Ablation of Ventricular Tachycardia in Coronary Artery Disease

Introduction

The development of sustained monomorphic ventricular tachycardia (VT) is one of the most significant late complications that can occur in a patient who has suffered a prior myocardial infarction (MI). Regardless of the hemodynamic tolerability of any index episode of VT in this setting, patients with a healed MI scar and significant left ventricular (LV) systolic dysfunction have substantially reduced survival and derive a demonstrable prognostic benefit from implantable cardioverter-defibrillator (ICD) placement, even before developing clinical VT. It is clear, however, that ICDs are deployed for sudden death risk mitigation and should not be considered a treatment or cure for VT. Repeated ICD shocks for recurrent VT can lead to significant morbidity and mortality, and repeated delivery of antitachycardia pacing may also be associated with adverse outcomes. Present-day medical therapy is incompletely effective in preventing ICD therapy and comes with the risk of significant adverse effects and additional extracardiac toxicity in the case of amiodarone. Few meaningful breakthroughs in antiarrhythmic drug development have occurred in recent times to suggest any change in this landscape is imminent.

In this light, catheter ablation assumes an important role in the overall management of ischemic cardiomyopathy (ICM) patients with VT. Although the suggestion of a prognostic benefit has been found in one trial, and although the prevention of ICD shocks may lead to a secondary survival benefit, the primary goal of the procedure is to improve quality of life by prevention of VT recurrences and ICD therapies without antiarrhythmic drug side effects.

Anatomy

Multiple intracardiac mapping studies have confirmed that the electrophysiologic mechanism of the vast majority of monomorphic VT in the setting of prior MI is reentry. As clearly demonstrated in the early seminal surgical studies, and confirmed subsequently by entrainment mapping data, critical portions of the reentry circuitry of postinfarct VT reside within a healed myocardial infarct scar, usually a large and confluent one ( Fig. 30.1 ). Such scars are often associated with advanced LV remodeling, areas of dyskinesis and aneurysm formation, and significant LV systolic dysfunction. Infarct scar formation and remodeling is not a uniform amorphous process; instead structural and ultrastructural heterogeneity within scar regions is universal ( Fig. 30.2 ). Collateral formation, endoluminal perfusion, acute reperfusion therapy, and ongoing collagen turnover all contribute to the formation of surviving (predominantly subendocardial) myocyte bundles of varying diameter interlaced in networks through the dense infarct core. These bundles are separated by insulating sheets of collagen that alter wave front propagation through scar in a manner conducive to the establishment of reentrant tachyarrhythmias. The extent of ventricular scar and LV systolic dysfunction in patients with ICM is an important determinant of arrhythmic risk. Sustained monomorphic VT is more likely seen in those with larger infarct scars. The advent of primary prevention medical therapy and earlier, more effective acute reperfusion therapy with primary percutaneous intervention have altered infarct scar characteristics. Patchy fibrosis is now seen more frequently, and aneurysm formation has become rare. This has altered the frequency and characteristics of VT seen in the chronic phase after MI with more rapid VT seen in such patients. It remains unclear whether the reduced late VT incidence expected with smaller healed infarcts will be balanced by an increased prevalence of VT as long-term post-MI survival improves.

Remember that not all patients with reentrant VT and coronary artery disease have a myocardial infarct-related ventricular scar and some may instead have a coexisting nonischemic dilated cardiomyopathy. Such patients tend to have basal VT sources as well as the frequent epicardial and intramural VT exits typical of that substrate, in direct contrast to postinfarct ICM patients whose pathology and VT circuitry characteristically lie in the subendocardial layer.

Pathophysiology

Disorders of repolarization or disorders of conduction (or both) may form the basis of the electrophysiologic substrate in any arrhythmogenic disease, but in the postinfarct context, abnormalities of conduction predominate. Myocardial necrosis at the time of the initial infarction and replacement of lost myocytes with collagen-based fibrous tissue leads to an overall reduction in the number and density of gap junctions between surviving cells within an infarct scar. Thus even though they are capable of generating recordable action potentials, these myocytes are poorly coupled electrically to nearby cells. Not only does this lead to a slowing of wave front conduction velocity in the scar, but also, because of source-sink mismatch, a greatly increased likelihood of conduction failure producing unidirectional block. In addition, electrical propagation is significantly more affected in the transverse direction orthogonal to myofiber axis as a result of an amplification of normal nonuniform anisotropy by layers of collagen between myocyte bundles. This slow, discontinuous wave front conduction within an infarct scar sets up the ideal milieu for the establishment of reentrant excitation, with the constrained diastolic isthmus usually located within the core of the scar. The exit of the VT wave front from this isthmus occurs at the scar border zone where inscription of the surface QRS commences. The wave front then propagates through the ventricle surrounding the scar, often in a figure-of-8 (dual loop) configuration, before reentering the protected isthmus within the scar again. The diastolic corridor may in some cases be constrained between dense infarct scar and an anatomic barrier such as a valve annulus or a surgical conduit. The contribution of functional barriers to the complete VT reentrant circuit have been underestimated but older resetting studies and recent ultrahigh resolution activation mapping studies confirm their importance, particularly at the entrance to and exit from the diastolic corridor. Approximately 40% of VTs have isthmuses that are shared with a second VT. Evidence that supports reentry as the dominant mechanism of postinfarct VT is summarized in Box 30.1 with some examples in Fig. 30.3 .

