Abstract
Ventricular tachycardia (VT) in the setting of structural heart disease, whether ischemic or nonischemic in etiology, is usually caused by reentry caused by the presence of scar. Catheter ablation has become an effective treatment for management of VT among such patients, especially with the recognition that arrhythmogenic substrate can be identified and targeted in sinus rhythm. As one third of patients have only hemodynamically tolerated VT, substrate-based ablation has become a routine part of most VT ablation procedures. Electroanatomic mapping systems, improved mapping and ablation tools, and imaging techniques, such as intracardiac echocardiography, have facilitated the development of improved techniques for ablation of VT substrate, with associated improvements in outcomes. Given the relative safety with which VT ablation can be performed, as well as the relative efficacy in VT-free survival that can be achieved using substrate-based approaches, VT ablation is no longer considered a treatment of last resort for patients with structural heart disease. This chapter aims to describe various approaches for performing substrate-based VT ablation, among both ischemic and nonischemic cardiomyopathies, for whom the VT mechanism of reentry is demonstrated or presumed to predominate clinical episodes.
Keywords
cardiomyopathy, catheter ablation outcomes, heart failure, ventricular tachycardia
Key Points
Mapping
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Arrhythmogenic substrate in ventricular tachycardia (VT) in the setting of structural heart disease is usually living but diseased myocardium within scar, which promotes reentry. This substrate can usually be identified and effectively targeted with ablation in sinus rhythm. Relevant substrate features are consistent with abnormal conduction and include (1) low-amplitude, high-frequency, bipolar signals, including late potentials in sinus rhythm or local abnormal ventricular activities provoked with pacing; (2) sites at which pace maps demonstrate exit or central isthmus characteristics; (3) lowamplitude unipolar signals from left or right ventricular endocardium. Substrate may also be directly visualized with preprocedure imaging or periprocedural intracardiac echocardiography (ICE).
Ablation Targets
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Ablation is targeted to regions identified on mapping, as aforementioned, to render the substrate electrically inexcitable. VT noninducibility following ablation is the most common end point. Others have evolved to include demonstration of entrance block (subsequent absence of conduction into the targeted region following ablation) and exit block (also known as “core isolation,” or absence of pace capture within a region that could be captured before ablation).
Special Equipment
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Electroanatomic mapping systems are critical for effective identification and visualization of substrate. ICE is not critical but is extremely helpful in identifying substrate as well as in confirming catheter location and facilitating safety. Multipolar catheters can assist with higher-resolution and higher density mapping. Irrigated-tip ablation catheters are essential for effective radiofrequency delivery.
Sources of Difficulty
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Presence of midmyocardial substrate, proximity of VT substrate to other critical anatomic structures, including coronary arteries and proximal His-Purkinje system, each add difficulty to effective VT control. However, at experienced centers, effective VT control can be achieved in the majority of patients
Introduction
Fibrotic tissue, and its ability to promote arrhythmogenic substrate when incorporated into living myocardium, was recognized decades ago among patients with prior myocardial infarction (MI) and ventricular tachycardia (VT). This concept was exemplified by the results obtained from the early cardiac surgical experiences in invasive VT management, which subsequently provided the framework for contemporary catheter-based strategies for substrate modification. Patients considered for treatment at that time were those with refractory VT following transmural MI that produced both left ventricular (LV) systolic dysfunction and aneurysm formation. The initial approach for surgical treatment included resection of densely scarred aneurysm only, sometimes with concomitant coronary arterial bypass grafting; however, VT recurrence rates using this approach were disappointingly high, approaching 80% in some series. Electrophysiologic (EP) data collected during the surgical era of post-MI VT treatment provided important information regarding (1) reentry as the mechanism in most cases and (2) localization to the subendocardium (1–2 mm thickness) of the most critical VT reentry elements, those areas of diseased but surviving myocytes contained within channels protected by surrounding scar or other electrically inert anatomic barriers ( Figs. 33.1 and 33.2 ). Guided by data as demonstrated in Fig. 33.3 , subendocardial resection among the patients who survived the surgery led to effective arrhythmia control in more than 90% over a mean follow-up time of more than 2 years, further validating the concepts generated from EP study and characterization.
