R7631_ElMapHeart_Cov_01.qxd
6/3/06
14:00
Page 1
Electro-anatomical Mapping of the Heart An Illustrated Guide to the Use of the CARTO™ System Josef Kautzner Anders Kirstein Pedersen Petr Peichl
Electro-anatomical Mapping of the Heart An Illustrated Guide to the Use of the CARTO™ System
Josef Kautzner Anders Kirstein Pedersen Petr Peichl
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page i
Electro-anatomical Mapping of the Heart An Illustrated Guide to the Use of the CARTO™ System
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page ii
CARTO™ system is a registered trademark of Biosense Webster, Inc., Diamond Bar, CA, USA. Published by Remedica Commonwealth House, 1 New Oxford Street, London, WC1A 1NU, UK Civic Opera Building, 20 North Wacker Drive, Suite 1642, Chicago, IL 60606, USA
[email protected] www.remedicabooks.com Tel: +44 20 7759 2999 Fax: +44 20 7759 2901 Publisher: Andrew Ward In-house editors: Nicky Fernando and Catherine Harris Booth Design and artwork: AS&K Skylight Creative Services © 2006 Remedica While every effort is made by the publisher to see that no inaccurate or misleading data, opinions, or statements appear in this book, they wish to make it clear that the material contained in the publication represents a summary of the independent evaluations and opinions of the authors. As a consequence, the authors, publisher, and any sponsoring company accept no responsibility for the consequences of any inaccurate or misleading data or statements. Neither do they endorse the content of the publication or the use of any drug or device in a way that lies outside its current licensed application in any territory. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the publisher. Remedica is a member of the AS&K Media Partnership ISBN-13: 978 1 901346 98 5 ISBN-10: 1 901346 98 6 British Library Cataloguing-in-Publication Data A catalogue record for this book is available from the British Library. Printed in Spain.
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page iii
Electro-anatomical Mapping of the Heart An Illustrated Guide to the Use of the CARTO™ System
Josef Kautzner, MD, PhD Professor of Medicine Department of Cardiology Institute for Clinical and Experimental Medicine Prague Czech Republic Anders Kirstein Pedersen, MD, PhD Associate Professor of Cardiology Skejby Sygehus Aarhus University Hospital Denmark Petr Peichl, MD Fellow in Cardiology Department of Cardiology Institute for Clinical and Experimental Medicine Prague Czech Republic
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page iv
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page v
CONTENTS Preface
ix
Abbreviations
xi
1.
Electro-anatomical Mapping
1
1.1 Basic Principles of Electro-anatomical Mapping 1.1A General concepts 1.1B Spectrum of electro-anatomical maps 1.1C Limitations of electro-anatomical mapping
2 2 5 7
1.2 Set-up for the Mapping Procedure 1.2A Location of the reference patch 1.2B Selection of the reference signal – the key to success 1.2C Setting up the window of interest
8 8 9 9
1.3 Mapping Technique 1.3A CARTO mapping of cardiac chambers 1.3B Maintaining endocardial contact with the mapping catheter
13 13 17
1.4 Annotation of Electro-anatomical Maps 1.4A How to annotate electrograms 1.4B How to differentiate atrial from ventricular local electrograms 1.4C How to define myocardial scar 1.4D How to evaluate a line of block
18 18 18 18 21
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page vi
CONTENTS
2.
3.
vi
1.5 Diagnosis of Arrhythmias 1.5A Mechanism of arrhythmias 1.5B The importance of entrainment mapping during CARTO procedures 1.5C New map or re-map?
22 22 24 25
1.6 Advanced Mapping Techniques 1.6A Qwikmapping 1.6B Image integration
26 26 26
Normal and Abnormal Conduction of the Heart
31
2.1 Virtual Model of the Heart
32
2.2 Normal Electrical Activation of the Atria and Ventricles
32
2.3 Activation Patterns in Ventricular Conduction Disturbances 2.3A Left bundle branch block and left ventricular conduction abnormalities 2.3B Left anterior hemiblock accompanied by right bundle branch block
35 35 35
2.4 Activation Patterns During Different Pacing Modes 2.4A Right ventricular apical pacing 2.4B Biventricular pacing 2.4C Right ventricular bifocal pacing 2.4D Single-site left ventricular pacing
37 37 38 38 38
Clinical Application of Electro-anatomical Mapping in the Treatment of Arrhythmias
41
3.1 Focal Atrial Tachycardias
43
3.2 Typical Atrial Flutter 3.2A Typical atrial flutter 3.2B Reverse typical flutter
45 45 47
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page vii
CONTENTS
3.3 Atypical Atrial Flutter 3.3A Non-surgical right atrial macro-reentrant tachycardias 3.3B Post-incisional right atrial tachycardias 3.3C Left atrial macro-reentrant tachycardias 3.3D Left septal atrial flutter 3.3E Post-ablation left atrial tachycardias 3.3F Macro-reentrant tachycardias after correction of complex congenital heart disease
49 49 50 51 51 52 52
3.4 Atrial Fibrillation 3.4A Segmental pulmonary vein isolation 3.4B Circumferential ablation around pulmonary vein ostia 3.4C Combined technique 3.4D Ablation of an electrophysiological substrate 3.4E The role of imaging
53 53 55 56 57 57
3.5 Atrioventricular Nodal Reentry
60
3.6 Inappropriate Sinus Tachycardia
62
3.7 Accessory Pathways
63
3.8 Idiopathic Focal Ventricular Tachycardia 3.8A Ventricular tachycardia originating from the right ventricular outflow tract 3.8B Ventricular tachycardia originating from the left ventricular outflow tract 3.8C Right ventricular outflow tract versus left ventricular outflow tract site of origin 3.8D Other locations of the arrhythmogenic focus in idiopathic ventricular tachycardias
65 65 67 67 67
3.9 Idiopathic Reentrant Ventricular Tachycardia (Fascicular)
70
vii
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page viii
CONTENTS
3.10 Post-myocardial Infarction Ventricular Tachycardia 3.10A Mapping during ventricular tachycardia 3.10B Ablation of stable ventricular tachycardia 3.10C Sinus rhythm substrate mapping 3.10D An integrated approach 3.10E Epicardial approach
71 71 72 72 73 73
3.11 Ventricular Tachycardias in Dilated Cardiomyopathy
75
3.12 Ventricular Tachycardias in Right Ventricular Arrhythmogenic Cardiomyopathy
76
3.13 Post-incisional Ventricular Tachycardias
78
3.14 Catheter Ablation of Ventricular Fibrillation
80
References
viii
83
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page ix
PREFACE Mapping of the heart is one of the principal techniques used in the diagnosis and treatment of cardiac arrhythmias. Electrical activity of the heart can be recorded from the body surface (ECG mapping), from the surface of the heart (epicardial mapping) or from the endocardium (endocardial mapping). Signals can be acquired simultaneously from various sites or sequentially, point-by-point, and these data can be visualized in different formats. The power of computer processing opened new horizons in cardiac mapping. The so-called electro-anatomical mapping system (CARTO™, Biosense Webster, Inc., Diamond Bar, CA, USA), developed in the mid-nineties, represents one of the most successful systems for detailed endocardial/epicardial mapping of cardiac arrhythmias. For the first time in history, it allowed superimposition of 3D anatomy and local electrograms. The major advantages of the system comprise direct visualization of the activation pattern of individual arrhythmias, catheter navigation to the desired arrhythmic substrate during radiofrequency ablation and minimal need for fluoroscopy. Since its introduction into the clinical arena, the use of the electro-anatomical mapping system has continued to grow. This book reviews the main clinical applications of the CARTO system, and provides recommendations for the mapping and treatment of a wide range of arrhythmias. We hope that the combined experience of our two centers will provide practical assistance to those just starting to use this system. Besides explanation of basic principles of the mapping procedure, major sections of the book deal with the use of the CARTO system in individual types of arrhythmias. For each arrhythmia, a review of published data is presented together with a recommended strategy for mapping and ablation. All sections are supported by images in order to facilitate the learning process. Finally, the text is accompanied by a selection of the most relevant references.
Josef Kautzner, MD, PhD Anders Kirstein Pedersen, MD, PhD Petr Peichl, MD March 2006
ix
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page x
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page xi
ABBREVIATIONS 3D = three-dimensional AF = atrial fibrillation Ant = anterior Ao = aorta ARVC = arrhythmogenic right ventricular cardiomyopathy AT = atrial tachycardia AV = atrioventricular aVF = augmented electrocardiographic leads from the foot aVL = augmented electrocardiographic leads from the left arm AVNRT = atrioventricular nodal reentrant tachycardia aVR = augmented electrocardiographic leads from the right arm CRT = cardiac resynchronization therapy CS = coronary sinus CT = computed tomography ECG = electrocardiogram EP = electrophysiological ICE = intracardiac echocardiography Inf = inferior IVC = inferior vena cava IVS = interventricular septum LA = left atrium Lat = lateral LATs = local activation times LBBB = left bundle branch block LCA = left coronary artery LIPV = left inferior pulmonary vein
LPB = left posterior bundle LSPV = left superior pulmonary vein LV = left ventricle LVOT = left ventricular outflow tract MA = mitral annulus MI = myocardial infarction MR = magnetic resonance Os = ostium PA = pulmonary artery PPI = post-pacing interval PVs = pulmonary veins RA = right atrium RB = right bundle RBBB = right bundle branch block RCA = right coronary artery RF = radiofrequency RIPV = right inferior pulmonary vein RSPV = right superior pulmonary vein RV = right ventricle RVOT = right ventricular outflow tract SVC = superior vena cava TA = tricuspid annulus VF = ventricular fibrillation VT = ventricular tachycardia WOI = window of interest
xi
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page xii
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page 1
ELECTRO-ANATOMICAL MAPPING 1.1 Basic principles of electro-anatomical mapping 1.2 Set-up for the mapping procedure 1.3 Mapping technique 1.4 Annotation of electro-anatomical maps 1.5 Diagnosis of arrhythmias 1.6 Advanced mapping techniques
R7631_ElMapHeart_03.qxd
6/3/06
16:08
Page 2
The CARTO™ (Biosense Webster, Inc., Diamond Bar, CA, USA) electro-anatomical system is a powerful tool for mapping cardiac arrhythmias. This chapter explains the basic concepts underlying the CARTO system, highlighting its advantages over conventional mapping techniques and its inherent limitations; recommends a strategy for system set-up; and provides guidance on arrhythmia recognition. Finally, it describes in detail the new advanced mapping features of the system.
1.1 Basic principles of electro-anatomical mapping 1.1A General concepts Conventional electrophysiologic mapping compares local activation times (LATs) at different mapping spots (ie, timing of the local electrograms) with a reference either on the surface electrocardiogram (ECG) or a selected intracardiac signal. A major limitation of this approach is the need for fluoroscopic control of the catheter position. Besides the risk associated with the use of X-rays, fluoroscopy does not provide exact information on the orientation and position of the catheter tip in a three-dimensional (3D) heart chamber. Such information is especially important when repeated catheter navigation to a desired location is required during radiofrequency (RF) ablation. In addition, conventional mapping is largely ineffective for complex reentrant arrhythmias, for which multipolar mapping catheters are required. The CARTO system [1,2] uses low energy electromagnetic fields (from 5 ǂ 10–6 to 5 ǂ 10–5 T) for placement of the catheter tip. Three such fields are generated by magnetic coils located under the examination table; this creates a non-homogeneous electromagnetic field around the patient’s chest (Figures 1 and 2). The mapping catheter contains a magnetic sensor that is located near the distal electrode (Navistar®, Biosense Webster, Inc., Diamond Bar, CA, USA) and permits precise positioning of the catheter in a given electromagnetic field. Resolution is <1 mm for catheter positioning and <1º for catheter tip orientation. In all of these respects, the design of the catheter is not significantly different from that of a conventional mapping catheter. It does, however, allow the recording of both unipolar and bipolar electrograms and contains a thermocouple or thermistor for temperature monitoring during catheter ablation. Catheters are supplied with 4 or 8 mm tips and irrigated tips. To avoid inaccuracies caused by movement of the patient, the position of another reference sensor (eg, an adhesive or ‘reference’ patch placed on the patient’s back) is monitored within the electromagnetic field. The mapping procedure generally consists of the systematic acquisition of points where the catheter tip touches the endocardium (or epicardium). At each of these touching points, both the exact position in space and the local electrogram are recorded. Through the sequential acquisition of new points, a 3D anatomical map is created in real-time. The greater the number of points acquired, the better the anatomical detail obtained. When mapping regular rhythms, each point is associated with a specific LAT (ie, the interval between the beginning of the local electrogram and the selected reference signal).
2
R7631_ElMapHeart_03.qxd
6/3/06
16:09
Page 3
ELECTRO-ANATOMICAL MAPPING
1.1
Figure 1. Components of the CARTO™ system. (A) workstation, (B) junction box, (C) location pad positioned under the cath table, (D) CARTO™ XP processing unit.
A)
B)
C)
D)
3
R7631_ElMapHeart_03.qxd
6/3/06
16:09
Page 4
1.1 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Figure 2. This is the view of the upper relevant hemisphere of the magnetic fields. The three distances determine the location, the orientation, and the rotation of the catheter.
Location of the sensor
D3 D1 S3 S1 D2
S2
4
R7631_ElMapHeart_03.qxd
6/3/06
16:09
Page 5
ELECTRO-ANATOMICAL MAPPING
1.1B Spectrum of electro-anatomical maps Anatomical reconstruction of the mapped cardiac structure is done in realtime, and the system allows for the immediate editing of acquired data. Besides a plain anatomical map (Figure 3), various electrophysiological (EP) data can be color-coded and superimposed on reconstructed 3D anatomy. Examples of other anatomical maps are as follows: •
•
Activation map: adding LATs to the anatomical reconstruction creates an activation map (Figure 4). This provides essential information about the activation sequence and the velocity of activation. Isochronal map: analogous to the activation map is the isochronal map, which depicts all the points with an activation time within a specific range (eg, 10 ms) with the same color. Depending on conduction velocity, each color layer will be of variable width (isochrones are narrow in areas of fast conduction and broad in regions of slow conduction).
Figure 3. An anatomical map of both atria during sinus rhythm (left anterior oblique view).
•
•
•
1.1
Propagation map: after finishing the activation map, the spread of electrical activation can be visualized on the propagation map (Figure 5). This is a two-colored, animated map that depicts the propagating wavefront. Voltage map: electro-anatomical mapping systems also allow visualization of local electrogram amplitudes and construction of a voltage map (Figure 6). This map distinguishes normal myocardium (high voltage signals) from scar tissue (low or no voltage signals). Areas with no electrical capture at 10 mA are considered to be dense scar, and are labeled in grey. Mesh map: a mesh map (Figure 7) shows the cardiac chambers as a fine transparent net. This facilitates visualization of points under the surface (ie, ablation points). An individualized map can be created by recording specific values for each point in the map (eg, a map of durations of local potential or a map of impedances obtained from reading an RF generator).
Figure 4. An activation map of both atria during sinus rhythm. The activation time is color-coded in the following sequence: red–yellow–green–blue–violet (left anterior oblique view).
5
R7631_ElMapHeart_03.qxd
6/3/06
16:09
Page 6
1.1 ELECTRO-ANATOMICAL MAPPING OF THE HEART
The acquired map provides a geometrical reconstruction of the shape and size of the specific cardiac structure (usually cavity), from which its volume can be calculated. In addition, the operator can determine the shape and size of specific anatomical structures, such as the tricuspid annulus (TA) or coronary sinus (CS) orifice, in detail. This is particularly useful in patients with structural heart disease and altered cardiac function.
Moreover, distances between acquired points can be measured, which is especially useful in the design of linear ablation lines. The electro-anatomical mapping system allows catheter navigation to the same position each time with high reproducibility and minimal need for fluoroscopy. RF energy at each site can be tagged directly in the map to depict the ablation lines.
Figure 5. (A–F) A propagation map of both atria during sinus rhythm (left anterior oblique view). Propagation of the wavefront is depicted in red.
6
A)
B)
C)
D)
E)
F)
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 7
ELECTRO-ANATOMICAL MAPPING
1.1C Limitations of electro-anatomical mapping Electro-anatomical mapping has a number of inherent limitations: • •
•
Firstly, the sequential, point-by-point mapping technique is time-consuming. Secondly, the system is only able to map cardiac rhythms with constant cycle lengths. This means that the CARTO system is not suitable for mapping unstable arrhythmias with variable cycle lengths. Similarly, when an arrhythmia is interrupted, a new map has to be created. Thirdly, the system has difficulties in mapping sharp ridges of tissue and/or ostia of the veins, as the mapping software interpolates between acquired points.
Figure 6. A voltage map of both atria (left anterior oblique view). Note: high-voltage areas (violet) reflect normal myocardium. Low-voltage areas and scars would be displayed in red.
•
1.1
Finally, it is important to appreciate that the electro-anatomical mapping system can only provide a map of those parts of the heart that are in fact mapped. If a particular part of a given cardiac chamber is not mapped, then it will not show up on the 3D electro-anatomical map. However, this limitation can be overcome by the addition of an image integration module, such as CARTOMerge™ (Biosense Webster, Inc., Diamond Bar, CA, USA). This software works by merging a computed tomography (CT) or magnetic resonance (MR) image with the 3D image of the mapped cardiac chamber, thereby providing a more accurate map of the heart [3].
Figure 7. A mesh map of both atria (left anterior oblique view).
7
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 8
1.2 ELECTRO-ANATOMICAL MAPPING OF THE HEART
1.2 Set-up for the mapping procedure 1.2A Location of the reference patch Electro-anatomical mapping requires the use of a location reference, ie, a sensor visible in the electromagnetic field. Movement of the location reference indicates movement of the patient’s chest, which must be corrected to prevent distortion of the 3D electro-anatomical map. The location sensor is placed in an adhesive reference patch that is secured to the patient’s back (around the 7th intercostal space paravertebrally). The position of the sensor within the heart should be checked using fluoroscopy prior to the procedure (Figure 8). The patch should be placed close to the chamber that is to be mapped, since there is a certain pre-defined range within which the tip of the mapping catheter can be localized.
The patient should be placed approximately 10 cm above the catheterization table (eg, by using a mattress of appropriate thickness), so that the patient’s chest is in alignment with the electromagnetic field that is emitted from below the table. A Reference Location Check dialog box is used to check the location of the reference patch in relation to the location pad. Positioning of the location pad should be adjusted in order to place the reference dot into the circle within the location pad scheme on the screen. Here, the dot changes color from red to green. The patient should try to avoid any chest movement after the location pad has been fixed. Although minor movements can usually be corrected within the Reference Location Check dialog box, even when placement of the reference sensor appears nearly perfect the points in the map might not correspond if previous and current His position tags are not equal. In such cases, it is better to start a new map.
Figure 8. (A) The reference patch mounted on the patient’s back in a typical location. (B) Location of the reference patch tip (arrows) positioned behind the LA in LA atypical flutter. For better visualization of the reference electrode, a paper clip may be temporarily attached to the end of the electrode.
A)
8
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 9
ELECTRO-ANATOMICAL MAPPING
1.2
1.2B Selection of the reference signal – the key to success In electro-anatomical mapping, selection of an appropriate reference signal is crucial. Which reference signal is selected is dependent on whether the tachycardia is atrial (AT) or ventricular (VT) in origin. For mapping of ATs, a stable intracardiac atrial signal such as a signal from the CS or a recording from the right atrium (RA) is preferred. The catheter should not be placed in the same cardiac cavity as the mapping catheter as this could cause accidental movement. The use of a temporary screw-in catheter lead is recommended if proximity to the presumed protected isthmus of slow conduction is necessary. However, it is mostly used in patients with post-incisional tachycardias (ie, to maintain a stable sensing reference and for verification of linear lesions through pacing close to the ablation line). For mapping of VTs, it is recommended that the QRS complex in a standard ECG lead be used as the sensing reference. Channels with a sharp R or S deflection (eg, at the pre-cordial lead) and leads with a polarity of P- and T-waves (opposite of a triggering wave) are preferred.
