Ablation of Unstable Ventricular Tachycardia and Ventricular Fibrillation

Key Points

Substrate mapping is performed to delineate the scarred myocardium in unstable ventricular tachycardia (VT).
For ventricular fibrillation (VF), mapping is performed to identify the focal origin of triggers.
Targets for substrate ablation include VT exit sites identified by pace mapping, sites identified by brief resetting and entrainment mapping, late and fractionated potentials, sites with local abnormal ventricular activity, and channels between dense (“electrically unexcitable”) scar. Ablation to “homogenize” the scar area is an alternative effective approach.
Targets for focal VF are premature ventricular complex (PVC) triggers preceded by Purkinje potentials or from the ventricular outflow tract or papillary muscle.
Preoperative imaging such as computed tomography scan or magnetic resonance imaging may help guide the mapping strategy. Special equipment includes an electroanatomic mapping system, which is necessary to construct a 3-dimensional rendering of ventricular geometry and scar location; irrigated-tip radiofrequency ablation catheter, which is optimal for mapping and ablation; intracardiac echocardiography, which may facilitate transseptal access to perform transmitral left ventricular mapping and monitoring of complications such as cardiac tamponade; and a percutaneous left ventricular assist device to optimize hemodynamic status.
Sources of difficulty include epicardial and intramyocardial VT circuits, and for VF ablation, PVC triggers that are difficult to induce.

Introduction

A parsimonious approach to catheter ablation of ventricular tachycardia (VT) is performed using classic methods of activation and entrainment mapping during arrhythmia to identify the critical isthmus during VT and minimize the number of ablation lesions. However, hemodynamic instability during VT often limits the extent to which these methods can be used. Approximately 33% of patients will have exclusively hemodynamically stable VTs induced at the time of electrophysiology study. The vast majority (∼66%) will have at least one hemodynamically unstable VT induced, preventing detailed entrainment or activation mapping. Even in those patients who have a mappable stable VT, it is almost invariably true that other unstable (that is, “unmappable”) VTs can also be induced. This is not surprising when one considers that the arrhythmogenic substrate is not a simple single circuit, but rather an extensive sheet of surviving myocardial fibers in a bed of scar tissue with multiple potential entry and exit points—allowing for different reentrant paths (that is, different VTs) to be operative at any given time ( Fig. 32.1 ). From a procedural perspective, it may be most appropriate to regard this substrate as a mass of arrhythmogenic tissue with multiple tracts of surviving tissue traversing through scar—many, or perhaps even all, of which might be appropriate to target for ablation to completely eliminate VT. For other cases, the presenting arrhythmia may be ventricular fibrillation (VF), which is intrinsically unstable. In this chapter, we discuss techniques that can be applied for catheter ablation of unstable VT and for VF.

Fig. 32.1, The substrate for ventricular tachycardia (VT) in postmyocardial infarction (post-MI) patients. Instead of a single bundle of myocardium forming the tachycardia circuit (A), surgical mapping studies of post-MI VT have revealed an extensive sheet of surviving myocardial fibers linked in the subendocardium through multiple “entrance” and “exit” points (B, C). This accounts for multiple potential reentrant paths (that is, different VT morphologies) at different times all originating from the same mass of infarcted tissue.

Pathophysiology of Scar-Related Ventricular Tachycardia

The techniques for ablation of VT rely on principles developed from studies that characterized the VT substrate postmyocardial infarction (post-MI). In the majority of patients with structural heart disease, the pathogenesis of VT is reentry in the area of scarred myocardium. Although most commonly seen in patients with a prior myocardial infarction (MI), VT may occur in any disease process that results in myocardial scar. Scar-related reentrant VT has been described in patients with dilated cardiomyopathy (DCM), arrhythmogenic right ventricular cardiomyopathy/dysplasia, hypertrophic cardiomyopathy, sarcoidosis, and following cardiac surgery such as in correction of tetralogy of Fallot. The techniques used for catheter ablation of scar-related VT have evolved from our understanding of post-MI VT and the surgical experience in this population.

The Anatomic Substrate of Postmyocardial Infarction Ventricular Tachycardia

After an MI, the tissue can be broadly divided into three zones: the dense scar, the surrounding live myocardial tissue, and the intervening “border zone.” It is important to note that this border zone is not necessarily physically located only at the periphery of the scar, but is rather located at any of the interfaces between the normal tissue and dense scar. In this border zone, electrically-active live myocardial fibrils are interspersed among the bed of infarcted, fibrotic tissue. These fibrils are characterized by abnormal electrophysiologic properties including slower conduction velocity and decreased cell-to-cell electrical coupling (e.g., because of altered Connexin 43 activity at the gap junction). As with reentrant circuits located in other regions of the heart, the initiation of VT is dependent on the development of unidirectional block and slow enough conduction to allow the recovery of excitability of the initially blocked region to initiate a self-perpetuating reentrant circuit. The initiators of scar-related VT are not well understood. Presumably, a well-timed premature beat or series of premature beats arise as a result of triggered activity from discrete regions of the heart, and this allows for the unidirectional block and slow conduction required to initiate reentrant VT.