The involvement of scar and associated reentry in monomorphic VT among patients with nonischemic etiologies for structural heart disease (SHD) has also now become well recognized. Therefore the invasive treatment of VT in these patients has mirrored the approaches taken for VT in the post-MI setting, focusing on modification of arrhythmogenic substrate.
The advent of catheter ablation using radiofrequency (RF) energy as an ablation source in the 1980s, followed by rapid advancements in electroanatomic mapping (EAM) tools, led to several important milestones in our ability to effectively manage these patients. First, it was now possible to “see” potentially arrhythmogenic substrate without the need for direct visualization with open heart surgery and attendant surgical risks. Secondly, and perhaps most importantly, many of these characteristics could be identified and ablated during sinus rhythm, without the need for repeated and sustained VT inductions and entrainment or activation mapping. Because less than one third of patients with VT have only hemodynamically tolerated VT that is able to be mapped with repeated entrainment maneuvers, substrate-based ablation has become a routine part of most VT ablation procedures among those with SHD. This technique has helped to increase the proportion of such patients that can be effectively treated and has provided incremental gains in preventing recurrent VT and implantable cardioverter-defibrillator (ICD) therapies. Given the relative safety with which VT ablation can be performed, as well as the relative efficacy in VT-free survival that can be achieved using substrate-based approaches, VT ablation is no longer considered a treatment of last resort for patients with SHD.
This chapter aims to describe various approaches for performing substrate-based VT ablation, among both ischemic and nonischemic cardiomyopathies for whom the VT mechanism of reentry is demonstrated or presumed to predominate clinical episodes.
Anatomy and Pathophysiology
The anatomic elements of a VT circuit are comprised of surviving myocardial tissue within a region of electrically inert fibrotic scar tissue. Although scar is usually implicated as the etiology of VT in patients with SHD, the scar tissue itself is electrically unexcitable and, in and of itself, is not the actual target for ablation; this is the likely reason that surgically-based resection of only dense scar had such poor efficacy in controlling VT. The true areas of interest in such patients are the regions of surviving myocytes that are usually contained within or are at the border zones of these areas of fibrosis (see Fig. 33.1 ). These myocytes contain disrupted and reduced numbers of gap junctions, which lead to nonuniform conduction, slowing of conduction velocity, and altered refractory periods. Differentially and abnormally conducting tissue connected in series, or channels, then provide the elements that allow for reentry to occur and sustain. These properties include the potential to develop unidirectional block and areas of slowed conduction through which reentrant wave fronts can propagate once initiated. An important feature of this substrate, especially in the context of understanding how modification is effective, is that these channels of conducting tissue that exist within abnormal and fibrotic substrate are numerous and are usually not fixed in conduction velocity or conduction vector. In other words, unidirectional block can be provoked within the same tissue in disparate directions depending on the site and method of initiating reentry; using various pathways of conduction, several distinctive VTs based on QRS morphology and even cycle length can thus result from varying exits or other components of VT circuits propagating differently but within the same abnormal substrate (see Fig. 33.3 ). Identifying areas containing potential channels of conduction and rendering them electrically inert with ablation, functionally making existing scar tissue more electrically homogeneous, is the ultimate goal of most forms of contemporary substrate modification.
The most common method used for identifying fibrotic myocardium has been to identify regions of reduced or absent electrogram (EGM) voltage during sinus rhythm using a roving mapping catheter. Use of an EAM system to record location and EGM voltage rendering a 3-dimensional model is critical to all substrate modification strategies. Of note, identifying areas with low-amplitude bipolar signals represents only a starting point for identification of relevant substrate. Signals within abnormal myocardium involved in reentry typically display other characteristics consistent with abnormal conduction, including high-frequency, multicomponent fractionation; prolonged duration (>80 ms); or activation continuing or occurring after global ventricular activation has occurred, as manifested by the completion of the surface QRS complex (see Figs. 33.1–33.3 and Fig. 33.4 ). The latter, so-called late potentials (LPs), have frequently been found at critical sites within reentrant VT circuits, including 89% of isthmus sites, 57% of entrance, and 20% of exit sites. Identification of EGMs with reduced voltage and abnormal characteristics forms the basis for substrate modification using catheter ablation.
