BACKGROUND: The optimal method to identify the arrhythmogenic substrate of scar-related ventricular tachycardia (VT) is unknown. Sites of activation slowing during sinus rhythm (SR) often colocalize with the VT circuit. However, the utility and limitations of such approach for guiding ablation are unknown. METHODS: We conducted a multicenter study in patients with infarct-related VT. The left ventricular (LV) was mapped during activation from 3 directions: SR (or atrial pacing), right ventricular, and LV pacing at 600 ms. Ablation was applied selectively to the cumulative area of slow activation, defined as the sum of all regions with activation times of ≥40 ms per 10 mm. Hemodynamically tolerated VTs were mapped with activation or entrainment. The primary outcome was a composite of appropriate implanted cardioverter-defibrillator therapies and cardiovascular death. RESULTS: In 85 patients, the LV was mapped during activation from 2.4±0.6 directions. The direction of LV activation influenced the location and magnitude of activation slowing. The spatial overlap of activation slowing between SR and right ventricular pacing was 84.2±7.1%, between SR and LV pacing was 61.4±8.8%, and between right ventricular and LV pacing was 71.3±9.6% (P<0.05 between all comparisons). Mapping during SR identified only 66.2±8.2% of the entire area of activation slowing and 58% critical isthmus sites. Activation from other directions by right ventricular and LV stimulation unmasked an additional 33% of slowly conducting zones and 25% critical isthmus sites. The area of maximal activation slowing often corresponded to the site where the wavefront first interacted with the infarct. During a follow-up period of 3.6 years, the primary end point occurred in 14 out of 85 (16.5%) patients. CONCLUSIONS: The spatial distribution of activation slowing is dependent on the direction of LV activation with the area of maximal slowing corresponding to the site where the wavefront first interacts with the infarct. This data may have implications for VT substrate mapping strategies.

Cardiac Electrophysiology Section Department of Cardiovascular Medicine Cleveland Clinic OH

Department of Cardiology Homolka Hospital Prague Czech Republic

Department of Pharmacology College of Physicians and Surgeons of Columbia University New York NY

Division of Cardiology Department of Internal Medicine Samsung Medical Center Sungkyunkwan university Seoul Republic of Korea

Harvard Thorndike Electrophysiology Institute Cardiovascular Division Department of Medicine Beth Israel Deaconess Medical Center Harvard Medical School

Helmsley Electrophysiology Center Division of Cardiology Icahn School of Medicine at Mount Sinai New York NY

Richard A and Susan F Smith Center for Cardiovascular Outcomes Research Division of Cardiovascular Medicine Beth Israel Deaconess Medical Center Harvard Medical School

Zobrazit více v PubMed

Josephson ME, Horowitz LN, Farshidi A. Continuous local electrical activity. A mechanism of recurrent ventricular tachycardia. Circulation. 1978;57:659–65. PubMed

Josephson ME, Horowitz LN, Farshidi A, Spielman SR, Michelson EL, Greenspan AM. Sustained ventricular tachycardia: evidence for protected localized reentry. Am J Cardiol. 1978;42:416–24. PubMed

de Bakker JM, van Capelle FJ, Janse MJ, Wilde AA, Coronel R, Becker AE, Dingemans KP, van Hemel NM, Hauer RN. Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation. Circulation. 1988;77:589–606. PubMed

de Bakker JM, Janse MJ, Van Capelle FJ, Durrer D. Endocardial mapping by simultaneous recording of endocardial electrograms during cardiac surgery for ventricular aneurysm. J Am Coll Cardiol. 1983;2:947–53. PubMed

Coronel R, Wilms-Schopman FJ, Opthof T, Janse MJ. Dispersion of repolarization and arrhythmogenesis. Heart Rhythm. 2009;6:537–43. PubMed

Anter E, Tschabrunn CM, Buxton AE and Josephson ME. High-Resolution Mapping of Postinfarction Reentrant Ventricular Tachycardia: Electrophysiological Characterization of the Circuit. Circulation. 2016;134:314–27. PubMed PMC

Marchlinski FE, Callans DJ, Gottlieb CD and Zado E. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation. 2000;101:1288–96. PubMed

Jais P, Maury P, Khairy P, Sacher F, Nault I, Komatsu Y, Hocini M, Forclaz A, Jadidi AS, Weerasooryia R, et al. Elimination of local abnormal ventricular activities: a new end point for substrate modification in patients with scar-related ventricular tachycardia. Circulation. 2012;125:2184–96. PubMed

de Chillou C, Groben L, Magnin-Poull I, Andronache M, MagdiAbbas M, Zhang N, Abdelaal A, Ammar S, Sellal JM, Schwartz J, et al. Localizing the critical isthmus of postinfarct ventricular tachycardia: the value of pace-mapping during sinus rhythm. Heart Rhythm. 2014;11:175–81. PubMed

Di Biase L, Santangeli P, Burkhardt DJ, Bai R, Mohanty P, Carbucicchio C, Dello Russo A, Casella M, Mohanty S, Pump A, et al. Endo-epicardial homogenization of the scar versus limited substrate ablation for the treatment of electrical storms in patients with ischemic cardiomyopathy. J Am Coll Cardiol. 2012;60:132–41. PubMed