Figure 9. (A) Schematic of a reentry circuit with scars forming a narrow channel of slow conduction. Propagation throughout this channel coincides with diastole and once the activation wavefront reaches the exit site, it forms the QRS complex/P-wave. (B) Set-up of the margins of the WOI. The margins should ideally coincide with the propagation of the activation wavefront throughout the zone of slow conduction. Thus, the WOI (backward window + forward window) can be set as backward window = interval between the mid-diastole preceding the reference signal and the reference signal itself, while forward window = remaining part of the 90% of cycle length. (Courtesy of Dr. De Ponti, University of Insubria-Varese, Italy).
A) Setting the WOI
The acquisition of ectopic beats should be avoided, even in patients in whom only a voltage map is acquired. The red dot placed on the reference signal that marks triggering of (fiducial) point signal will show whether the triggering is stable. It could either be a maximum/minimum deflection, or a maximum/minimum slope whenever appropriate.
1.2C Setting up the window of interest Defining the window of interest (WOI) is the most important step in the set-up as it determines the time frame of the cardiac cycle during which the acquisition of the mapping points will occur. Typically, the WOI is centered around the reference signal, such that the margins of the WOI both precede and follow the reference (Figure 9). Generally, the total duration of the WOI should match the tachycardia cycle length, however, the individual set-up varies depending on the origin of tachycardia (ie, AT or VT).
B)
There is also a difference when mapping focal versus macro-reentrant tachycardias.
WOI
9
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 10
1.2 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Atrial tachycardias In focal ATs with distinct P-waves, the beginning of the WOI should precede the onset of the P-wave (typically by 100 ms). However, in macro-reentrant ATs, the margins of the WOI should coincide with the propagation of the activation wavefront throughout the zone of slow conduction. Differentiation or identification (whether focal or macro-reentrant), however, might be difficult prior to mapping (Figures 10 and 11).
If the AT mechanism is unknown, the following steps are recommended: •
Map with a selected WOI less than or equal to the AT cycle length (ie, 90–99%). Allow 100 ms to the left of the P-wave onset. Since this set-up works for most ATs, re-annotating and/or re-mapping a new WOI is not required. If, however, the cycle length changes during mapping, there are two choices:
Figure 10. Activation maps of the RA after surgical correction of tetralogy of Fallot (posteroanterior view). Both maps were acquired during the same AT (cycle length of 360 ms); however, each was annotated using a different WOI. (A) An improperly selected WOI. Since the whole cycle length of the arrhythmia has been covered by the RA activation, the arrhythmia may appear to be reentry. However, precise analysis of the map indicates that the activation starts in the roof of the RA (blue), and then propagates downwards (blue–violet–red–yellow–green). (B) The same map with different annotation of activation times. The beginning of the WOI has been shifted backwards to coincide with the activation in the superior portion of the RA, and all points have been re-edited according to this new WOI. The true focal origin (white arrow) of the arrhythmia then becomes apparent, as only a portion of the AT cycle length is covered.
A)
10
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 11
ELECTRO-ANATOMICAL MAPPING
a) If only a slight increase in cycle length is observed, the WOI can still be used by annotating all late signals to the right of the WOI. Check whether the spectrum of all acquired LATs covers the entire tachycardia cycle length. A period of no electrical activity might represent conduction through the zone of slow conduction. b) Try to locate the zone of slow conduction using a voltage map and fractionated signals. Their participation in the circuit can be assessed by entrainment mapping.
•
1.2
Shift the beginning and end of the WOI to coincide with activation of the above areas and re-map the atrium; alternatively, repeat the procedure with a new WOI setting.
When mapping during atrial pacing (eg, for creation of a voltage map or validation of a block in the atria), the CARTO system usually triggers on the pacing artifact in the reference channel. Excluding the pacing spike from the WOI (eg, by setting the beginning of the WOI from +10 to +30 ms) avoids automatic triggering of the LAT in the mapping channel by the pacing spike. It is also recommended that the WOI be shortened in order to avoid automatic triggering of a ventricular electrogram.
Figure 11. Activation maps in a patient with reentry encircling the central atriotomy scar on the RA wall (right lateral view). Both maps were acquired during the same tachycardia; however, each was annotated using a different WOI. (A,B) Although the distribution of colors is shifted in both maps, the reentrant origin of the tachycardia remains obvious as all colors of the scale (red–yellow–green–blue–violet) encircle the centrally positioned scar (double white line). (B) Annotation clearly delineates the channel of conduction between the atriotomy scar and an additional line of block located more posteriorly.
A)
B)
11
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 12
1.2 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Ventricular tachycardias For mapping of both focal and reentry ventricular arrhythmias, the beginning of the WOI should slightly precede the onset of the QRS complex on the 12-lead ECG (Figure 12). With this approach, the earliest activation within the cycle (either single focus or exit site in the case of a reentry circuit) will be displayed in red as the hot spot. For reentrant VTs, the WOI should be long enough to cover almost the entire cycle length of the VT.
Figure 12. Selection of the WOI for slow-tolerated VT with a cycle length of 420 ms. (A) The peak deflection of the QRS complex in lead V2 (red dot) was chosen as the trigger channel. The beginning of the WOI was set to slightly precede the onset of the QRS complex (–170 ms), and the end of the WOI was calculated to match the cycle length of +250 ms. (B) The activation map of the LV (left lateral view). The close relationship of the earliest and latest activations (red and violet) effectively shows the isthmus of slow conduction. Application of RF energy within that area successfully terminated the VT.
A)
12
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 13
ELECTRO-ANATOMICAL MAPPING
1.3 Mapping technique The software creates a continuous surface map of the chamber depending on the number of mapping points. The quality of the map is a reflection of the number of points acquired – the more points, the greater the detail of the map. The ‘fill threshold’ is the function that determines the level of interpolation (and hence detail). For detailed maps, the threshold is usually set at 15 units; higher values lead to increased fill and hence a decrease in detail (Figure 13).
By pulling the catheter into the RA, additional points can be acquired until the inferior vena cava (IVC) is reached. More points are acquired by rotating the catheter in the vein. The position of the bundle of His is noted and the catheter is bent towards the CS ostium. By rotating the catheter counterclockwise, the cavotricuspid isthmus is reached where more points are obtained from its annular part, as well as from the Eustachian ridge and the areas in-between. Further rotation of the catheter allows a few more points to be obtained around the TA. The annulus is then marked by using a special software tool (Figure 14).
Right atrium Mapping of the superior vena cava (SVC) should begin with the location of the SVC. Mapping of the circumference of the SVC at its entry point permits circumferential mapping of the SVC without the need for fluoroscopy. Alternatively, a vessel tag can be used to indicate the SVC.
Subsequent mapping of the cavity can be performed with minimal use of fluoroscopy by adding points in new areas and checking endocardial signals. New points are acquired only when the tip of the catheter comes into contact with the endocardium. Tagging the SVC, IVC, and CS as vessel tubes facilitates interpretation of the 3D map created.
1.3A CARTO mapping of cardiac chambers
1.3
Figure 13. Activation map of the RA during typical atrial flutter in left anterior oblique view. Panels show different levels of fill threshold. When low fill threshold is selected (A), acquisition of many other points would be required to construct the anatomy of the atrium. When a higher level of fill threshold is chosen (B, C), the system interpolates activation times between the points and fills blank areas. In such cases, less mapping points are necessary; however, the resulting map is anatomically less precise and activation is more interpolated.
A)
B)
C)
13
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 14
1.3 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Left atrium Mapping of the left atrium (LA) begins with marking the circumference of the mitral valve and the region of the left appendage. Individual pulmonary veins (PVs) are tagged using a vessel tag and the ostium of each vein is mapped around the proximal end of each vessel tag. Additional points are obtained by rotating the catheter around the posterior, superior, and inferior wall. The septal aspect is mapped by bending the catheter in the left atrial cavity and rotating the shaft counterclockwise so that the bent tip is against the septum. In order to better depict individual anatomy of the PVs, additional maps can be created (ie, one map for each PV) (Figure 15).
Right ventricle Mapping of the right ventricle (RV) begins with tagging the bundle of His, entering the outflow tract, and obtaining several points circumferentially from the pulmonary valve. Additional points are obtained by withdrawing the catheter and bending it in the midseptal area so that it enters the RV apex. Counterclockwise rotation and further bending of the catheter allow mapping of the free wall. The circumference of the tricuspid valve can be mapped by fully bending the catheter and withdrawing it from the valve. Finally, additional points are obtained from the outflow tract, the septum, and the free wall (Figure 16). The RV is generally the most difficult chamber to map. When the RV becomes enlarged, access to regions within the RV becomes difficult. In such a case, a supporting sheath such as the SR 0™ (Daig, Minnetonka, MN, USA) is recommended.
Figure 14. Anatomical map of the RA in the left anterior oblique (A), posteroanterior (B) and right anterior oblique (C) view. Note that both SVC and IVC could be labeled by means of vessel tags. Alternatively, SVC can be mapped as a tubular extension of the RA (see lower part of the SVC adjacent to the RA).
A)
14
B)
C)
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 15
ELECTRO-ANATOMICAL MAPPING
1.3
Figure 15. Anatomical map of the LA in postanterior view. The PVs can be tagged either by dragging the mapping catheter within the vein using ‘vessel tagging’ software tool (A), or each vein can be mapped three-dimensionally using an individual map (B). The second option enables a more realistic depiction of PVs, their oval diameter and the level of their ostia. 3D CT construction of the LA and PVs in a given patient (C).
A)
B)
C)
Figure 16. Anatomical map of the RV in the left anterior oblique (A), posteroanterior (B) and right anterior oblique (C) view. Map shows characteristic pyramid-like shape of the RV with pulmonary valve (PA) at superior aspect and TA posteriorly.
A)
B)
C)
15
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 16
1.3 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Left ventricle The left ventricle (LV) is mapped either retrogradely via the aortic valve or antegradely via the mitral valve after trans-septal access. In our view, the retrograde approach allows for easier mapping, especially in dilated ventricles. Mapping and the acquisition of points can begin from the apex, and progress towards the mitral valve and the mitral annulus (MA). Points are added by rotating the bent catheter around the various regions of the ventricle. The anterior wall, particularly close to the outflow tract, remains the least accessible part of the ventricle. Therefore, to retrogradely map the entire anterior wall, a large curve has to be made in the ventricle by repeatedly bending the tip and pushing the shaft inside (Figures 17 and 18).
To map a normal LV, manipulation with a straightened or mildly bent catheter is often required. A trans-septal approach is needed in case of aortic stenosis or prosthesis. This approach affords more detailed mapping, from the ventricular septum to the apex, and also provides an alternative route of access to the LV in cases where other routes are compromised (eg, in patients with obliterated iliac arteries in whom arterial vascular access is impossible). Access to the high anterior wall, however, might remain somewhat limited.
Figure 17. Anatomical map of the LV with the proximal part of ascending aorta (Ao) in the right anterior oblique (A), right lateral (B) and left anterior oblique (C) view. Ascending aorta is constructed as a separate map. MA is depicted by tagging several points at the level of the annulus.
A)
16
B)
C)
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 17
ELECTRO-ANATOMICAL MAPPING
Figure 18. A fluoroscopic image showing the course of the mapping catheter inserted via the aorta into the LV and bent within the apex. Such a maneuver is usually necessary in order to map the anterior wall, especially in patients with a dilated LV. On the left of the figure, there is an RV pacing lead positioned in the apex.
•
•
•
1.3
Contact of the ablation catheter with the endocardium can be verified by the appearance of a small protrusion of the catheter tip icon above the surface of the electro-anatomical map. EP markers of adequate contact include recordings of sharp, highfrequency local electrograms, the appearance of an ‘injury’ current in unipolar recordings, and/or an increase in impedance. In some cases, catheter contact can be monitored by intracardiac echocardiography.
It is important to note the appearance of electrograms on conventional electrophysiology recording systems, since differences in filtering and amplifiers can lead to differences in the visual quality of signals received by the CARTO system.
Figure 19. In good contact, the catheter tip will protrude above the surface of the map reconstruction and the signals will usually be sharp and of high amplitude. In poor contact, the catheter will be projected only as a mesh and the signals will have far-field characteristics.
Good Contact
Poor Contact
CARTO map
1.3B Maintaining endocardial contact with the mapping catheter To obtain quality electrograms that can be analyzed both quantitatively and qualitatively, it is crucial that endocardial contact with the mapping catheter be maintained. This is particularly important in voltage mapping as inadequate contact can result in inaccurate or false maps.
Signals
The indices used for checking adequate electrode contact with the endocardium are as follows (Figure 19): •
The catheter position should be checked by fluoroscopy, especially synchronous movements with cardiac pulsation and the position within the cardiac contour. 17
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 18
1.4 ELECTRO-ANATOMICAL MAPPING OF THE HEART
1.4 Annotation of electro-anatomical maps 1.4A How to annotate electrograms Most investigators annotate signals at the earliest deflection of the near-field bipolar electrogram. Inspection of the corresponding unipolar electrogram can reveal whether a soft, far-field electrogram is present, especially in the early part of the signal, and, if so, caution must be exercised. Fractionated electrograms are usually annotated at the start of the signal. A visual, qualitative inspection with high gain and a check of the signal quality on a conventional electrophysiology system are useful. For low amplitude electrograms, long duration signals and entrainment pacing (ie, pacing at a cycle length of 30–50 ms shorter than that of the tachycardia) should assist in deciding where to annotate the electrogram (ie, pacing capture locates the part of the signal that corresponds to local activation closest to the catheter tip).
Figure 20. Schematic of signal distribution along the line of block. The double potentials beside the barrier are constituted by a sharp signal (black arrow) that represents the local activation and lowamplitude far-field potential that reflects activation of the opposite site of the block. At the gap within the line of block, a narrow-spaced double potential with a high-frequency signal in-between can be recorded.
Annotation of double potentials
Double potentials are signals with two components separated by an isoelectric line that reflects local activation block. In general, ‘sharper’ and higher amplitude components represent local activation, while ‘wider’ and lower amplitude components represent the far-field potential from the opposite side of the block. However, the amplitude of these components might not always assist with the annotation process, since it is based on the amount of myocardium activated (eg, activation within a narrow channel can result in recordings of a low amplitude, high frequency signal, followed by a higher amplitude, low frequency signal representing the surrounding endocardium). The component that coincides with the capture is annotated through entrainment pacing. All double potentials should be tagged during the mapping process so that the entire line of block can be analyzed. The components get closer to each other towards the end of the block and almost merge at the turning point (Figure 20). At this stage, individual mapping points can be reviewed and reannotated to either the first or second component, depending on the course of activation.
1.4B How to differentiate atrial from ventricular local electrograms Closer to the atriovenous annuli, recordings from the mapping catheter show both atrial and ventricular local electrograms. The ventricular electrograms can be mistaken for atrial local activation and thus corrupt the developing activation map. However, with the CARTO system, as ventricular components coincide with the QRS complex (Figure 21), only cycles without such components are selected. This reduces the possibility of creating a distorted and inaccurate activation map.
1.4C How to define myocardial scar To assess voltage maps and locate scar areas, the voltage range should be changed from automatic to a manual set-up with a pre-defined voltage range. The values for the upper and lower limits of this set-up differ for atria and ventricles and are not standardized. The most commonly selected ranges are from 0.5 to 1.5 mV for ventricles and from 0.3 to 1.0 mV for atria. In such cases, all voltage values <0.5 mV and/or <0.3 mV will be shown in red and are deemed to correspond to scar tissue. In order to fully understand the arrhythmia substrate, it is important to determine whether there are channels of slow conduction within the low voltage area where the signals are both fragmented and of low voltage 18
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 19
ELECTRO-ANATOMICAL MAPPING
Figure 21. Recordings from a mapping catheter (M1–M2) obtained during mapping of atrial arrhythmia. The large component in the mapping channel is ventricular (V), since it coincides with a QRS complex in the pre-cordial lead V5. The second high-frequency component represents local atrial activation (A). The LAT should therefore be annotated at the beginning of the second component (yellow dot).
1.4
(<0.1 mV). Therefore, pacing at a higher output is necessary irrespective of the selected cut-off value for scar tissue. All sites with no capture at 10–20 mA are then annotated as dense scars (in grey); this allows the delineation of slow-conducting channels in between the grey zones (Figures 22 and 23).
Figure 22. An activation map of the RA during pacing from a temporary screw-in lead positioned on the right atrial free wall (asterisk) in a patient after surgical correction of tetralogy of Fallot and paroxymal AT (right lateral view). The map shows a narrow channel of slow conduction located within two scar areas (grey). The first application within the channels interrupted conduction and prevented induction and recurrences of AT.
19
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 20
1.4 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Figure 23. (A) A voltage map of the LV after anteroseptal MI. Note that signals <0.5 mV cover a large area; however, two dense scars (grey) form a channel of slow conduction. Two VTs with similar cycle length and opposing axes were inducible in this patient. (B) Using pacemapping the exit sites (marked by *, #) for both arrhythmias were located at opposing poles of the scar area, while both shared a common central pathway. An ablation line across this central isthmus abolished both VTs.
A)
20
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 21
ELECTRO-ANATOMICAL MAPPING
1.4D How to evaluate a line of block In conventional EP mapping, a line of block is validated by recordings separated by an isoelectric line when pacing close to the ablation line. While the first component represents direct early local activation, the second component shows the wavefront originating from the opposite side of the block. To assess the block across the cavotricuspid isthmus in the RA, other methods such as differential pacing or validation of unipolar electrograms can be used.
1.4
The CARTO system records early activation points on one side of the line (ie, adjacent to the pacing site), followed by points from the opposite side of the line (Figure 24). Therefore, while one side of the line would be red, the opposite side would be purple. It is critical to pace close to the ablation line. To achieve stable positioning of the pacing catheter on the RA lateral wall, a temporary screw-in lead can be used.
Figure 24. Activation maps of the RA during pacing from (A) the lateral isthmus and (B) the septum (inferior view). Note: the latest activation (violet) is present in both cases on the opposite side of the ablation line, and is consistent with the presence of the bi-directional complete block.
A)
B)
21
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 22
1.5 ELECTRO-ANATOMICAL MAPPING OF THE HEART
1.5 Diagnosis of arrhythmias
Figure 26. (A–C) Propagation maps of the LV (anteroposterior view) during focal VT originating from the apex (red arrow).
1.5A Mechanism of arrhythmias The CARTO system records the spatial positioning of relevant EP information on the mapped cardiac chamber. This provides electrophysiologists with a precise tool to accurately diagnose the origin of focal and macro-reentrant arrhythmias.
A)
In focal arrhythmias (Figures 25 and 26), the earliest activation within the heart has to be mapped. This site is seen as a ‘hot spot’ region within the relevant chamber, with centrifugal endocardial activation. As the impulse originates from one focus and travels to the other mapped chambers (ie, either atria or ventricles) and finally extinguishes, it is worth noting that the LATs of acquired points in these chambers do not cover the entire cardiac cycle. The fact that the arrhythmia is focal in origin does not provide information regarding its etiopathogenesis. Focal arrhythmias can have different mechanisms:
B) Figure 25. An activation map showing focal atrial arrhythmia arising from the anterior LA wall near to the MA (left anterior oblique view). Although the tachycardia cycle length was 350 ms, only 78 ms (from –72 ms to +6 ms) is mapped, which suggests its focal origin.
C)
22
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 23
ELECTRO-ANATOMICAL MAPPING
• • •
triggered activity abnormal automaticity micro-reentry
Differential diagnosis is based on such factors as clinical presentation, response to different drugs, and programmed electrical stimulation.
1.5
Figure 28. (A–F) depict the propagation of activation during the same arrhythmia-encircling atriotomy as in Figure 27. The propagation map reveals another loop of reentry that runs via the cavotricuspid isthmus. Both loops share a common channel between the atriotomy scar (white line) and the IVC.
A)
D)
B)
E)
C)
F)
In macro-reentrant tachycardias (Figures 27 and 28), the impulse circulates around central obstacle(s). There is no site of earliest activation and the colors are dispersed around the central obstacle from the earliest to the latest activation. As a result, a wide range of LATs covering the entire cycle length of the arrhythmia can be recorded, while maintaining close spatial relationships between the earliest and latest activations. Figure 27. An activation map of the RA after surgical closure of an atrial septal defect with persistent AT (cycle length of 240 ms) (lateral view). The blue tags on the lateral wall correspond to the scar after atriotomy (white line), which creates a central barrier for the reentrant circuit. Note: activation times of acquired points (from –115 ms to +106 ms) cover almost the entire AT cycle length.