Nonischemic Versus Ischemic Ventricular Tachycardia Substrate
Most of the research discussed thus far has been based on work performed in the context of ischemic heart disease. Although these concepts have also been demonstrated to be useful and applicable to VT ablation in nonischemic heart disease, several important differences exist in ischemic versus nonischemic substrates that should be highlighted.
In contrast to the fairly predictable scar distribution encountered in patients with ischemic heart disease and VT, scar characteristics and distribution among patients with nonischemic cardiomyopathy (NICM) can be far more heterogeneous and, relatively speaking, more 3-dimensional ( Fig. 33.5 ). A periannular location of substrate has been identified to be relatively common, around the mitral valve among patients with idiopathic dilated LV cardiomyopathy and around the tricuspid valve among those with arrhythmogenic right ventricular cardiomyopathy (ARVC). However, there is a wide variation of other presentations, especially when taking into account other nonischemic etiologies for SHD, including prior myocarditis, cardiac sarcoidosis, or other infiltrative cardiomyopathies. Notably, NICM substrates more often involve the epicardium as well as the mid-myocardium. In some instances, the substrate is entirely localized within the mid-myocardium or septum ( Fig. 33.6 ). Increasingly recognized is that NICM substrate for VT can be present among patients with a known history of coronary artery disease and even with a known history of prior MI, at a rate that likely exceeds a previously reported rate of 1.2%. Recognizing this potential in planning for ablation is important because of the far greater challenges that are encountered in ablation of VT in NICM.
Presentations such as these confound our ability to identify substrate using conventionally accepted mapping techniques. Standard bipolar voltage mapping, for instance, provides great detail with respect to the tissue with which a mapping catheter’s electrodes are in direct contact, but it provides limited information regarding tissue that is deeper to the tip–tissue interface. Limitations in identifying such substrate may be especially enhanced when using contemporary multipolar catheters with small interelectrode spacing, as these bipoles reflect an even narrower field of view than those with larger interelectrode spacing. Use of unipolar mapping, during which signals are recorded between the distal electrode (cathode) and an anode placed at an electrically inert and remote location, for instance at Wilson’s central terminus, widens the field of view substantially. This type of mapping compromises the ability to assess EGM detail but may allow for gross appreciation of deeper substrate abnormalities ( Fig. 33.7 ).
Therefore potentially epicardial or mid-myocardial substrate can still be identified from endocardial mapping, but with assessment of unipolar EGMs instead of bipolar signals. This concept was demonstrated to be valid among cohorts of VT patients with LV NICM and ARVC who underwent detailed endocardial and epicardial mapping with modest to no identifiable endocardial substrate and among whom endocardial unipolar voltage cutoffs could be validated with bipolar epicardial signal analysis. Use of adjunctive imaging, for instance with preprocedural cardiac magnetic resonance imaging (cMRI) or with intraprocedural ICE, has also been demonstrated to be of particular value among patients with NICM and VT, based on challenges that exist in identifying substrate using only EP mapping tools ( Fig. 33.8 ).
However, even once identified or recognized, additional challenges exist in effectively penetrating to regions of interest using standard ablation techniques, and achieving effective VT control in such patients has been repeatedly demonstrated to be challenging in observational studies and clinical trials. Despite challenges, scar within myocardium has been demonstrated to produce a compartmentalization effect, delaying transmural conduction times and often disrupting intramural activation patterns ( Fig. 33.9 ). This compartmentalization effect can sometimes confer an advantage; the scar tissue that provides a barrier to transmural conduction can also sometimes be used as a reinforcing anchor for ablation lesions, assuming that the lesions can penetrate to the scar. Often times, repeated ablations or use of adjunctive ablation techniques (discussed later in this chapter) are necessary to achieve success comparable to what can be achieved with less effort among patients who have had VT related to prior MI.