Di Biase L, Burkhardt JD, Lakkireddy D, Carbucicchio C, Mohanty S, Mohanty P, Trivedi C, Santangeli P, Bai R, Forleo G, et al. Ablation of Stable VTs Versus Substrate Ablation in Ischemic Cardiomyopathy: The VISTA Randomized Multicenter Trial. J Am Coll Cardiol. 2015;66:2872–82. PubMed

Tzou WS, Frankel DS, Hegeman T, Supple GE, Garcia FC, Santangeli P, Katz DF, Sauer WH, Marchlinski FE. Core isolation of critical arrhythmia elements for treatment of multiple scar-based ventricular tachycardias. Circ Arrhythm Electrophysiol. 2015;8:353–61. PubMed

Sacher F, Lim HS, Derval N, Denis A, Berte B, Yamashita S, Hocini M, Haissaguerre M, Jais P. Substrate mapping and ablation for ventricular tachycardia: the LAVA approach. J Cardiovasc Electrophysiol. 2015;26:464–71. PubMed

Peters NS, Wit AL. Gap junction remodeling in infarction: does it play a role in arrhythmogenesis? J Cardiovasc Electrophysiol. 2000;11:488–90. PubMed

Peters NS and Wit AL. Myocardial architecture and ventricular arrhythmogenesis. Circulation. 1998;97:1746–54. PubMed

Rohr S Myofibroblasts in diseased hearts: new players in cardiac arrhythmias? Heart Rhythm. 2009;6:848–56. PubMed

Ciaccio EJ, Coromilas J, Costeas CA, Wit AL. Sinus rhythm electrogram shape measurements are predictive of the origins and characteristics of multiple reentrant ventricular tachycardia morphologies. J Cardiovasc Electrophysiol. 2004;15:1293–301. PubMed

Anter E, Kleber AG, Rottmann M, Leshem E, Barkagan M, Tschabrunn CM, Contreras-Valdes FM, Buxton AE. Infarct-Related Ventricular Tachycardia: Redefining the Electrophysiological Substrate of the Isthmus During Sinus Rhythm. JACC Clin Electrophysiol. 2018;4:1033–1048. PubMed

Child N, Bishop MJ, Hanson B, Coronel R, Opthof T, Boukens BJ, Walton RD, Efimov IR, Bostock J, Hill Y, et al. An activation-repolarization time metric to predict localized regions of high susceptibility to reentry. Heart Rhythm. 2015;12:1644–53. PubMed PMC

Irie T, Yu R, Bradfield JS, Vaseghi M, Buch EF, Ajijola O, Macias C, Fujimura O, Mandapati R, Boyle NG, et al. Relationship between sinus rhythm late activation zones and critical sites for scar-related ventricular tachycardia: systematic analysis of isochronal late activation mapping. Circ Arrhythm Electrophysiol. 2015;8:390–9. PubMed PMC

Aziz Z, Shatz D, Raiman M, Upadhyay GA, Beaser AD, Besser SA, Shatz NA, Fu Z, Jiang R, Nishimura T, et al. Targeted Ablation of Ventricular Tachycardia Guided by Wavefront Discontinuities During Sinus Rhythm: A New Functional Substrate Mapping Strategy. Circulation. 2019;140:1383–1397. PubMed

Kawara T, Derksen R, de Groot JR, Coronel R, Tasseron S, Linnenbank AC, Hauer RN, Kirkels H, Janse MJ, de Bakker JM. Activation delay after premature stimulation in chronically diseased human myocardium relates to the architecture of interstitial fibrosis. Circulation. 2001;104:3069–75. PubMed

Peters NS, Coromilas J, Hanna MS, Josephson ME, Costeas C, Wit AL. Characteristics of the temporal and spatial excitable gap in anisotropic reentrant circuits causing sustained ventricular tachycardia. Circ Res. 1998;82:279–93. PubMed

Dillon SM, Allessie MA, Ursell PC, Wit AL. Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts. Circ Res. 1988;63:182–206. PubMed

Berruezo A, Fernandez-Armenta J, Andreu D, Penela D, Herczku C, Evertz R, Cipolletta L, Acosta J, Borras R, Arbelo E, et al. Scar dechanneling: new method for scar-related left ventricular tachycardia substrate ablation. Circ Arrhythm Electrophysiol. 2015;8:326–36. PubMed

Martin CA, Martin R, Maury P, Meyer C, Wong T, Dallet C, Shi R, Gajendragadkar P, Takigawa M, Frontera A, et al. Effect of Activation Wavefront on Electrogram Characteristics During Ventricular Tachycardia Ablation. Circ Arrhythm Electrophysiol. 2019;12:e007293. PubMed

Kuck KH, Schaumann A, Eckardt L, Willems S, Ventura R, Delacretaz E, Pitschner HF, Kautzner J, Schumacher B, Hansen PS, group Vs. Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomised controlled trial. Lancet. 2010;375:31–40. PubMed

Sapp JL, Parkash R, Tang AS. Ventricular Tachycardia Ablation versus Antiarrhythmic-Drug Escalation. N Engl J Med. 2016;375:1499–1500. PubMed

Patient selection, ventricular tachycardia substrate delineation, and data transfer for stereotactic arrhythmia radioablation: a clinical consensus statement of the European Heart Rhythm Association of the European Society of Cardiology and the Heart Rhythm Society