Author + information
- Edward P. Gerstenfeld, MD⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Edward P. Gerstenfeld, University of California, San Francisco, MU-East 4th Floor, 500 Parnassus Avenue, San Francisco, California 94143
The use of implantable cardioverter-defibrillators (ICD) in patients with reduced ejection fraction after myocardial infarction (MI) has been shown to reduce cardiovascular death and total mortality (1). However, defibrillator shocks for recurrent ventricular tachycardia (VT) can be painful and anxiety provoking for patients. Antiarrhythmic therapy can be used to prevent recurrent episodes of VT. However, such therapy may be incomplete and is often associated with adverse effects. Catheter ablation has the potential to prevent recurrent VT without the need for long-term antiarrhythmic therapy. According to the American Heart Association consensus statement, catheter ablation is recommended “for symptomatic sustained monomorphic VT, including VT terminated by an ICD, that recurs despite antiarrhythmic drug therapy or when antiarrhythmic drugs are not tolerated or not desired” (2).
The mechanism of VT after MI in the vast majority of patients is re-entry, which is facilitated by slow conduction and block within a heterogeneous scar. Progressive fibrosis and remodeling may lead to the development of VT many years after the index event. Catheter ablation of VT seeks to interrupt the critical channel or “isthmus” of slow conduction within a scar that supports the development and maintenance of VT. Significant advances in VT mapping and ablation have occurred over the past decade. In addition to pacing maneuvers (entrainment) that allow one to map the critical isthmus during tolerated VT, the advent of three-dimensional mapping systems has allowed ablation of poorly tolerated or “unstable” VTs. Voltage maps can delineate the scar boundaries, allowing the targeting of the VT isthmus and exit sites during sinus rhythm (3). Newer techniques may also target “channels” of relatively higher voltage within scars (4) or signals containing “late potentials” indicative of viable myocardium in a zone of slow conduction. Percutaneous ventricular assist devices are also being used to facilitate mapping during poorly tolerated VT or in patients who have significant left ventricular dysfunction (5).
Despite these advances, however, the long-term success rate of catheter ablation, when measured in terms of freedom from any recurrent VT, remains suboptimal. The VTACH (Ventricular Tachycardia Ablation in Addition to Implantable Defibrillators in Coronary Heart Disease) study reported by Kuck et al. (6) randomized patients with VT after MI to receive ICD implantation alone versus catheter ablation followed by ICD implantation. Although recurrent VT was clearly reduced in the ablation arm, the VT recurrence rate at 2 years was still 53%. Jaïs et al. (7) recently reported a new technique of catheter ablation, primarily targeting late fractionated potentials during sinus rhythm. Although complete elimination of these late potentials portended a better prognosis, the rate of recurrent VT or death at 2 years in the successful group was 45%.
Little is known about the reason for recurrent VT after acutely “successful” catheter ablation. We know the success rate is better for mappable VTs compared with unmappable VTs (8) and that the success rate is best when all induced VTs are targeted for ablation. However, there are several reasons VT may recur after ablation. The remodeling process after MI is a complex one, and continued infarct remodeling may lead to the formation of new VT circuits that were not present during the initial ablation session. It is also possible, given the poor reproducibility of programmed stimulation, that VTs which are not induced during the initial ablation session are clinically relevant and become manifest much later. Although we know the majority of re-entry circuits after MI are subendocardial, ablation lesions may be limited by the presence of subendocardial fibrosis or thrombus, and incomplete lesions may lead to recurrences of the same clinical VT after ablation. Some VT circuits may be midmyocardial or epicardial, limiting endocardial access to the critical isthmus. Finally, it is possible that ablation lesions are proarrhythmic, and that the creation of islands of unexcitable myocardium may create a barrier for the development of new VTs after ablation.
Determining the reasons for recurrent VT after ablation is challenging because it requires tracking electrocardiogram, mapping, and ablation data over many years. In this issue of the Journal, Yokokawa et al. (9) try to understand the reasons for VT recurrences after ablation in patients with prior MI.
