1 Catheter Ablation of 0 Supraventricular and Ventricular ...extras.springer.com/2007/978-1-84628-715-2/fs... · and surgical5 or catheter ablation to cure or control cardiac arrhythmias.6,7

213 9

Catheter Ablation of Supraventricular and

Ventricular ArrhythmiasLuz-Maria Rodriguez, Carl Timmermans, and

Hein J.J. Wellens

Key Points

• Catheter ablation has become the fi rst truly curative treatment for many supraventricular and some ventricu-lar 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 negli-gible. The recurrence rate after ablation of accessory path-ways 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 fl utter ranges between 65% and 98%. There is a risk of recurrence of ablated atrial fl utter of 10% to 55%.

• In general, catheter ablation for atrial tachycardia is effec-tive and safe.

• In ablation procedures to treat atrial fi brillation, 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 fi stula.

• Atrioventricular nodal ablation followed by pacemaker implantation is limited to patents in whom catheter abla-tion cannot cure the supraventricular arrhythmia, such as left atrial fl utter, multifocal atrial tachycardia, and some atrial fi brillation. It is an accepted modality in patients with atrial fi brillation with a very rapid ventric-ular response that cannot be controlled with antiarrhyth-mic medication, external and internal cardioversion, and perhaps the atrial implantable defi brillator.

• 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 fi brillation is character-ized 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 revolu-tionized 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 under-standing 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 fi rst 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) abla-tion catheter with a large (4 mm) distal electrode, the success rate improved dramatically.9,10 To date, catheter ablation has become the fi rst truly curative treatment for many supraven-tricular 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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Historical Aspects . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2139Indications for Catheter Ablation of Tachycardias. . . . 2140

Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2158

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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 specifi c arrhythmia of the patient.

Indications for Catheter Ablation of Tachycardias

The effi cacy and the safety profi le 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.

Catheter Ablation of Supraventricular Tachycardias

Accessory Pathways

As also discussed in Chapter 93 on preexcitation, an acces-sory 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 connec-tions 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 local-ization of the accessory pathways in the AV groove (Fig. 102.1). Free wall accessory pathways are subdivided in a pos-terior, lateral, and anterior localization. Posteroseptal acces-sory pathways may also be found in the wall of the coronary sinus and in some cases in the middle cardiac vein.13 Antero-septal 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 Classifi cation Level of evidence

Accessory pathwaysWPW syndrome (preexcitation symptomatic arrhythmias, well-tolerated I BWPW syndrome (with AF and rapid-conduction or poorly tolerated AVRT) I BAVRT, poorly tolerated (concealed accessory pathway) I BSingle or frequent AVRT episode(s) (concealed accessory pathway) IIa BPreexcitation, asymptomatic IIa BAV nodal reentry tachycardia (AVNRT)Recurrent AVNRT I BAVNRT with frequent episodes in patients who desired complete control of arrhythmias I BInfrequent, well-tolerated AVNRT I BFocal atrial tachycardia (AT)Asymptomatic or symptomatic incessant AT(s) I BNonsustained and asymptomatic AT III BAtrial fl utter (AFL)First episode and well-tolerated AFL IIa BRecurrent and well-tolerated AFL I BPoorly tolerated AFL I BAFL appearing after use of class IC agents or amiodarone for the treatment of AF I BSymptomatic non-CTI dependent AFL after failed antiarrhythmic drugs therapy IIa BSupraventricular tachycardia after repaired congenital heart diseaseFocal AT or scar macro reentry tachycardia I CClassifi cation 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/effi cacy of a procedure or treatment IIa: Weight of evidence is in favor of the procedure or treatmentIII: There is evidence and/or general agreement that the procedure or treatment is not useful/effective and in some cases may be harmfulLevel A: (highest) derived from multiple randomized clinical studiesLevel B: (intermediate) data are on the basis of a limited number of randomized trials, nonrandomized studies, or observational registriesLevel C: (lowest): primary basis for the recommendation was expert consensus

AVRT, atrial ventricular reentry tachycardia; CTI, cavotricuspid isthmus; WPW, Wolff-Parkinson-White syndrome.


c at h e t e r a b l at ion of s u p r av e n t r ic u l a r a n d v e n t r ic u l a r a r r h y t h m i a s 2141

tions (anterogradely and retrogradely), or only anterogradely, or only retrogradely. The latter pathway is called a “con-cealed” pathway. Concealed pathways are of two types, the rapidly and the slowly conducting one.

