
10 2
93-2038
93871
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
RF
HBE
CS d
100 mm/sec
FIGURE 102.24. The 12-lead ECG of an idiopathic left ventricular
tachycardia having a right bundle branch block–like morphology
and left axis. Note the very sharp potential (the posterior fascicle)
preceding the QRS complex in the endocardial recording from the
radiofrequency ablation catheter (RF). CS d, distal coronary sinus;
HBE, His bundle electrogram; RF, radiofrequency catheter.
V1
V1
II
V2
II
V2
III
III
V3
V3
aVR
V4
aVR
V4
V5
aVL
V5
aVL
aVF
V6
aVF
V6
400 ms
FIGURE 102.23. (A) The 12-lead ECG of a patient with an idiopathic ventricular tachycardia originating in the left ventricle in the
inferoposterior aspect of the septum close to the posterior fascicle.
Note that the ventricular tachycardia has a right bundle branch
block–like configuration and a left axis deviation. (B) The 12-lead
ECG of an idiopathic ventricular tachycardia originating more anteriorly in the apicoseptal aspect of the left ventricle. That ventricular
tachycardia shows a right bundle branch block–like configuration
and a northwest QRS axis.
CAR102.indd 2154
there were four recurrences (14%) in patients with RVOT VT
and none in patients with left ventricular VT. Unsuccessful
ablation of right and left VT was characterized by more than
one VT morphology and the presence of a delta wave-like
beginning of the QRS (Fig. 102.25), suggesting an epicardial
origin, and a pace map showing a correlation in fewer than
11 out of the 12 ECG leads. Other series of RVOT and left
ventricular VT have shown similar success rate and rare
complications.81,82 In patients who cannot be ablated from the
right ventricle, specific characteristics of the QRS complex
during VT may point to an origin in the left ventricular
outflow tract or aortic root.83 In idiopathic VT, catheter ablation is a curative technique, and therefore, should be offered
early in the treatment of symptomatic patients.
Catheter Ablation of Postinfarction
Ventricular Tachycardia
Monomorphic VT due to the presence of scar tissue, most
often after myocardial infarction, is commonly based on a
reentry mechanism.11 Interruption of the reentry circuit by
catheter ablation requires identification of an essential part
of the reentry circuit. A reentry circuit varies in size, configuration, and location (subendocardial, midmyocardial,
subepicardial). The region where the wave front emerges
from the circuit is termed the exit site. The region proximal
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215 5
c a t h e t e r a b l a t i o n o f s u p r av e n t r i c u l a r a n d v e n t r i c u l a r a r r h y t h m i a s
A
I
II
III
V1
V2
V3
B
I
II
94579
V1
V2
III
V3
aVR
V4
aVL
V5
aVR
V4
aVL
V5
aVF
aVF
V6
V6
400 ms
931381
FIGURE 102.25. Example of a patient in whom RF catheter ablation
failed. (A) The 12-lead ECG during sinus rhythm. (B) The 12-lead
ECG during ventricular tachycardia with a left bundle branch
block–like morphology and right axis. Note the slow (delta wavelike) beginning of the QRS complex.
tion, all inducible stable VT were targeted. Ten of 52 patients
died (19%) and 16 patients (31%) had VT recurrences. In
general, the long-term success ranges from 45% to
75%.85–90 In the majority of the patients reported in those
studies and also in our patients, antiarrhythmic drugs were
continued.
A new approach that allows better localization of the
reentry circuit(s) has been described to treat patients with
multiple unstable VT morphologies.91 This approach consists
of localizing the area of scarred tissue, and the regions of
residual “viable” myocardium in the scar during sinus
rhythm using the CARTO system (voltage mapping) (Fig.
102.28). The success rate using this approach varies from
70% to 88%. The success rate in postinfarction VT may be
improved by using new ablative sources (cryotechnology)
that can produce deeper lesions in case of calcified and
fibrotic scars.
In postinfarction patients who, after implantable cardioverter-defibrillator (ICD) implant require frequent shocks,
catheter ablation may substantially reduce the number of
shocks. Additionally, in patients who present with an electrical storm after an acute myocardial infarction, and in whom
antiarrhythmic drugs and sedation failed to control the
arrhythmia, catheter ablation of the triggering ventricular
premature beats may be a bailout therapy.92 An uncommon
form of VT that can be cured by catheter ablation is the
Outer loop
Exit
CAR102.indd 2155
Proximal
to the exit consists of a central and a proximal part (Fig.
102.26). After the wave front emerges from the exit, it propagates through a loop, back to the proximal region of the
circuit. The outer loop is a broad pathway along the margin
of the scar.11 Identification of the central part of the reentry
circuit, which in general, exhibits slow conduction, is of
importance to obtain successful ablation. If the zone of slow
conduction is not too broad, a single ablation may terminate
the VT. However, in some cases a broad portion of the reentry
circuit has to be interrupted by a series of energy applications
in a manner similar to that used for ablation of atrial
flutter.84
Stevenson et al.11 have proposed criteria to identify the
central part (slow conduction zone) of the reentry circuit.