The authors studied 98 patients referred for catheter ablation of VT between 2004 and 2011 (9). All patients had a history of anterior (33%) or inferior (66%) MI and VT that recurred despite antiarrhythmic therapy. In these patients, they were able to induce 725 VTs, 105 “clinical” and the remaining “nonclinical” as determined predominantly from intracardiac electrogram morphology and cycle-length analysis. Critical endocardial sites were identified in 71% of the clinical VTs and only 45% of the nonclinical VTs. These critical sites were identified by entrainment mapping in 15% of the clinical VTs and 4% of the nonclinical VTs; the remainder were identified with pace-mapping. Ablation was directed focally to the VT isthmus during tolerated VT or clustered around areas of good pace-maps (10 of 12 match) for poorly tolerated VTs. After ablation, there was no inducible VT with up to 4 extrastimuli at 2 right ventricular sites in 63% of patients. Impressively, none of the clinical VTs were inducible after ablation. After ablation, VT recurred in 33 patients (34%): a new VT in 16 (48%), the clinical VT only in 7 (21%), and both clinical and nonclinical VTs in 10 (30%). Fourteen of the patients with recurrent VT underwent repeat ablation. Interestingly, new VTs that were not documented in the prior study were inducible in all patients. The critical isthmus for the recurrent VT was “adjacent” to prior ablation lesions in the majority (53%) of patients, at sites of a prior VT isthmus in 15%, and new sites remote from the original VT in the remaining 32%. After repeat ablation, the final success rate with catheter ablation was 77%.
There are certainly several limitations to the study (9): use of intracardiac electrogram morphology is far from perfect for distinguishing clinical from nonclinical VTs. The vast majority of VTs were targeted based on pace-map criteria, and these criteria (match of 10 of 12 leads) were not very specific. Therefore, many of the so-called critical sites may not have really represented the true VT isthmus. It is also unclear why no critical site could be found for nearly 45% of the induced VTs. The authors used an ablation approach of placing “clusters” of lesions at these critical sites, rather than the more commonly described “linear” ablation through sites of good pace-maps. In addition, there is some disconnect between the described strategy and the ablation lesions shown in the maps depicted in Figures 2 and 3 of Yokakawa et al. (9). The lesions placed in this large infarct seem to be more extensive than those described by the authors' approach targeting areas of late potentials and pace-map matches, making a clear understanding of their approach to ablation difficult. The alignment of 2 left ventricular electroanatomic maps recorded years apart, accounting for changes in sampling density and left ventricular volume, which can account for 6-mm differences in the location of “critical” isthmus sites, is certainly prone to error.
Nevertheless, maintaining the intracardiac electrograms for all the clinical and induced VTs, maintaining a uniform stimulation protocol, and maintaining detailed enough maps over 7 years such that a comparison of VT isthmus location was possible for patients undergoing repeat ablation represents a truly Herculean effort. The authors should be congratulated for providing new information about VT recurrence after ablation.
So what have we learned from this ambitious study (9)? The major learning points are the following: 1) the most common origin of recurrent VT after catheter ablation is adjacent to prior ablation lesions; and 2) the second most common site of origin is from a new region not identified during the original ablation session. The question is, how can we use this information to improve outcome after VT ablation? The origin of recurrent VTs “adjacent” to prior ablative lesions raises 2 possibilities. Either ablation altered the exit of the original VT circuit or ablation lesions created proarrhythmic boundaries that supported the development of new VTs in an already remodeled substrate. The authors describe an ablation approach that applies “clusters” of lesions at sites of good pace-maps. It is possible that a linear pattern of lesions through sites of good pace-maps might be less proarrhythmic. Achieving transmural lesions with complete block in the left ventricle is challenging; however, an endpoint of block across a linear lesion set may improve ablation outcome by preventing the development of future VTs. Use of intracardiac echocardiography and/or contact force catheters could also improve the efficacy of ablation lesions by ensuring adequate catheter stability during ablation.
Preventing the development of newly identified VTs at distant sites is more challenging. This may occur either because the recurrent VT was not induced during the initial procedure or because evolving changes to the left ventricular substrate over time led to the development of new VT circuits. Some have advocated ablating all late potentials in sinus rhythm as a strategy for VT ablation (7); this might result in the prevention of future VTs by ablating regions of slow conduction that might later support VT. Conversely, such lesions may also have proarrhythmic potential. A more extensive approach would involve ablation to “homogenize” the entire scar, because the scar does not contribute to left ventricular function, and any heterogeneous region might serve to support a future VT. Use of cardiac magnetic resonance imaging (10) or direct visualization to guide ablation of heterogeneous zones capable of supporting VT has also been described.
We have witnessed several innovations specific to pulmonary vein isolation for treating atrial fibrillation over the past few years, including development of the cryoballoon, laser balloon, and the phased radiofrequency energy multielectrode catheters. New technology specific to VT ablation has been lacking. Technologies that allow more detailed mapping of unstable VT, contiguous linear ablation with confirmation of adequate lesion formation, and better endpoints beyond programmed stimulation are needed. There are also few randomized trials comparing the many available VT ablation strategies. The 77% freedom from VT after ablation achieved by Yokakawa et al. (9) is indeed laudable, but the authors have also reminded us that our current understanding of VT in the setting of structural heart disease remains incomplete. This is an area that should become a priority for investigation in the next decade.
Dr. Gerstenfeld has reported that he has no relationships relevant to the contents of this paper to disclose.
↵⁎ Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology.
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