Ablation Procedure

To perform an ablation procedure, catheters are inserted through both femoral veins or the subclavian vein and posi-tioned in the heart under fl uoroscopy. 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 fl uoroscopic 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 abla-tion 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 specifi c 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 electro-grams. 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 102.1. The location of accessory pathways along the tri-cuspid and mitral annulus. AS, anteroseptal; CS, coronary sinus; LA, left anterior; LL, left lateral; LP, left posterior; LPS, left postero-septal; RA, right anterior; RL, right lateral; RP, right posterior; RPS, right posteroseptal.

His bundle

1

2

3CS

ostium

AVN

anterior

perinodal

posterior

FIGURE 102.2. The location of the three types of midseptal acces-sory pathways (anterior, perinodal, posterior) in the space between the ostium of the coronary sinus (CS) inferiorly, and the His bundle superiorly. AVN, atrioventricular node.

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).


214 2 c h a p t e r 10 2

energy is delivered at the atrial insertion of the accessory pathway. The catheter inserted in the coronary sinus ana-tomically marks the AV groove and helps in mapping left-sided accessory pathways.

In patients with right-sided accessory pathways, the pro-cedure 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 loca-tion of the accessory pathway. Posteroseptal accessory path-ways 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 fi rst centimeters of the coronary sinus and its posterior branches.13 Because of the vicinity of the conduc-tion system (right bundle for anteroseptal accessory path-ways; 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 pace-maker 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 poten-tial (Fig. 102.4). Certain morphologies of the unipolar elec-trogram and an early intrinsic defl ection of the unipolar

recording relative to the delta wave onset may also indicate an optimal ablation site.18 The atrial insertion of an acces-sory pathway is usually localized by identifying the site of the shortest ventriculoatrial (VA) interval during ventricular pacing or during circus movement tachycardia or by record-ing an accessory pathway potential. In general, the following criteria are considered to select the optimal site for deliver-ing ablative energy in preexcited rhythms: the presence of an accessory pathway potential, the onset of a local ventriculo-gram preceding the delta wave by 5 to 20 ms, a local AV interval less than 40 ms, and a PQS morphology in the uni-polar 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 inter-ruption 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 experi-ence of the operator. The success rate for left free wall acces-sory 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

95-2286IIIIII

aVRaVLaVFV1V2V3V4V5V6

HRAHIS

RFRFU1RFU2

AP

AV

200 mm/sec

A-V = –20 ms

95-2286 99512

A V

A B

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 suc-cessful 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.

97-0153IIIIII

aVRaVLaVF

V1V2V3V4V5V6

RFd

RF1

RF2

25 mm/sec

start

99518

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 (*).


c at h e t e r a b l at ion of s u p r av e n t r ic u l a r a n d v e n t r ic u l a r a r r h y t h m i a s 214 3

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 diffi cult. 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 tachycar-dia, using a slowly conducting accessory pathway for ven-triculoatrial conduction, the success rate is as high as 95% to 100%.22

Recurrence of Conduction of Accessory Pathways

In our institution, the incidence of reappearance of conduc-tion 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 fi gures 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

rate. Based on this information, patients should be followed for 6 months after ablation.

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 signifi cant 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 Electrophysi-ology27 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 pneu-mothorax. A multivariate analysis showed three indepen-dent factors for recognizing patients with a high probability

IIIIII

aVRaVL

aVFV1

V2

V3

V4

V5

V6

RF

RB

HBED

HBEF

RVA

100 mm/sec

RB RB

A AM M

96-0419

HBEP

HBED AF

PF

RBMahaim

FIGURE 102.6. An electrophysiologic study in a patient with a preexcited tachycardia with atrioventricular conduction over an atriofascicular (Mahaim) fi ber, and ventriculoatrial conduction over the His-AV node pathway. Note the presence of a Mahaim potential

(M) recorded with the tip of the RF catheter where successful abla-tion was performed. RB, right bundle; HBED, distal His bundle electrogram; HBEF, proximal His bundle electrogram.