These criteria include the presence of a mid-diastolic potential, and the demonstration of concealed entrainment (Fig.
102.27). The strategy in these patients varies from center to
center. Some centers advocate ablating all inducible stable
VTs.11,85,86 Other groups87,88 prefer only to target the clinically
stable one. In our institution, we prefer to target only the
clinical VT(s). Sixty-one patients underwent catheter ablation in our institution. Successful ablation was obtained in
79%. After a mean follow-up period of 20 ± 10 months, 11
patients had a VT recurrence and 10 patients died (four
patients from pump failure, three from sudden cardiac death,
and three from noncardiac death).89 Our results are comparable to those reported by Stevenson et al.11 In their popula-
Central
Inner loop
A
B
Outer loop
FIGURE 102.26. The parts of a reentry circuit with an inner
loop (A) and a broad outer loop (B) in scarred myocardium.
11/24/2006 10:52:56 AM
215 6
chapter
99520/1
10 2
aVF
I 99-1344
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
V1
HISd
V2
HISp
V3
RV
V4
RFd
99-1344
I
II
III
aVR
aVL
99520/2
25 mm/sec
V5
D
V6
25 mm/sec
A
B
I 99-1344
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
HISd
99520/4
470
470
S-QRS = 270
450
HISp
RV
RFd
100 mm/sec
PPI = 450
Eg-QRS = 270
C
A
start
FIGURE 102.27. (A) The 12-lead ECG during ventricular tachycardia
in a patient with an old inferoposterior infarction. The ventricular
tachycardia shows a left bundle branch block–like morphology with
QR complexes in lead II, III, and aVF. (B) Sinus rhythm with incomplete left bundle branch block. (C) Ventricular pacing in the infarcted
area by way of the RF ablation catheter. Pacing is performed 20 ms
faster than the ventricular tachycardia rate (fi rst four QRS complexes).
Note that the morphology of the QRS during ventricular pacing is
identical to that during ventricular tachycardia indicating concealed
entrainment. The pacing spike-QRS (S-QRS) interval is 270 ms and is
equal to the mid-diastolic electrogram-QRS interval (Eg-QRS). The
postpacing interval (PPI) is the same as the pacing cycle length
(450 ms). This suggests that the RF catheter is located in the zone of
slow conduction. (D) RF ablation at the site shown in C terminates
the ventricular tachycardia within 3 seconds. Note the appearance of
complete left bundle branch block after VT ablation. This was due to
catheter manipulation in the left ventricle.
B
C
VT1
y+
PM
010985
Blpolar voltage
≥1.50 mV
VT2
VT
PM
VT
I
II
Exit VT1
III
aVR
≤0.50 mV
aVL
aVF
LV
V1
V2
V3
V4
V5
1.46 cm
V6
25 mm/sec
25 mm/sec
Exit VT2
25 mm/sec
25 mm/sec
(amplitude >1.5 mV); gray, dense scar (amplitude <0.5 mV) and range
FIGURE 102.28. (A) A bipolar voltage map during sinus rhythm of
between purple and red; border zone (signals amplitudes between
the left ventricle (LV) in a posterior-anterior view of a patient with
0.5 and 1.5 mV). The 12-lead ECG during VT and pace map (B,C)
an old inferoposterolateral infarction. The patient had two different
directed the linear ablation. Arrows indicate the site where the exit
ventricular tachycardias: VT1 with a left bundle branch block morpoint of the VTs was found. Linear lesions (red dark dots) were
phology and left axis, VT2 with right bundle branch block morpholextended from dense scar and cross-border zone.
ogy and northwest QRS axis. Color range indicates the ventricular
electrogram amplitude (mV). Purple represents normal myocardium
CAR102.indd 2156
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c a t h e t e r a b l a t i o n o f s u p r av e n t r i c u l a r a n d v e n t r i c u l a r a r r h y t h m i a s
so-called bundle branch reentry VT.93 These VTs are observed
in patients with extensive interventricular septal damage
leading to conduction disturbances in the bundle branches
and the septum (as in patients with ischemic or dilated
cardiomyopathy after aortic valve replacement, myotonic
dystrophy, and following chest trauma). The reentrant
circuit in this type of VT may utilize one bundle branch as
an anterograde limb of the circuit with after transseptal
conduction retrograde conduction over the other bundle
branch. These VTs, therefore, may show a left or a right
bundle branch block-like morphology.94 They can be cured by
ablating one of the bundle branches. Another possibility is
that the reentry circuit uses the anterior fascicle and posterior fascicle of the left bundle branch. This is called “interfascicular” VT. In the latter situation, the VT shows a right
bundle branch block-like configuration with right or left axis
deviation.95 Catheter ablation of one of the fascicles can cure
this type of VT.
