The Shape of Ventricular Tachycardia

HomeCirculationVol. 148, No. 18The Shape of Ventricular Tachycardia Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBThe Shape of Ventricular Tachycardia William G. Stevenson, Harikrishna Tandri and Dan M. Roden William G. StevensonWilliam G. Stevenson Correspondence to: William G. Stevenson, MD, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, 1215 21st Ave South, Nashville, TN 37212. Email E-mail Address: [email protected] https://orcid.org/0000-0002-2118-7893 Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN. , Harikrishna TandriHarikrishna Tandri Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN. and Dan M. RodenDan M. Roden https://orcid.org/0000-0002-6302-0389 Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN. Originally published30 Oct 2023https://doi.org/10.1161/CIRCULATIONAHA.123.066574Circulation. 2023;148:1368–1370is related toIdentification of Human Ventricular Tachycardia Demarcated by Fixed Lines of Conduction Block in a 3-Dimensional Hyperboloid CircuitThe heart functions as an electrical syncytium, producing a coordinated sequence of depolarizations for effective contraction 100 000 times daily. Even in a homogenous syncytium, however, reentrant arrhythmias are possible. In mathematical simulations, Winfree et al1 showed that reentry can occur when a critically timed premature stimulus launches a wavefront that collides with tissue that has not yet recovered from the preceding beat, forms an arc of conduction block that lengthens until the wavefront encounters excitable elements, propagates around behind the arc of block, and arrives at the center of the arc as it is recovering excitability, to allow reentry. This forms a figure-of-8 type of circuit with clockwise and counterclockwise loops and a central isthmus (Figure [A]). The lines of block are not fixed, but functional, because of refractoriness of the tissue, and are maintained during tachycardia by collision of wavefronts from either side of the line. Reentry is maintained if the wave circulates with a sufficiently long revolution time to allow the tissue in front of the advancing wave of depolarization to recover excitability after its last depolarization. Thus, even this modeling in the normal heart emphasizes the principle that slow conduction, which increases revolution time, facilitates reentry.Article, see p 1354Download figureDownload PowerPointFigure. Reentry circuits. A, A double-loop (figure-of-8) reentry circuit defined by functional block (heavy black lines) maintained by collision of wavefronts (small arrows) from the circulating reentry wavefronts (thick arrow). B, A cross-section of the ventricular wall with fibrosis (white hatched area) and a myocardial conducting channel through the scar (blue and purple) allowing for reentry (yellow arrows). The myocardial channel with its entrance and exit connecting to larger adjacent myocardium can be viewed as a hyperboloid shape (black dashed lines).Sustained ventricular tachycardia (VT) is a very rare event in the normal heart, and emerges most commonly in hearts with fibrotic scar from previous myocardial infarction or nonischemic cardiomyopathy. Indeed, the extent of fibrosis, captured as areas of late gadolinium enhancement on magnetic resonance imaging, is associated with the risk of sudden death, presumably because of scar-related VT.2,3 Figure-of-8 reentry is inducible after myocardial infarction in experimental models4–6 and in humans with VT.7,8 Fibrosis can facilitate reentry in several ways. A decrease in coupling between myocyte bundles slows conduction velocity and alters susceptibility to conduction block.5 Fibrosis that completely separates myocyte bundles produces fixed conduction block that may define part of the reentry circuit path, and in particular the isthmus.9Electroanatomic mapping systems now allow rapid reconstruction of the anatomy and electrical activation sequence of the endocardium and the epicardium, such that mapping during VT is often possible. Complete reentry circuits are usually not identified, and confusing activation patterns are common.8,10 In this issue of Circulation, Nishimura et al11 present an interesting approach to thinking about the geometry of reentrant circuits and in particular the constraints on critical isthmuses that maintain VT. They consider that figure-8 reentry realized in 3 dimensions would resemble a hyperboloid (Figure [B]). The wavefront propagates through a central isthmus, emerging from an exit region, and circulates through loops back to the entrance of the isthmus. The parts of the shape that are confined within the wall and not accessible to recording from endocardial or epicardial catheters are obscured. Thus, what is recorded from the endocardial or epicardial surface may be a slice through the hyperboloid shape. The endocardial or epicardial surface or regions of fibrosis extending to the epicardial or endocardial surface may