214 4 c h a p t e r 10 2

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 fl uoroscopy time was an important concern for eventual complications. To date, with more experience, procedure and fl uoroscopy times have shortened, thereby reducing the risk of complications due to radiation.

Atrioventricular Nodal Reentrant Tachycardia

Catheter ablation in patients suffering from AV nodal reen-trant 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-

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 poste-rior 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

Two techniques have been used to ablate the slow pathway: the anatomic technique30,32 and the electrophysiologic tech-nique.28,29 In the anatomic technique, fl uoroscopic landmarks are used to guide the positioning of the ablation catheter. Using the posterior approach, the ablation catheter is posi-tioned in the posterior third of Koch’s triangle (Fig. 102.8). An atrial/ventricular (A/V) ratio of 0.5 or <1 in the electro-gram 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 induc-ibility 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 deliv-ered. When using the electrophysiologic technique, ablation is performed based on specifi c electrograms representing slow pathway conduction.

Two distinct morphologies of slow pathway potentials have been described. Jackman et al.28 described a sharp spike-like potential preceded by a lower frequency, lower ampli-tude 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.

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.

FIGURE 102.8. The catheter position used for ablation of AV nodal reentrant tachycardia in two fl uoroscopic views: (A) right anterior oblique view; (B) left anterior oblique view. CS, coronary sinus; CSO,

coronary sinus ostium; HRA, high right atrium; RF, radiofrequency catheter; RV, right ventricle.



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 labora-tory) 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 fl utter, the so-called common or typical atrial fl utter, occurs in the right atrium and may rotate in a counterclockwise (CCW) or clockwise (CW) manner.34,35 Nonfl uoroscopic mapping36 and the use of mul-tiple endocardial electrograms37 have identifi ed the circuit of the right atrial common fl utter. The CCW atrial fl utter is a broad band of peri-tricuspid activation that enters the isthmus [the atrial tissue between the inferior vena cava (IVC) orifi ce 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 fl utter, while running in the opposite direction, shares the same circuit with the same endocardial borders as the CCW atrial fl utter. On the 12-lead ECG, the common atrial fl utter shows the so-called sawtooth appearance.

Ablation Procedure

An atrial fl utter 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 acti-vation of the coronary sinus ostium–TA isthmus, the His bundle, and the coronary sinus. During the electrophysio-logic study, the atrial fl utter 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 fl uoroscopy or a three-dimensional mapping system (Fig. 102.9).

Two approaches have been described to ablate common atrial fl utter: the anatomic approach39–42 and the electrophys-iologic approach.43 The anatomic approach uses fl uoroscopic landmarks to localize the right atrial isthmus, and the elec-trophysiologic approach targets areas with critical isthmus conduction determined on the basis of concealed entrain-ment or the presence of double potentials.43 Two isthmi have been described38: 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 pro-duces complete conduction block from the TA to the coro-nary sinus ostium and to the IVC, eliminating both CCW

and CW atrial fl utter.38 A linear ablation is performed in one of the previously mentioned isthmi, either by applying point-by-point radiofrequency energy or cryothermia, or by drag-ging the catheter during the radiofrequency application.

Regardless of the approach used, the end point for suc-cessful ablation is the noninducibility of atrial fl utter 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 abla-tion, 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 con-trast, 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 confi rm the non-inducibility of atrial fl utter and bidirectional isthmus con-duction block. Using this methodology, the acute success rate of catheter ablation for common atrial fl utter ranges between 65% and 98%.38–43

In a number of patients with atrial fi brillation, the arrhythmia may organize into atrial fl utter while treating these patients with class III45 or class IC46,47 antiarrhythmic drugs. Catheter ablation of the right atrial isthmus may sig-nifi cantly reduce the incidence of atrial fi brillation in these patients.45–47 After ablation, these patients should continue to take the medication that changed atrial fi brillation into atrial fl utter.

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 abla-tion procedures.

Recurrences of Right Atrial Common Flutter

A high recurrence rate (10% to 55%) has been reported if noninducibility of atrial fl utter 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 con-duction 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 fl utter have been recognized. Spontaneous atrial fl utter and atrial


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fl utters occurring after ablation of atrial fi brillation. Recently, by mapping the spontaneous atrial fl utter with the CARTOTM Biosense system, electrical silent areas or zones of block in the left atrium were demonstrated.51 Different types of reen-trant 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 Ter-mination of the perimitral fl utter 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 peripul-monary vein circuits can be ablated by joining the pulmo-nary vein to the mitral annulus. Ablation of atrial fl utters with small reentry circuits should be performed at the area of the slow conduction. The chronic success rate in this type

of atrial fl utter is around 75%. Atrial fl utter after linear abla-tion for atrial fi brillation 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 fl utter.

