Fast and the Furious

HomeCirculation: Arrhythmia and ElectrophysiologyVol. 11, No. 4Fast and the Furious Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBFast and the FuriousElectrogram Drift: Dynamic Analysis of Acquired Electrograms to Optimize Discrimination of Ventricular Tachycardia Substrate Ammar M. Killu, MBBS, Danesh Kella, MBBS and Suraj Kapa, MD Ammar M. KilluAmmar M. Killu Department of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN. , Danesh KellaDanesh Kella Department of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN. and Suraj KapaSuraj Kapa Department of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, MN. Originally published13 Apr 2018https://doi.org/10.1161/CIRCEP.118.006391Circulation: Arrhythmia and Electrophysiology. 2018;11:e006391See Article by Kuroki et al"It don't matter if you win by an inch or a mile. Winning's winning."—Dom Toretto | The Fast and The Furious (2001)The foundation for ablation of ventricular tachycardia (VT) in patients with structural heart disease lies in (1) identifying relevant substrate, (2) proving that said substrate contributes to arrhythmogenesis, and (3) ablating that substrate. Many investigators, however, espouse pure substrate-guided approaches that may supplant step 2, wherein targeting of perceived substrate, as defined by voltage cut offs or signal characteristics, is performed in lieu of proving the relevance of that site or region to arrhythmogenesis. In fact, pure substrate-guided approaches to ablation, particularly in infarct-related VT, have been shown to have a reasonable likelihood of success in both retrospective studies and clinical trials.1–4 However, the best method for defining substrate, either before or during invasive electrophysiological procedures, remains an area of active study. The publication in this issue of Circulation: Arrhythmia and Electrophysiology by Kuroki et al5 present yet another approach to using acquired electrogram signals to optimize identification of critical targets for ablation. Understanding the relevance of their findings needs to be considered in the context of work to date on defining substrate for ventricular arrhythmogenesis and the associated pitfalls of existing approaches.What Drives VT?In structural heart disease, it is the existence of electrically active circuits with conductive properties sufficiently different from that of surrounding normal myocardium that drives VT. Generally, but not always, these potential circuits exist in regions of the otherwise dense scar as complex connections between variably healthy regions of the myocardium. Thus, in the structurally diseased heart, these circuits may present themselves to the electrophysiologist as fractionated signals, late potentials (reflecting slow or complex wavefront propagation) or low-voltage regions. However, the presence of such attributes does not necessarily guarantee that these regions necessarily contribute to arrhythmia. Therefore, ablation is often extensive, including targeting all apparently abnormal signals, even if the contribution to arrhythmogenicity cannot be proven.How Do We Define Relevant Circuits Among the Greater Milieu?The fundamental precept of substrate mapping lies in the acquisition of electrogram signals during creation of the 2-dimensional shell (reflecting the endocardial or epicardial surface) which is, in turn, reflected by the computer in 3-dimensions. Point density partly defines map accuracy, especially given the complex endocardial topography of the cardiac chambers. Traditionally, on electrogram acquisition, those signals demonstrating clear morphological abnormalities (fractionation, late potentials, split potentials, etc) are tagged, and voltage amplitudes are automatically determined. Given work was done by several investigators, bipolar voltage amplitude cut offs are then used to help define regions of likely abnormal tissue, reflecting a mix of cells of variable viability and potential to conduct. Proof of conduction along certain circuits is achieved by any of a variety of approaches, including altering voltage limits to identify channels within the denser scar region, pace mapping to identify local and global capture, or activation and entrainment mapping during VT.6–9 However, these are surrogate end points given the various factors that can define voltage amplitude, the potential for far-field capture with local pacing, and often hemodynamically intolerable VT that may limit the ability to map during arrhythmia. In turn, all of these approaches are fundamentally limited by our inability to map transmurally, as circuits can exist in any orientation and length within the 3-dimensional cellular milieu.What Can We Do to Scout Our Competition Better?There are several approaches that exist to map substrate and define relevant components of that substrate. Several reported approaches to defining substrate and their associated pitfalls are summarized in the Table. Recent data from several groups have supported the use of preoperative imaging and intraoperative image integration to help