Catheter Ablation of Ventricular Tachycardia Late After Myocardial Infarction: Techniques, Indications, and Recent Advances

Tristram D. Bahnson, MD
Tristram D. Bahnson, MD
Topic: Catheter Ablation of Ventricular Tachycardia After Myocardial Infarction: Techniques, Indications, and Recent Advances Faculty/Credentials: Tristram D. Bahnson, MD, Duke University Medical Center, Durham, North Carolina Learning Objectives: At the conclusion of this activity, the participant should be able to:

1. Understand how prior myocardial infarction changes the heart to produce ventricular tachyarrhythmias and how ventricular tachycardia occurs.

2. Understand the evolution of therapeutic catheter ablation for ventricular tachycardia, including the procedural success rates, principles that guide how the procedure is done, and techniques for identifying areas that should be ablated during these procedures.

3. Understand which patients are eligible for catheter ablation for ventricular tachycardia and how new technologies are being applied to expand patient eligibility. Activity instructions. Successful completion of this activity entails reading the article, answering the test questions and obtaining a score of over 70%, and submitting the test and completed evaluation form to the address listed on the form. Tests will be accepted until the expiration date listed below. A certificate of completion will be mailed to you within 60 days. Estimated time to complete this activity: 1 hour Initial release date: October 30, 2003 Expiration date: October 30, 2004. Target audience. This educational activity is designed for physicians, nurses and cardiology technologists who treat patients with ventricular tachycardia. Accreditation statement This activity is sponsored by HMP Communications.

Physicians: HMP Communications is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

HMP Communications designates this continuing medical education activity for a maximum of 1 category 1 credit toward the AMA Physician s Recognition Award. Each physician should claim only those credits that he/she actually spent in the educational activity.

This activity has been planned and produced in accordance with the ACCME Essential Areas and Policies. Nurses: Provider approved by the California Board of Registered Nursing, Provider Number 13255 for 1 contact hour. Radiologic Technologists: Activities approved by the American Medical Association (AMA Category 1) are eligible for ARRT Category B credit as long as they are relevant to the radiologic sciences. Radiologic Technologists, registered by the ARRT, may claim up to 12 Category B credits per biennium. SICP: Society of Invasive Cardiovascular Professionals (SICP) approved for 1 CEU. Commercial support disclosure This educational activity has been supported by an educational grant from Biosense Webster, a Johnson and Johnson company. Faculty disclosure information All faculty participating in Continuing Medical Education programs presented by HMP Communications are expected to disclose to the meeting audience any real or apparent conflict(s) of interest related to the content of their presentation.

Tristram D. Bahnson, MD, has disclosed that he has received research grants from Guidant Corporation, Medtronic Corporation, St. Jude Medical, Inc., and Biosense-Webster Inc.