Catheter Ablation of “Incisional Tachycardia”

Atrial arrhythmias are a frequent clinical problem after sur-gical correction of congenital heart disease. Hemodynamic impairment and pressure overload, together with the pres-ence of surgical scars and prosthetic material, may result in an arrhythmogenic combination of fi xed artifi cial obstacles and electrophysiologic abnormalities that cause scar fl utters or macroreentrant incisional tachycardia.53 These tachycar-dias 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

AP LAO

HaloHalo

His

HisCS

CS

CryoCryo

SVCTV

CSIVC

TVCS

Halo

Halo

IVC

SVC

PS

His

His

A

C

B

FIGURE 102.9. The catheter posi-tions for ablation of a common atrial fl utter in the right anterior (A), and the left anterior oblique view (B). A duodecapolar catheter (Halo) is posi-tioned 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 cath-eter 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 antero-posterior (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.



011425I

IIIHBEdHBEp

H1920H1718H1516H1314H1112H0910

H0708H0506H0304H0102CS78CS56CS34CS12

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A B C D E

FIGURE 102.10. (A,B) Atrial pacing during sinus rhythm before ablation. (A) Pacing at the coronary sinus ostium. (B) Pacing at the low lateral right atrium. Note a dual wave front of right atrial activa-tion with bidirectional conduction, which collides in H.9.10. (C,D) Bidirectional conduction block with the presence of double poten-tials in the cavotricuspid isthmus. (C) Pacing at the coronary sinus ostium. (D) Pacing at the low lateral right atrium. The surface ECG

lead III is shown. Intracardiac electrograms are recorded from the His bundle area. H1.2 to H19.20 indicate 10 bipoles of the duode-capolar (Halo) catheter positioned around the tricuspid annulus, and CS1.2 to CS7.8 represent four bipoles of a decapolar catheter placed in the coronary sinus (CS). (E) Sinus rhythm with the presence also of double potential.

397 ms

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FIGURE 102.11. An example of a clock-wise perimitral fl utter (cycle length, 400 ms) bounded by an anterior silent area (gray color) in the left anterior oblique (LAO) (A) projection. The pos-teroanterior (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.

mitral valve surgery. The electrocardiogram (ECG) pattern of these scar fl utters or “incisional tachycardia” is variable; the rate is often slightly below the lower limit usually accepted for common atrial fl utter. The localization and the size of the scar may vary from patient to patient. Endocardial mapping of the entire reentrant circuit is sometimes diffi cult or impossible (especially after the Mustard and Senning pro-cedures). Catheter ablation in these patients is targeted to areas forming a critical part (isthmus) of the circuit, identi-fi ed 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%. Seventy-two percent of the patients had a long-term clinical improve-ment 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 conduc-tion cannot be localized. In these cases, areas in proximity to anatomic or surgical barriers showing concealed entrain-ment 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 isthmus-dependent common atrial fl utter in most of these patients.57,59 With new mapping techniques, like the three-dimensional, nonfl uoroscopic mapping (CARTO) system, the scar can be more precisely located and the ablation site can be better directed and verifi ed (Fig. 102.13).


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FIGURE 102.12. (A) Left atrial electroanatomic map of a patient with a “gap-related” left atrial fl utter recorded during the tachycar-dia 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

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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 fl utter with positive fl utter 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 acti-vated in tandem with the halo catheter, and double potentials, as a

result of a previous ablation attempt, were recorded on the cavotri-cuspid 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.

before the left pulmonary veins and down the posterior left atrial wall, passing a gap with slow conduction in the ablation line encircl-ing the left pulmonary veins. The red points show the gap in the ablation line. (B) The 12-lead during tachycardia showing positive fl utter waves in the inferior leads and V1 (stars).