23
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 24
1.5 ELECTRO-ANATOMICAL MAPPING OF THE HEART
1.5B The importance of entrainment mapping during CARTO procedures Slow conduction zones in reentrant tachycardias often consist of relatively narrow channels of conduction within scar areas. Such zones can be identified using an activation map acquired during tachycardia. However, the exact definition of the circuit might be difficult to predict, especially during the mapping of complex atrial arrhythmias. Thus, entrainment mapping should always be done to check whether the specific region participates in the arrhythmia circuit or if it merely serves as a bystander in the process. Entrainment mapping (Figure 29) involves suprathreshold pacing from the tip of the mapping catheter at a cycle length 30–50 ms shorter than that of the tachycardia. Unipolar pacing is preferred, but in practice it is mostly bipolar
due to lower distortions in the recorded return electrograms. If the pacing site is within the circuit, pacing speeds up the circulation of the impulse (without changing the morphology of the P-waves or QRS complexes) and/or other intracardiac signals (ie, concealed fusion or concealed entrainment). In addition, the post-pacing interval (ie, the first return cycle after termination of pacing) should be identical in cycle length to that of the tachycardia. The interval between the stimulus artifact and the P-wave (or QRS complex) is also equal to the interval between local activation and the P-wave (or QRS complex) during tachycardia. Finally, entrainment pacing allows annotation of the exact timing of activation in low amplitude, long duration fractionated signals (ie, where the LAT corresponds with the timing of the pacing stimulus, leading to capture with minimum energy at that site).
Figure 29. Schematic of a model arrhythmia reentry circuit that consists of scar areas with channels of slow conduction. The identification of each part of the reentry circuit can be made using entrainment mapping (see text for details).
Schematic arrhythmia Reentry circuit
1. Entrance 2. Central zone 3. Exit
24
4. Bystander 5. Outer loops 6. Inner loops
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 25
ELECTRO-ANATOMICAL MAPPING
1.5
In AT, if a distinct P-wave is not visible, the sequence of atrial electrograms recorded by other catheters can be used as a guide to determine whether entrainment is with fusion (a change in P-wave morphology or atrial activation sequence indicates the fusion) or concealed (identical P wave morphology). With atrial macro-reentrant tachycardias (except typical atrial flutter), determining whether the arrhythmia originated from the LA or the RA may be difficult. In such a case, mapping typically begins in the RA. Activation times less than 50% of the tachycardia cycle length and a lengthy postpacing interval during entrainment pacing (>40 ms) indicate that the reentry circuit is located in the LA. An activation map of the RA usually shows passive activation from two separate sites: a) the ostium of the CS and b) a region of Bachmann’s bundle, with earliest activation on the lateral side (Figure 30). To prevent the termination of an arrhythmia during entrainment pacing and/or a change in morphology of the arrhythmia, regions with fractionated signals should be annotated first and entrainment pacing performed when the activation map is complete or nearly complete.
Figure 30. An activation map of the RA during tachycardia originating from the LA (anterior view). The earliest activation (red) is located within the ostium (os) of the CS. It then separates into two wavefronts around the TA and again merges on the RA free wall (violet).
1.5C New map or re-map? Generally, one map per cardiac chamber should be sufficient to depict the necessary anatomy. Special structures such as an enlarged CS and other vessels can be mapped separately. If an arrhythmia changes or breaks into sinus rhythm, the mapped chamber will inevitably change its volume. In practice, however, this is insignificant compared to the inaccuracies inherent in creating a new map. Therefore, when re-mapping, appropriate changes in the reference and WOI set-up should be taken into consideration, detailed information on the chamber anatomy should be provided, and all maps should be comparable.
SVC
His
TA
CS os IVC
25
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 26
1.6 ELECTRO-ANATOMICAL MAPPING OF THE HEART
1.6 Advanced mapping techniques 1.6A Qwikmapping
1.6B Image integration
A limitation of the CARTO system is that electro-anatomical maps are created point-by-point. This can be time-consuming and precludes the mapping of unstable or non-sustained arrhythmias. Qwikmapping was introduced to speed up the mapping procedure.
Advances in catheter ablation of AF have stimulated particular interest in the anatomy of the LA and PVs. The most valuable data have been obtained from modern imaging modalities such as CT and MR angiography [3,4]. The results suggest that the anatomy of the PVs is complex and varies considerably between patients. The most important fact discovered thus far, is that, in a large proportion of patients, left-sided PVs merge into the common vestibule or antrum. The shape of the antrum is oblong, with a much smaller anteroposterior than superoinferior diameter. In contrast, right-sided PVs are usually discrete and more circular in shape. Approximately 30% of patients possess supernumerary PVs: these occur most frequently on the right side, and typically have a diameter <1 cm.
The Qwikmap™ catheter (Biosense Webster, Inc., Diamond Bar, CA, USA) is a multipolar catheter with 6 quadripolar, orthogonally arranged electrode sets located on the shaft. This supplements the benefits derived from a standard catheter and enables the acquisition of near-field electrograms from a relatively large area. The catheter is also equipped with 2 magnetic-field sensors on the shaft, which enable the precise calculation of catheter location, orientation, and trajectory. Using these electrodes and sensors, the CARTO system can directly visualize the entire Qwikmap catheter shaft during the mapping procedure. It can locate not only the position of the tip of the catheter, but also the trajectory of the catheter shaft, which enhances the geometrical information available for the mapped chamber (Figure 31). By using 6–10 ‘regular’ tip points, the trajectory of the catheter shaft can delineate 60–100 additional points within the chamber, thereby increasing the geometrical accuracy of the derived map. The ability to visualize the entire catheter also reduces the need for fluoroscopy. In addition, the multi-electrode array embedded in the catheter shaft can obtain LATs from all electrodes at each time point. This simultaneous acquisition of electrical activation then facilitates the mapping of a nonsustained tachycardia or transient event. The complex construction of the catheter, however, requires a connector handle with 70 pins.
26
The electro-anatomical mapping system can be used to obtain a 3D anatomical map of the atrium, and to tag individual PVs by using either vessel tags or additional 3D maps. This delineates the anatomy of the proximal segments of each vein. However, the ability of the CARTO system to map ostia of the PVs and carina between the appendage and the left-sided veins remains limited. Hence, mapping and ablation of the PVs might require a combination of electro-anatomical maps with 3D images obtained by CT or MR angiography: a process known as image integration. The simplest form of image integration consists of the presentation of preacquired CT or MR images on a 3D electro-anatomical mapping system screen; and the synchronization of its movements with electro-anatomical maps (using CARTOSync™ software, Biosense Webster, Inc., Diamond Bar, CA, USA). This technique allows direct comparison of a virtual 3D electroanatomical map with real images (Figure 32). A similar technique is used to support catheter ablation of VTs, in which a LV electro-anatomical map is placed side-by-side with a pre-acquired CT or MR image.
R7631_ElMapHeart_03.qxd
6/3/06
16:10
Page 27
ELECTRO-ANATOMICAL MAPPING
1.6
Figure 31. Mapping the RA with the Qwikmap™ catheter. The catheter is bent along the top of the RA. (A–F) Acquisition of six points along the catheter shaft without moving the catheter. All points contain information on the LAT. Thus, a map of the entire atrium can be created with only a few positions of the catheter.
A)
B)
C)
D)
E)
F)
27
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 28
1.6 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Figure 32. Parallel visualization of a CT reconstruction (A) and an electro-anatomical map (B) using the CARTOSync™ software.
A)
The advanced level of image integration superimposes the acquired electroanatomical map with segmented CT/MR images using CARTOMerge software. To achieve this, the pre-acquired 3D CT/MR datasets must be correctly registered with the electro-anatomical system. The procedure, in phases, is as follows: Image processing 1) 3D volume rendering: reconstruction of CT/MR images of multiple 2D slices into 3D volume. 2) Segmentation: definition and separation of the 3D structure of interest (eg, individual heart chambers and associated structures such as the aorta and the pulmonary artery [PA]), based on user-selected markers or ‘seeds’. The seeds are then placed in different anatomical structures in the 3D reconstruction (Figure 33). The ‘region competing’ algorithm then attempts to competitively grow each seed within the surrounding volume, incorporating all voxels (volume units of CT/MR imaging) next to the seed location. 3) Shell creation (export process): conversion of 3D structures into ‘shell’ or ‘surface’ images to depict the internal surface and endoscopic images.
B)
Registration This refers to the process of merging the CT/MR image with the corresponding electro-anatomical map (Figure 34). At this stage, the electroanatomical map should, at least roughly, reproduce the actual volume of a given structure. 1) Landmark definition: a landmark pair is a set of two points (noted by small flags) that annotate the same fiducial structure (eg, lower or upper rim of the PV ostia, aortic cusps, or LV apex) on both the CT/MR surface images and the CARTO map. 2) Visual alignment: superimposition of the CARTO map on the CT/MR shell. The alignment can be done manually or by two available algorithms: a) Landmark registration: the software calculates the minimum average distance between all participating landmarks. In order to activate this feature, at least three landmark pairs must be applied. The accuracy increases when using intracardiac echocardiography since it allows the exact visualization of fiducial intracardiac structures.
28
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 29
ELECTRO-ANATOMICAL MAPPING
1.6
Figure 33. (A) A complete 3D reconstruction of the heart. (B) Individual cardiac chambers may be segmented (separated) from the model by placing selective markers (seeds) in the middle of each chamber. (C) Subsequently, any of the segmented portions (eg, the aorta, LV, and LA) can be toggled and registered for mapping using the CARTOMerge™ software.
A)
B)
C)
Figure 34. The registration of a segmented CT reconstruction and an electro-anatomical map using the CARTOMerge™ software. (A) A grossly mapped LA with a high density of points on the posterior wall. To enable registration, four ‘landmark’ points were annotated on the PV ostia (white arrows). (B) Corresponding points were tagged on the CT-segmented reconstruction. (C) A superimposed CT reconstruction and electro-anatomical map. (D) Final layout of the ablation points on the CT image. For better visualization of the ablation points, the fill threshold of the electro-anatomical map was decreased to zero.
A)
B)
D)
C)
LS
LS
RS
RS
LS RS
RI RI
LI
LS
LI
RS RI
RI LI
LI
29
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 30
1.6 ELECTRO-ANATOMICAL MAPPING OF THE HEART
b) Surface registration: the software uses an algorithm that calculates the smallest average distance between the shells created from CARTO map points and the corresponding 3D shells reconstructed from the CT images. This process registers the images based on all acquired points. A 3D CT or MR anatomical map can be used for subsequent navigation of the catheter tip. Visualization of the CARTO map can be totally suppressed. Virtual endoscopy images can also be used to assess the position of the catheter tip and specific anatomical structures such as the PV ostia (see Chapter 3.4 on ‘Atrial fibrillation’). New image integration techniques are currently under development that will allow quality anatomical images to be obtained during the mapping procedure.
30
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 31
NORMAL AND ABNORMAL CONDUCTION OF THE HEART 2.1 Virtual model of the heart 2.2 Normal electrical activation of the atria and ventricles 2.3 Activation patterns in ventricluar conduction disturbances 2.4 Activation patterns during different pacing modes
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 32
Knowledge of cardiac anatomy and normal cardiac activation is essential for appropriate diagnosis and treatment of arrhythmias. This chapter demonstrates how both normal and abnormal activation patterns of the atria and ventricles can be visualized by an electro-anatomical system.
2.1 Virtual model of the heart Electro-anatomical mapping enables the reproduction of a virtual 3D image of the anatomy of individual cardiac chambers, as well as the recording of relevant local electrograms. To reproduce the anatomy of a given chamber, it is helpful to be familiar with its characteristic shape and topography. In this respect, the most instructive images for electrophysiologists can be obtained from 3D reconstruction of multi-slice CT angiography and/or MR angiography. Based on a multi-slice CT scan of a healthy individual, we have created a ‘virtual model of the heart’ composed of thin, 3D slices displayed in three perpendicular views (cranial, left, and right anterior oblique). Browsing through these cardiac slices affords a comprehensive exploration of cardiac topography (Figure 35). The virtual model can be viewed on the CD accompanying this book.
2.2 Normal electrical activation of the atria and ventricles Atrial activation originates from the area of the sinus node that is localized in the high RA (sulcus terminalis). This area is roughly between the base of the right appendage and the SVC. Activation then spreads in two wavefronts, along the crista terminalis and along the interatrial septum, towards the atrioventricular (AV) nodal area. The LA is activated mainly from Bachmann’s bundle (ie, from the upper anterior septum), and to a lesser extent by posterior fibers (posteromedial tracts) [5]. From the septum, the activation spreads towards the lower lateral side of the LA, where it finally extinguishes (Figure 36). The normal ventricular activation sequence starts when the electric impulse travels from the AV node to the bundle of His. The bundle then divides into the right and left bundles of Tawara with subsequent branching into separated fascicles that finally terminate in the larger network of subendocardially positioned Purkinje cells. Impairment at any level of this system (AV node, His bundle, fascicles or distal network of Purkinje cells) can lead to specific changes in the activation sequence and prolongs the QRS duration. Activation of both ventricles under normal circumstances is rapid and essentially synchronous, with LV activation slightly preceding RV activation
32
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 33
NORMAL AND ABNORMAL CONDUCTION THE HEART
2.2
Figure 35. CT scans of the heart in three perpendicular views: (A) cranial; (B) left anterior oblique; and (C) right anterior oblique..
A)
B)
C)
Figure 36. Isochronal maps of the atria in (A) left anterior oblique and (B) posteroanterior views. Note the early activation of the LA anterior wall by Bachmann’s bundle.
A)
B)
33
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 34
2.2 ELECTRO-ANATOMICAL MAPPING OF THE HEART
by about 10 ms (Figure 37). In addition, an electrical impulse is conducted from the endocardium to the epicardium [6]. Within the LV, activation starts from three separate sites that correspond to where the fascicles terminate:
Activation then spreads radially, so that the apex and LV lateral wall are activated within the terminal portion of the QRS complex [7]. The total LV endocardial activation time accounts for about 50 ms.
• • •
In the RV, activation spreads from the interventricular septum (IVS) and anterior wall (ie, the site of insertion of the moderator band). Activation of the IVS occurs mainly from the left bundle, resulting in negative deflection of the initial portions of the QRS complex in limb leads I and aVL (septal Q-wave). The latest activation occurs within the RVOT and laterally near the TA.
the lower portion of the septum the midseptum the anterior wall near the base of the papillary muscle
Figure 37. (A) Isochronal and (B–E) propagation maps of both ventricles (left anterior oblique view). In patients without conduction disturbances, activation of both ventricles is rapid and synchronous. LV activation precedes RV activation by 10 ms. Pink tags depict sites with fascicular potentials and a black line has been added to schematically illustrate the course and terminations of bundles under the endocardium.
A)
34
B)
D)
C)
E)
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 35
NORMAL AND ABNORMAL CONDUCTION THE HEART
2.3 Activation patterns in ventricular conduction disturbances
2.3
Figure 38. Activation maps of both ventricles (left anterior oblique view) with a corresponding 12-lead ECG, showing typical LBBB. The depolarization of the ventricles starts on the right ventricular free wall at the termination of the RB; the latest activation occurs on the LV lateral wall (black arrow).
In addition to the clinical benefit derived from the interventional treatment of arrhythmias, the CARTO™ system provides a precise description of activation patterns during conduction abnormalities and ventricular pacing. Such mapping studies are as important as a standard ECG in identifying complex conduction disturbances in patients with congestive heart failure who are potential candidates for cardiac resynchronization therapy (CRT). To date, several publications have focused on the electrical activation sequence in patients with heart failure and conduction abnormalities using the CARTO system [8–10]. These studies provide detailed descriptions of the spectrum of conduction disturbances and factors that can affect the electrical activation pattern. Although the electro-anatomical mapping system cannot be used in clinical practice on a routine basis, it offers an instructive background for understanding the principles and mechanisms that underlie CRT.
2.3A Left bundle branch block and left ventricular conduction abnormalities Uncomplicated left bundle branch block (LBBB) is often used as an illustration of a ‘model’ conduction abnormality. LBBB results in considerable mechanical desynchronization between the IVS and the left lateral wall (Figure 38). Activation in LBBB begins on the right lateral free wall and the septum, and spreads slowly towards the LV via the IVS. LV activation then begins in the midseptum and is delayed by 64±12 ms. Both the velocity and the character of subsequent LV conduction depend on the nature of the underlying myocardial pathology. However, several conditions can result in ECG morphology that resembles LBBB, despite different activation patterns (Figures 39 and 40). In such cases, electroanatomical mapping can be used for exact characterization of the conduction defect and identification of the last activated region.
Figure 39. Activation maps of both ventricles (left anterior oblique view) with a corresponding 12-lead ECG in a patient with LV conduction delay and a leftward shift of the electrical axis. In contrast to complete LBBB, the LV is activated with a delay via the left posterior bundle (LPB). In addition, QRS widening is caused by slow propagation throughout the LV.
2.3B Left anterior hemiblock accompanied by right bundle branch block The presence of right bundle branch block (RBBB) on a baseline ECG is often associated with a higher probability of CRT failure [11]. However, selected patients with RBBB can benefit from CRT, especially when their RBBB is accompanied by LV conduction disturbances (eg, hemiblocks) [12]. In bifascicular block, the activation spreads from the termination of the left 35
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 36
2.3 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Figure 40. Activation and voltage maps in an anterior aneurysm. (A,C) Left anterior oblique and (B,D) left lateral views. In contrast to complete LBBB, the conduction delay is confined within the LV. Note: activation of each chamber begins nearly simultaneously, and the scar on the anterior wall (grey) represents a barrier for impulse propagation, which encircles the LV. The latest activation (violet on activation maps, black arrows) is present on the lateral side of the scar.
36
A)
C)
B)
D)
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 37
NORMAL AND ABNORMAL CONDUCTION THE HEART
posterior fascicle, and is then conducted throughout the LV, and then via the IVS towards the RV (Figure 41). Note that the last activated region might be located in either the LV or RV, depending on the degree of dilatation or impairment. In such cases, electroanatomical mapping can be employed to characterize the resulting activation pattern.
2.4
2.4 Activation patterns during different pacing modes In light of recent knowledge on the deleterious effects of RV apical pacing, alternative pacing sites have been studied [13,14]. Although electrical activation itself may not necessarily correspond with mechanical activation, such studies help us to understand abnormal activation patterns in different pacing modes.
2.4A Right ventricular apical pacing Electro-anatomical activation maps in this pacing mode demonstrate prolonged ventricular activation that is the reverse of normal activation: it spreads from the RV apex to the LV apex, and then towards the base of the heart (Figure 42).
Figure 42. (A–D) A propagation map (left anterior oblique view rotated cranially) of both ventricles during RV apical pacing (position of RV lead is indicated by black arrow). Note: late activation is present basally on the lateral LV wall.
Figure 41. An activation map during bifascicular block (left anterior oblique view) with a corresponding 12-lead ECG. Note: the latest activation (violet on activation map, black arrow) is present in both the RV and LV. Thus, a significant activation delay is also present within the LV.
A)
C)
B)
D)
37
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 38
2.4 ELECTRO-ANATOMICAL MAPPING OF THE HEART
2.4B Biventricular pacing The main principle of biventricular pacing is the creation of an electrical ‘bypass’ to the site of last activation (usually the lateral wall) (Figure 43). The LV is then activated from the two separate activation wavefronts, which subsequently fuse. However, the resulting activation pattern is highly dependent on the lead positioning. In cases where the RV lead is located in the apical position and the LV lead is in the left lateral free wall region, both wavefronts spread from these opposite sites and merge in the middle of the LV. This activation pattern can be modified by different positions of both the RV and LV leads. A midseptal location of the RV lead results in a more basal shift of the septal wavefront and earlier merging of both wavefronts in the central part of the LV. Activation then spreads towards the LV apex. In contrast, a more apical position of the LV lead provides a wavefront that spreads from the LV apex back to its base. The pattern of merging with activation from the RV lead is again dependent on its position.
Figure 43. (A–D) A propagation map of both ventricles during biventricular pacing (left anterior oblique view), with close positioning of the ventricular pacing leads (position is indicated by black arrows – the RV lead is placed in the apex and the LV lead distally in the anterior interventricular vein). (E–H) Propagation maps with a distant location of both leads (position is indicated by black arrows – the RV on the mid-septum and the LV laterally). See text.