define substrate. Preoperative imaging may optimize mapping and minimize missing relevant regions by defining the transmural and 3-dimensional distribution of potentially arrhythmogenic tissue. However, ability to target substrate purely based off of noninvasively acquired data and real-time magnetic resonance imaging is limited, though work in this regard is actively evolving in the form of noninvasive ablation and magnetic resonance imaging-enabled invasive approaches. Intraoperatively, conventional bipolar voltage cut offs are used to define our attribution of scar versus normal tissue. However, use of set cut offs has profound limitations, particularly given that in some patients, regions with a local bipolar voltage below the presumed cut off for scar may still contain viable myocardial tissue that can contribute to arrhythmia. This has led to the approach of voltage limit adjustment (VLA) wherein channels within the broader scar region are identified by toggling the bipolar voltage limits.7,8 However, these approaches may be suboptimal because of poor specificity as Kuroki et al5 indicate in their study. However, such approaches may also have limited sensitivity given the VLA approach still presumes that given channels need to consistently lie within similar voltage ranges in the same patient, though voltage may have a little direct relationship to conduction characteristics. Mountantonakis et al8 previously demonstrated that multiple adjustments may be needed until all potential VT channels may be identified and even then the majority of perceived channels did not necessarily correlate with the existence of an isthmus.8 Our dependence on voltage is a false arbiter of conduction because the voltage is really just a surrogate measure of myocardial health that, in turn, may or may not associate with arrhythmogenic potential.Table. Approaches to Defining Arrhythmogenic Ventricular SubstrateStrategies for Defining the VT Circuit or the Underlying SubstrateConcept and Value PrinciplesScenarios Where Most Often UsedLimitationsEntrainment mappingConsidered gold-standard to identify the critical isthmus using pacing maneuvers during VT.Stable hemodynamics during VT with or without support.Readily inducible VT.Hemodynamically unstable VT.Noninducible VT.VT may be terminated with pacing.Activation mappingIdentify the area of slow conduction, that is, the critical isthmus during VT.Stable hemodynamics with or without support during VT.Readily inducible VT.Hemodynamically unstable VT.Noninducible VT.Can be open to interpretation based on activation map.Absence of entire circuit may be because of incomplete mapping, midmyocardial scar, or excluded components (eg, endocavitary structures).Pace mappingPaced QRS morphology and capture latency used to identify the VT exit site. Inexcitability of tissue suggests scar.Hemodynamically unstable VT.Difficult to induce VTCannot exclude bystander sites in the scar.Limited resolution because of far-field capture.Assumes that the pacing wavefront always follows the same path as the VT circuit (may get orthodromic capture resulting in a different morphology QRS but along a critical path).Voltage-based substrate identification (including voltage limit adjustment)Areas of low-voltage suggest diseased tissue and slow conduction, with potential involvement in the VT circuit.Hemodynamically unstable VT.Difficult to induce VT.Multiple VTs induced.Arbitrary cut offs used may exclude surviving myocardial cells within areas considered scar by certain voltage cut offs.Assumes that all diseased areas are involved in the VT circuit.Limited resolution and may require endo- and epicardial mapping.Topographical characteristics may limit spatial resolutionMidmyocardial substrate may not be accounted for (n.b. unipolar voltages have been suggested to overcome this limitation).Signal amplitude may seem low because of epicardial fat but in fact, reflect.LAVA (local abnormal ventricular activation) and late potentials (including electrogram processing techniques such as FFT to further characterize substrate)Delayed activation of areas in reference to the QRS and high-frequency low-amplitude signals suggest slow conduction, with potential involvement in the VT circuit.Hemodynamically unstable VT.Difficult to induce VT.Multiple VTs induced.Characterization of signal-of-interest as late potential or LAVA may change with different activation wavefront (sinus vs ventricular pacing) and thus may be arbitrary.Assumes that the signal-of-interest is of clinical relevance to the arrhythmia.Signals may seem abnormal because of spatially close but electrically distant structures existing in the vicinity of the catheter tip during mapping.MRI-guided mappingAreas of scar reconstruction from late gadolinium enhancement on MRI integrated in the 3-dimensional electroanatomic mapping to guide ablation.Substrate may be identified before the ablation including distribution of intramural and epicardial foci.Identify relationship of other critical structures (eg, coronary arteries) relative to perceived substrate.Hemodynamically