Atrial Tachycardia

Atrial tachycardia can be classifi ed according to its mecha-nism into automatic, triggered activity and reentry. As pointed out in Chapter 91, supraventricular tachycardias may be paroxysmal or incessant. Results from a meta-analysis study show that the clinical and electrophysiologic characteristics of atrial tachycardia may vary between dif-ferent age groups.60 This study demonstrated that pediatric patients have more often automatic and incessant forms, whereas the adult patients present more often the nonauto-matic forms with a paroxysmal pattern.60 Furthermore, right-sided atrial tachycardia and multifocal atrial tachycar-dia were more common in adults. It is important to know that in patients with incessant atrial tachycardia the inabil-ity 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 coro-nary 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 fi brillation (Fig. 102.15).63

As shown in Chapter 91 on supraventricular tachycar-dias, the P wave axis and width can be very helpful in local-izing the likely site of origin of atrial tachycardia.

ABLATION PROCEDURE

Currently, two techniques are used to localize the site of origin of atrial tachycardia: the technique using multielec-trode catheters and the three-dimensional, nonfl uoroscopic 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 entrain-ment. 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 abla-tion. Although the left atrium is easily accessed using the transseptal technique, left-sided mapping may be more dif-fi cult than right-sided mapping. In general, catheter ablation for atrial tachycardia is effective and safe. No procedure-related complications have been reported.

Atrial Fibrillation

To date, catheter ablation of atrial fi brillation has been shown to be most effective in patients with symptomatic paroxys-mal atrial fi brillation resistant to antiarrhythmic drugs. Strategies aimed at treating atrial fi brillation are trigger elimination and substrate modifi cation.

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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

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, tri-cuspid valve.


215 0 c h a p t e r 10 2

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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 acti-vation spreading gradually from that region over the entire LA. Right atrial activation occurs through a superior connection (Bach-mann’s bundle) activating the left septum and the rest of the RA from superior to inferior. This activation is blocked in a bidirec-tional manner in the cavotricuspidal isthmus, as a result of a previ-ous RF ablation. Red dots indicate radiofrequency applications. CS, coronary sinus; LIPV, left inferior pulmonary vein; LMPV, left inter-mediate pulmonary vein; LSPV, left superior pulmonary vein; MV,

mitral valve; TV, tricuspid valve. (C) The 12-lead ECG shows iso-electric p waves in lead I and aVL and positive in the inferior and precordial leads with 2 : 1 atrioventricular conduction. (D) Endocar-dial recordings during atrial tachycardia of the RA and LA. The cycle length of the tachycardia is 320 ms. Note the Marshall poten-tial (*) 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 duode-capolar catheter positioned around the tricuspid annulus; distal (CSd), medial (CSm), and proximal (CSp).

TRIGGER ELIMINATION

As demonstrated by Haïssaguerre et al.,65 the majority of the triggers for atrial fi brillation originate from the pulmo-nary 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 fi rst 45 patients studied by Haïssaguerre et al., a single focus of atrial ectopy was identifi ed in 29 patients, two foci were identifi ed in nine patients, and three or four foci were identifi ed in seven

patients. Focal ablation, inside the pulmonary vein(s), was performed in this population. This approach has been aban-doned 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 pulmo-nary 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



isolation can be performed either by recording the pulmo-nary vein potential electrograms using circular mapping catheters with fl uoroscopy guidance (Fig. 102.16) or, empiri-cally, 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 fi stula.71 Therefore, other ablative energies for ablation of atrial fi brillation (see New Ablative Energy Sources, below) need to be considered.

SUBSTRATE MODIFICATION

In patients with chronic atrial fi brillation (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 essen-tial 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 fi brillation (Fig. 102.21).72 However, complications may occur with the fi rst technique, such as pulmonary vein stenosis and atrioesopha-geal fi stula.71 The latter is due to the vicinity of the esopha-gus to the left pulmonary veins and to the thickness of the

posterior wall of the left atrium (3 mm). A longer follow-up is needed to evaluate the impact of substrate modifi cation on the arrhythmia burden in patients with chronic atrial fi brillation.

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BFIGURE 102.16. This is an example of mapping of the pulmonary veins (PVs) using circular catheters (Lasso) in a patient with parox-ysmal atrial fi brillation who underwent PV isolation with cryother-mia. (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

decapolar catheter is inserted in the LIPV (recording/pacing). (C) Initiation of a paroxysm of atrial fi brillation 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.

