EDITORIAL COMMENT
"The Older the Broader"
Electrogram Characteristics Help Identify the Critical Isthmus During Catheter Ablation of Postinfarct Ventricular Tachycardia*
Helmut U. Klein, MD* and
Sven Reek, MD
Division of Cardiology, University Hospital Magdeburg, Magdeburg, Germany
* Reprint requests and correspondence: Dr. Helmut U. Klein, Division of Cardiology, University Hospital Magdeburg, Leipziger Strasse 44, 39120 Magdeburg, Germany (Email: Helmut.Klein{at}medizin.uni-magdeburg.de).
During the past 10 years, significant progress has been achieved in the treatment of supraventricular as well as ventricular tachycardia (VT) with radiofrequency (RF) catheter ablation. In particular, RF catheter ablation became the treatment of choice for atrioventricular-nodal re-entrant tachycardia, atrioventricular re-entry tachycardia, ectopic atrial tachycardia, atrial flutter, and idiopathic right or left VT. In contrast to a high success rate accomplished in the aforementioned tachycardias, ablation of atrial fibrillation and postinfarct VT is far less successful and still a matter of intensive research. The reason for may be the heterogeneous structural abnormalities of the underlying tissue from which the electrical abnormality originates, the lack of a fixed anatomic structure that is involved in the onset or maintenance of a macro–re-entrant or micro–re-entrant circuit, the possibility of multiple tachycardia morphologies using different exit or entry points within a large "arrhythmogenic" area and, most importantly, a continuous structural remodeling of the atrial or ventricular myocardium caused by the underlying disease process (1,2).
Postinfarction VTs arise in areas of fibrosis that contain surviving myocardial strands, producing a "zig-zag" course of activation leading to inhomogeneous anisotropy (3). Hidden in the arrhythmogenic area is the common central pathway, the critical isthmus, causing slowing of impulse conduction, allowing re-entry to occur. The isthmus itself may be surrounded by "dead ends" or branching of impulses that do not participate in the common pathway of the leading re-entrant circuit and may be misinterpreted when recorded with roving mapping electrodes (4).
In the early studies of patients with postinfarct VT who underwent intraoperative "point-by-point" passive mapping of endocardial and epicardial myocardium, bipolar electrograms within the infarcted area demonstrated abnormally broadened and fractionated electrograms as well as delayed isolated potentials and double potentials during sinus rhythm (5). They were considered as "arrhythmogenic," and by either removing or encircling them, it was hoped that surgical techniques such as large endocardial resection would abolish VT (6,7).
With the introduction of catheter ablation for VT, new mapping strategies to identify the critical isthmus within or at the border of the infarcted area were designed. The target site of ablation is identified by activation mapping and stimulation techniques using concealed entrainment criteria in an area where mid-diastolic potentials are recorded (8). This, however, requires induction of the "clinical" VT, which may not be inducible or give rise to many "nonclinical" VTs. Often, the induced VT is hemodynamically unstable, and thorough activation mapping becomes impossible. New computer-assisted mapping tools, such as the three-dimensional electroanatomic (CARTO, Biosense Webster, Diamond Bar, California) (9) or the noncontact mapping system (EnSite 3000, Endocardial Solutions Inc., St. Paul, Minnesota) (10), have been developed to either facilitate activation mapping or to create voltage maps to delineate the arrhythmogenic substrate (i.e., the low-voltage zone during sinus rhythm looking for very low-amplitude electrograms, fractionation, and late potentials) (11). Applying linear lesions with RF energy along an identified border between scar and normal voltage tissue or anatomic boundaries encircles or isolates the critical arrhythmogenic substrate (12). This approach is most promising, and identifying only abnormal electrograms during sinus rhythm within the infarcted area may be more successful than sophisticated entrainment mapping to pinpoint one or multiple critical isthmus spots of potential re-entrant circuits. Activation mapping in postinfarct VT could probably be replaced by "substrate" mapping.
The findings presented by Bogun et al. (13) in this issue of the Journal support the importance of electrographic characteristics in patients with postinfarct VT. Sites with the broadest electrograms or isolated potentials detected during sinus rhythm mapping were identical with the critical isthmus of the re-entrant circuit during induced VT. The application of RF energy was most successful when delivered within the area of abnormal electrograms.