Ventricular tachyarrhythmias late after myocardial infarction (MI) present an important clinical problem. This review will focus on the pathophysiology and treatment of ventricular tachyarrhythmias (VT) late after a myocardial infarction including application of new technologies and techniques for catheter ablation of ventricular tachycardia in this patient population. Catheter ablation of ventricular tachycardia in structurally normal hearts (idiopathic ventricular tachycardia) is established1 and will not be considered. Mechanism of Ventricular Tachycardia Late After Myocardial Infarction Myocardial infarction results in myocardial cell death and subsequent formation of a scar where necrotic myocardial tissue is replaced by connective tissue and extra cellular matrix proteins. Connective tissue replacement of myocardial tissue is often patchy, with areas of viable myocytes dispersed within the scar zone.2 Channels of functioning myocytes bounded by electrically unexcitable regions form conductive isthmuses within the scar border through which impulse propagation travels over a circuitous route and results in slow conduction and conduction block.3 Slow conduction through isthmuses of surviving myocytes allows for classical reentry to occur in association with the infarct scar.4,5 These slow-conducting isthmuses are critical to initiation and maintenance of scar-associated re-entry and can exist between nonconducting regions within the infarct scar, between a non-conducting region and region of functional block, or between two regions of functional block.5,6 Tachycardia initiation usually occurs when the advancing activation wave front from a premature ventricular beat enters the scar area and is sufficiently delayed through a scar isthmus to allow for recovery of myocardium outside the scar. When the impulse exits the scar region, ventricular myocardium is activated again (Figure 1). A sustained re-entrant rhythm is established when the advancing wave front of activation re-enters the infarct scar and successfully traverses the course of the tachycardia circuit once more. Ventricular tachycardia late after MI results from this scar-associated re-entry and causes heart failure, syncope or sudden cardiac death. The hallmark of treatment for ventricular tachycardia after myocardial infarction is the implantable cardioverter defibrillator (ICD). The ICD is superior to antiarrhythmic drug therapy in preventing death in patients with documented ventricular arrhythmias.7 Furthermore, the use of ICDs for primary prevention in individuals deemed to be at high risk for ventricular arrhythmias late after MI has also received wide acceptance.8,9 Importantly, ICDs do not prevent occurrence of VT, but simply terminate significant episodes when they occur. The experience of frequent painful ICD shocks is clinically significant, and oftentimes requires adjunctive therapy for suppression of VT and ventricular fibrillation (VF).7,10 A large, multi-center trial of ICD therapy for secondary prevention demonstrated that between 69 and 85 percent of individuals had greater than one ICD shock for VT or VF during three years of follow-up.7 These results are consistent with that of many other ICD trials.11 Trials of ICD implantation for primary prevention of sudden cardiac death also demonstrate a shock prevalence of up to 75% of patients at 3-year follow-up.8 Antiarrhythmic drug therapy and non-pharmacologic therapies, such as catheter ablation and arrhythmia surgery, have been developed to treat recurrent ventricular tachycardia late after MI. In general, any of these treatments aim to alter the substrate for VT to prevent arrhythmia initiation. Antiarrhythmic drugs alter the electrophysiology of the heart to produce conduction block within infarct scar tissue. Randomized trials of drug therapy in post-MI patients failed to demonstrate a mortality benefit.12-15 While antiarrhythmic drugs suppress ventricular tachycardia, these drugs can also produce new areas of slow conduction in association with infarct scars that produces a substrate for arrhythmia initiation and maintenance where none previously existed. Accordingly, several antiarrhythmic drugs have been shown to increase mortality in patients late after myocardial infarction, despite demonstrated efficacy at suppressing ventricular arrhythmias.14,15 Antiarrhythmic drugs have remained the first-line therapy to treat recurrent ventricular arrhythmias which precipitate ICD shocks when the arrhythmia burden is deemed to be excessive.16 In the AVID trial of ICDs for secondary prevention of VT/VF, 26% and 34% of individuals treated with ICDs required additional antiarrhythmic drug therapy for VT suppression at two and three years, respectively.7 Despite crossover to antiarrhythmic drug therapy, more than 60% of these individuals experienced ventricular arrhythmia consistent with drug inefficacy.17 Forty-two percent of these patients received amiodarone as the adjunctive antiarrhythmic agent.7 Another trial using sotalol for primary suppression of recurrent VT after ICD implant for prevention of sudden cardiac death showed suppression of recurrent arrhythmias with sotalol; however, 30% of patients experienced shocks despite sotalol therapy during the 12 months of follow-up.16 Thus, antiarrhythmic drugs appear to have only moderate efficacy for arrhythmia suppression in ICD patients. Additional problems with the use of antiarrhythmic drugs in ICD patients includes elevation of defibrillation thresholds, which is commonly seen with amiodarone,18 amiodarone induced extra-cardiac toxicity,12,13 proarrhythmia, and drug-induced bradycardia.16 (continued below)