unstable VT.Difficult to induce VT.Multiple VTs induced.Limited data.Assumes that the substrate houses the clinical VT circuit.Does not necessarily demonstrate most critical elements within broader scar region that contribute to arrhythmogenesis.Listed are various approaches to defining ventricular substrate during ablation for ventricular tachycardia, situations in which there may be utility, and associated limitations. FFT indicates fast-Fourier transform; MRI, magnetic resonance imaging; and VT, ventricular tachycardia.Another approach is the use of local signal characteristics in the form of fractionated, split, or late potentials instead of voltage alone.7,8,10 The presence of a locally sensed multicomponent bipolar signal implies that there are multiple electrically depolarizing cells contributing to the local signal at relatively different time points throughout a single cardiac cycle, thus implying a locally complex cardiac milieu. However, each signal at an individual site needs to be considered in the context of surrounding sites in the case of reentry, as reentry is defined by the path a circuit may take and not by a single spot alone. Mountantonakis et al8 and Arenal et al7 have previously supported the use of isolated late potentials as a surrogate marker for the existence of critical VT circuits, though their identification may be dependent on point density and the rhythm in which mapping is performed.7,8 Thus, some investigators have supported using a broader late activation ablation approach wherein all abnormal potentials are targeted. However, these approaches are still limited because of the dependence on stationary signal characteristics often taken independent of surrounding signals and thus driving more ablation than what may be otherwise necessary.Can Mathematical Transformation of Electrograms Inject Some NITROUS Into Our Ablative Approach?In this issue of Circulation: Arrhythmia and Electrophysiology, Kuroki et al5 present a retrospective analysis depicting the incremental utility of fast-Fourier transform analysis in combination with VLA to identify critical isthmi on the basis of apparent high-voltage and high-frequency channels. Their work builds on a prior study assessing time- and frequency-domain analysis of endocardial mapping by Campos et al11 which showed that automated analysis by time-domain analysis may rapidly quantify electrogram fragmentation and guide substrate-based ablation of VT. They reported that frequency-domain analysis was suboptimal with only 60% of VT isthmus sites identified by this approach.11 In contrast, the current study suggests that fast-Fourier transform combined with VLA carries a high sensitivity and high specificity in identifying relevant VT isthmi.Consideration of the incremental utility of such electrogram transformations needs to be considered in the context of the information it is providing us. Essentially, they rely on the precept that such transformations allow us to see deeper into the signal by converting the signal over a period of time into its frequency components, with each temporal component being characterized by a unique amplitude and phase. This technique, when applied to electrogram or electrocardiographic signals, says nothing about arrhythmic mechanism but only offers a transformed representation of the local signal which can be used to demonstrate the stability of local activation characteristics. Unfortunately, the approach is governed by similar limitations to that of standard electrogram acquisition, in which spatially close but electrically distant structures may contribute to perceived local electrogram fractionation (as when a catheter may be adjacent to an endocavitary structure and the endocardial surface simultaneously), wavefront collision from multisite activation (as during activation over the His-Purkinje system when multiple wavefronts may converge on single sites resulting in extinguishing or revelation of local potentials), and inadequate catheter contact. Despite these limitations, the ability to use novel mathematical approaches to distinguishing relevant components of the electrogram signal holds promise to reveal more about cardiac activation than has been previously imagined in traditional substrate evaluation approaches. More research is needed to understand exactly what is being revealed, however—namely are we better visualizing elements of transmural activation, further characterizing relevant endocardial circuits, or something else. This need is further revealed in the requirement of multiple ranges for the fast-Fourier transform ratio used by Kuroki et al5 to ultimately fit in all isthmuses identified during entrainment mapping. Thus, similar to the limitation of VLA, the technique used by Kuroki et al5 still does not offer a completely automated means of defining relevant substrate, with some dynamic manual adjustment yet needed.5Will Our Approach to the Finish Line Be Any Different?In the publication by Kuroki et al,5 identification of channels as portrayed by the presence of both high-frequency