Most interesting in the study by Bogun et al. (13) was the fact that they found a significant positive correlation between infarct age and the duration of the broadest endocardial electrograms (>200 ms) during sinus rhythm mapping in the peri-infarct zone. The older the infarct, the broader the electrograms, the longer the delay between the electrogram and the isolated potentials. There was no correlation with left ventricular ejection fraction, number of old infarctions, the infarct location, and the area of infarct size. However, other hemodynamic parameters or ventricular dilation parameters were not assessed. The authors explain their time-dependent findings by a continuous remodeling process after the acute infarction event with gradual formation of areas with surviving myocardial strands separated by fibrous tissue deposition. There are experimental data to confirm this (14), and clinical experience also tells us that growing time after myocardial infarction increases the likelihood of developing sustained VT or life-threatening ventricular tachyarrhythmias (15).
A word of caution is necessary not to oversimplify their interesting and important findings. In the report of Bogun et al. (13), the time of first infarction to the time of the electrophysiologic study and ablation procedure ranged from 1 to 31 years, with a mean of 16 years after the index event. The reported series included only 23 patients, but in 5 patients the time of infarction could not be determined, and 10 patients had a second infarction before the study. Is there a continuous uninterrupted remodeling process over the years to come after myocardial infarction, and when is the formation of the arrhythmogenic substrate finished to originate a sustained VT? If the formation of the arrhythmogenic substrate is time dependent, how do we explain that some patients may develop VT after a few weeks, some after many years after myocardial infarction, whereas others will never experience VT episodes although suffering from the same amount of ventricular dilation and ventricular dysfunction?
Remodeling after myocardial infarction is a multiform and complex mechanism involving molecular and cellular components, causing early and late changes in ventricular size, architecture, function, and electrical stability in infarcted but also noninfarcted areas (14). Experimental data from healing myocardial infarction are mostly derived from early postinfarct periods (15), and information on the late genetic and molecular process that perpetuates remodeling and may cause arrhythmias is scarce (16,17).
The major limitation of the study is that we have no insight into the electrogram characteristics in patients with similar functional remodeling late after myocardial infarction who did not develop VT. They may have the same electrogram characteristics.
The specificity of the described electrogram changes is unknown, and further studies with a larger patient cohort are needed to prove the authors' conclusion that the older the myocardial infarction, the broader the potentially arrhythmic electrograms, and the easier it will be to use them as target sites for ablation.
To widely apply the described technique of VT ablation by targeting the sites of broadest electrograms during sinus rhythm, a generally accepted definition of electrogram duration, fractionation, and isolated potentials is mandatory. Defined cut-off points of beginning and ending of electrograms as well as agreement on signal filtering, amplitude, amplification, and sampling rate of bipolar signals from low voltage areas are needed.
Because we did not learn from Bogun et al. (13) how many broad electrogram sites were ablated with RF energy until the clinical VT became uninducible, further studies are needed to demonstrate if encircling the areas of broad electrograms with linear lesions is sufficient or if each critical isthmus site must be destroyed separately. If, however, broad electrograms are the consequence of a perpetuating remodeling process after myocardial infarction, there is little hope that permanent suppression of VT may be achieved because new critical isthmus sites will arise unless the remodeling process can be stopped by other approaches such as drugs, revascularization, or non-pharmacologic techniques. Applying sophisticated entrainment techniques and mapping the earliest breakthrough during induced VT may become unnecessary in the future, if we target the broadest electrograms within the low-voltage infarction zone during sinus rhythm (18). Applying efficient energy with the appropriate electrode tool that is able to delineate and destroy the most critical arrhythmogenic electrograms, either endocardially or epicardially, will certainly increase the success rate of currently still unsatisfactory results of VT ablation.
Because structural remodeling is the basic underlying mechanism of both VT and atrial fibrillation, it is time to look for similar electrographic characteristics in patients with atrial fibrillation to improve results of extensive and time-consuming ablation procedures in patients with persistent or chronic atrial fibrillation (19).
