Localizing the critical isthmus of postinfarct ventricular tachycardia: The value of pace-mapping during sinus rhythm Christian de Chillou, MD, PhD,*† Laurent Groben, MD,* Isabelle Magnin-Poull, MD,*† Marius Andronache, MD, PhD,*† Mohamed Magdi Abbas, MD,* Ning Zhang, MD,* Ahmed Abdelaal, MD,* Sonia Ammar, MD,* Jean-Marc Sellal, MD,* Jérôme Schwartz, MD,* Béatrice Brembilla-Perrot, MD,* Etienne Aliot, MD, FHRS,* Francis E. Marchlinski, MD, FHRS‡ From the *CHU de Nancy, Département de Cardiologie, Vandœuvre lès-Nancy, France, †INSERM-IADI, Vandœuvre lès-Nancy, France, and ‡Cardiovascular Division, Electrophysiology Section, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania. BACKGROUND Most postinfarct ventricular tachycardias (VTs) are sustained by a reentrant mechanism. The “protected isthmus” of the reentrant circuit is critical for the maintenance of VTs and the target for catheter ablation. Various techniques based on conventional electrophysiology and/or detailed three-dimensional (3D) reconstruction of the VT circuit are used to unmask this isthmus.
to scar border in the outer entrance zones (23% ⫾ 28%), in the entrance zones (39% ⫾ 34%), and in the entrance part of the isthmus (32% ⫾ 26%). The color-coded sequence (from the best to the poorest matching sites) on the PMs revealed figure-of-eight pictures matching the VT activation time maps and identifying VT isthmuses.
OBJECTIVE The purpose of this study was to assess pace-maps (PMs) to identify postinfarct VT isthmuses. We hypothesized that an abrupt change in paced QRS morphology may be used to identify a VT isthmus and be targeted for successful ablation.
CONCLUSION Pace-mapping is useful for unmasking VT isthmuses in patients with well-tolerated postinfarct endocardial reentrant VTs.
METHODS High-density 3D PMs were matched to the subsequent 3D endocardial reentrant VT activation mapping in 10 patients (8 men; age 70.7 ⫾ 10.8 years) who underwent successful postinfarct VT ablation. At each pacing site in a given patient, the 12-lead ECG recorded during pacing was compared to that of VT, with the resulting matching percentage (up to 100% for perfect matches) allocated to this point to generate color-coded PMs. RESULTS With respect to VT isthmuses, the best percentages of matching were found in the exit zones and isthmus exit part (89% ⫾ 8% and 84% ⫾ 7%, respectively) and the poorest adjacent
A reentrant mechanism1–3 explains most postinfarct ventricular tachycardias (VTs). The so-called “protected isthmus” of the reentrant circuit is the critical element for the maintenance of these VTs and, therefore, the target for ablation.4 Identifying such a protected isthmus can be performed either by a conventional electrophysiologic approach based on VT entrainment techniques or by electroanatomic activation mapping using a three-dimensional (3D) mapping system.4–6 However, such techniques cannot be used to define the protected VT isthmus in the presence of a poorly Drs. de Chillou, Andronache, Aliot, and Marchlinski have received lecture fees from Biosense Webster. Dr. Abdelaal is currently an employee of Biosense Webster. Address reprint requests and correspondence: Dr. Christian de Chillou, Département de Cardiologie, Hôpitaux de Brabois, 1, rue du Morvan, 54511 Vandœuvre lès Nancy, France. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
KEYWORDS Catheter ablation; Electroanatomic mapping; Electrophysiologic mapping; Ischemic cardiomyopathy; Pacemapping; Ventricular tachycardia ABBREVIATIONS 3D ¼ three-dimensional; ECG-AC ¼ ECG average correlation; EGM ¼ electrogram; ICD ¼ implantable cardioverterdefibrillator; LOB ¼ line of functional conduction block; LV ¼ left ventricle; PM ¼ pace-map; RF ¼ radiofrequency; SR ¼ sinus rhythm; VT ¼ ventricular tachycardia (Heart Rhythm 2014;11:175–181) I 2014 Heart Rhythm Society. All rights reserved.
tolerated unmappable VT. Several investigators have proposed a substrate-based approach that either relies on sinus rhythm (SR) scar definition using bipolar voltage and pacemapping to create linear lesions or targets electrograms (EGMs) showing late potentials (or fractionation).7–11 The techniques and response of pace-mapping during SR have been incompletely correlated with the actual definition of isthmus location and boundaries. We hypothesized that abrupt transitions in paced QRS morphology when pacing the endocardium of infarcted myocardium from one that matches VT to one that has little similarity should help identify VT isthmuses.
Methods Patients Of the 82 consecutive patients who underwent a postinfarct sustained VT ablation procedure in our institution between http://dx.doi.org/10.1016/j.hrthm.2013.10.042
176 2004 and 2007 (4-year period), 10 fulfilled the following criteria and were included in the present retrospective study: (1) presence of a monomorphic clinical VT documented by 12-lead ECG, which subsequently was inducible, sustained, and well tolerated during electrophysiologic study; (2) availability of SR 3D electroanatomic mapping of the left ventricle (LV) along with high-density pace-mapping; (3) performance of 3D activation mapping of the clinical VT confirming a reentrant mechanism and allowing precise definition of the critical isthmus boundaries; and (4) confirmation that radiofrequency (RF) catheter ablation lesions applied across the isthmus prevented induction of VT. All 10 patients (8 men, mean age 70.7 ⫾ 10.8 years) included in the study had a remote (19.2 ⫾ 5.6 years) myocardial infarction. Infarct locations were anterior (n = 4), inferior (n = 5), or anterior and inferior (n = 1). Mean LV ejection fraction was 0.37 ⫾ 0.14. Four patients were equipped with an implantable cardioverter-defibrillator (ICD) at the time of the ablation procedure, and another four underwent ICD placement after the ablation procedure.