Figure 1. Mechanism of VT late after MI and potential ablation targets. A hypothetical infarct scar as viewed from the endocardial surface. Areas of light grey represent regions where low amplitude fragmented potentials are recorded and black areas represent regions of dense scar where high output pacing failed to capture ventricular myocardium. Low amplitude fragmented potentials are often evident at un-excitable sites due to recording of activity of neighboring tissue63 (far-field potentials). A possible tachycardia circuit is depicted by the thick line traversing the scar. Slow conduction is depicted by the zig-zag course of conduction through the isthmus area which is bounded by un-excitable tissue. Note that impulses can propagate into "dead end" paths with or without slow conduction as depicted by the thin lines. Catheter recordings at any of these sites would be expected to reveal low amplitude fragmented potentials; however, the areas marked as bystander pathways (white asterisk) do not participate in the tachycardia circuit. Pacing from any of these sites during sinus rhythm would reveal long stimulation to QRS onset times (stim-QRS). Pacing from any of these sites during tachycardia at pacing rates faster than the tachycardia rate would be expected to capture heart tissue and accelerate the rate of the tachycardia as measured on the surface ECG (entrain the tachycardia); however, the time between the local electrogram and onset of the surface QRS will equal the time between the pacing stimulus and onset of the surface QRS only when tissue that is part of the tachycardia circuit has been captured. When pacing during tachycardia from sites within the tachycardia circuit there is no change in the QRS morphology during pacing compared with VT (entrainment with concealed fusion). Furthermore, when pacing with entrainment ceases, the interval between the last stimulus and the next local electrogram measured on the mapping/pacing catheter (the return cycle length or post-pacing interval) will equal the tachycardia cycle length only when pacing from sites within the tachycardia circuit. In this way, bystander sites can be distinguished from sites within the tachycardia circuit such as the central isthmus of slow conduction.5,6,31 In this hypothetical example, a common central isthmus is part of the tachycardia circuit for two distinct VTs (VT1 and VT2) which would likely demonstrate different cycle lengths and different QRS morphologies. Targets for catheter ablation for ventricular tachycardia after MI are depicted by the red solid or dotted lines. Ablation of the common isthmus (solid line perpendicular to the central isthmus) would eliminate both VT1 and VT2. An alternative strategy is to produce lines of block at the tachycardia exits sites depicted by the dotted lines at "A" and "B". Clinically, exit sites are demonstrated by entrainment with concealed fusion during tachycardia, or by pacing during normal sinus rhythm to identify sites where the paced QRS morphology matches the VT QRS morphology. Pacing from the exit regions at "A" would produce a 12-lead ECG QRS morphology near identical to the morphology of VT1 (a pace map match) whereas pacing at "B" would match the QRS morphology of VT2. Pacing from either site would be expected to produce capture with a modest delay in the stim-QRS time. In this hypothetical case both exit sites would need to be successfully targeted to eliminate both VTs.
Nonpharmacologic Therapy for Ventricle Tachycardia Late After Myocardial Infarction Catheter ablation for treatment of VT late after myocardial infarction is evolving as an important therapy option for patients with recurrent VT. As Figure 1 depicts, isthmus regions of the tachycardia circuit within the infarct scar, if identified, would be excellent targets for catheter ablation owing to the critical dependence of VT on conduction through these regions. Early research demonstrated efficacy of surgical endocardial resection in the region of the infarct scar to control incessant ventricular tachycardia late after myocardial infarction, suggesting that critical sites of the tachycardia circuit were often located in the subendocardial region in close association with the infarct scar. Surgical endocardial resection in patients with refractory ventricular tachycardia resulted in VT suppression in 83-95% of patients, although operative mortality was as high as 10-15%.19-21 The curative potential of endocardial resection for ventricular tachycardia gave added impetus to research on percutaneous endocardial mapping and ablation for ventricular tachycardia late after MI. Initial studies suggested that areas of the infarct scar could be identified by recording low amplitude and fractionated endocardial electrograms during percutaneous catheter mapping22 and that significant