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Footnotes
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* 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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References
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1. Akar FG, Rosenbaum DS. Transmural electrophysiological heterogeneities underlying arrhythmogenesis in heart failure Circ Res 2003;93:638-645.[Abstract/Free Full Text]
2. de Bakker JM, van Capelle FJ, Janse MJ, et al. Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation Circulation 1988;77:589-606.[Abstract/Free Full Text]
3. de Bakker JM, von Capelle FJ, Janse MJ, et al. Slow conduction in the infarcted human heart. "Zigzag" course of activation Circulation 1993;88:915-926.[Abstract/Free Full Text]
4. Khan HH, Stevenson WG. Activation times in and adjacent to reentry circuits during entrainment: implications for mapping ventricular tachycardia Am Heart J 1994;127:833-842.[CrossRef][Web of Science][Medline]
5. Klein H, Karp RB, Kouchoukos NT, et al. Intraoperative electrophysiologic mapping of the ventricles during sinus rhythm in patients with a previous myocardial infarctionIdentification of the electrophysiologic substrate of ventricular arrhythmias. Circulation 1982;66:847-853.[Free Full Text]
6. Kienzle MG, Miller J, Falcone RA, et al. Intraoperative endocardial mapping during sinus rhythm: relationship during sinus rhythm: relationship to site of origin of ventricular tachycardia Circulation 1984;70:957-965.[Abstract/Free Full Text]
7. Bourke JP, Campbell RW, Renzulli A, et al. Surgery for ventricular tachyarrhythmias based on fragmentation mapping in sinus rhythm alone Eur J Cardiothorac Surg 1989;3:401-406.[Abstract]
8. Stevenson WG, Friedman PL, Kocovic D, et al. Radiofrequency catheter ablation of ventricular tachycardia after myocardial infarction Circulation 1998;98:308-314.[Abstract/Free Full Text]
9. Gepstein L, Hayam G, Ben-Haim SA. A novel method for nonfluoroscopic catheter-based electroanatomical mapping of the heartIn vitro and in vivo accuracy results. Circulation 1997;95:1611-1622.[Abstract/Free Full Text]
10. Schilling R, Peters N. Davies DFeasibility of a noncontact catheter for endocardial mapping of human ventricular tachycardia. Circulation 1999;99:2543-2552.[Abstract/Free Full Text]
11. Marchlinski FE, Callans DJ, Gottlieb CD, et al. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy Circulation 2000;101:1288-1296.[Abstract/Free Full Text]
12. Soejima K, Suzuki M, Maisel WH, et al. Catheter ablation in patients with multiple and unstable ventricular tachycardias after myocardial infarction: short ablation lines guided by reentry circuit isthmuses and sinus rhythm mapping Circulation 2001;104:664-669.[Abstract/Free Full Text]
13. Bogun F, Krishnan S, Siddiqui M, et al. Electrogram characteristics in postinfarction ventricular tachycardia: effect of infarct age J Am Coll Cardiol 2005;46667–74.
14. Prabhu SD. Post-infarction ventricular remodeling: an array of molecular events (editorial) J Mol Cell Cardiol 2005;38:547-550.[CrossRef][Web of Science][Medline]
15. Gardner PJ, Ursell PC, Fenoglio JJ, Wit AL. Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts Circulation 1985;72:596-611.[Abstract/Free Full Text]
16. St. John Sutton M, Lee D, Rouleau JL, et al. Left ventricular remodeling and ventricular arrhythmias after myocardial infarction Circulation 2003;107:2577-2582.[Abstract/Free Full Text]
17. Adamson PB, Vanoli E. Early autonomic and repolarization abnormalities contribute to lethal arrhythmias in chronic ischemic heart failure J Am Coll Cardiol 2001;37:1741-1748.[Abstract/Free Full Text]
18. Wrobleski D, Houghtaling C, Josephson ME, et al. Use of electrogram characteristics during sinus rhythm to delineate the endocardial scar in a porcine model of healed myocardial infarction J Cardiovasc Electrophysiol 2003;14:524-529.[CrossRef][Web of Science][Medline]
19. Konings KT, Smeets JL, Penn OC, et al. Configuration of unipolar atrial electrograms during electrically induced atrial fibrillation in humans Circulation 1997;95:1231-1241.[Abstract/Free Full Text]
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References