A)
E)
B)
F)
C)
G)
D)
H)
2.4C Right ventricular bifocal pacing RV bifocal pacing has been suggested as an alternative to biventricular pacing [15]. With RV bifocal pacing, a lead is positioned in the RV apex and outflow tract (Figure 44). Since both leads are located on the right side of the IVS, the resulting activation pattern resembles LBBB with slow trans-septal, right-to-left activation. The last activated region is typically in the middle of the LV free wall.
2.4D Single-site left ventricular pacing Early studies on the hemodynamic effects of different pacing modes revealed that single-site LV pacing is more beneficial than biventricular pacing [16,17]. Single-site LV pacing produces an activation sequence that is highly dependent on the degree of fusion, with spontaneous conduction via the conduction system. If there is fusion, a pattern of two opposing wavefronts as in biventricular pacing can be observed. If there is no fusion, LV activation originates only from the LV pacing site and spreads to the rest of the LV, and finally to the RV. Hence, the resulting ventricular activation pattern with delayed conduction via IVS resembles that of ‘minor’ LBBB (Figure 45).
38
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 39
NORMAL AND ABNORMAL CONDUCTION THE HEART
Figure 44. A propagation map of both ventricles during (A–D) LBBB and (E–H) after implantation of RV bifocal pacing (left anterior oblique view). The location of RV electrodes positioned within the RV apex and right ventricular outflow tract is indicated by black arrows. Note: activation of the LV is in a right-to-left direction and resembles LBBB.
2.4
Figure 45. A propagation map of the ventricular activation sequence during single-site LV pacing in (A–D) a patient with complete AV block and (E–H) a patient with a normal PR interval leading to the phenomenon of fusion. In (A–D), activation propagates in a left-to-right direction, creating a ‘reversed LBBB’ pattern. In (E–H), spontaneous activation via the fascicular system causes early septal activation and the LV is activated from two opposing wavefronts, as seen during biventricular pacing.
A)
E)
A)
E)
B)
F)
B)
F)
C)
G)
C)
G)
D)
H)
D)
H)
39
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 40
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 41
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS 3.1 Focal atrial tachycardias 3.2 Typical atrial flutter 3.3 Atypical atrial flutter 3.4 Atrial fibrillation 3.5 Atrioventricular nodal reentry 3.6 Inappropriate sinus tachycardia 3.7 Accessory pathways 3.8 Idiopathic focal ventricular tachycardia 3.9 Idiopathic reentrant ventricular tachycardia (fascicular) 3.10 Post-myocardial infarction ventricular tachycardia 3.11 Ventricular tachycardias in dilated cardiomyopathy 3.12 Ventricular tachycardias in right ventricular arrhythmogenic cardiomyopathy 3.13 Post-incisional ventricular tachycardias 3.14 Catheter ablation of ventricular fibrillation
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 42
The CARTO™ electro-anatomical mapping system can be used to guide catheter ablation in most cardiac arrhythmias. In unselected arrhythmias, however, it does not result in a significantly different duration and/or outcome. As a result, conventional procedures are preferred [18]. The mapping system, however, significantly reduces fluoroscopy time and radiation dose; once the 3D anatomy is mapped, it navigates the catheter tip within a given cardiac chamber to accurately locate the source of the arrhythmia. The main use of the electro-anatomical mapping
42
system is, therefore, to support catheter ablation in complex cardiac arrhythmias. This section provides a systematic description of the most important indications for using the CARTO system. For each arrhythmia, a brief review of the published data is provided, together with a recommended strategy for mapping and ablation. Note that more cases, including propagation maps, can be found on the accompanying CD-ROM entitled ‘Electro-anatomical Mapping of the Heart’.
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 43
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.1
3.1 Focal atrial tachycardias Focal AT is a relatively rare type of supraventricular arrhythmia: the primary mechanism is abnormal automaticity or triggered activity [19,20]. As a result, ectopic tachycardias tend not to respond to programmed atrial stimulation, exhibit a ‘warm-up’ phenomenon (eg, the arrhythmia rate accelerates following onset), and are not terminated by vagal maneuvers or drugs that affect the AV node. The only exception is an arrhythmia of micro-reentrant origin, where programmed atrial stimulation is effective in inducing or terminating the arrhythmia. Focal AT is characterized by atrial activation that begins in a small region (or focus) and spreads centrifugally. Ectopic activity usually originates from typical anatomical locations such as the crista terminalis and/or the PVs (Figure 46). Other locations of foci include the posterior LA wall, SVC, ligament of Marshall, ostium of the CS, and/or the interatrial septum [21]. The cycle length of focal AT is typically ≥250 ms and varies depending on autonomic tone. Sympathetic activation generally accelerates the rate of focal discharge.
Figure 46. An electrogram showing a short burst of atrial ectopy. In the first sinus beat, the activation occurs from proximal to distal CS (black arrow). During the following ectopic beats, the activation sequence reverses (black arrows) being the earliest within the mapping catheter positioned in the left upper PV. The source of ectopy was located deep within the vein.
While catheter ablation of focal AT using conventional fluoroscopic mapping techniques has demonstrated only limited success (due to an inability to identify the arrhythmogenic focus), electro-anatomical mapping is able to precisely locate the arrhythmogenic focus, and hence, provides more accurate results (Figure 47) [22]. Electro-anatomical mapping also allows for easier catheter navigation in the atrium and re-navigation to the target position for RF ablation [23]. Not only is there a high success rate when ablation of atrial foci is guided by electro-anatomical mapping, but the procedure can be performed using only one or two applications of RF energy [24–27].
43
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 44
3.1 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Tips and tricks for mapping and ablation of focal ATs
•
Unipolar recordings can confirm that the tip of the ablation catheter is on target (the absence of R-waves suggests that there is no intervening myocardium between the catheter and the focus).
•
If the earliest activity is found on the upper RA septum, the ectopy might originate from right-sided PVs and a trans-septal puncture might be required for LA access.
The beginning of the WOI should be set 60–100 ms before the onset of the P-wave on the surface ECG.
•
The earliest activity in a successful ablation site usually precedes P-wave onset by 40 ms (range 20–100 ms).
Low density activation map is quickly able to identify the early activation area; higher density mapping is required to more precisely locate the focus (eg, the ‘hot and cold approach’).
•
RF energy application at the earliest activation point is usually associated with an acceleration of tachycardia.
•
After ablation, remapping of the atria may be used to verify a shift in the earliest activation site towards the sinus node.
•
Mapping of the RA is usually performed first, unless P-wave morphology and intracardiac signals clearly indicate that the arrhythmia is of LA origin.
•
An intracardiac reference should be selected for triggering (eg, CS catheter).
•
•
Figure 47. (A) An activation map of the LA (anteroposterior view), with an ectopic focus firing from the left upper PV. (B) The change in activation after elimination of ectopy. Note: the earliest activation is in the interatrial septum region.
A)
44
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 45
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.2
3.2 Typical atrial flutter Generally the term macro-reentrant AT refers to all reentrant tachycardias with a large central obstacle, irrespective of ECG pattern [28]. The central obstacle can be fixed, functional, or a combination of both. As the impulse circulates, there is no single point of origin of activation and atrial tissues are activated from various parts of the circuit. As a result, endocardial atrial activation can be recorded continuously throughout the cycle – hence, the concept of early activation does not apply here. The participation of different sites in the reentrant circuit can be confirmed through entrainment pacing.
3.2A Typical atrial flutter The most common type of macro-reentrant AT is typical atrial flutter, which has a cycle length of 190–250 ms and minimum variation [28]. During flutter, activation of the RA enables the impulse to travel around the TA. In a typical ‘counterclockwise’ variant, the impulse activates the septum in a caudocranial direction, and travels along the crista terminalis towards the cavotricuspid isthmus. The latter is localized between the TA and IVC, and is a critical component in the macro-reentrant circuit (Figures 48 and 49).
Figure 48. An ECG recording during typical counterclockwise atrial flutter. Note: the saw-tooth pattern in the inferior leads.
Concealed entrainment can be produced by pacing within the isthmus. However, it was electro-anatomical mapping that confirmed previous mapping observations that the entire RA is activated during atrial flutter. This activation results in the characteristic (saw-toothed) flutter waves in leads II, III, and aVF of the ECG. These consist of a down-sloping plateau followed by a sharp negative then positive deflection, leading to the next down-sloping segment.
45
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 46
3.2 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Figure 49. (A–F) A propagation map of both atria during typical counterclockwise atrial flutter (left anterior oblique view). Note: activation circulates around the TA in a counterclockwise direction. The creation of a line of block across the isthmus terminated the arrhythmia.
46
A)
B)
C)
D)
E)
F)
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 47
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.2
3.2B Reverse typical flutter In reverse typical flutter, the direction of activation is reversed (ie, ascending over the anterior wall and descending on the posterior and septal walls). It occurs in approximately 10% of cases (Figures 50 and 51). Anatomical and functional barriers are similar to those of typical atrial flutter. The ECG pattern consists of broad, positive deflections in the inferior leads, and wide, negative deflections in V1. Catheter ablation of atrial flutter is now a standard procedure with a very high success rate, minimum recurrences, and a low complication rate. Despite many modifications to the technique, the end point remains the creation of a bi-directional conduction block across the cavotricuspid isthmus. In routine clinical practice, electro-anatomical mapping is rarely used for this indication, due to the high success rate of conventional methods. However, electro-anatomical mapping can reduce X-ray exposure and facilitate the creation of a linear lesion across the cavotricuspid isthmus [29,30].
Figure 50. An ECG recording during reverse (clockwise) typical atrial flutter.
Furthermore, the electro-anatomical mapping system has significant potential for the catheter ablation of typical atrial flutter in specific patient populations. Firstly, the system provides precise anatomical localization of the catheter tip affording precise ablation in patients with significant distortion to the RA anatomy (eg, after heart transplant). Secondly, it can assist with ablation of the cavotricuspid isthmus for post-incisional arrhythmias (eg, after surgery for congenital heart disease) (see Chapter 3.3B).
Tips and tricks for mapping and ablation of typical atrial flutter Three strategies are generally employed for catheter ablation of atrial flutter: 1. Mapping the entire RA. 2. Selective mapping of the isthmus by disarming the 3D imaging capability (ie, surface reconstruction). 3. A simplified approach with three points at the TA and three corresponding points on the Eustachian ridge (where the ablation line interconnects with the mid-points of each of the three points, on both sides of the isthmus).
47
R7631_ElMapHeart_03.qxd
6/3/06
16:11
Page 48
3.2 ELECTRO-ANATOMICAL MAPPING OF THE HEART
•
An intracardiac reference should be selected for triggering (eg, CS catheter).
•
Ablation can be performed during atrial flutter and/or during atrial or CS pacing.
•
A point-by-point lesion delivery is preferred when deploying the RF current (consisting of 30- to 60-second applications at each point on the ablation line).
•
Remapping both sides of the ablation line during pacing, from either the low RA and/or the proximal CS, clearly indicates a complete block on the isthmus.
•
When impulses travel through the crista terminalis, circumferential mapping around the caval vein shows conduction posteriorly around the IVC.
Figure 51. (A–F) A propagation map of the RA during reverse (clockwise) typical atrial flutter (left anterior oblique view). The activation circulates around the TA in a clockwise direction.
48
A)
B)
C)
D)
E)
F)
R7631_ElMapHeart_03.qxd
6/3/06
16:12
Page 49
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.3 Atypical atrial flutter Other forms of macro-reentrant ATs or ‘atypical flutter’ include a wide range of variable arrhythmias that differ from typical and reverse typical atrial flutter. If the arrhythmia is stable enough to allow for mapping and entrainment studies, a description of the mechanism is often preferred to the term ‘atypical’ [31].
3.3A Non-surgical right atrial macro-reentrant tachycardias Tachycardias due to macro-reentrant circuits in the RA that do not involve the cavotricuspid isthmus are rare in patients without surgical scars. The main obstacles include low voltage areas (indicating myocardial scarring or infiltration) and/or lines of double potentials (indicating functional block) (Figure 52). The term ‘upper loop reentry’ refers to circuits involving the
3.3
SVC, while ‘lower loop reentry’ refers to circulation of the impulse around the IVC using the cavotricuspid isthmus. There are areas of slow conduction either between low-voltage areas or between low-voltage areas and anatomical barriers such as the TA. Electrograms are broad and fragmented in these areas and concealed entrainment can confirm their participation in the circuit. Due to variable and highly individual anatomical substrates, little is known about the long-term prognosis of catheter ablation. Ablation of the cavotricuspid isthmus is indicated in all cases, since a large barrier resulting from ablation of the substrate in the lateral part of the atrium may favor reentry around the TA, ie, typical atrial flutter.
Figure 52. (A) An activation map and (B) a voltage map of the RA during AT with a cycle length of 240 ms (right anterior oblique view). Although the patient’s medical history was negative for any heart disease, large low-voltage (red) and scar areas (grey) of unknown origin were found within the atrium. The AT circuit was confined to the scar area on the lateral wall. Two applications of slow conduction within the isthmus successfully interrupted the AT. Additionally, ablation of the cavotricuspid isthmus was performed to abolish all possible reentrant circuits within the RA. The parallel white lines show a line of block extending from the scar area.
A)
B)
49
R7631_ElMapHeart_03.qxd
6/3/06
16:12
Page 50
3.3 ELECTRO-ANATOMICAL MAPPING OF THE HEART
3.3B Post-incisional right atrial tachycardias Macro-reentrant tachycardias associated with surgical scars are a common problem for patients who have previously had surgery for congenital or valvular heart disease. The reentrant circuits are typically located on the lateral RA wall (ie, the site of atriotomy and scar after cannulation of the IVC) [32–37]. The scar is often marked by a line of double potentials, and activation moves in the opposite direction on to the sides of the obstacle (Figure 53).
The critical isthmus of the reentry is often located between the inferior end of the double potential line and the IVC, or between the two scar areas. At this site, fragmented, low-amplitude potentials are recorded. The pressure of the catheter tip can terminate the arrhythmia and thus entrainment mapping may not be possible. Catheter ablation at such a site is most likely to create a complete line of block and abolish the reentry circuit. Care should be taken to avoid damage to the right phrenic nerve; pacing from the ablation catheter at high output should be used before the RF current is applied to the
Figure 53. An activation map of the RA after correction of tetralogy of Fallot with right atriotomy. Two reentrant circuits and loops are present (A) around the atriotomy and (B) around the TA via the cavotricuspid isthmus. Ablation of the common isthmus between the atriotomy and the IVC, or, alternatively, ablation of the cavotricuspid isthmus together with ablation from the atriotomy scar towards the TA, are required to terminate both loops.
A)
50
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:12
Page 51
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.3
RA free wall. Furthermore, ablation in the upper part of the RA can cause damage to the sinus node, and heart rate should be observed during application as acceleration of sinus rhythm may indicate proximity to the sinus node. In all cases, cavotricuspid isthmus ablation should be performed, as typical flutter can occur. The atriotomy on the right atrial lateral wall creates a posterior barrier for impulse propagation, which favors reentry around the TA, ie, atrial flutter.
3.3C Left atrial macro-reentrant tachycardias Unless a pathological process creates large obstacles and areas of slow conduction, the anatomy of the LA, unlike that of the RA, provides less favorable conditions for macro-reentrant tachycardias. Studies using electroanatomical mapping have identified electrically silent areas of myocardium in the circuit center [38,39]. These low-voltage areas usually have to be located in proximity to anatomical structures such as the PV ostia to form larger central obstacles to sustain a reentry circuit (Figure 54). Barriers can also be extended by lines of functional block. As a result, LA reentrant tachycardias present with a spectrum of reentry patterns, depending on the size, number, and location of the electrically silent areas and barriers. Complex reentry paths can show double or triple loop appearances. In addition, the musculature around the CS can be a part of the circuit.
Figure 54. LA flutter in a patient with mitral valve disease and LA scars (posterior oblique view of both atria). The activation map reveals the presence of large scar areas in the LA and an isthmus of slow conduction between them, with annotation of the ablation site. Two applications within the isthmus terminated the tachycardia.
The resulting ECG pattern varies, and can even resemble focal AT with discrete P-waves and an isoelectric baseline. RA mapping shows simultaneous activation of the superior and inferior septal RA. Activation sequence within the CS can vary, based on the location of the circuit. Mapping of the LA should cover the entire cycle length of the tachycardia, and entrainment mapping will confirm participation of different portions of the LA within the circuit. In order to define the critical isthmuses for subsequent catheter ablation, it is crucial to integrate activation mapping data with virtual 3D anatomy provided by the electro-anatomical mapping system. Deployment of RF lesions across the isthmus or between anatomical obstacles and low-voltage areas leads to interruption of the arrhythmia. The electro-anatomical mapping system can then be used to validate the completeness of the lines of block.
3.3D Left septal atrial flutter Marrouche et al. described a specific form of atypical flutter from the left side of the interatrial septum [40]. Using electro-anatomical mapping, a reentrant circuit was identified revolving around the LA septum primum, with a critical isthmus between the PVs and/or the MA and the septum primum. The ECG 51
R7631_ElMapHeart_03.qxd
6/3/06
16:12
Page 52
3.3 ELECTRO-ANATOMICAL MAPPING OF THE HEART
morphology varies based on the direction in which the impulse travels around the central obstacle (ie, clockwise or counterclockwise). The activation map of the LA should cover the whole cycle length of the tachycardia. Entrainment mapping can be used to confirm whether the circuit circles around the fossa ovalis. The ablation strategy in these patients consists of the creation of linear lesions between the fossa ovalis and the right-sided PVs and/or the MA.
3.3E Post-ablation left atrial tachycardias Figure 55. An activation map of both atria in a patient with Mustard’s correction (anteroposterior view). The LA with systemic venous blood was accessed via the IVC. The RA (PV atrium) was mapped retrogradely via the aorta and systemic RV. Despite limited mapping, the activation pattern indicates a macro-reentrant circuit proceeding counterclockwise around the TA: atrial flutter. The cavotricuspid isthmus was divided by an intra-atrial patch into proximal (venous) and distal (arterial) parts, and ablation lesions had to be deployed on both sides to create a continuous line of block.
The widespread use of both surgical and catheter-based techniques for atrial fibrillation ablation has resulted in a growing number of cases of macroreentrant tachycardias related to gaps in the ablation lines. As with other post-incisional tachycardias, previous ablation lines may, together with anatomical structures, form barriers of variable size and shape. The location of conduction gaps or channels varies and depends on the ablation strategy used. In our experience, these critical isthmuses most frequently occur either around the MA and/or between the right and left-sided PVs. Similar to other atypical flutters, entrainment mapping plays an important role in identification of the circuit.
3.3F Macro-reentrant tachycardias after correction of complex congenital heart disease A history of complex atrial surgery, such as Mustard, Senning, or Fontan procedures, predisposes a patient to various ATs. The mechanism of tachycardia is primarily dependent on the extent of surgery, fibrosis, and myocardial hypertrophy. Typically, reentrant arrhythmias circulate around central obstacles, which are highly variable: double loops are common. Mapping and ablation are particularly challenging in patients who have undergone a baffle procedure. In addition to the complexity of the substrate, the need for bi-atrial access and, often, hemodynamic compromise during tachycardia make mapping extremely challenging. Ablation should be guided by entrainment mapping. The electro-anatomical mapping system provides an excellent tool for delineating both the anatomy and the course of activation (Figure 55). Often, a typical flutter circuit is involved. In these patients, however, the cavotricuspid isthmus consists of two parts, each located in a different atrium and separated by a baffle. The PV atrium can be accessed either retrogradely via the aorta and RV, and/or antegradely via the puncture of the baffle. Catheter ablation of the cavotricuspid isthmus is then performed from the tricuspid valve to the baffle in the PV atrium, and from the baffle to the IVC in the systemic venous atrium. 52
R7631_ElMapHeart_03.qxd
6/3/06
16:12
Page 53
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
Tips and tricks for catheter ablation of atypical flutter
3.4 Atrial fibrillation
•
It is possible to determine whether the circuit is localized in the RA or LA by activation mapping of the CS and RA. Mapping of the RA is usually performed first, unless P-wave morphology and intracardiac signals clearly indicate an LA origin.