truncate the hyperboloid, and they designated this truncation a depth boundary. In addition, the orientation of the hyperboloid within the wall may vary. For example, the isthmus exit may be at the endocardium and entrance closer to the epicardium, further complicating the representation of the reentry circuit on the mapping surface. This interesting exercise may lead to new ways of thinking about VT maps that could help infer the location of the isthmus when it is intramural, helping to guide ablation.During VT, lateral lines of block that define the isthmus, which Nishimura et al11 refer to as lateral boundaries, have wavefronts moving in opposite directions on either side of the line. Are these lateral boundaries a functional block present only during VT, as in mathematic simulations and early postinfarction models, or a fixed block that would be anticipated from fibrosis and that would also be present during sinus rhythm? Because fixed block would most likely represent fibrosis without myocytes, definition of the reentry path would lend itself to identification by imaging techniques and mapping during sinus rhythm. To address this question, Nishimura et al11 marked lines of block identified during VT and assessed conduction in the absence of VT during sinus rhythm or relatively slow pacing. Because fixed block can escape detection when the myocardium on both sides of the block is activated by a sinus rhythm wavefront traveling longitudinally relative to the line of block,12 Nishimura et al11 paced to alter the direction of activation through the region, and in some cases paced adjacent to the line while recording on the opposite side of it. Split potentials characteristic of block were observed in 74% of VTs, supporting the frequent existence of fixed, rather than functional, conduction block defining at least a portion of the isthmus.These findings are consistent with the seminal observations of de Bakker et al13 in explanted human hearts showing that some reentry paths were defined by fibrosis. A narrow bundle of fibers could traverse dense fibrosis, creating a channel or isthmus from which the reentry wavefront emerges, producing an apparent focal site of endocardial activation. The wavefront propagates away in all directions, and may travel in broad loops back to the entrance of the isthmus. Thus, the concept of a smooth broad isthmus defined by a regular hyperboloid is a first approximation only of a much more complex structure in which, for example, an isthmus can be a narrow irregular path.The frequent presence of fixed conduction block in regions defining the VT isthmus is consistent with previous studies showing that ablation targeting areas of abnormal conduction and electrograms identified by "substrate mapping" during stable sinus or paced rhythm is effective for ablation of VT in some patients.12,14,15 In this study, areas of slow conduction identified from isochronal crowding that have been associated with successful sites for catheter ablation were also shown to be associated with regions of fixed conduction block.There are several caveats. These studies come from a selected population of patients who had recurrent sustained monomorphic VT that was inducible and allowed mapping. It is possible that functional block plays more of a role in faster VTs and those that are more difficult to induce. Whereas fixed conduction block was present for the majority of areas where block defined a VT isthmus, the specificity of fixed conduction block for identifying successful ablation sites was not defined. Some of the putative reentry paths defined on the basis of activation alone may have been bystanders. Not every area of fixed block is necessarily arrhythmogenic. Thus, the specificity of finding a region of fixed block is uncertain and this study did not test ablation guided by these mapping findings. Furthermore, fixed blocks closer to the perivalvular regions and late activated regions may behave differently from similar blocks occurring in the septal and apical ventricles.The idea of conceptualizing the critical isthmus of a reentrant circuit as the neck of a hyperboloid structure will provoke further questions about the 3-dimensional nature of reentry and the usefulness of this model: some of those may include how best to reconstruct or visualize hyperboloids and their orientation, how their boundaries are determined by anatomic barriers or fibrosis, and whether they are fixed or can change over time or with different stimulation sites or rates. Answering questions such as these may lead to improved methods to treat or prevent reentrant arrhythmias.Disclosures Dr Stevenson has received speaking honoraria from Medtronic, Biotronik, Abbott, Johnson & Johnson, and Boston Scientific, and consulting honoraria from Novartis; and holds a patent for irrigated needle ablation that is consigned to Brigham Hospital. Dr Tandri has received research support from Abbott. Dr Roden reports no conflicts of interest.