and high-voltage channels (whether partial or full) may include all relevant isthmuses and, thus, reflect optimal ablation targets among the larger milieu of perceived substrate. However, there are several limitations, including the limited number of patients included, the retrospective nature of the study, the question of whether any channels may have been missed, and the lack of long-term outcomes.Furthermore, whether novel electrogram processing techniques may actually impact overall outcomes is unclear. Ideally, these approaches will have 2 overall aims: (1) avoid missing relevant substrate (ie, being more sensitive) and (2) avoid targeting substrate that may be otherwise nonarrhythmogenic (ie, being more specific). Whether the finish line will be any differently realized between more targeted or broader substrate-based approaches is unclear and requires randomized prospective studies comparing different methods. However, the study by Kuroki et al5 represents a welcome addition to the VT mapping literature as it yields another measure of slow conduction within potentially critical isthmuses that could hold the potential for not just bringing the finish line closer but by also making it more clear.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.http://circep.ahajournals.orgSuraj Kapa, MD, Department of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905. E-mail [email protected]References1. Sacher F, Lim HS, Derval N, Denis A, Berte B, Yamashita S, Hocini M, Haissaguerre M, Jaïs P. Substrate mapping and ablation for ventricular tachycardia: the LAVA approach.J Cardiovasc Electrophysiol. 2015; 26:464–471. doi: 10.1111/jce.12565.CrossrefMedlineGoogle Scholar2. Berruezo A, Fernández-Armenta J, Andreu D, Penela D, Herczku C, Evertz R, Cipolletta L, Acosta J, Borràs R, Arbelo E, Tolosana JM, Brugada J, Mont L. Scar dechanneling: new method for scar-related left ventricular tachycardia substrate ablation.Circ Arrhythm Electrophysiol. 2015; 8:326–336. doi: 10.1161/CIRCEP.114.002386.LinkGoogle Scholar3. 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; 8:353–361. doi: 10.1161/CIRCEP.114.002310.LinkGoogle Scholar4. Kumar S, Baldinger SH, Romero J, Fujii A, Mahida SN, Tedrow UB, Stevenson WG. Substrate-based ablation versus ablation guided by activation and entrainment mapping for ventricular tachycardia: a systematic review and meta-analysis.J Cardiovasc Electrophysiol. 2016; 27:1437–1447. doi: 10.1111/jce.13088.CrossrefMedlineGoogle Scholar5. Kuroki K, Nogami A, Igarashi M, Masuda K, Kowase S, Kurosaki K, Komatsu Y, Naruse Y, Machino T, Yamasaki H, Xu D, Murakoshi N, Sekiguchi Y, Aonuma K. New substrate-guided method of predicting slow conducting isthmuses of ventricular tachycardia: preliminary analysis to the combined use of voltage limit adjustment and fast-Fourier transform analysis.Circ Arrhythm Electrophysiol. 2018; 11:e005705. doi: 10.1161/CIRCEP.117.005705.LinkGoogle Scholar6. 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.LinkGoogle Scholar7. Arenal A, del Castillo S, Gonzalez-Torrecilla E, Atienza F, Ortiz M, Jimenez J, Puchol A, García J, Almendral J. Tachycardia-related channel in the scar tissue in patients with sustained monomorphic ventricular tachycardias: influence of the voltage scar definition.Circulation. 2004; 110:2568–2574. doi: 10.1161/01.CIR.0000145544.35565.47.LinkGoogle Scholar8. Mountantonakis SE, Park RE, Frankel DS, Hutchinson MD, Dixit S, Cooper J, Callans D, Marchlinski FE, Gerstenfeld EP. Relationship between voltage map "channels" and the location of critical isthmus sites in patients with post-infarction cardiomyopathy and ventricular tachycardia.J Am Coll Cardiol. 2013; 61:2088–2095. doi: 10.1016/j.jacc.2013.02.031.CrossrefMedlineGoogle Scholar9. Hsia HH, Lin D, Sauer WH, Callans DJ, Marchlinski FE. Anatomic characterization of endocardial substrate for hemodynamically stable reentrant ventricular tachycardia: identification of endocardial conducting channels.Heart Rhythm. 2006; 3:503–512. doi: 10.1016/j.hrthm.2006.01.015.CrossrefMedlineGoogle Scholar10. Bogun F, Good E, Reich S, Elmouchi D, Igic P, Lemola K, Tschopp D, Jongnarangsin K, Oral H, Chugh A, Pelosi F, Morady F. Isolated potentials during sinus rhythm and pace-mapping within scars as guides for ablation of post-infarction ventricular tachycardia.J Am Coll Cardiol. 2006; 47:2013–2019. doi: 10.1016/j.jacc.2005.12.062.CrossrefMedlineGoogle Scholar11. Campos B, Jauregui ME, Marchlinski FE, Dixit S, Gerstenfeld EP. Use of a novel fragmentation map to identify the substrate for ventricular tachycardia in postinfarction cardiomyopathy.Heart Rhythm. 2015; 12:95–103. doi: 10.1016/j.hrthm.2014.10.002.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails April 2018Vol 11, Issue 4 Advertisement Article InformationMetrics © 2018 American Heart Association, Inc.https://doi.org/10.1161/CIRCEP.118.006391PMID: 29654137 Originally publishedApril 13, 2018 Keywordsretrospective studiesprospective studieselectrophysiologymyocardiumheartEditorialsPDF download Advertisement SubjectsArrhythmiasElectrophysiology