Mapping Ventricular Tachycardia Substrate
Several mapping approaches have been developed to identify relevant substrate for ablation and effective ventricular arrhythmia control, many of which have substantial overlap, and many of which then guide subsequent ablation strategies. The following sections and Tables 33.1 and 33.2 highlight the approaches that have come to form the foundation of contemporary substrate modification for VT management.
| Identified During Sinus or Paced Rhythm |
|---|
| Low-Amplitude Electrograms (EGMs) on Voltage Map Bipolar signals:
|
Sites Demonstrating Abnormal Local Conduction
|
| Sites With Favorable Pace Map Characteristics One or more of the following:
|
Identified While Mapping in Ventricular Tachycardia, if Tolerated
|
| Ablation Strategy | Ablation End Point in Addition to VT Noninducibility | Outcomes From Index Publications |
|---|---|---|
| Direct Ablation at All Sites of Interest | ||
| Local abnormal ventricular activity (LAVA) ablation | Elimination of all LAVAs, including but not limited to late potentials |
|
| Late potential abolition | Elimination of all late potentials |
|
| Scar homogenization | Elimination of all evidence for abnormal local conduction (late potentials and abnormal EGMs), within regions of bipolar EGM amplitude ≤1.5 mV | Ischemic cardiomyopathy:
|
| Selective Ablation | ||
| Scar dechanneling: Ablation at presumed conducting channel (CC) entrance sites within scar, characterized byLate potentials of shortest delay following global ventricular activation and Bipolar signal voltage ≤ 1.5 mV | Elimination of all identified CCs into scar following targeted ablation at entrance sites |
|
| Core isolation: ablation encircling sites within scar with VT circuit isthmus features characterized byBipolar signal amplitude ≤ 1.5 mV (≤ 1.0 mV when possible) and Late potentials, abnormal EGMs, or dense scar regions with channels of conduction and Pace capture with favorable pace map characteristics or Isthmus sites identified on limited activation or entrainment during VT |
|
|
Mapping Tools
Tools that are essential for substrate-based VT mapping and ablation include an EAM system and associated mapping catheter(s), which can be comprised of a single bipolar electrode for point-to-point mapping (typically the ablation catheter is used in this instance) or multiple electrodes. The advantage of mapping with the ablation catheter is that simultaneous mapping and ablation can occur; to ablate in concert with mapping using multipolar catheters, either multiple access sites to the chamber being mapped must be obtained (i.e., retrograde aortic and transseptal accesses in the case of endocardial LV mapping) or catheter exchanges need to be performed. However, multipolar mapping catheters confer the additional advantage of smaller electrode sizes and interelectrode spacing, which allow for greater precision, detail, and speed in mapping.
Not required but usually helpful for both mapping and ablation is phased-array ICE. ICE provides real-time imaging to confirm catheter location and contact; assess for anatomic variations and structures such as papillary muscles that may challenge catheter movement or alter ablation approach; assess for acute complications such as cardiac perforation and effusion or worsening systolic function; and to reduce use of fluoroscopy. ICE is especially useful when epicardial or mid-myocardial substrate is present. Scar often appears as regions of increased echogenicity on ICE and can be quickly identified with initial catheter placement and image acquisition and even before any EP mapping has occurred. Hyperechoic regions within the mid-myocardium or epicardium often correlate with unipolar voltage abnormalities (see Fig. 33.8B ) and can substantiate the need for additional mapping (and ablation) on the surface opposite to that which has already been mapped (i.e., the epicardium or right ventricular [RV] side of the septum). ICE can be used in conjunction with any of the commercially available EAM systems. However, currently only the CARTO system (Biosense Webster, Diamond Bar, CA) has the capability of integrating ICE images into the EAM, using the CARTO Sound catheter (see Fig. 33.8E ). This feature can be helpful in facilitating rapid 3-dimensional anatomic reconstruction of the chamber of interest, based on fusion of 2-dimensional ICE images taken at different angles. It can also incorporate locations and anatomy of papillary muscles or other anatomic variations directly into the map, as well as superimpose a visual substrate reference into the map, all of which facilitate mapping and ablation.