Once initiated, to maintain the reentrant circuit, the wavelength of the tachycardia circuit must be short enough, or the path of myocardial circuit long enough such that the wave front is constantly encountering excitable tissue. This can occur because of either (1) an anatomically-determined circuit of the appropriate length or (2) a partial anatomic barrier combined with a functional barrier. For example, a functional barrier may result from ischemia, electrophysiologic changes resulting from treatment with antiarrhythmic drugs, or electrolyte and pH changes ( Fig. 32.2 ). The anatomic compartmentalization combined with altered cell-to-cell electrical coupling of the diseased tissue sets the stage for local micro- (or macro-) reentrant circuits that result in VT and have the potential to culminate in VF.

$Fig. 32.2, The importance of the excitable gap to maintain a reentrant tachycardia circuit. A, The wave front traverses within the scarred tissue along a surviving tract of myocardial tissue. Conduction through this pathway is slow because of a number of potential factors including the arrangement of the myocardial fibers (side-to-side instead of end-to-end), alterations in gap junctions between myocardial fibrils, a meandering path of the tract, and slow conduction velocity at certain regions (e.g., areas of extreme wave front curvature). The wavelength of the circuit is short enough that the leading edge of the wave front constantly encounters excitable myocardial tissue. This “excitable gap” allows the circuit to perpetuate and manifest as ventricular tachycardia (VT). B, The wavelength of the tachycardia circuit is longer than the tissue tract that it must follow. The leading edge of the wave front encountered refractory tissue so the circuit extinguished, and VT was not maintained. C, However, functional block can supervene in certain situations such as ischemia, increased heart rates, administration of drugs that alter conduction velocity or ventricular repolarization, electrolyte changes, acid-base imbalances, etc. In this situation, the combination of functional block to the preexisting anatomical block creates an excitable gap, allowing for sustained VT.$

Surgical Experience With Postmyocardial Infarction Ventricular Tachycardia

The approach to ablation of unstable VTs developed directly from the extensive experience since the late 1970s with surgical modification of the arrhythmogenic substrate in post-MI patients. Because the reentrant circuit is most often located in the subendocardium at the junction of normal and scarred myocardium, the initial surgical experience with simple aneurysmectomy was disappointing. However, two effective general strategies were developed over time: (1) subendocardial resection—involving surgical removal of the subendocardial layer containing the arrhythmogenic substrate in this border zone; and (2) encircling endocardial ventriculotomy—consisting of the placement of a circumferential surgical lesion through the border zone, presumably interrupting potential VT circuits. Because of its distinct advantage in destroying myocardial cells without disrupting the fibrous stroma, cryoablation has also been used both as a stand-alone intervention during surgery, and as an adjunct to subendocardial resection. Encircling cryoablation is an efficacious procedure incorporating cryoablation into the concept of an encircling endocardial ventriculotomy. When performed at experienced centers, the long-term freedom from malignant VT/VF after surgery is more than 90% ( Fig. 32.3 ).

Fig. 32.3, Surgical substrate modification to eliminate ventricular tachycardia (VT). The border between the normal and infarcted/aneurysmal wall contains a stylized VT circuit—predominantly endocardial, and partially intramural. The surgical procedures, subendocardial resection and ventriculotomy, are thought to either remove or transect critical endocardial portions of the VT circuit, respectively. During catheter ablation, the border zone is mapped using the electroanatomic mapping system, the putative exit site of the VT is identified by pace mapping, and catheter-based linear lesions are placed in an attempt to interrupt the circuit. Because mapping is performed during sinus rhythm instead of during VT, this allows for greater patient safety and comfort.

It is interesting to note that in the initial surgical experience, intraoperative mapping was performed to help guide the surgical resection. After open surgical bypass, multielectrode plaques were used to precisely identify the origin of the VT. This area of endocardium was either surgically removed, or surgically transected using a scalpel blade. However, VT surgery then evolved such that in many cases, equivalent results were obtained by visualizing the scar and either simply resecting it, or by placing surgical cryoablation or laser ablation lesions along its border. These “empiric” lesions are thought to eliminate critical portions of the circuit and thus render VT noninducible ( Fig. 32.4 ).