Catheter ablation of atrial fibrillation (AF) is a viable therapeutic alternative for symptomatic patients who are resistant to anti-arrhythmic drugs. Since its introduction a decade ago, several techniques have evolved. These reflect the principal mechanisms of AF.
•
An intracardiac reference should be selected for triggering (eg, CS catheter).
3.4A Segmental pulmonary vein isolation
•
Due to the unpredictable nature of the circuits, it is difficult to guide the setting of the WOI prior to mapping.
•
If the tachycardia is of LA origin (assuming passive activation of the RA and triggering on the catheter in the CS), the beginning of the WOI should be set to occur after the reference signal.
•
If the reentrant circuit is unclear and multiple lines of block and/or scar are present within the atria, cardioversion and remapping should be performed during sinus rhythm, or pacing should be employed.
•
If the tachycardia cycle changes, remapping should be strongly considered.
•
Tag all sites with double potentials and fractionated signals, as these might be related to a critical part of the circuit.
•
Use pacing techniques such as entrainment only after the map is completed. This helps to avoid tachycardia interruption or a transformation of the tachycardia into a different morphology. In such a case, a new map has to be started.
•
In case of multiple loops within the RA, first ablate the cavotricuspid isthmus (in case of multiple reentrant loops) to facilitate mapping.
•
For surgically corrected congenital heart disease, compare the acquired voltage map with a protocol describing the surgical procedure in order to allocate the number and location of scar areas.
•
3.4
In early catheter ablation attempts to reproduce a scheme of linear lesions analogous to the Maze procedure, Haissaguerre et al. described three patient cases of focal mechanisms of AF [41]. Foci of spontaneous electrical activity that triggered AF were noted predominantly within the PVs, and these became the target for ablative attempts [42]. Subsequent anatomical studies confirmed previous observations on the presence of atrial muscular sleeves around the ostia of the PVs [43,44], and a more recent publication revealed the presence of node-like cells in these muscular extensions [45]. Haissaguerre et al. pioneered the concept of selective electrical isolation of arrhythmogenic or all PVs [46]. This concept was based on the variable arrangement of muscular fibers around the ostia, with some preferential routes of conduction from the vein and vice versa. Using a purpose-constructed, circular mapping catheter (Lasso™, Biosense Webster, Inc., Diamond Bar, CA, USA), they were able to map the sites of conduction and destroy them selectively, instead of burning the entire circumference of the PV ostia (Figure 56). The success rate of this procedure is between 60 and 80%, with the best results in patients with paroxysmal AF but without structural heart disease. There are, however, several limitations to this approach. Firstly, the technique appears to be most effective in patients with clear evidence of focus-triggered AF (ie, those with multiple runs of selfterminating AF, initiated by frequent premature ectopic beats) and less well in patients with persistent or permanent AF. This is perhaps because AF in the latter group is more dependent on a myocardial substrate and hence PV isolation alone might not be enough. The second limitation is that there is a 1–3% risk of PV stenosis, which can be clinically significant and for which the optimal treatment is yet unknown [47].
Verify the completeness of ablation lines during pacing from sites adjacent to the line (in order to force the conduction of the impulse towards the line, or, in case of a gap, through the line).
53
R7631_ElMapHeart_03.qxd
6/3/06
16:12
Page 54
3.4 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Finally, the long-term success of the technique is impaired by frequent recovery of conduction and many subjects require repeat procedures [48]. This might reflect the use of the lowest possible RF energy delivery in the proximal segments of the PVs in an attempt to eliminate the risk of PV stenosis. Further development of this treatment strategy and additional ablation lines have been proposed, especially in subjects with persistent AF and/or associated congestive heart failure [49].
Figure 56. (A) A fluoroscopic image of the LASSO™ catheter positioned within the PV. (B) Stepwise abolition of the PV potentials and complete isolation of the vein during pacing from the distal CS.
A)
54
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:12
Page 55
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.4B Circumferential ablation around pulmonary vein ostia Pappone et al. developed a different strategy for the treatment of AF [50,51]. Using the CARTO electro-anatomical mapping system, they circumferentially deployed RF lesions around the PV ostia (Figure 57). The endpoint for ablation was signal amplitude abatement to ≤0.1 mV and LAT difference of >30 ms between points on both sides of a line (as confirmed by repeat mapping around the ostia). Although complete electrical isolation of the PVs is rarely achieved with this technique, it substantially modifies the substrate and/or partially denervates the heart. The effectiveness of this technique is probably due to the abolition of the stable rotors situated close to the PVs, that are thought to maintain AF. The success rate of this procedure is 75–90% [52].
3.4
A non-randomized comparison of medical treatment with catheter ablation indicated a better prognosis for subjects treated interventionally [53]. When circumferential ablation around the PV ostia was compared with segmental isolation within the proximal segments of the PVs, a greater long-term success rate was noted with the former technique [54]. At 6 months, 88% of patients who underwent circumferential ablation and 67% who underwent segmental isolation were free of symptomatic AF in the absence of antiarrhythmic drug therapy. At the same time, the risk of PV stenosis is reduced when RF energy is applied around the ostia. However, a new and serious complication to this approach – atrio-esophageal fistula – has been noted [55].
Figure 57. An electro-anatomical reconstruction of the LA in the (A) anteroposterior and (B) posteroanterior views. Ablation lines were designed to encircle the PVs. An additional line was then created from the left-sided PVs towards the MA.
A)
B)
55
R7631_ElMapHeart_03.qxd
6/3/06
16:12
Page 56
3.4 ELECTRO-ANATOMICAL MAPPING OF THE HEART
3.4C Combined technique Due to the limited success rates of both the segmental isolation and circumferential ablation techniques, combined techniques have emerged. Mansour et al. described a novel method of circumferential extra-ostial isolation of the PVs, combining electro-anatomical mapping and the Lasso catheter [56]. Isolation of the right and left PVs was achieved by a single encirclement of the ipsilateral veins. This approach eliminated AF in 75% of patients versus 60% of patients treated with segmental isolation within the PV ostia. Ouyang et al. used a similar approach with two Lasso catheters [57]. Marrouche et al. described yet another combined technique that uses intracardiac echocardiography (ICE) to visualize PV ostia, and the Lasso mapping catheter for the assessment of local signals and complete electrical isolation of the veins (Figure 58) [58]. The position of the Lasso catheter is controlled by ICE and is continuously adjusted to eventually cover the entire circumference of the veno-atrial junction or antrum. This allows for the deployment of the lesions at the level of the veno-atrial junction, and also allows assessment of the electrical isolation of the relevant PV (ie, antrum isolation).
During initial experiences with this novel approach, ‘microbubbles’ were observed during RF energy delivery. The appearance of microbubbles suggested the overheating of tissue. This preceded a sudden increase in impedance and/or a ‘pop’ phenomenon. Experimental evidence now suggests that microbubble formation is related to tissue temperature [59]. Brisk showers of microbubbles can be observed when the temperature reaches around 90°C. Monitoring of the catheter tip–tissue interface using intracardiac ultrasound is recommended throughout application of RF energy until the desired effect is achieved or until microbubbles appear. If microbubbles appear, RF energy should be decreased by 5–10 W. When brisk showers of microbubbles appear, RF energy needs to be terminated immediately if a sudden impedance rise and ‘pop’ are to be avoided. This approach minimizes complications and allows for the administration of a relatively high energy level to the tissues with maximum efficacy. The potential advantages might explain the high efficacy of this strategy, both in patients with and without structural heart disease, and in patients with paroxysmal and persistent AF. The overall reported success rates for all patient groups reached above 90% and 70%, respectively [58,60].
Figure 58. (A) An intracardiac echocardiograph of the common ostium of the left-sided PVs. (B) Monitoring the microbubbles (arrow) during RF application enables the operator to avoid overheating the tissue and the ‘pop’ phenomenon.
A)
56
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:12
Page 57
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.4
3.4D Ablation of an electrophysiological substrate The theory that AF is sustained by mother rotors with subsequent fibrillatory conduction, and previous experimental data, have led to attempts to modify the electrophysiological substrate for these reentry circuits. Nademanee et al. used electro-anatomical mapping of both atria to denote areas with complex and fragmented local electrograms in an anatomical map [61]. These areas were localized predominantly in the posterior LA wall and/or in the septal region. Catheter ablation within these areas led to an interruption of AF in 115 of 121 patients. It also prevented the recurrence of arrhythmia at 1-year follow-up in 92 of 121 patients (76%) after the first procedure, and in 110 of 121 patients (91%) after the second procedure. The mechanism by which ablation within the areas of fragmented potential prevents the recurrence of AF is not clear. However, extensive ablation might eliminate some triggers in the peri-ostial area, eliminate or modify the abnormal atrial substrate needed for the maintenance of AF, and/or modulate cardiac parasympathetic activity.
Figure 59. Different types of PV branching patterns as assessed by 3D reconstructions of MR imaging with virtual endoscopic views. (A) Four separate ostia; (B) short common left vestibule and additional right-top PV with separate ostium; and (C) long common left trunk and additional right-middle PV.
A)
3.4E The role of imaging Imaging techniques such as MR and CT angiography indicate that the anatomy of the LA and PVs is very complex and highly variable. Arguably the most important discovery is that, in up to 80% of patients, the left-sided PVs merge into the common vestibule or antrum (Figure 59) [62,63]. Ablation at this level provides better efficacy and a much lower risk of PV stenosis. In addition, recognition of additional PVs allows successful isolation around their ostium. This emphasizes the need for either preprocedural 3D imaging (and image integration) or intra-procedural imaging using ICE, or both methods (Figure 60). A new software CARTOMerge™, integrates pre-procedural 3D images (either 3D CT or MR angiography) with the virtual electro-anatomical CARTO map constructed during the procedure. After the initial process of registration, the imported 3D anatomical map of the LA and PVs can be used for catheter navigation (Figure 61). ICE guidance can be used to improve the registration process. Our early experience with this software indicates that it is possible to obtain a reliable correlation between anatomical reconstructions and real-time CARTO maps of the LA and PVs in an adequate proportion of patients (Figure 62).
B)
C)
57
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 58
3.4 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Figure 60. (A) A voltage map of the LA (posteroanterior view) with circumferential ablation lesions around the PV ostia to prevent AF. This ‘virtual’ map shows four vein ostia. Ablation was believed to be deployed at the ostial level. Due to recurrence of the arrhythmia, the patient was scheduled for a reablation supported by an MR angiography. (B) A 3D reconstruction of the LA which clearly demonstrates a common ostium of left-sided PVs along with a long common trunk. Using this information, high-density mapping was deployed to delineate the anatomy (C). It documented that the previous ablation was performed relatively deeply in the common trunk. This example highlights the necessity for imaging in order to obtain a detailed understanding of the anatomy of individual patients. The dotted lines in (B,C) indicate the ostium of the PVs.
A)
B)
C)
Figure 61. Registration of 3D CT image and electro-anatomical map using the CARTOMerge™ software. (A) Anatomical map of the LA in the posteroanterior view. Firstly, four ‘landmarks’ have to be tagged at specific sites around the ostia of the PVs. Secondly, corresponding sites (B) are selected for each landmark on the CT reconstruction. Finally, both maps can be ‘merged’ together using the registration software tool (C). Subsequently, the CARTO map can be suppressed by a decrease in the fill threshold and a 3D CT image alone would be sufficient.
A)
58
B)
C)
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 59
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
Tips and tricks for ablation of AF
•
It is recommended that pacing from the CS is used for reference when ablation is performed in sinus rhythm (in AF, use QRS as the reference channel).
•
For visualization of the LA, we recommend using the anatomical map.
•
Electro-anatomical mapping of the LA can start with PV construction using a vessel tool, after which several points around the MA are collected and the rest of the atrium is mapped with minimal use of fluoroscopy.
•
For precise allocation of the edge between the left-sided PVs and the appendage, we prefer to annotate the points within the appendage as floating points (the appendage is identifiable by high voltage local electrograms, with characteristically more organized activity in fibrillating patients).
As there are different approaches to catheter ablation of AF and the technique is still under development, it is impossible to give a clear step-by-step method for ablation. Hence, we suggest some useful tips to help during the procedure. •
•
•
Pre-procedural 3D imaging (MR or CT angiography) is helpful for understanding the anatomy and the selection of appropriate tools (eg, size of the Lasso catheter used to confirm isolation of PVs). To obtain better access to both left- and right-sided PVs, trans-septal puncture is preferable in the mid portion of the fossa ovalis, posteriorly, in the craniocaudal direction. Optimum selection of puncture site can be obtained with the use of intracardiac echocardiography. Rather aggressive anticoagulation is recommended in order to prevent thromboembolic events, especially in patients with enlarged atria and persistent arrhythmia (activated clotting time approximately 350 s).
3.4
Figure 62. Circumferential ablation of the PVs using CARTOMerge™ software. The panels show the LA (posteroanterior view) of the CT reconstruction with virtual endoscopic views (A), the left PVs (B), and the right PVs (C).
A)
B)
C)
59
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 60
3.5 ELECTRO-ANATOMICAL MAPPING OF THE HEART
•
To obtain a more detailed anatomy around the PV ostia, high density mapping is recommended. The best results can be obtained with simultaneous use of intracardiac echocardiography. Alternatively, CARTOSync™ software can be used to reproduce the anatomy of the LA and PV ostia.
•
Some operators prefer creating a shell of the LA first and subsequently mapping individual PVs in the form of separate maps, providing a more accurate anatomy of PVs and their ostia.
•
Tagging at the level of the ostia supports subsequent catheter ablation.
•
For ablation around the PV ostia, it is preferable to hide pulmonary vessel tags or additional maps in order to better visualize the tip of the catheter.
•
Watch for a high impedance rise that can indicate the catheter is positioned too distally within the vein.
•
Whenever using CARTOMerge software, the registration process appears to provide the best results when several landmarks (3–4) are fitted to the upper and lower parts of the PV ostia. The merge is subsequently improved by mapping of the posterior left atrial and PV ostial walls.
3.5 Atrioventricular nodal reentry Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common type of paroxysmal supraventricular tachycardia. It is more prevalent in females than in males, and is usually not associated with structural heart disease. A large body of evidence suggests that the reentry circuit is not confined to the compact AV node itself, but employs peri-nodal tissue. Pathophysiologically, tachycardia involves reciprocation between two functionally and anatomically distinct pathways: the slow pathway extends inferoposteriorly to the compact AV node and spreads around the septal margin of the TA, while the fast pathway is located around the apex of Koch’s triangle [64,65]. Typically, AVNRT is characterized by antegrade conduction via the slow pathway, while the fast pathway conducts retrogradely (ie, slow–fast AVNRT). Following conduction through the slow pathway to the bundle of His, the impulse travels retrogradely to the atria. As a result, the P-wave is hidden inside the QRS complex and/or in its terminal part (pseudo r´ in V1). In approximately 5–10% of cases, the impulse travels in the opposite direction (ie, fast–slow, or atypical, AVNRT) and shows a long RP pattern (eg, the P-wave is negative in leads II, III, and aVF, and precedes the next QRS complex). In another rare variant, both limbs of the reentrant circuit are composed of slow conducting tissue (ie, slow–slow AVNRT), where the P-wave is inscribed with a variable interval after the QRS complex. Catheter ablation targeting the slow pathway in the posteroseptal to midseptal region along the TA is the preferred approach, since it reduces the risk of inadvertent heart block and results in a high success rate. With typical AVNRT, ablation is performed in sinus rhythm; with the atypical variant, the earliest retrograde activation can be mapped and ablated during tachycardia. In the typical variant, the electro-anatomical mapping system can be used to annotate the area of the bundle of His and the ostium of the CS – this method of treatment has been found to shorten the total procedure time and X-ray exposure versus the conventional approach [66]. However, the main potential use of the CARTO system lies in the treatment of atypical AVNRT [67]. In this type of arrhythmia, it allows real-time mapping of the earliest retrograde activation superimposed on the anatomy of the CS ostium and Koch’s triangle. This approach appears to facilitate safe ablation in this region (Figure 63).
60
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 61
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.5
Tips and tricks for mapping and ablation of AVNRT •
As most arrhythmias arise in Koch’s triangle (ie, between the bundle of His, CS ostium, and TA), only the anatomical landmarks in this area need to be defined.
•
Tag all sites exhibiting a bundle of His potential to create the ‘His cloud’. This should be avoided during subsequent ablation.
•
During atypical AVNRT, briefly map the entire RA, the region of the CS ostium, and Koch’s triangle in order to annotate the site of the earliest retrograde activation and, thus, the target for ablation.
Figure 63. (A) Intracardiac recordings during atypical AVNRT. The earliest activity can be recorded in the ablation catheter that is positioned below the AV node. (B) An activation map of both ventricles during atypical AV nodal reentry showing the earliest activation below the bundle of His, within the ostium of the CS, and corresponding to the exit of the slow pathway.
A)
B)
61
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 62
3.6 ELECTRO-ANATOMICAL MAPPING OF THE HEART
3.6 Inappropriate sinus tachycardia Inappropriate sinus tachycardia refers to an abnormally elevated heart rate at rest or to a disproportionate increase in heart rate on minimal exertion, where the P-wave morphology is identical to that seen during normal sinus rhythm. The diagnosis of this clinical entity has to be made by exclusion, as secondary causes of sinus tachycardia and/or an etopic focus near the area of the sinus node must always be ruled out. First-line therapy for inappropriate sinus tachycardia is pharmacologic. Beta-blockers and/or sotalol can relieve symptoms. If drug therapy fails, RF modification of the sinus node region can be used to suppress heart rate.
The sinus node is a longitudinal structure situated along the crista terminalis in the region of the sulcus terminalis; the upper part of the node is more sensitive to adrenergic stimulation. The ablation strategy specifically takes account of these features. Identification of the site of earliest activation during catecholamine stimulation (usually a continuous infusion of isoproterenol) provides the target for RF ablation; elimination of this area alone should ensure that some degree of chronotropic competence is retained [68]. This can be achieved by placing a multipolar mapping catheter along the crista terminalis and observing a shift in the earliest activation during isoproterenol infusion.
Figure 64. Isochronal activation maps of the RA (right lateral view), (A) before and (B) after sinus node modification for inappropriate sinus tachycardia. Note: the caudal shift of the earliest activation after the ablation procedure (arrow).
A)
62
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 63
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
The electro-anatomical mapping system has recently been used to increase the accuracy of mapping and reduce fluoroscopy time [69]. Marrouche et al. reported on the use of the electro-anatomical mapping system in 35 patients for identification and targeting of the earliest activation site within the sinus node area [70]. This strategy helped to achieve target heart rate in all patients in the long-term (although repeated sessions were required in 21%) and none required pacemaker implantation. Our experience is similar to this study (Figure 64). The electro-anatomical mapping system can also be used for a combined epicardial–endocardial treatment approach, when an endocardial procedure alone is ineffective [71,72].
Tips and tricks for mapping and ablation of inappropriate sinus tachycardia •
As a reference channel, use an intracardiac signal for triggering (eg, CS catheter).
•
Mapping of the RA during baseline rhythm is recommended in order to exclude focal atrial tachycardia.
•
Re-map the atrium under adrenergic stimulation (eg, isoproterenol infusion) to locate a shift in the earliest activation and delineate the target for ablation.
•
Pacing at 10 mA before each application is recommended to exclude local capture and avoid phrenic nerve injury during RF energy delivery.
•
Energy application in the area of the sinoatrial tissue is usually associated with an accelerated heart rate, with a subsequent drop in rate during delivery or after termination of delivery.