Ventricular Tachycardia Induction
VT induction is usually attempted at multiple junctures during a case, even for substrate-based ablation cases. At the beginning of the case, either before or after a substrate map is created, this is performed for several reasons: (1) to gain a gross understanding of the number of monomorphic VTs that may need to be targeted, which is especially relevant in the frequent instances in which 12-lead electrocardiograms (ECGs) of spontaneously occurring (“clinical”) VTs are unavailable; (2) to estimate potential exit sites (and potential sites to focus mapping and ablation) based on 12-lead morphology of induced VTs and acquire 12-lead templates from which subsequent mapping can be based; and (3) to confirm that substrate-based, reentrant VT can account for the clinical tachycardias experienced by the patient, thus justifying proceeding with substrate modification. At subsequent intervals during ablation, VT induction is also often attempted to determine the end point for ablation (discussed in greater detail later).
Programmed electrical stimulation (PES) methods can vary, but a widely used protocol is to pace for 8 beats using constant pacing drive cycle lengths of 600 and 400 ms followed by the introduction of one to three extrastimuli until VT is induced or the ventricular effective refractory period is reached. Performing PES at multiple ventricular sites other than the RV apex, such as the RV outflow tract or the LV, also can be useful in some patients in whom stimulation from the RV apex fails to induce VT. The ability to induce sustained monomorphic VT increases successively with the introduction of up to three extrastimuli. Beyond three extrastimuli, the probability of inducing monomorphic VT increases only marginally whereas the potential to induce polymorphic VT or ventricular fibrillation (VF) increases more substantially.
Voltage Mapping
Reference values for “normal” bipolar voltage were defined by mapping the right ventricle and left ventricle among six patients without SHD and with the use of the CARTO EAM system. Specifically, the nadir-to-peak amplitudes of all bipolar ventricular EGM signals obtained with a mapping catheter comprised of a 4-mm-tip electrode, 2-mm-ring electrode, separated by 1-mm interelectrode distance were measured from the endocardial right ventricle and left ventricle. Among normal right ventricles, the mean ± standard deviation EGM amplitude was 3.7 ± 1.7 mV; although the range of normal values obtained varied from 0.4 to 11.5 mV, 95% or more of all signals were higher than 1.44 mV. In normal LV endocardium, mean EGM amplitude was 4.8 ± 3.1 mV, with a range of 0.6 to 20.5 mV; 95% or more of all signals were higher than 1.55 mV. For ease of use, an average normal value of greater than 1.5 mV was then generated, and this value has persisted as the standard for identifying normal bipolar endocardial ventricular EGM amplitude or voltage. Using a similar approach among eight patients with structurally normal hearts, a reference value of greater than 1.0 mV was determined to be consistent with normal epicardial EGM amplitude, after taking care to exclude areas of major coronary arterial distribution and associated epicardial fat (within 1 cm of these regions), both of which can lead to artificially low-amplitude signals because of poor contact with myocardium rather than reflect true abnormality of tissue. Abnormal endocardial bipolar signal amplitude correlating with “dense scar” was derived from intraoperative VT mapping data and defined as less than 0.5 mV. Remember that signal analysis based on voltage alone is insufficient for identifying relevant substrate—poor catheter contact can produce low voltage that does not correlate with substrate of interest. Other features indicating abnormal conduction must also be present, including fractionation, or late or prolonged duration of activation, as described previously in the Anatomy and Pathophysiology section.
Interrogated sites can be color-coded based on voltage amplitude and displayed on the EAM, producing a 3-dimensional reconstruction of the chamber of interest with EGM information at each site sampled by the catheter, and visually highlighting relevant substrate within which more detailed mapping and ablation should be focused. Although these values were developed and validated using the magnetic-based CARTO system (Biosense Webster, Diamond Bar, CA), other mapping systems incorporating impedance-based methods for sensing intracardiac catheter position and visualization have also been developed and are used clinically, including EnSite (Abbott, Minneapolis, MN) and Rythmia (Boston Scientific, Minneapolis, MN). The accuracy in location, activation, and scar identification in each of these systems has been validated with in vivo, imaging, or histopathologic correlation studies.