The anatomic substrate in the postinfarct patient can be inferred from the presence of Q waves on the surface electrocardiogram (ECG), demonstrated by scar imaging techniques such as late gadolinium enhancement (LGE) on magnetic resonance imaging (MRI) or even visualized directly during surgical subendocardial resection. However, the electrophysiologic substrate can really only be defined by the use of invasive catheter-based electrode recordings at an electrophysiology study (EPS).

At EPS, the induction of sustained monomorphic VT with the use of programmed stimulation implies that the electrophysiologic substrate for VT exists although this does not necessarily predict the presence of spontaneous clinical VT because specific triggers such as ventricular ectopy, heart failure, or changes in autonomic tone are required for this to occur. In addition, at EPS, catheter-based electrode recordings from the infarct region show characteristic abnormalities reflective of the loss of functioning cardiomyocytes and the slow and discontinuous wave front conduction present in ventricular scar. Normal ventricular myocardial bipolar electrograms are sharp, biphasic or triphasic signals of greater than 1.5 mV peak-to-peak amplitude, 70 ms or less duration, and/or greater than 0.046 amplitude:duration ratio ( Fig. 30.4 ). A loss of cardiomyocyte mass in the scar results in attenuation of the bipolar electrogram amplitude with dense scar showing bipolar voltage less than 0.5 mV and regions of bipolar voltage between 0.5 and 1.5 mV typically being seen in the scar border. Slow conduction in the infarct scar causes prolongation of the local bipolar electrogram with multiple low-amplitude deflections ( Fig. 30.5 ). Such electrograms are called fractionated and are defined by a bipolar voltage less than 0.5 mV, a duration of more than 133 ms, and/or an amplitude:duration ratio of less than 0.005 ²⁹ (see Fig. 30.4 ). The multiple deflections of fractionated electrograms have been shown to each correspond to delayed activation of surviving islands of myocyte separated by dense collagen sheets within the field of view of the recording electrode. When activation of a discrete surviving myocyte bundle is sufficiently delayed, a low-amplitude isolated late potential (ILP) may be recorded following an isoelectric interval after the larger initial, usually far-field, ventricular electrogram ( Figs. 30.4 and 30.5 ). Such a bundle may form an anatomically constrained conducting channel in the scar that has the potential to serve as the protected diastolic isthmus of a VT circuit (see Fig. 30.5 ).

In the setting of coronary disease, polymorphic VT may suggest the presence of acute ischemia. There may be multiple operative mechanisms, including abnormal automaticity or Purkinje fiber mediated reentry or triggered activity from diastolic calcium overload in compromised but still viable cells. Polymorphic VT does not require the presence of a healed anatomic infarct substrate as it can occur in patients with no prior ventricular scar presenting with acute coronary syndromes for the first time. It may occur in the very early phase of infarct repair and remodeling where Purkinje fiber triggers at the border of the necrotic zone may be important in its initiation ( Fig. 30.6 ).

Arrhythmia Diagnosis and Differential Diagnosis

The vast majority of patients with sustained postinfarct VT can be diagnosed by a 12-lead ECG recorded at the bedside during tachycardia. It is almost axiomatic that a broad complex tachycardia in the setting of a patient with a prior MI is VT, but multiple published algorithms have been suggested to help exclude the other less likely differential diagnoses, namely supraventricular tachycardia with aberrant conduction (including atrial flutter with 1:1 conduction), preexcited tachycardia, paced tachycardias, and artifact ( Fig. 30.7 ).

The diagnostic criteria for postinfarct scar-related VT are listed in Box 30.2 . The diagnosis of myocardial scar-related VT hinges on the demonstration of atrial, atrioventricular nodal, and His-Purkinje dissociability from the tachycardia (which excludes all forms of supraventricular, preexcited, and fascicular tachycardias, including bundle branch reentry VT). Such proof can be obtained at the bedside with the surface 12-lead ECG or in the laboratory during EPS with pacing maneuvers. In the presence of a dual-chamber ICD system, the presence of ventriculoatrial dissociation on ICD interrogation is essentially conclusive. The diagnosis of VT can also be strongly suggested in patients with single-chamber ICDs as stored electrogram morphology in tachycardia should be different from the sinus rhythm conducted morphology in VT. However, right bundle branch block aberrance during supraventricular tachycardia can alter the wave front vector by which the sensing bipole in the right ventricle (RV) is activated and hence also changes the ICD electrogram morphology. Such ICD intracardiac electrograms may be useful in matching induced VTs to clinical arrhythmias as well as potentially even in pace mapping ( Fig. 30.8 ). The latter maneuver may be the only mapping option in the uncommon scenario in which no VT is inducible at EPS in a patient in whom there are no 12-lead ECG recordings of clinical VT.