•
•
•
3.7
3.7 Accessory pathways Typical accessory pathways are extra-nodal connections between atrial and ventricular myocardium localized around the AV groove or within the posteroseptal space. Sinus rhythm pathways usually present with a variable degree of pre-excitation on the surface ECG, although pathway conduction might be intermittent. Pathways that conduct only retrogradely do not manifest in sinus rhythm and are referred to as concealed pathways. Accessory pathways are classified based on their relationship to the MA or TA and the type of conduction (decremental versus non-decremental). Typically, accessory pathways exhibit rapid, non-decremental conduction. Less commonly (approximately 8% of pathways), they show decremental antegrade or retrograde conduction. The term ‘permanent junctional reciprocating tachycardia’ describes a rare clinical syndrome that involves a slow conducting, concealed pathway that is usually localized posteroseptally [73,74]. While conventional technology supports successful catheter ablation of most accessory pathways, electro-anatomical mapping can minimize fluoroscopic exposure and the number of vascular accesses (Figure 65). This is particularly relevant in the pediatric population [75]. In addition, the electroanatomical mapping system is useful in patients with multiple accessory pathways, especially concealed pathways [76]. It can also be useful in less frequent variants of accessory pathways, such as those associated with Ebstein’s anomaly [77], those with an epicardial course of treatment, and where the atrial insertion is more distant from the TA and/or MA (eg, in the right appendage) [78]. In the latter case, electro-anatomical mapping and ablation can successfully be performed using the epicardial approach.
Tips and tricks for mapping and ablation of accessory pathways •
After several applications, the earliest activation site usually shifts caudally. If no clinical effect is found, perform another mapping procedure to obtain a new target site with early activation.
The primary step in accessory pathway mapping is the careful reproduction of the anatomy of the AV annulus (or annuli).
•
The AV annulus is best identified by the presence of both atrial and ventricular signals (the A/V ratio should be about 1:1).
Maintain this strategy until a significant reduction in the sinus rate is achieved.
•
In case of recurrences leading to repeated ablation sessions, it might be necessary to ablate the sinoatrial node region completely, resulting in escape junctional rhythm.
The CARTO software is not designed for the annotation of short AV intervals or accessory pathways. Instead, it provides an anatomical shell for the manual annotation of early ventricular or atrial activation.
•
Ventricular pacing appears to be the preferable strategy for annotating the earliest atrial activation, and, thus, the target for ablation. 63
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 64
3.7 ELECTRO-ANATOMICAL MAPPING OF THE HEART
•
A typical ablation site shows the appropriate A/V ratio.
•
When ablation close to the annulus fails, electro-anatomical mapping of atrial insertion during ventricular pacing and/or during orthodromic reentrant tachycardia might reveal that the atrial insertion is distant from the annulus due to an atypical course of the pathway.
•
The electro-anatomical mapping system can even support circumferential ablation around the atypical atrial origin of the pathway, thereby excluding it from the rest of the myocardium (see accompanying CD).
B)
Figure 65. (A) An activation map of the RA and RV during sinus rhythm in a patient with a delta wave. The earliest activation of the RV is present on the lateral wall (arrow), and corresponds to the ventricular insertion of the pathway. (B) Abolition of the antegrade conduction during RF application at the site of the earliest ventricular activation. (C) Remap of the RA and RV after ablation of the antegrade conduction. Note: the delayed activation (violet) of the right lateral wall as compared to (A).
A)
64
C)
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 65
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.8 Idiopathic focal ventricular tachycardia Approximately 10% of patients with VT who are referred for evaluation in specialized electrophysiology centers are diagnosed with idiopathic VT [79]. Although these arrhythmias can be asymptomatic, about two-thirds of patients suffer from symptoms such as palpitations, dizziness, and/or syncope. Cardiac arrest has also been anecdotally reported; however, these arrhythmias are generally considered to be benign. Potential mechanisms of idiopathic VT, together or separately, include [80]: • • •
triggered activity mediated by cyclic AMP (and thus catecholamine-sensitive) abnormal automaticity micro-reentry
Conceptually, most of these arrhythmias can be considered as focal in origin. This notion has implications for selecting a strategy for catheter ablation. Due to incomplete understanding of the arrhythmia mechanism, an acceptable classification of these tachycardias has not been proposed. Therefore, VTs can be classified based on their clinical pattern, such as repetitive monomorphic VT or paroxysmal VT. Another classification reflects the site of origin. The majority of these arrhythmias originate in the RV (predominantly in the outflow tract) and the morphology of the QRS resembles that seen in LBBB; about 30% of idiopathic VTs originate in the LV and show RBBB morphology. Finally, idiopathic VTs can be classified by their response to pharmacologic provocations such as catecholamines, verapamil, and adenosine, or to physiologic stimuli such as exercise. Due to the focal nature of their origin, most idiopathic VTs are amenable to catheter ablation.
3.8A Ventricular tachycardia originating from the right ventricular outflow tract VT originating from the RV outflow tract (RVOT) has a typical morphology of LBBB, with a transitional zone in chest leads V3 and beyond (ie, transition from a small, positive R-wave to an R-wave that is larger than the S-wave in a given lead). The frontal plane of the QRS axis is usually close to 90º with relatively narrow QRS complexes (around 140 ms) that are often tall in the II, III, and aVF leads. The most common location of the arrhythmia focus is on the IVS beneath the pulmonary valve. However, it can also be on the free wall of the RVOT and/or close to the bundle of His.
3.8
The two common mapping techniques used to localize the origin of RVOT VT are activation mapping (because of its focal origin) and pace mapping. Activation mapping is effective for identifying the earliest activation in the RVOT during isolated ectopic beats and/or during VT. Local ventricular activation that precedes the onset of the QRS by 20–50 ms usually identifies a site where ablation should be successful. In addition, the morphology of the unipolar recording from the tip of the mapping catheter can help to differentiate between optimal and sub-optimal ablation sites: a QS pattern without an R-wave suggests that the tip is at the focus, without tissue inbetween. Pacing from the endocardium at the origin of the VT results in QRS morphology identical to that of the VT (pace mapping). Pace mapping can be used either as an adjunct to activation sequence mapping, or as the primary mapping technique. The success rate of catheter ablation of RVOT VT is approximately 90%. There is limited information available on the use of the electro-anatomical mapping system in guiding catheter ablation of RVOT VT. Dixit et al. reported on a series of patients who underwent electro-anatomical mapping to create anatomical maps of the RVOT, and also to relate ECG morphologies to specific sites within the RVOT [81]. This study provided useful information that helped to differentiate septal and free-wall origins of VT: all free-wall sites demonstrated monophasic R-waves that were shorter, broader, and had a notched morphology (especially in lead II) [81]. The CARTO system provides two options for the navigation of catheter ablation in RVOT: 1. Perform activation mapping during sustained VT and/or isolated ectopic beats with the same morphology as the clinical VT. 2. Perform anatomical mapping in sinus rhythm and tag the location of the best activation sequence mapping site and/or pace mapping site in case of the requirement for subsequent re-navigation of the ablation catheter (Figure 66). Due to potential ectopic activity caused mechanically by the ablation catheter, which would impair the accuracy of mapping in the former technique, we prefer the latter strategy, and use the electro-anatomical mapping system mostly for creating an anatomical shell of the RV and for subsequent annotation of the earliest activation site. This approach also decreases the need for fluoroscopy. 65
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 66
3.8 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Figure 66. An anatomical map of the RV during sinus rhythm (anteroposterior view). The map was created to obtain gross RV anatomy; subsequently, pace mapping was deployed to allocate the site that produces the same QRS morphology as that observed during ectopy.
A)
66
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 67
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
In addition to depicting the 3D anatomy of the RV and annotating points of interest for subsequent re-navigation of the ablation catheter, the electroanatomical mapping system provides another potential advantage. It can be used to differentiate between idiopathic right outflow tract tachycardia and the initial stages of arrhythmogenic right ventricular cardiomyopathy (ARVC) [82]. The latter is characterized by lower amplitude, prolonged duration electrograms that can be depicted on voltage maps (Figure 67). In some patients, these scar areas might be limited to the RVOT and/or to regions adjacent to the TA.
3.8B Ventricular tachycardia originating from the left ventricular outflow tract Some patients present with repetitive, monomorphic VT suggestive of outflow tract origin, where the ECG configuration points towards a location of the focus in the left ventricular outflow tract (LVOT). In the first study on this topic, Callans et al. noted that, in 12% of patients with a clinical syndrome of idiopathic outflow tract VT, the origin of the VT was in the LV [83]. Tachycardias from the region of aortomitral continuity (ie, the left fibrous trigone) were characterized by a dominant R-wave in lead V1. VTs with a LBBB configuration and a pre-cordial R-wave transition at lead V2 arose from the basal aspect of the superior LV septum or from an epicardial location [83]. The former can be successfully ablated from the region of aortomitral continuity. The latter form of VT is ablatable from either the aortic or pulmonary cusps, the sub-aortic region, and/or the great cardiac vein (Figure 68) [84,85]. Intracardiac echocardiography provides the advantage of non-invasive monitoring of the catheter tip in order to avoid damage to the coronary artery ostium. Otherwise, coronary angiography is recommended to visualize the ostia of coronary arteries. In any case, the electro-anatomical mapping system has proved useful in reconstructing the anatomy of the LVOT and the aortic root, as well as in supporting successful catheter ablation [86].
3.8C Right ventricular outflow tract versus left ventricular outflow tract site of origin Although several authors have suggested that the transition of the QRS complex in V1–V3 is a reliable predictor that the area of origin lies outside of the RVOT, there is evidence that the situation is more complex. Tanner et al. observed that R/S transition in lead V3 was present in 58% of patients; despite this, mapping and ablation of the RVOT successfully stopped the arrhythmia in 58% of these patients [85]. The remaining patients (42%)
3.8
required detailed mapping in other areas such as the PA trunk, CS, LVOT, aortic cusps, and/or epicardium. On these occasions, the electro-anatomical mapping system has proved very useful for establishing the anatomy of and relationships between different structures. A stepwise approach has been advocated where mapping begins in the RVOT, followed by the PA, CS, and the great cardiac vein. If transvenous access is not successful, retrograde mapping of the LVOT and the aortic sinus of Valsalva is recommended. If all anatomical accesses are unsuccessful, epicardial mapping via percutaneous access should be considered.
3.8D Other locations of the arrhythmogenic focus in idiopathic ventricular tachycardias Although most focal idiopathic VTs originate from outflow tracts, arrhythmogenic foci can also originate in other regions, such as the septum near the His bundle area and/or from the MA [86,87]. VTs originating in the latter can be identified based on the presence of an S-wave in lead V6 and the morphology of the QRS, depending on the location around the annulus. The electro-anatomical mapping system can be employed to annotate the sites of origin (Figure 69).
Tips and tricks for ablation of focal idiopathic VTs •
The creation of an anatomical map in sinus rhythm with tagging of relevant structures, subsequent pace mapping, and annotation of appropriate sites, is preferred to direct mapping of the ectopic focus.
•
When attempting to map the ectopic focus, care should be taken to avoid incorporating false ectopic beats (made by catheter movement) into the map since these may distort the activation map.
•
When mapping during VT, stable triggering and precise annotation are crucial in allocating the ectopic source; add proximal and unipolar recordings to the annotation window.
•
A selected surface ECG lead is usually used as a reference channel, and stability of triggering in this channel is important. To obtain stable triggering avoid using a lead with double spikes (eg, with RR morphology).
67
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 68
3.8 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Figure 67. Voltage maps of the RV in (A) idiopathic RVOT tachycardia and (B) ARVC. Note: the difference between both maps with a large low-voltage area in (B).
A)
68
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:13
Page 69
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.8
Figure 68. An electro-anatomical activation map of the RV and simplified anatomical map of the left and right aortic cusps in the left lateral (A) and posteroanterior view (B) in patient with idiopathic ventricular tachycardia. The earliest activation site during the ectopy was found in the left aortic cusp (black arrow), below the ostium of the left main coronary artery. Intracardiac echocardiography was used to guide safe RF energy delivery in the left aortic cusp, remote from the coronary ostium (C).
A)
B)
Figure 69. (A) An ECG recording with ventricular bigeminy of RBBB morphology. (B) An activation map of the LV during ectopy (left lateral view). The earliest activation was identified laterally, close to the base (arrow). (C) The corresponding voltage map. In contrast to arrhythmias after MI, the focus is not associated with any scars.
A)
B)
C)
69
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 70
3.9 ELECTRO-ANATOMICAL MAPPING OF THE HEART
3.9 Idiopathic reentrant ventricular tachycardia (fascicular) The second important category of idiopathic VTs is fascicular or ‘verapamilsensitive’ VT. It has an RBBB QRS morphology and usually a superior and leftward frontal plane axis, and occurs predominantly in young or middleaged male patients without structural heart disease. It has been demonstrated that the underlying mechanism is reentry. The circuit is confined to the Purkinje system (posterior fascicle), which consists of Ca2+-dependent tissue – this explains the ‘verapamil sensitivity’. Less often, the reentrant circuit is located within the anterior fascicle. In such cases, QRS morphology shows an inferior axis. RF ablation can successfully be performed on the left side of the IVS following identification of the ectopic focus by pace mapping, the earliest pre-systolic Purkinje potential, or a diastolic potential during VT [88–90]. The electro-anatomical mapping system is increasingly used to support catheter ablation, allowing superimposition of 3D anatomy and tagged sites of interest. It may be useful in evaluating multiple breakthrough sites from the reentrant circuit to the ventricular myocardium, and in annotating the earliest Purkinje potential [91].
B)
70
Figure 70. (A) An ECG recording during fascicular tachycardia. Note: the morphology of RBBB and left anterior hemiblock, which suggest that the origin is from the left posterior fascicle. The sharp signal in the mapping catheter positioned on the left posterior fascicle preceding each QRS complex reflects the early activation of the conduction system (arrows). (B) Propagation maps show, from left to right, the ventricle during idiopathic fascicular VT (right anterior oblique view).
A)
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 71
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
More recently, the system has been used to map abnormal short, sharp, highfrequency potentials that correspond to retrograde Purkinje potentials within the Purkinje network during sinus rhythm [92]. The earliest retrograde Purkinje potential appears to be a critical site for the VT substrate, and has been found to correspond with the earliest activation during VT. Therefore, it might also be used to guide successful ablation when VT is non-inducible (eg, during transient catheter mechanical trauma). Mapping during VT can show a focal origin with a slow conduction area and high-frequency potentials preceding ventricular activation (Figure 70). These sharp potentials represent activation of the left bundle and Purkinje system, which are typically noted progressively later, when moving from the earliest activation site. Hence, early diastolic potentials can be mapped and mechanical trauma may terminate arrhythmia.
Tips and tricks for mapping and ablation of idiopathic fascicular VTs •
The creation of an activation map of the LV in sinus rhythm, with subsequent detailed mapping and annotation of the Purkinje fiber network, is recommended.
•
Abnormal, high-frequency, low-amplitude potentials can be mapped in some areas of sinus rhythm in diastole. These are suggestive of retrograde Purkinje potentials.
3.10
3.10 Post-myocardial infarction ventricular tachycardia In this setting, the role of catheter ablation is usually as adjunctive therapy to implantation of a cardioverter defibrillator, often indicated for recurrent VTs in patients after device implantation. Catheter ablation may be a life-saving procedure in arrhythmic storm, and it is also the first-line therapy for incessant monomorphic VTs, although it is usually followed by the implantation of a cardioverter defibrillator. Currently, catheter ablation only can be considered a definitive treatment, ie, without the need for subsequent cardioverter defibrillator implant, in patients with preserved LV function. Areas of post-myocardial infarction (MI) scar typically form an anatomical substrate for reentrant VTs. Isthmuses of slow conduction, bordered by scar areas or a valvular annulus, are critical components of most of these reentry circuits [93]. The reentry circuits can be quite large, with endocardial isthmuses ranging 18–41 mm in length and 6–36 mm in width. Although predominantly localized sub-endocardially, they can, in some patients, be deep in the myocardium and/or sub-epicardial. Multiple morphologies of inducible monomorphic VTs are common and can originate from different regions or share the same critical isthmus [94,95].
3.10A Mapping during ventricular tachycardia
•
Ablation can be guided by either the earliest Purkinje potential mapped during tachycardia, and/or the site of the earliest retrograde Purkinje potential in sinus rhythm (ie, when no tachycardia can be induced).
Until the introduction of electro-anatomical mapping, catheter ablation was primarily performed in patients who were able to hemodynamically tolerate ablation during the VT [96]. A successful procedure required localization of the area of slow conduction, which is critical for the maintenance of VT. Generally, the following conventional mapping techniques were used:
•
Voltage mapping also helps to differentiate between idiopathic VT and other variants that could be associated with undiagnosed structural heart disease, such as myocardial scars.
•
Endocardial activation mapping focuses on endocardial electrograms preceding the onset of the QRS complex on the surface ECG. This is based on the assumption that the beginning of the QRS complex coincides with the exit of the impulse from the area of slow conduction. Location of this exit influences the morphology of the QRS complex as the impulse then initiates the depolarization of the main mass of myocardium outside of the scar. Therefore, electrical activity from the critical isthmus of slow conduction can be recorded with variable timing before the QRS complex. The electrograms are recorded from closely spaced bipolar electrodes using conventional filtering, and are often fractionated and of low amplitude. In some patients, these electrograms are located in mid-diastole (ie, with mid-diastolic potentials). 71
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 72
3.10 ELECTRO-ANATOMICAL MAPPING OF THE HEART
•
•
Entrainment mapping consists of pacing from the tip of the mapping catheter with a cycle length 30–50 ms shorter than that of the VT. Participation of a given region in the circuit is reflected by concealed entrainment, ie, by entrainment of VT without any evidence of fusion. In this case, the morphology of the paced QRS complexes is identical to clinical VT and the first return cycle is equal to the VT cycle length. Based on the duration of the interval between stimulus and the beginning of the QRS complex, the position of the mapping catheter can be specified in more detail (ie, the entrance, central, or exit zone, and/or bystander areas or outer loops). Pace mapping during sinus rhythm at similar rates to clinical VT can be used to identify zones of slow conduction (with a stimulus-to-QRS complex duration ≥40 ms) and sites at which the clinical VT morphology could be reproduced. Note that the accuracy of the morphology match in this setting does not always predict the result of catheter ablation. This may be due to the fact that epicardial breakthrough sites are often at a considerable distance from the critical portion of the circuit.
3.10B Ablation of stable ventricular tachycardia By identifying critical reentry circuit isthmuses using the above techniques, clinical VTs can be successfully ablated with a limited number of RF current applications in >70% of patients [93,96,97]. Despite the high acute success rate, about 20–40% of patients experience VT recurrence during follow-up. Another limitation is the need for hemodynamic stability during mapping and catheter ablation. However, the CARTO electro-anatomical mapping
system’s ability to better visualize the anatomy of the ventricle and precisely locate the critical isthmus improves the success of catheter ablation of stable VT (Figure 71).
3.10C Sinus rhythm substrate mapping Most post-MI patients have multiple VTs and, frequently, some of these patients are hemodynamically unstable [97–99]. Electro-anatomical mapping provides a unique tool for characterizing the arrhythmia substrate during sinus rhythm and to guide catheter ablation [100]. This ‘substrate mapping’ is based on experimental studies on the identification of scarred myocardium using voltage maps. In addition, an electrically unexcitable scar within a low-voltage area can be identified by pacing at >10 mA at 2 ms pulse width; such scars often form the border of reentry paths [95]. The localization of the exit zone from the arrhythmogenic substrate can be predicted by stimulation in the border zone with late potentials and by comparison of paced electrogram morphology with ECG morphology during arrhythmia (Figures 72 and 73). A stimulusto-QRS (S-QRS) delay >40 ms during pace mapping is an indication of abnormal conduction that is often associated with reentry circuits [101]. In some circuits, the critical path can be reconstructed by pace mapping (ie, pacing at different sites and comparing the paced ECG morphology with the targeted VT). In case of a match, a shorter S-QRS interval indicates the exit site of the reentry, while a longer S-QRS may indicate the central zone of the reentry.
Figure 71. A propagation map of the LV in the posteroanterior view during slow, tolerated VT. The critical isthmus for reentry is located between the dense scar area (grey) on the lateral wall and the MA. Ablation line (red points) is designed to trans-sect this isthmus. Ablation in this region terminated VT and prevented its induction.
72
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 73
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.10D An integrated approach
Tips and tricks for mapping and ablation of post-MI VTs
The electro-anatomical mapping system combines substrate mapping with limited entrainment mapping in hemodynamically tolerated forms of VT [94,99]. It allows the annotation of mid-diastolic potentials and/or entrainment sites during VT, and/or late potential regions during sinus rhythm. Ablation within the central zone, in combination with linear lesions through the exit regions of all inducible VTs, abolishes the inducibility of VTs in 70–80% of cases.