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.For Disclosures, see page 1370.Circulation is available at www.ahajournals.org/journal/circCorrespondence to: William G. Stevenson, MD, Division of Cardiovascular Medicine, Vanderbilt University Medical Center, 1215 21st Ave South, Nashville, TN 37212. Email william.g.stevenson@vumc.orgREFERENCES1. Winfree AT. Electrical instability in cardiac muscle: phase singularities and rotors.J Theor Biol. 1989; 138:353–405. doi: 10.1016/s0022-5193(89)80200-0CrossrefMedlineGoogle Scholar2. Grani C, Benz DC, Gupta S, Windecker S, Kwong RY. Sudden cardiac death in ischemic heart disease: from imaging arrhythmogenic substrate to guiding therapies.JACC Cardiovasc Imaging. 2020; 13:2223–2238. doi: 10.1016/j.jcmg.2019.10.021CrossrefMedlineGoogle Scholar3. Di Marco A, Brown PF, Bradley J, Nucifora G, Claver E, de Frutos F, Dallaglio PD, Comin-Colet J, Anguera I, Miller CA, et al. Improved risk stratification for ventricular arrhythmias and sudden death in patients with nonischemic dilated cardiomyopathy.J Am Coll Cardiol. 2021; 77:2890–2905. doi: 10.1016/j.jacc.2021.04.030CrossrefMedlineGoogle Scholar4. 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. doi: 10.1161/01.res.63.1.182LinkGoogle Scholar5. Ciaccio EJ, Anter E, Coromilas J, Wan EY, Yarmohammadi H, Wit AL, Peters NS, Garan H. Structure and function of the ventricular tachycardia isthmus.Heart Rhythm. 2022; 19:137–153. doi: 10.1016/j.hrthm.2021.08.001CrossrefMedlineGoogle Scholar6. Mehra R, Zeiler RH, Gough WB, El-Sherif N. Reentrant ventricular arrhythmias in the late myocardial infarction period 9: electrophysiologic-anatomic correlation of reentrant circuits.Circulation. 1983; 67:11–24. doi: 10.1161/01.cir.67.1.11LinkGoogle Scholar7. Downar E, Kimber S, Harris L, Mickleborough L, Sevaptsidis E, Masse S, Chen TC, Genga A. Endocardial mapping of ventricular tachycardia in the intact human heart: II: evidence for multiuse reentry in a functional sheet of surviving myocardium.J Am Coll Cardiol. 1992; 20:869–878. doi: 10.1016/0735-1097(92)90187-rCrossrefMedlineGoogle Scholar8. Tung R, Raiman M, Liao H, Zhan X, Chung FP, Nagel R, Hu H, Jian J, Shatz DY, Besser SA, et al. Simultaneous endocardial and epicardial delineation of 3D reentrant ventricular tachycardia.J Am Coll Cardiol. 2020; 75:884–897. doi: 10.1016/j.jacc.2019.12.044CrossrefMedlineGoogle Scholar9. Soejima K, Stevenson WG, Maisel WH, Sapp JL, Epstein LM. Electrically unexcitable scar mapping based on pacing threshold for identification of the reentry circuit isthmus: feasibility for guiding ventricular tachycardia ablation.Circulation. 2002; 106:1678–1683. doi: 10.1161/01.cir.0000030187.39852.a7LinkGoogle Scholar10. Hadjis A, Frontera A, Limite LR, Bisceglia C, Bognoni L, Foppoli L, Lipartiti F, Paglino G, Radinovic A, Tsitsinakis G, et al. Complete electroanatomic imaging of the diastolic pathway is associated with improved freedom from ventricular tachycardia recurrence.Circ Arrhythm Electrophysiol. 2020; 13:e008651. doi: 10.1161/CIRCEP.120.008651LinkGoogle Scholar11. Nishimura T, Shatz N, Weiss JP, Zawaneh M, Bai R, Beaser AD, Upadhyay GA, Aziz ZA, Naya HM, Shatz DY, et al. Identification of human ventricular tachycardia demarcated by fixed lines of conduction block in a 3-dimensional hyperboloid circuit.Circulation. 2023; 148:1354–1367. doi: 10.1161/CIRCULATIONAHA.123.065525LinkGoogle Scholar12. Anter E, Neuzil P, Reddy VY, Petru J, Park KM, Sroubek J, Leshem E, Zimetbaum PJ, Buxton AE, Kleber AG, et al. Ablation of reentry-vulnerable zones determined by left ventricular activation from multiple directions: a novel approach for ventricular tachycardia ablation: a multicenter study (PHYSIO-VT).Circ Arrhythm Electrophysiol. 2020; 13:e008625. doi: 10.1161/CIRCEP.120.008625LinkGoogle Scholar13. 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. doi: 10.1161/01.cir.77.3.589LinkGoogle Scholar14. 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. doi: 10.1161/CIRCULATIONAHA.119.042423LinkGoogle Scholar15. Acosta J, Soto-Iglesias D, Jauregui B, Armenta JF, Penela D, Frutos-Lopez M, Arana-Rueda E, Pedrote A, Mont L, Berruezo A. Long-term outcomes of ventricular tachycardia substrate ablation incorporating hidden slow conduction analysis.Heart Rhythm. 2020; 17:1696–1703. doi: 10.1016/j.hrthm.2020.05.017CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesIdentification of Human Ventricular Tachycardia Demarcated by Fixed Lines of Conduction Block in a 3-Dimensional Hyperboloid CircuitTakuro Nishimura, et al. Circulation. 2023;148:1354-1367 October 31, 2023Vol 148, Issue 18 Advertisement Article InformationMetrics © 2023 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.123.066574PMID: 37903185 Originally publishedOctober 30, 2023 KeywordsEditorialshearttachycardia, ventricularPDF download Advertisement SubjectsArrhythmiasCatheter Ablation and Implantable Cardioverter-DefibrillatorMechanisms