$Fig. 32.4, Electroanatomic mapping of the effect of arrhythmia surgery. A, Left ventriculography reveals a large inferobasal aneurysm in the setting of three-vessel coronary artery disease and clinical ventricular tachycardia (VT). During a presurgical electrophysiology study, programmed ventricular stimulation revealed easily-inducible VT. B, Left ventricular (LV) electroanatomic mapping was performed during sinus rhythm. The bipolar voltage amplitude maps shown in right anterior oblique caudal (left) and left lateral-caudal (right) projections reveal a large inferobasal aneurysmal scar with electrograms containing abnormal fractionated and late potentials (not shown). C, During surgery, the LV was opened through the aneurysm, the aneurysm was resected, cryoablation was applied to the margins of the scar, and the ventricle was closed with the support of a patch. D, Months after the surgery, a repeat electrophysiology study revealed (1) a smaller homogeneous scar without evidence of fractionated and late potentials (right posterior oblique and inferior projections on left and right , respectively); (2) a more favorable ventricular geometry without an aneurysmal component; and (3) no inducible VT with programmed ventricular stimulation. The color range is set such that purple represents normal tissue (>1.5 mV), red the most severely disease tissue (<0.1 mV), and gray represents pure scar with no identifiable electrical activity. AV , Aortic valve; MV , mitral valve.$

The effect of arrhythmia surgery on the myocardial substrate was examined in a study of 18 patients undergoing successful subendocardial resection procedures. These patients had all previously sustained anterior wall MIs and manifested multiple morphologies of drug-refractory monomorphic VT. During the operative procedure, a 20-electrode rectangular plaque array was used to obtain electrical data from the apical septum during VT as well as during normal sinus rhythm immediately before and immediately after resection of subendocardial tissue ( Fig. 32.5 ). Electrograms (EGMs) could be compared from 298 of 360 (83%) of the electrodes. Before resection, split EGMs were present in 130 (44%) and late potentials in 81 (27%) of the recordings. However, the postresection recordings revealed a complete absence of the split EGMs, as well as elimination of all of the previously recorded late potentials. The mean EGM duration decreased from 112 ± 38 to 65 ± 27 ms, primarily caused by the loss of these split and late potentials. Histologic studies revealed that the subendocardial tissue removed in this procedure contains bundles of surviving muscle fibrils separated by dense connective tissue. These data suggest that the direct effect of the subendocardial resection procedure is to eliminate the tissue containing these abnormal EGM components.

Fig. 32.5, The electrophysiologic effect of subendocardial resection surgery. Recordings were made using a 20-bipole plaque array (A) before and (B) after resection as well as after replacement of (and recording through) the resected tissue specimen (C). The dotted line in (A) denotes the end of the QRS complex. The split and late electrogram (EGM) components ( arrows ) before resection are absent in the postresection recordings. In addition, most channels show an increase in amplitude of the remaining early EGM component, which maintains the same general morphology as before resection. After replacement of the specimen, these early EGMs appear similar to those obtained before resection, but note the absence of split and late electrograms (channels 5 and 20 did not record properly).

The surgical experience provided several important lessons that are relevant for modern catheter ablation of VT: (1) critical portions of the VT circuit reside on the endocardial surface of the scar (allowing access via a percutaneous endoluminal approach); (2) the majority of VTs exit from the border of the scarred myocardium; (3) during normal sinus rhythm, the “anatomy” of the scar can be delineated by certain criteria distinguishing abnormal endocardial EGM—low voltage amplitude, prolonged EGM duration, and the presence of late potentials; and (4) empiric disruption of the arrhythmogenic substrate containing these abnormal fractionated, discrete, split or late potentials in this “border zone” area can eliminate VT.

Other Scar-Related Ventricular Tachycardias

Reentrant VT also occurs from myocardial scar in the setting of other forms of cardiac pathology such as dilated cardiomyopathy (DCM). Histologic studies of myocardial tissue from patients with DCM have revealed multiple patchy areas of interstitial and replacement fibrosis and myofibrillar disarray with variable degrees of myocyte hypertrophy and atrophy. A necropsy study in patients with idiopathic DCM revealed that despite a relative paucity of visible scar (14%), a high incidence of mural endocardial plaque (69%–85%) and myocardial fibrosis (57%) was found. As with post-MI VT, the mechanism of VT related to DCM is also most commonly reentrant and is related to scarred substrate. Unlike post-MI scar, there is no predilection for an endocardial location. Delayed contrast enhanced magnetic resonance imaging (MRI) has demonstrated that scar in DCM may also be found in the epicardium and midmyocardium. Therefore a combined epicardial and endocardial ablation is often necessary to successfully abolish VT. In addition, in our experience, and that of other investigators, by electroanatomic mapping, the scar tends to be predominantly localized to the basal regions of the left ventricle (LV) and ventricular septum. Clinical studies of VT mapping and ablation in the setting of DCM have revealed that a substrate-based approach is also useful to eliminate these arrhythmias.

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