•
Programmed ventricular stimulation should be performed before the initiation of electro-anatomical mapping as possible patient movement during cardioversion could distort the acquired map.
•
Either the retrograde trans-aortic or antegrade trans-septal approach can be used for detailed electro-anatomical mapping of the LV.
•
A high-density voltage map of the LV during baseline rhythm and/or during ventricular pacing should be created with the manual voltage scale set from 0.5 to 1.5 mV.
•
Areas of fragmented and late potentials should be annotated with color tags.
3.10E Epicardial approach Failure of endocardial catheter ablation might reflect an epicardial or intramural location of reentrant circuits. The technique developed by Sosa et al. for percutaneous access to the pericardial space has been used by various investigators to enable epicardial mapping and ablation [102]. Proximity to the coronary artery or the phrenic nerve might limit this approach in some patients.
3.10
Figure 72. A voltage map of the LV in a patient with an anterior aneurysm and multiple morphologies of unstable VT (anteroposterior view). During mapping, areas without any electrical activity and no capture at 10 mV were labeled as dense scar (grey). Exit sites for all inducible VTs were allocated using the pace map. Subsequent transsection of these isthmuses by linear lesions abolished the inducibility of VTs.
73
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 74
3.10 ELECTRO-ANATOMICAL MAPPING OF THE HEART
•
•
Pacing (preferably unipolar) should be systematically employed within the scar and around the border zone to identify zones of slow conduction associated with specific exit sites (according to the resulting morphology of the QRS complex). Areas without electrical activity and with no capture at 10 mA should be tagged, in grey, as dense scar.
•
In tolerated ‘slow’ VTs, mapping may be performed during tachycardia.
•
In such a case, a search should be made for mid-diastolic signals, and entrainment mapping should be used to ascertain the location of the catheter tip within the circuit.
•
Entrainment mapping might not capture the tiny diastolic potential, or it might terminate the arrhythmia.
•
A Cool tip™ ablation catheter is preferred for the ablation of VTs in patients after MI.
•
When ablation from an endocardial approach is not successful, epicardial mapping and ablation should be considered.
Figure 73. A voltage map of the LV after an inferior MI (caudal view). Exit sites for two inducible VTs were allocated using the pace map. Those isthmuses were transected using short ablation lines, and an additional line was extended towards the MA.
74
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 75
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.11 Ventricular tachycardias in dilated cardiomyopathy In contrast to post-infarction scars in patients with coronary artery disease, little is known about the arrhythmogenic substrate for sustained VT in patients with non-ischemic cardiomyopathy. Recent data suggest that intra-myocardial fibrosis, especially the patchy pattern, transforms continuous conduction into discontinuous conduction [104]. As a result of conduction delay, the arrhythmogenic mechanism induced by fibrosis is usually reentry. However, Pogwizd et al. noted a focal mechanism for clinical tachycardias in patients diagnosed with idiopathic dilated cardiomyopathy [105]. The origin included sites that revealed muscle bundles embedded in connective tissue, suggesting that fibrosis promotes focal activation. In this respect, anisotropy was found to facilitate the development of ectopic focal activity [106].
3.11
Hsia et al. used the electro-anatomical mapping system to characterize the arrhythmogenic substrate in patients with idiopathic VT [107]. With the exception of some focal VTs and bundle branch reentry, the majority of ventricular arrhythmias were due to intra-myocardial reentry associated with relatively limited myocardial scars [108]. Importantly, the scars were mostly positioned basally, adjacent to the annulus and deep in the sub-endocardium (Figure 74). Epicardial ablation may often be required to reach critical components of the circuit.
Tips and tricks for mapping and ablation in dilated cardiomyopathy •
Use a similar strategy to that for post-MI VTs.
•
When ablation from the endocardial side is not successful, consider epicardial mapping and ablation. An epicardial location of critical regions of the reentrant circuit appears to be more frequent in idiopathic dilated cardiomyopathy as compared with post-MI patients.
Figure 74. Voltage maps of the LV in non-ischemic, dilated cardiomyopathy in (A) anteroposterior and (B) posteroanterior views. The low-voltage area is located basally, near the MA. (C) Two morphologies of VT were inducible in the patient. Note: R-waves in all the pre-cordial leads suggest a basal origin of the VTs.
A)
B)
C)
75
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 76
3.12 ELECTRO-ANATOMICAL MAPPING OF THE HEART
3.12 Ventricular tachycardias in right ventricular arrhythmogenic cardiomyopathy ARVC is a myocardial disease that primarily affects the RV, often resulting in VT and sudden cardiac death. Histologically, the syndrome is characterized by the gradual replacement of myocytes within the RV by adipose and fibrous tissue [109]. Previous studies have confirmed that RF catheter ablation of hemodynamically tolerated VT in ARVC can be performed using a similar strategy to that of post-MI patients, including entrainment mapping
techniques. More recently, electro-anatomical mapping has been used to support catheter ablation, even in untolerated VT [110]. The regions of the RV that are most frequently involved are the RV inflow area near the TA, the apex, and the outflow tract (Figure 75). Electro-anatomical mapping in these areas will reveal low-amplitude, fractionated potentials [111]. In addition, the activation map of the RV might display an extremely delayed activation along the TA corresponding with the epsilon wave in the right precordial leads (Figure 76). The CARTO system can therefore be used for both confirmation of the diagnosis of ARVC and to support catheter ablation, especially in patients with multiple episodes of VT [112].
Figure 75. A voltage map of the RV in ARVC in (A) right and (B) left anterior oblique views. Note: the low-voltage areas present within the outflow tract and near the TA, but the LV is not affected. In contrast to the typical presentation of ARVC, there is no low-voltage area within the RV apex.
A)
76
B)
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 77
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
Tips and tricks for mapping and ablation in ARVC •
Programmed ventricular stimulation should be performed prior to initiating electro-anatomical mapping since the patient might move during possible cardioversion and this could distort the acquired map.
•
A long guiding sheath (eg, PREFACE™, Biosense Webster, Inc., Diamond Bar, CA, USA and/or SR 0™, Daig, Minnetonka, MN, USA) enables easier mapping of the dilated RV.
•
A high-density voltage map of the RV during baseline rhythm and/or during ventricular pacing should be created with the manual voltage scale set from 0.5 to 1.5 mV.
•
Areas of fragmented and late potentials should be annotated with color tags.
•
Pacing (preferably unipolar) should be systematically employed within the scar and around the border zone in order to identify the specific exit site for all zones of slow conduction within the scar. This represents the primary target for RF ablation.
3.12
Figure 76. An isochronal map of the RV in ARVC (right oblique view). Due to delayed propagation of the activation, the wavefront is throughout the scarred myocardium and the lateral wall near the TA is activated after the end of the QRS complex, forming an epsilon wave in the right pre-cordial leads (red arrows).
77
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 78
3.13 ELECTRO-ANATOMICAL MAPPING OF THE HEART
•
Areas without electrical activity and with no capture at 10 mA should be tagged as dense scar, in grey.
•
For tolerated ‘slow’ VTs, mapping may be performed during tachycardia.
•
In such a case, a search should be made for mid-diastolic signals, and entrainment mapping should be used to ascertain the location of the catheter tip within the circuit.
•
Entrainment mapping might not capture the tiny diastolic potential, or it might terminate the arrhythmia.
•
For ablation of VTs in patients with ARVC, either a Cool tip or an 8-mm tip ablation catheter is preferred.
3.13 Post-incisional ventricular tachycardias The incidence of VTs in patients treated late after correction for congenital heart disease is relatively high, varying between 4–8% [113,114]. The scar tissue (eg, post-ventriculotomy) and patches after the surgical procedure can form an arrhythmogenic substrate for multiple reentrant circuits and VTs. Besides reentry, other mechanisms have to be considered as up to 30% of patients with previously documented clinical VT are not inducible during programmed ventricular stimulation. To date, most published data refer to patients with corrected tetralogy of Fallot. In a study by Gonska et al., catheter ablation successfully eliminated the inducibility of VT in 11 out of 16 patients [115]. The reentry circuit was confined to the RVOT scar area, and successful ablation sites were placed along its border zone (Figure 77). Alternatively, the creation of a line of block
Figure 77. A voltage map of the RV after correction of tetralogy of Fallot in (A) the left anterior oblique, (B) anteroposterior, and (C) right anterior oblique views. The low-voltage area in the RVOT corresponds to the scar after ventriculotomy. Fractionated, late potentials were present in the border zone of the scar area, and the ablation line was deployed along its lateral portion towards the TA.
A)
78
B)
C)
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 79
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
between the ventriculotomy and the TA has been advocated to prevent reentry (Figure 78). The potential of the electro-anatomical mapping system in supporting catheter ablation of VTs after correction for congenital heart disease was revealed soon after this technology was introduced into clinical practice [116]. It enabled reconstruction of the reentry circuit around the ventriculotomy scar in a patient with a history of correction for tetralogy of Fallot. Nevertheless, experience with this method remains anecdotal [117]. Based on our experience with a series of patients, the application of electroanatomical mapping in this indication offers the advantage of precise characterization of the arrhythmogenic substrate.
3.13
Tips and tricks for mapping and ablation in patients after surgical correction for congenital heart disease •
It is important to review the scheme of repair for a given congenital heart disease and to become familiar with the location of incisions and/or prosthetic material before beginning mapping.
•
Programmed ventricular stimulation should be performed before the initiation of electro-anatomical mapping; the mechanical trauma caused by the mapping catheter can result in temporary non-inducibility of VT.
•
Since, in the majority of cases, tachycardia is confined to the RV, mapping should begin in this chamber.
Figure 78. (A) A 12-lead ECG tracing during VT in a patient after correction of tetralogy of Fallot. Note: the LBBB morphology suggests an RV origin. (B) An activation map of the RV showing the VT circuit with a narrow protected channel (asterisk) between the scar in the RVOT and the IVS (right lateral view). (C) A mid-diastolic signal (arrow) recorded within the channel of slow conduction. Two applications of RF current within this area abolished the VT.
A)
B)
C)
79
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 80
3.14 ELECTRO-ANATOMICAL MAPPING OF THE HEART
80
•
A long guiding sheath (eg, PREFACE and/or SR 0) enables easier mapping of the RV.
•
A high-density voltage map of the RV during baseline rhythm and/or during ventricular pacing should be created with the manual voltage scale set from 0.5 to 1.5 mV.
•
Areas of fragmented and late potentials should be annotated with color tags.
•
Pacing (preferably unipolar) should be systematically employed within the scar and around the border zone to identify zones of slow conduction associated with specific exit sites (according to the resulting morphology of the QRS complex).
•
Areas without electrical activity and with no capture at 10 mA should be tagged as dense scar, in grey (corresponding to ventriculotomy scars or prosthetic material).
•
In tolerated ‘slow’ VTs, mapping can be performed during tachycardia.
•
In such a case, a search should be made for mid-diastolic signals and entrainment mapping should be used to ascertain the location of the catheter tip within the circuit.
•
Entrainment mapping might not capture the tiny diastolic potential, or it might terminate arrhythmia.
•
To minimize the recurrence of arrhythmia, all potential conduction channels between scars, and/or scars and the TA, should be transected by ablation lines.
•
A Cool tip ablation catheter is preferred for the ablation of VTs in patients with previous repair for congenital heart disease.
3.14 Catheter ablation of ventricular fibrillation Until recently, catheter ablation of polymorphic VT and/or ventricular fibrillation (VF) seemed unrealistic. However, we have shown that polymorphic VT/VF can be triggered from a single ectopic focus, originating from the Purkinje system within the LV, and, thus, might be amenable to catheter ablation [118]. This report initiated collaborative efforts in this area. The first study on the role of the Purkinje conducting system in triggering idiopathic VF suggested that focal catheter ablation of the ectopic focus could successfully eliminate frequent attacks of VF [119]. A more extensive study revealed that, in the majority of patients, the ectopic focus is housed within the Purkinje conduction system [120] and could trigger VF, even in subjects with long QT syndrome and/or Brugada syndrome [121]. From our viewpoint, the electro-anatomical mapping system is useful for supporting catheter mapping and for annotation of the Purkinje system in these selected cases (Figure 79). More recently, ectopic foci originating from LV Purkinje fibers were observed to trigger arrhythmic storm shortly after acute MI and catheter ablation was shown to cure drug-refractory patients [122]. This is consistent with experimental data on the survival of Purkinje fibers in extensive anteroseptal MIs in dogs [123]. Monomorphic ectopic beats from Purkinje fibers in the border zone of a post-infarct scar were shown to initiate arrhythmic storm, even remote from MI [124]. The electro-anatomical mapping system was used to delineate scar areas and to support the mapping of ectopic foci. In addition, in some patients with less frequent ectopy, substrate mapping and ablation of Purkinje potentials close to the border zone of the infarct appeared to be a successful approach. Therefore, electro-anatomical mapping might enable catheter ablation even in patients without ectopy during the procedure.
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 81
CLINICAL APPLICATION OF ELECTRO-ANATOMICAL MAPPING IN THE TREATMENT OF ARRHYTHMIAS
3.14
Figure 79. (A) A short paroxysm of polymorphic VT triggered by monomorphic ectopy. (B) An activation map of the LV during sinus rhythm (right anterior oblique view). The source of the ectopy (arrow) was allocated using pace mapping near the termination of the left posterior fascicle. (C) Intracardiac recordings at the earliest site. The first ectopy beat (arrow) is preceded by a sharp deflection (from the Purkinje system). Note: the second sinus beat is followed by the same sharp signal, which is then blocked and not conducted to the working myocardium. Application at that site both abolished ectopy and prevented recurrence of ventricular arrhythmias.
A)
B)
C)
81
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 82
3.14 ELECTRO-ANATOMICAL MAPPING OF THE HEART
Tips and tricks for mapping and ablation of VF
82
•
Consider this mechanism in all cases of arrhythmic storm leading to VF, and analyze the triggering ectopy.
•
When arrhythmic episodes are triggered by identical ectopic beats, attempt to record their morphology on a 12-lead ECG.
•
If the patient is resistant to anti-arrhythmic drugs, consider mapping the suspected focus with support from the electro-anatomical mapping system.
•
Depending on the ECG morphology of the ectopic beats, either the LV or the RV should be mapped, aiming to identify the earliest activation site, often with preceding Purkinje potential.
•
Catheter ablation of the earliest activated site has the potential to eliminate the trigger.
•
Alternatively, in patients with coronary artery disease, elimination of the trigger can be performed by ablation of the sites near the Purkinje potentials close to the border zone of the scar in sinus rhythm.
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 83
REFERENCES 1.
Gepstein L, Hayam G, Ben-Haim SA. A novel method for nonfluoroscopic catheter-based electroanatomical mapping of the heart. In vitro and in vivo accuracy results. Circulation 1997;95:1611–22.
17. Auricchio A, Stellbrink C, Block M, et al. Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heart failure. The Guidant Congestive Heart Failure Research Group. Circulation 1999;99:2993–3001.
2.
Gepstein L, Evans SJ. Electroanatomical mapping of the heart: basic concepts and implications for the treatment of cardiac arrhythmias. Pacing Clin Electrophysiol 1998;21:1268–78.
18. Sporton SC, Earley MJ, Nathan AW, et al. Electroanatomic versus fluoroscopic mapping for catheter ablation procedures: a prospective randomized study. J Cardiovasc Electrophysiol 2004;15:310–15.
3.
Tops LF, Bax JJ, Zeppenfeld K, et al. Fusion of multislice computed tomography imaging with three-dimensional electroanatomic mapping to guide radiofrequency catheter ablation procedures. Heart Rhythm 2005;2:1076–81.
19. Gillette PC, Garson A Jr. Electrophysiologic and pharmacologic characteristics of automatic ectopic atrial tachycardia. Circulation 1977;56:571–5.
4.
Wittkampf FH, Vonken EJ, Derksen R, et al. Pulmonary vein ostium geometry: analysis by magnetic resonance angiography. Circulation 2003;107:21–3.
5.
De PR, Ho SY, Salerno-Uriarte JA, et al. Electroanatomic analysis of sinus impulse propagation in normal human atria. J Cardiovasc Electrophysiol 2002;13:1–10.
6.
Durrer D, van Dam RT, Freud GE, et al. Total excitation of the isolated human heart. Circulation 1970;41:899–912.
7.
Cassidy DM, Vassallo JA, Marchlinski FE, et al. Endocardial mapping in humans in sinus rhythm with normal left ventricles: activation patterns and characteristics of electrograms. Circulation 1984;70:37–42.
8.
9.
Rodriguez LM, Timmermans C, Nabar A, et al. Variable patterns of septal activation in patients with left bundle branch block and heart failure. J Cardiovasc Electrophysiol 2003;14:135–41. Auricchio A, Fantoni C, Regoli F, et al. Characterization of left ventricular activation in patients with heart failure and left bundle-branch block. Circulation 2004;109:1133–9.
10. Peichl P, Kautzner J, Cihak R, et al. The spectrum of inter- and intraventricular conduction abnormalities in patients eligible for cardiac resynchronization therapy. Pacing Clin Electrophysiol 2004;27:1105–12. 11. Reynolds MR, Joventino L, Josephson ME. Relationship of baseline electrocardiographic characteristics with the response to cardiac resynchronization therapy for heart failure. Pacing Clin Electrophysiol 2004;27:1513–18.
20. Kall JG, Kopp D, Olshansky B, et al. Adenosine-sensitive atrial tachycardia. Pacing Clin Electrophysiol 1995;18:300–6. 21. Lin WS, Tai CT, Hsieh MH, et al. Catheter ablation of paroxysmal atrial fibrillation initiated by non-pulmonary vein ectopy. Circulation 2003;107:3176–83. 22. Marchlinski F, Callans D, Gottlieb C, et al. Magnetic electroanatomical mapping for ablation of focal atrial tachycardias. Pacing Clin Electrophysiol 1998;21:1621–35. 23. Hoffmann E, Reithmann C, Nimmermann P, et al. Clinical experience with electroanatomic mapping of ectopic atrial tachycardia. Pacing Clin Electrophysiol 2002;25:49–56. 24. Kottkamp H, Hindricks G, Breithardt G, et al. Three-dimensional electromagnetic catheter technology: electroanatomical mapping of the right atrium and ablation of ectopic atrial tachycardia. J Cardiovasc Electrophysiol 1997;8:1332–7. 25. Nademanee K, Kosar EM. A nonfluoroscopic catheter-based mapping technique to ablate focal ventricular tachycardia. Pacing Clin Electrophysiol 1998;21:1442–7. 26. Natale A, Breeding L, Tomassoni G, et al. Ablation of right and left ectopic atrial tachycardias using a three-dimensional nonfluoroscopic mapping system. Am J Cardiol 1998;82:989–92. 27. Wetzel U, Hindricks G, Schirdewahn P, et al. A stepwise mapping approach for localization and ablation of ectopic right, left, and septal atrial foci using electroanatomic mapping. Eur Heart J 2002;23:1387–93. 28. Waldo AL. Treatment of atrial flutter. Heart 2000;84:227.
12. Garrigue S, Reuter S, Labeque JN, et al. Usefulness of biventricular pacing in patients with congestive heart failure and right bundle branch block. Am J Cardiol 2001;88:1436–41, A8.
29. Kottkamp H, Hugl B, Krauss B, et al. Electromagnetic versus fluoroscopic mapping of the inferior isthmus for ablation of typical atrial flutter: a prospective randomized study. Circulation 2000;102:2082–6.
13. Tse HF, Yu C, Wong KK, et al. Functional abnormalities in patients with permanent right ventricular pacing: the effect of sites of electrical stimulation. J Am Coll Cardiol 2002;40:1451–8.
30. Willems S, Weiss C, Ventura R, et al. Catheter ablation of atrial flutter guided by electroanatomic mapping (CARTO): a randomized comparison to the conventional approach. J Cardiovasc Electrophysiol 2000;11:1223–30.
14. Wilkoff BL, Cook JR, Epstein AE, et al. Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial. JAMA 2002;288:3115–23.
31. Saoudi N, Cosio F, Waldo A, et al. A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomical bases. A Statement from a Joint Expert Group from The Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Eur Heart J 2001;22(14):1162–82.