delay between a pacing stimulus and onset of ventricular activation, as represented by delayed onset of the surface QRS after pacing (Figure 2D, 2E), could identify areas of slow conduction in or around the infarct scar.23 While patients demonstrating large areas of abnormal endocardial electrograms were at higher risk of developing VT,24,25 only a small subset of endocardial sites with abnormal electrograms actually participated in the VT circuits.26,27 Accordingly, additional mapping criteria were developed to distinguish endocardial sites that were critical to arrhythmogenesis from bystander endocardial sites not involved with the VT circuit (Figure 1).5,6,27,28 Table 1 lists endocardial mapping criteria to identify target sites for ablation in the initial clinical series of catheter ablation for post-MI VT.5,6,28-31 Importantly, all mapping criteria to distinguish bystander sites from critical isthmuses of the tachycardia circuit required mapping during sustained ventricular tachycardia.27 Thus, the initial approach to percutaneous catheter ablation of VT late after MI (henceforth called standard mapping) included the following: 1) systematic manipulation of the mapping catheter tip around the endocardial surface of the heart during ventricular tachycardia to identify low-amplitude, high-frequency pre-systolic electrograms; 2) testing to determine whether or not sites with abnormal electrograms were participating in the tachycardia circuit by observing the response to pacing maneuvers during tachycardia; and 3) applying radiofrequency (RF) energy to sites thought to be participating in the tachycardia circuit. Catheter ablation for VT using standard mapping criteria in the patients with a dominant hemodynamically stable clinical VT demonstrated good initial success ranging from 73-81%.5,28-30 More recent studies continue to validate the specificity of these standard mapping criteria for identification of critical portions of the VT circuit.32 (continued below)
Figure 2. Mapping data from a patient with VT late after myocardial infarction (A) Six different VT morphologies induced in a patient late after MI. (B, Left) Voltage map of the postero-basal infarct region generated during mapping and ablation using the CARTO system (Biosense Webster, Inc., Diamond Bar, California) in a patient exhibiting the multiple VT morphologies depicted in panel A. A scale for color coding of endocardial electrogram voltage amplitude appears to the right. Purple areas represent sites with normal (> 1.5 mV) peak to peak bipolar endocardial electrograms. Red areas represent sites with low amplitude ((B, Right) The mesh view on the right allows better visualization of tagged points which were annotated during mapping. Endocardial electrograms demonstrating fragmented potentials and stim-QRS times > 40 ms are tagged as blue circles. Areas consistent with exit sites were also defined by a pace map match to an inducible VT (black arrows). Red circles represent sites where RF lesions were delivered targeting both the central isthmus as well as tachycardia exit sites. All ablation sites were located within the infarct scar. In this case, all inducible VT morphologies were eliminated. (C) Endocardial recording from the central isthmus region (white arrow, panel B) during VT and during sinus rhythm demonstrated fractionated potentials (FP). During VT, a mid-diastolic low-amplitude potential is recorded, which also appears at the end of the far-field ventricular electrogram during normal rhythm. There is a large difference in timing of the FP relative to the far-field electrogram during VT as opposed to sinus rhythm. (D) Pacing from the isthmus site induces VT with the first stim-QRS interval equal to the FP-QRS interval during tachycardia verifying that this site participates in the tachycardia circuit. The first paced beat also matches the QRS morphology of VT. Ablation at this site eliminated VT4. Additional ablation extending toward the infero-septal scar margin eliminated VT5. (E) Pace mapping near the basal and septal margin of the infarct scar matched VT2. Note the prolonged stim-QRS interval. Addition ablation toward the septal side of the unexcitable scar areas eliminated VT 1 and 2. Linear ablation guided by pace maps for remaining VT morphologies were made in the lateral region of the infarct scar and eliminated the remainder of the induced VT morphologies.
Reports of long-term follow-up after catheter ablation for monomorphic VT suggest that recurrence of clinically significant VT is common despite acute success targeting the dominant monomorphic VT. O Callighan et al. reported that 82% of 55 patients selected for stable monomorphic VT had their arrhythmia successfully ablated; however, 28% had recurrence by 5 years.33 Despite some arrhythmia recurrences, the majority of patients with initial success continued to derive clinic benefit with only rare ICD shocks during follow-up, supporting an important role for catheter ablation in patients with ICDs.33-35 Additional studies with patient follow-up greater than 2.5-3.0 years report initial successes of 73-79% and recurrence rates of 14-27%.36,37 All these trials limited patient enrollment to those with hemodynamically tolerated monomorphic VT.