In a method similar to that which was used to determine normal bipolar endocardial signal amplitudes, reference values for normal LV and RV endocardial unipolar voltage were determined by assessing voltage characteristics among patients without SHD (six in the LV endocardial unipolar validation study and eight in the RV endocardial unipolar validation study). More than 95% of unipolar endocardial EGMs acquired from normal left ventricles had an amplitude higher than 8.27 mV (mean, 19.6 ± 6.9 mV), and more than 95% of those acquired from normal right ventricles had an amplitude greater than 5.5 mV (see Fig. 33.7 ). Using these reference values, endocardial LV unipolar voltage less than 8.3 mV accurately identified 82% of patients with confirmed epicardial scar abnormalities as defined by bipolar epicardial mapping. Among four patients in whom disparities were identified with regard to extent of endocardial unipolar and epicardial bipolar abnormalities, cMRI in two identified the presence of mid-myocardial substrate that correlated with the endocardial unipolar abnormality, thus lending support to the idea that unipolar signal analysis may be more effective in identifying mid-myocardial substrate compared with bipolar mapping. We have additionally found that sometimes increasing the threshold for abnormal may be necessary to further bring out mid-myocardial or epicardial abnormalities on unipolar voltage assessment (see Fig. 33.8 ). Among ARVC and RV VT patients, endocardial RV unipolar voltage reference less than 5.5 mV in prospective validation significantly correlated with epicardial bipolar voltage area both with respect to size and location (r = 0.81, P =.008).
Therefore a voltage map created in sinus (or nontachycardia rhythm) can provide starting information with minimal hemodynamic compromise regarding presence of substrate localized toward the ventricular endocardial surface (using bipolar voltage cutoffs of <1.5 mV to define scar and <0.5 mV to define dense scar), epicardial surface (bipolar signal amplitude <1.0 mV), or potentially within the mid-myocardium (LV or RV unipolar signal amplitude <8.3 mV or <5.5 mV, respectively).
Pace Mapping to Identify Ventricular Tachycardia Circuit Components
VT exit sites, from which the rest of the ventricles are activated producing the 12-lead ECG morphology observed during VT, can usually be reasonably and quickly localized based on ECG characteristics (see Table 33.1 ). The process of pace mapping involves (1) using 12-lead ECG “templates” of spontaneously occurring or induced VTs to approximate exit sites within areas of abnormal substrate, as defined earlier and (2) pacing at such sites to produce a QRS complex that either mimics the QRS complex during VT (consistent with an exit site) or has features suggestive of other central isthmus sites. Good pace map sites, meaning sites at which pacing produces a QRS complex that is similar to the VT QRS, have often been defined as those where the paced QRS matches the VT QRS complex in 10 or more leads. However, a more liberal definition that accounts for limitations in this type of mapping, and described in greater detail later, is one in which the paced QRS matches the VT QRS morphology in bundle branch block configuration, frontal plane axis, and precordial transition (i.e., qualitatively but not exactly). Even using the more liberal definition, good pace map matches are observed less than 30% of the time at sites demonstrated by entrainment to be central isthmus sites.
Perhaps more important is the timing of the pacing stimulus, at which time local myocardial capture occurs, to the onset of the evoked QRS complex, which represents the activation of the global ventricular myocardium beyond the substrate; the temporal difference, when capturing myocardium that is relatively insulated by surrounding scar tissue, is a marker for relative location within a potentially critical isthmus ( Fig. 33.10 ). For instance, pacing at a VT exit site should lead to more immediate activation of normal myocardium and produce a QRS complex very similar to the VT morphology with relatively short (<40 ms) stimulus-QRS time. Pacing more proximally within a protected isthmus should produce progressively longer stimulus-QRS times. However, the more proximally within a VT isthmus that pacing is performed, especially when at early isthmus or entrance sites, the less likely the paced QRS complex will match the VT QRS, and, in fact, the more likely that multiple paced morphologies reflecting multiple potential exits may be produced. The reason for this phenomenon is that pacing during sinus rhythm, in the absence of functional unidirectional block that is present during VT, can lead to multidirectional wave front propagation, which will produce a different ventricular activation and QRS morphology than when VT is ongoing and wave front propagation within the same region is unidirectional. Furthermore, if high output is used for pacing capture, the pattern of ventricular activation can change and produce a different QRS morphology because of a greater virtual electrode size or anodal capture, even if pacing is performed within a critical site within the VT circuit. Nevertheless, despite these limitations, pace mapping can approximate the exit site of VT circuits, and therefore can lead operators to the associated and more critical central isthmus components to which the exits are adjacent.
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