Substrate-Based Ablation for Ventricular Tachycardia

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.