The results of catheter ablation of VT in patients with
right ventricular dysplasia are frequently disappointing in
the long term because of the progressive nature of the disease.
Only a limited number of cases of VT ablation in patients
with hypertrophic96 and dilated cardiomyopathy have been
reported.
In some patients with small and circumscribed subepicardial reentry circuits, like patients with cardiomyopathy
secondary to Chagas’ disease or inferior wall myocardial
infarction, epicardial catheter ablation has shown favorable
results.97
Catheter Ablation of Ventricular Fibrillation
Recently, catheter ablation of idiopathic ventricular fibrillation has been described in 27 patients. The initiating beat
of ventricular fibrillation had an identical electrocardiographic morphology and coupling interval compared to the
preceding isolated premature beats typically noted in the
aftermath of resuscitation. The initiating ventricular premature beats were preceded by distal Purkinje activity in
the majority of the patients and originated predominantly
in the septum of the left ventricle. Interestingly, these
triggers were also found in the right ventricle and were
also preceded by Purkinje activity. After a mean follow-up
215 7
of 24 months, 89% of the patients had no recurrence of
ventricular fibrillation as confirmed by the defibrillator
memory. Primary idiopathic ventricular fibrillation is characterized by dominant triggers from the distal Purkinje
system. The triggers can be eliminated by focal energy
delivery.98 Larger series of patients and longer follow-up are
needed to confirm the efficacy of catheter ablation of this
type of arrhythmia.
New Ablative Energy Sources
While the vast majority of arrhythmia substrates can be successfully ablated using radiofrequency energy, this energy
source has its limitations. For example, radiofrequency ablation may induce complete AV block when ablating focal
tachycardia or accessory pathways close to the conduction
system, or perforation of the coronary sinus if the accessory
pathway is located in this anatomic structure. As mentioned
in the section on ablation of atrial fibrillation, radiofrequency
energy may produce pulmonary vein stenosis in patients
undergoing ablation of paroxysmal atrial fibrillation. Pulmonary vein stenosis may lead to life-threatening pulmonary
hypertension or hemorrhage.99 Furthermore, radiofrequency
energy produces pain when ablating the cavotricuspidal
isthmus,100 the coronary sinus, and the atria. Because radiofrequency energy produces endocardial disruption, cardiac
perforation may occur. Another potential hazard of radiofrequency energy is the occurrence of a fistula between the left
atrium and the esophagus.71 This complication may develop
3 weeks after radiofrequency ablation. It has become vital,
therefore, to study other energy sources that could avoid
these disadvantages. Table 102.2 compares current catheterbased systems that can be applied to treat cardiac arrhythmias with especial emphasis on the treatment of atrial
fibrillation. We and other investigators have demonstrated
that in contrast to radiofrequency energy, cryoablation does
not produce acute or chronic pulmonary vein stenosis,101 is
painless,100 and less thrombogenic.102 Furthermore, we have
recently demonstrated that the long-term results of catheterbased cryoablation for supraventricular and ventricular
arrhythmias are comparable to those reported with radiofrequency energy.103
TABLE 102.2. Comparison between radiofrequency (RF) and new ablative energy sources
Clinical experience
Endothelial
disruption (e.g.,
PV stenosis)
Thrombogenicity
Mapping capability
Ability to create
transmural lesion
Lesion size
Perforation rate
CAR102.indd 2157
RF
Cryothermia
Ultrasound
Laser
Microwave
+++
Increased
++
Minimal
+
Increased
+
Increased
+
Increased
High
Yes
Requires
optimal
contact
+
Low
Low
Yes
Requires optimal
contact
(cryoadherence)
+
Very Low
Medium
No
Requires
optimal
contact
++
Low
High
No
Excellent,
contact
forgiving
+++
High
High
No
Excellent,
contact
forgiving
+++
High
11/24/2006 10:52:57 AM
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chapter
10 2
Summary
During the past 15 years, catheter ablation developed into an
effective and safe curative treatment for patients with different types of supraventricular arrhythmias including paroxysmal atrial fibrillation. This is also true in patients with
idiopathic ventricular tachycardia and patients with bundle
branch reentrant ventricular tachycardia. The technique,
therefore, should be considered early in the therapy of these
arrhythmias. Catheter ablation provides palliative treatment
in patients with recurrent episodes of spontaneous welltolerated postinfarction VT. In atrial fibrillation ablation,
new catheter designs, new ablative energy sources, and better
understanding of how to define and localize the substrate are
needed to improve results and to expand the indications for
other subsets of atrial fibrillation (persistent, permanent).
Catheter ablation should be restricted to centers where an
experienced clinical electrophysiologist performs these often
complicated and time-consuming procedures.
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