FIGURE 102.17. This fi gure shows an example of an isochronal activation map during coronary sinus pacing after anatomically isolation of all four pulmonary veins. Color coding represents acti-vation 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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FIGURE 102.18. An example of entrance block between the left atrium and the left superior pulmonary vein (LSPV) after isolation with cryoablation. During coro-nary sinus (CS) pacing the left atrium and the PV poten-tials are dissociated (arrows). From top to bottom: leads I, II, and V1, HBED, His bundle electrogram distal, cir-cumferential mapping from the ostium of the LSPV (LSPV12 to LSPV910). Cryo, cryocatheter.

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FIGURE 102.19. This fi gure 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).

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 orifi ces. In addition, two linear lesions were placed, one connecting the cir-cular lesions in the posterior wall and one connecting the left cir-cular lesion with the mitral valve (MV) (so-called left atrial isthmus).

Catheter Ablation of the Atrioventricular Junction

Currently, AV junctional ablation followed by pacemaker implantation is limited to patients in whom catheter abla-tion cannot cure the supraventricular arrhythmia (such as in left atrial fl utter, multifocal atrial tachycardia, and atrial fi brillation). It is an accepted treatment for symptomatic patients with atrial fi brillation in whom the arrhythmia and the ventricular response cannot be controlled by the cur-rently existing treatment modalities, like antiarrhythmic drugs, external or internal cardioversion, and the implant-able atrial defi brillator.73 Atrioventricular junctional abla-tion 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 defl ection. The success rate of this technique is close to 100%. On rare occasions, interrup-tion of conduction over the AV node–His-Purkinje system cannot be achieved from the right side, and a left-sided approach is necessary. Modifi cation or partial, instead of complete, AV nodal conduction74 has a moderate long-term success rate; therefore, complete interruption of the AV junc-tion 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.



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 hypertro-phied), valvular heart disease, and arrhythmogenic right ven-tricular 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 outfl ow tract, and is in or close to the specifi c 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 idio-pathic 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 ventric-ular outfl ow tract typically have a left bundle branch block-like confi guration with an intermediate or vertical QRS axis

in the extremity leads (Fig. 102.22). The mechanism of this VT is considered to be triggered activity. These VTs are fre-quently exercise related and catecholamine sensitive, and can be terminated by intravenous adenosine or beta-blocker

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FIGURE 102.21. A biatrial map (mesh presentation) in the anterior-posterior view. The arrow points to the electro-gram 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 fi brillation.

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FIGURE 102.22. A typical example of an idiopathic right ventricu-lar outfl ow 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 outfl ow tract.


215 4 c h a p t e r 10 2

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 outfl ow tract (RVOT). The VTs arising in the inferoposterior aspect of the septum of the left ventricle have a right bundle branch block-like confi gu-ration 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. Fur-thermore, 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 outfl ow 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,

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, specifi c characteristics of the QRS complex during VT may point to an origin in the left ventricular outfl ow tract or aortic root.83 In idiopathic VT, catheter abla-tion 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 identifi cation of an essential part of the reentry circuit. A reentry circuit varies in size, con-fi guration, 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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FIGURE 102.23. (A) The 12-lead ECG of a patient with an idio-pathic 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 confi guration and a left axis deviation. (B) The 12-lead ECG of an idiopathic ventricular tachycardia originating more ante-riorly in the apicoseptal aspect of the left ventricle. That ventricular tachycardia shows a right bundle branch block–like confi guration and a northwest QRS axis.

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.



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 calcifi ed and fi brotic scars.

In postinfarction patients who, after implantable cardio-verter-defi brillator (ICD) implant require frequent shocks, catheter ablation may substantially reduce the number of shocks. Additionally, in patients who present with an electri-cal 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

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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 wave-like) beginning of the QRS complex.

FIGURE 102.26. The parts of a reentry circuit with an inner loop (A) and a broad outer loop (B) in scarred myocardium.

to the exit consists of a central and a proximal part (Fig. 102.26). After the wave front emerges from the exit, it propa-gates 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 Identifi cation 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 fl utter.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 poten-tial, 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 abla-tion 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 compa-rable to those reported by Stevenson et al.11 In their popula-


215 6 c h a p t e r 10 2

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 incom-plete 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.