15. Pachon JC, Pachon EI, Albornoz RN, et al. Ventricular endocardial right bifocal stimulation in the treatment of severe dilated cardiomyopathy heart failure with wide QRS. Pacing Clin Electrophysiol 2001;24:1369–76. 16. Blanc JJ, Etienne Y, Gilard M, et al. Evaluation of different ventricular pacing sites in patients with severe heart failure: results of an acute hemodynamic study. Circulation 1997;96:3273–7.
32. Delacretaz E, Ganz LI, Soejima K, et al. Multi atrial maco-reentry circuits in adults with repaired congenital heart disease: entrainment mapping combined with three-dimensional electroanatomic mapping. J Am Coll Cardiol 2001;37:1665–76.
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 84
REFERENCES
33. Dorostkar PC, Cheng J, Scheinman MM. Electro-anatomical mapping and ablation of the substrate supporting intraatrial reentrant tachycardia after palliation for complex congenital heart disease. Pacing Clin Electrophysiol 1998;21:1810–19. 34. Nakagawa H, Shah N, Matsudaira K, et al. Characterization of reentrant circuit in macroreentrant right atrial tachycardia after surgical repair of congenital heart disease: isolated channels between scars allow “focal” ablation. Circulation 2001;103:699–709. 35. Peichl P, Kautzner J, Cihak R, et al. Clinical application of electro-anatomical mapping in the characterization of ‘incisional’ atrial tachycardias. Pacing Clin Electrophysiol 2003;26:420–5. 36. Triedman JK, Alexander ME, Berul CI, et al. Electroanatomic mapping of entrained and exit zones in patients with repaired congenital heart disease and intra-atrial reentrant tachycardia. Circulation 2001;103:2060–5. 37. Triedman JK, Alexander ME, Love BA, et al. Influence of patient factors and ablative technologies on outcomes of radiofrequency ablation of intra-atrial re-entrant tachycardia in patients with congenital heart disease. J Am Coll Cardiol 2002;39:1827–35. 38. Jais P, Shah DC, Haissaguerre M, et al. Mapping and ablation of left atrial flutters. Circulation 2000;101:2928–34. 39. Ouyang F, Ernst S, Vogtmann T, et al. Characterization of reentrant circuits in left atrial macroreentrant tachycardia: critical isthmus block can prevent atrial tachycardia recurrence. Circulation 2002;105:1934–42. 40. Marrouche NF, Natale A, Wazni OM, et al. Left septal atrial flutter: electrophysiology, anatomy, and results of ablation. Circulation 2004;109:2440–7. 41. Haissaguerre M, Marcus FI, Fischer B, et al. Radiofrequency catheter ablation in unusual mechanisms of atrial fibrillation: report of three cases. J Cardiovasc Electrophysiol 1994;5:743–51. 42. Haissaguerre M, Jais P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998;339:659–66. 43. Kholova I, Kautzner J. Anatomic characteristics of extensions of atrial myocardium into the pulmonary veins in subjects with and without atrial fibrillation. Pacing Clin Electrophysiol 2003;26:1348–55. 44. Saito T, Waki K, Becker AE. Left atrial myocardial extension onto pulmonary veins in humans: anatomic observations relevant for atrial arrhythmias. J Cardiovasc Electrophysiol 2000;8:888–94. 45. Perez-Lugones A, McMahon JT, Ratliff NB, et al. Evidence of specialized conduction cells in human pulmonary veins of patients with atrial fibrillation. J Cardiovasc Electrophysiol 2003;8:803–9. 46. Haissaguerre M, Shah DC, Jais P, et al. Electrophysiological breakthroughs from the left atrium to the pulmonary veins. Circulation 2000;102:2463–5. 47. Saad EB, Rossillo A, Saad CP, et al. Pulmonary vein stenosis after radiofrequency ablation of atrial fibrillation: functional characterization, evolution, and influence of the ablation strategy. Circulation 2003;108:3102–7. 48. Cappato R, Negroni S, Pecora D, et al. Prospective assessment of late conduction recurrence across radiofrequency lesions producing electrical disconnection at the pulmonary vein ostium in patients with atrial fibrillation. Circulation 2003;108:1599–1604. 49. Jais P, Hocini M, Hsu LF, et al. Technique and results of linear ablation at the mitral isthmus. Circulation 2004; 110:2996–3002.
84
52. Kottkamp H, Tanner H, Kobza R, et al. Time courses and quantitative analysis of atrial fibrillation episode number and duration after circular plus linear left atrial lesions: trigger elimination or substrate modification: early or delayed cure? J Am Coll Cardiol 2004;44:869–77. 53. Pappone C, Rosanio S, Augello G, et al. Mortality, morbidity, and quality of life after circumferential pulmonary vein ablation for atrial fibrillation: outcomes from a controlled non-randomized long-term study. J Am Coll Cardiol 2003;43:185–97. 54. Oral H, Scharf C, Chugh A, et al. Catheter ablation for paroxysmal atrial fibrillation: segmental pulmonary vein ostial ablation versus left atrial ablation. Circulation 2003;108:2355–60. 55. Pappone C, Oral H, Santinelli V, et al. Atrio-esophageal fistula as a complication of percutaneous transcatheter ablation of atrial fibrillation. Circulation 2004;109:2724–6. 56. Mansour M, Ruskin J, Keane D. Efficacy and safety of segmental ostial versus circumferential extra-ostial pulmonary vein isolation for atrial fibrillation. J Cardiovasc Electrophysiol 2004;15:532–7. 57. Ouyang F, Antz M, Ernst S, et al. Recovered pulmonary vein conduction as a dominant factor for recurrent atrial tachyarrhythmias after complete circular isolation of the pulmonary veins: lessons from double Lasso technique. Circulation 2005;111:127–35. 58. Marrouche NF, Martin DO, Wazni O, et al. Phased-array intracardiac echocardiography monitoring during pulmonary vein isolation in patients with atrial fibrillation: impact on outcome and complications. Circulation 2003;107:2710–16. 59. Wood MA, Shaffer KM, Ellenbogen AL, et al. Microbubbles during radiofrequency catheter ablation: composition and formation. Heart Rhythm 2005;2:397–403. 60. Chen MS, Marrouche NF, Khaykin Y, et al. Pulmonary vein isolation for the treatment of atrial fibrillation in patients with impaired systolic function. J Am Coll Cardiol 2004;43:1004–9. 61. Nademanee K, McKenzie J, Kosar E, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol 2004;43:2044–53. 62. Jongbloed MR, Bax JJ, Lamb HJ, et al. Multislice computed tomography versus intracardiac echocardiography to evaluate the pulmonary veins before radiofrequency catheter ablation of atrial fibrillation: a head-to-head comparison. J Am Coll Cardiol 2005;45:343–50. 63. Mlcochova H, Tintera J, Porod V, et al. Magnetic resonance angiography of pulmonary veins: implications for catheter ablation of atrial fibrillation. Pacing Clin Electrophysiol 2005;28:1073–80. 64. Haissaguerre M, Jais P, Shah DC, et al. Analysis of electrophysiological activity in Koch’s triangle relevant to ablation of the slow AV nodal pathway. Pacing Clin Electrophysiol 1997;20:2470–81. 65. Kwaku KF, Josephson ME. Typical AVNRT: an update on mechanisms and therapy. Card Electrophysiol Rev 2002;6:414–21. 66. Cooke PA, Wilber DJ. Radiofrequency catheter ablation of atrioventricular nodal reentry tachycardia utilizing nonfluoroscopic electro-anatomical mapping. Pacing Clin Electrophysiol 1998;21:1802–9. 67. Pollak SJ, Dreifus LS. Ablation of nonparoxysmal A-V nodal tachycardia. J Electrocardiol 2002;35:75–80. 68. Lee RJ, Kalman JM, Fitzpatrick AP, et al. Radiofrequency catheter modification of the sinus node for ‘inappropriate’ sinus tachycardia. Circulation 1995;92:2919–28.
50. Pappone C, Rosanio S, Oreto G, et al. Circumferential radiofrequency ablation of pulmonary vein ostia: a new anatomic approach for curing atrial fibrillation. Circulation 2000;102:2619–28.
69. Leonelli F, Richey M, Beheiry S, et al. Tridimensional mapping: guided modification of the sinus node. J Cardiovasc Electrophysiol 1998;9:1214–17.
51. Pappone C, Oreto G, Rosanio S, et al. Atrial electroanatomic remodeling after circumferential radiofrequency pulmonary vein ablation: efficacy of an anatomic approach in a large cohort of patients with atrial fibrillation. Circulation 2001;104:2539–44.
70. Marrouche NF, Beheiry S, Tomassoni G, et al. Three-dimensional nonfluoroscopic mapping and ablation of inappropriate sinus tachycardia. Procedural strategies and long-term outcome. J Am Coll Cardiol 2002;39:1046–54.
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 85
REFERENCES
90.
Tsuchiya T, Okumura K, Honda T, et al. Significance of late diastolic potential preceding Purkinje potential in verapamil-sensitive idiopathic left ventricular tachycardia. Circulation 1999;99:2408–13.
91.
Yano K, Keida T, Suzuki K, et al. Catheter ablation of idiopathic left ventricular tachycardia with multiple breakthrough sites guided by an electroanatomical mapping system. J Interv Card Electrophysiol 2001;5:211–14.
92.
Ouyang F, Cappato R, Ernst S, et al. Electroanatomic substrate of idiopathic left ventricular tachycardia: unidirectional block and macroreentry within the purkinje network. Circulation 2002;105:462–9.
93.
de Chillou C, Lacroix D, Klug D, et al. Isthmus characteristics of reentrant ventricular tachycardia after myocardial infarction. Circulation 2002;105:726–31.
94.
76. Weng KP, Wolff GS, Young ML. Multiple accessory pathways in pediatric patients with Wolff–Parkinson–White syndrome. Am J Cardiol 2003;91:1178–83.
Soejima K, Suzuki M, Maisel WH, et al. Catheter ablation in patients with multiple and unstable ventricular tachycardias after myocardial infarction: short ablation lines guided by reentry circuit isthmuses and sinus rhythm mapping. Circulation 2001;104:664–9.
95.
77. Ai T, Ikeguchi S, Watanuki M, et al. Successful radiofrequency current catheter ablation of accessory atrioventricular pathway in Ebstein’s anomaly using electroanatomic mapping. Pacing Clin Electrophysiol 2002;25:374–5.
Soejima K, Stevenson WG, Maisel WH, et al. Electrically unexcitable scar mapping based on pacing threshold for identification of the reentry circuit isthmus: feasibility for guiding ventricular tachycardia ablation. Circulation 2002;106:1678–83.
96.
Delacretaz E, Stevenson WG. Catheter ablation of ventricular tachycardia in patients with coronary heart disease. Part II: Clinical aspects, limitations, and recent developments. Pacing Clin Electrophysiol 2001;24:1403–11.
97.
Kottkamp H, Wetzel U, Schirdewahn P, et al. Catheter ablation of ventricular tachycardia in remote myocardial infarction: substrate description guiding placement of individual linear lesions targeting non-inducibility. J Cardiovasc Electrophysiol 2003;14:675–81.
98.
Reddy VY, Neuzil P, Taborsky M, et al. Short-term results of substrate mapping and radiofrequency ablation of ischemic ventricular tachycardia using a saline-irrigated catheter. J Am Coll Cardiol 2003;41:2228–36.
81. Dixit S, Gerstenfeld EP, Callans DJ, et al. Electrocardiographic patterns of superior right ventricular outflow tract tachycardias: distinguishing septal and free-wall sites of origin. J Cardiovasc Electrophysiol 2003;14:1–7.
99.
Kautzner J, Cihak R, Peichl P, et al. Catheter ablation of ventricular tachycardia following myocardial infarction using three-dimensional electro-anatomical mapping. Pacing Clin Electrophysiol 2003;26:342–7.
82. Boulos M, Lashevsky I, Gepstein L. Usefulness of electroanatomical mapping to differentiate between right ventricular outflow tract tachycardia and arrhythmogenic right ventricular dysplasia. Am J Cardiol 2005;95:935–40.
100. Marchlinski FE, Callans DJ, Gottlieb CD, et al. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation 2000;101:1288–96.
83. Callans DJ, Menz V, Schwartzman D, et al. Repetitive monomorphic tachycardia from the left ventricular outflow tract: electrocardiographic patterns consistent with a left ventricular site of origin. J Am Coll Cardiol 1997;29:1023–7.
101. Brunckhorst CB, Delacretaz E, Soejima K, et al. Identification of the ventricular tachycardia isthmus after infarction by pace mapping. Circulation 2004;110:652–9.
71. Schweikert RA, Saliba WI, Tomassoni G, et al. Percutaneous pericardial instrumentation for endo-epicardial mapping of previously failed ablations. Circulation 2003;108:1329–35. 72. Koplan BA, Parkash R, Couper G, et al. Combined epicardial-endocardial approach to ablation of inappropriate sinus tachycardia. J Cardiovasc Electrophysiol 2004;15:237–40. 73. Chen SA, Tai CT. Ablation of atrioventricular accessory pathways: current technique-state of the art. Pacing Clin Electrophysiol 2001;24:1795–809. 74. Cosio FG, Anderson RH, Kuck KH, et al. Living anatomy of the atrioventricular junctions. A guide to electrophysiologic mapping. A Consensus Statement from the Cardiac Nomenclature Study Group, Working Group of Arrhythmias, European Society of Cardiology, and the Task Force on Cardiac Nomenclature from NASPE. Circulation 1999;100:e31–7. 75. Drago F, Silvetti MS, Di Pino A, et al. Exclusion of fluoroscopy during ablation treatment of right accessory pathway in children. J Cardiovasc Electrophysiol 2002;13:778–82.
78. Goya M, Takahashi A, Nakagawa H, et al. A case of catheter ablation of accessory atrioventricular connection between the right atrial appendage and right ventricle guided by a three-dimensional electroanatomic mapping system. J Cardiovasc Electrophysiol 1999;10:1112–18. 79. Josephson ME. Electrophysiology of ventricular tachycardia: an historical perspective. J Cardiovasc Electrophysiol 2003;14:1134–48. 80. Lerman BB, Stein K, Engelstein ED, et al. Mechanism of repetitive monomorphic ventricular tachycardia. Circulation 1995;92:421–9.
84. Sadanaga T, Saeki K, Yoshimoto T, et al. Repetitive monomorphic ventricular tachycardia of left coronary cusp origin. Pacing Clin Electrophysiol 1999;22:1553–6.
102. Sosa E, Scanavacca M, d’Avila A, et al. Nonsurgical transthoracic epicardial catheter ablation to treat recurrent ventricular tachycardia occurring late after myocardial infarction. J Am Coll Cardiol 2000;35:1442–9.
85. Tanner H, Hindricks G, Schirdewahn P, et al. Outflow tract tachycardia with R/S transition in lead V3: six different anatomic approaches for successful ablation. J Am Coll Cardiol 2005;45:418–23.
103. Soejima K, Stevenson WG, Sapp JL, et al. Endocardial and epicardial radiofrequency ablation of ventricular tachycardia associated with dilated cardiomyopathy: the importance of low-voltage scars. J Am Coll Cardiol 2004;43:1834–42.
86. Dixit S, Gerstenfeld EP, Lin D, et al. Identification of distinct electrocardiographic patterns from the basal left ventricle: distinguishing medial and lateral sites of origin in patients with idiopathic ventricular tachycardia. Heart Rhythm 2005;2:485–91.
104. de Bakker JM, Stein M, van Rijen HV. Three-dimensional anatomic structure as substrate for ventricular tachycardia/ventricular fibrillation. Heart Rhythm 2005;2:777–9.
87. Tada H, Ito S, Naito S, et al. Idiopathic ventricular arrhythmia arising from the mitral annulus: a distinct subgroup of idiopathic ventricular arrhythmias. J Am Coll Cardiol 2005;45:877–86. 88. Nakagawa H, Beckman KJ, McClelland JH, et al. Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a Purkinje potential. Circulation 1993;88:2607–17. 89. Zardini M, Thakur RK, Klein GJ, et al. Catheter ablation of idiopathic left ventricular tachycardia. Pacing Clin Electrophysiol 1995;18:1255–65.
105. Pogwizd SM, McKenzie JP, Cain ME. Mechanisms underlying spontaneous and induced ventricular arrhythmias in patients with idiopathic dilated cardiomyopathy. Circulation 1998;98:2404–14. 106. Wilders R, Wagner MB, Golod DA, et al. Effects of anisotropy on the development of cardiac arrhythmias associated with focal activity. Pflugers Arch 2000;441:301–12. 107. Hsia HH, Callans DJ, Marchlinski FE. Characterization of endocardial electrophysiological substrate in patients with nonischemic cardiomyopathy and monomorphic ventricular tachycardia. Circulation 2003;108:704–10.
85
R7631_ElMapHeart_03.qxd
6/3/06
16:14
Page 86
REFERENCES
108. Delacretaz E, Stevenson WG, Ellison KE, et al. Mapping and radiofrequency catheter ablation of the three types of sustained monomorphic ventricular tachycardia in nonischemic heart disease. J Cardiovasc Electrophysiol 2000;11:11–17.
116. Stevenson WG, Delacretaz E, Friedman PL, et al. Identification and ablation of macroreentrant ventricular tachycardia with the CARTO electro-anatomical mapping system. Pacing Clin Electrophysiol 1998;21:1448–56.
109. Corrado D, Basso C, Thiene G. Arrhythmogenic right ventricular cardiomyopathy: diagnosis, prognosis, and treatment. Heart 2000;83:588–95.
117. Rostock T, Willems S, Ventura R, et al. Radiofrequency catheter ablation of a macroreentrant ventricular tachycardia late after surgical repair of tetralogy of Fallot using the electroanatomic mapping (CARTO). Pacing Clin Electrophysiol 2004;27:801–4.
110. Marchlinski FE, Zado E, Dixit S, et al. Electroanatomic substrate and outcome of catheter ablative therapy for ventricular tachycardia in setting of right ventricular cardiomyopathy. Circulation 2004;110:2293–8. 111. Boulos M, Lashevsky I, Reisner S, et al. Electroanatomic mapping of arrhythmogenic right ventricular dysplasia. J Am Coll Cardiol 2001;38:2020–7.
119. Haissaguerre M, Shah DC, Jais P, et al. Role of Purkinje conducting system in triggering of idiopathic ventricular fibrillation. Lancet 2002;359:677–8.
112. Reithmann C, Hahnefeld A, Remp T, et al. Electroanatomic mapping of endocardial right ventricular activation as a guide for catheter ablation in patients with arrhythmogenic right ventricular dysplasia. Pacing Clin Electrophysiol 2003;26:1308–16.
120. Haissaguerre M, Shoda M, Jais P, et al. Mapping and ablation of idiopathic ventricular fibrillation. Circulation 2002;106:962–7.
113. Gatzoulis MA, Balaji S, Webber SA, et al. Risk factors for arrhythmia and sudden cardiac death late after repair of tetralogy of Fallot: a multicentre study. Lancet 2000;356:975–81. 114. Harrison DA, Harris L, Siu SC, et al. Sustained ventricular tachycardia in adult patients late after repair of tetralogy of Fallot. J Am Coll Cardiol 1997;30:1368–73. 115. Gonska BD, Cao KM, Raab JM, et al. Heart disease in the young: radiofrequency catheter ablation of right ventricular tachycardia late after repair of congenital heart defects. Circulation 1996;94:1902–8.
86
118. Kautzner J, Bytesnik J. Catheter ablation of arrhythmogenic focus in ‘short coupled’ variant of torsade de pointes. Pacing Clin Electrophysiol 2000;23:717 (abstract).
121. Haissaguerre M, Extramiana F, Hocini M, et al. Mapping and ablation of ventricular fibrillation associated with long-QT and Brugada syndromes. Circulation 2003;108:925–8. 122. Bansch D, Oyang F, Antz M, et al. Successful catheter ablation of electrical storm after myocardial infarction. Circulation 2003;108:3011–6. 123. Friedman PL, Stewart JR, Fenoglio JJ Jr, et al. Survival of subendocardial Purkinje fibers after extensive myocardial infarction in dogs. Circ Res 1973;33:597–611. 124. Marrouche NF, Verma A, Wazni O, et al. Mode of initiation and ablation of ventricular fibrillation storms in patients with ischemic cardiomyopathy. J Am Coll Cardiol 2004;43:1715–20.