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≤0.50 mV

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VT PM VT

25 mm/sec 25 mm/sec 25 mm/sec 25 mm/sec

LV

Exit VT1

Exit VT2

y+ Blpolar voltage

1.46 cm

A B C

FIGURE 102.28. (A) A bipolar voltage map during sinus rhythm of the left ventricle (LV) in a posterior-anterior view of a patient with an old inferoposterolateral infarction. The patient had two different ventricular tachycardias: VT1 with a left bundle branch block mor-phology and left axis, VT2 with right bundle branch block morphol-ogy and northwest QRS axis. Color range indicates the ventricular electrogram amplitude (mV). Purple represents normal myocardium

(amplitude >1.5 mV); gray, dense scar (amplitude <0.5 mV) and range between purple and red; border zone (signals amplitudes between 0.5 and 1.5 mV). The 12-lead ECG during VT and pace map (B,C) directed the linear ablation. Arrows indicate the site where the exit point of the VTs was found. Linear lesions (red dark dots) were extended from dense scar and cross-border zone.

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

I 99-1344IIIII

aVRaVLaVFV1V2V3V4V5V6

HISdS-QRS = 270

450

PPI = 450 Eg-QRS = 270

470 470

99520/4

HISp

RV

RFd

100 mm/sec

99-1344

25 mm/sec

99520/1

A

C

B

I 99-134499520/2

IIIII

aVRaVLaVF

V1V2V3V4V5V6

HISd

HISp

RV

RFd

25 mm/sec

startD



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 poste-rior fascicle of the left bundle branch. This is called “inter-fascicular” VT. In the latter situation, the VT shows a right bundle branch block-like confi guration 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 subepi-cardial 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 fi brilla-tion has been described in 27 patients. The initiating beat of ventricular fi brillation had an identical electrocardio-graphic morphology and coupling interval compared to the preceding isolated premature beats typically noted in the aftermath of resuscitation. The initiating ventricular pre-mature 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

of 24 months, 89% of the patients had no recurrence of ventricular fi brillation as confi rmed by the defi brillator memory. Primary idiopathic ventricular fi brillation is char-acterized 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 confi rm the effi cacy of catheter ablation of this type of arrhythmia.

New Ablative Energy Sources

While the vast majority of arrhythmia substrates can be suc-cessfully ablated using radiofrequency energy, this energy source has its limitations. For example, radiofrequency abla-tion 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 fi brillation, radiofrequency energy may produce pulmonary vein stenosis in patients undergoing ablation of paroxysmal atrial fi brillation. Pulmo-nary 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 radio-frequency energy produces endocardial disruption, cardiac perforation may occur. Another potential hazard of radiofre-quency energy is the occurrence of a fi stula 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 catheter-based systems that can be applied to treat cardiac arrhyth-mias with especial emphasis on the treatment of atrial fi brillation. 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 catheter-based cryoablation for supraventricular and ventricular arrhythmias are comparable to those reported with radiofre-quency energy.103

TABLE 102.2. Comparison between radiofrequency (RF) and new ablative energy sources

RF Cryothermia Ultrasound Laser Microwave

Clinical experience + + + + + + + +Endothelial Increased Minimal Increased Increased Increased disruption (e.g., PV stenosis)Thrombogenicity High Low Medium High HighMapping capability Yes Yes No No NoAbility to create Requires Requires optimal Requires Excellent, Excellent, transmural lesion optimal contact optimal contact contact contact (cryoadherence) contact forgiving forgivingLesion size + + + + + + + + + +Perforation rate Low Very Low Low High High


215 8 c h a p t e r 10 2

Summary

During the past 15 years, catheter ablation developed into an effective and safe curative treatment for patients with differ-ent types of supraventricular arrhythmias including parox-ysmal atrial fi brillation. 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 well-tolerated postinfarction VT. In atrial fi brillation ablation, new catheter designs, new ablative energy sources, and better understanding of how to defi ne and localize the substrate are needed to improve results and to expand the indications for other subsets of atrial fi brillation (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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1 Catheter Ablation of 0 Supraventricular and Ventricular ...extras.springer.com/2007/978-1-84628-715-2/fs... · and surgical5 or catheter ablation to cure or control cardiac arrhythmias.6,7