Electrophysiologic study, mapping, and ablation Procedures were performed after informed consent was obtained. Systemic anticoagulation was achieved with heparin (initial bolus of 50 U/kg intravenous, followed by 1000– 2000 U/h) throughout the procedure. Sedation was obtained with 10 mg nalbuphine intravenous with incremental doses of 5 mg as necessary.
Step 1: Ventricular programmed electrical stimulation Endocardial signal and surface ECG were recorded using the BARD LabSystem PRO (CR Bard Inc, Lowell, MA). ICDs were programmed off during the procedure. In brief, a bipolar catheter was inserted via the femoral vein and positioned at the right ventricular apex. With this catheter, ventricular programmed electrical stimulation was used to induce VT, applying up to three extrastimuli during spontaneous rhythm and during paced rhythm (600-ms then 400-ms basic cycle length). Programmed electrical stimulation was delivered through an external stimulator (Micropace III EPS-320 Cardiac Stimulator 3.18, Micropace EP Inc, Sidney, Australia) with 2-ms pulse width at twice diastolic threshold. Failure to obtain the clinical VT promoted the same protocol in the right ventricular outflow tract. The clinical VT was eventually induced and sustained in all patients (see inclusion criteria). SR was restored by overdrive pacing after the original induction in order to pass on to the next stage.
Step 2: LV electroanatomic mapping and pace-mapping during SR The CARTO XP nonfluoroscopic electrophysiologic mapping and navigation system (Biosense Webster, Diamond Bar, CA) as well as the technique used for postinfarct VT mapping have been described previously.6,12,13 In brief, the
Heart Rhythm, Vol 11, No 2, February 2014 LV was approached in retrograde fashion via the aorta. Detailed endocardial bipolar SR mapping was performed in SR. The left atrioventricular junction (sites showing both an atrial and a ventricular EGM with an 1:1 amplitude ratio) was delineated. Infarct regions were identified, and more datapoints were acquired within and around these areas. Defining the area under more intense investigation relied on the usual clinical indicators, such as echocardiography, Q-wave topography, and VT morphology on 12-lead ECG as well as the presence of low (o1.5 mV) bipolar voltage EGMs.14,15 LV mapping was considered completed when the color-coded 3D shell showed no gap in both the infarct region (fill threshold set to 10) as well as the rest of the LV (fill threshold set to 20). Pace-mapping (10- to 15-second duration with 2-ms pulse width at twice diastolic threshold and maximum output of 25 mA) was performed at a pacing cycle length equal to that of the clinical VT at each site where a point was acquired during LV electroanatomic mapping within the area of interest (i.e., the scar region). Pacing threshold was repeatedly checked to set the stimulus strength at twice threshold. Each 12-lead ECG generated by pace-mapping was compared with that of the VT induced prior to mapping and confirmed based on 12-lead ECG comparison to represent the clinical VT. This comparison was done automatically by the data processing template matching software integrated into the Bard workstation. In brief, a reference QRS is selected on the 12-lead ECG obtained during the induced clinical VT and the one to be compared with the reference is selected on a pacemapping 12-lead ECG. The Bard software “slides” the reference over the incoming data until the best local match is found by using a correlation calculation. This calculation is repeated at multiple positions for each of the ECG leads. The position that yields the highest average correlation across all of the leads is the best local match. This position is marked, and the values for each lead are calculated and displayed along with an average correlation value for the entire ECG. As a result, an ECG average correlation (ECG-AC) value toward 99% to 100% means a perfect match between two 12-lead ECG morphologies, whereas an ECG-AC value toward zero (or even negative values) identifies a poor match between the two 12-lead ECG morphologies compared beforehand. For each lead-to-lead comparison, both the polarity and the amplitude of the QRS complexes play an important role as to the resulting value of the percentage of correlation calculated by the Bard software. Two QRS complexes with similar polarities and amplitude will have a positive percentage of correlation, up to 100%, which is the maximum possible value indicating a perfect match. In contrast, the percentage of correlation may have a negative value, down to –100%, which is the minimum possible value indicating the worst possible match, for example, in the case of similar amplitude but complete reversion of polarity (e.g., a “QS” and a “R” pattern) between the two QRS complexes. Because the CARTO XP system cannot integrate the ECG-AC values calculated by the Bard template matching software onto a 3D map, we took the effort to generate such
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Figure 1 Example of a pace-mapping (PM) map in a patient with an anterior wall myocardial infarction. The 12-lead ECG during ventricular tachycardia (VT) as well as four ECGs resulting from PM at four different sites (PM1 to PM4) are shown (left, right) with their location shown on the three-dimensional reconstruction (CARTO picture of the left ventricle in the left anterior oblique projection; middle). The percentage of correlation using the QRS matching algorithm is shown on each 12-lead ECG as well as the CARTO picture. Color-coding (from red to purple) relates to the percentage of matching between the 12lead ECG during VT and that during PM (from 99% to –46% in the examples shown).
maps using the CARTO LAT-map by changing the LAT value of each point acquired during SR by its corresponding ECG-AC value. To do so, the caliper marking the LAT was manually moved to a new LAT position whose value corresponds to the measured ECG-AC value but, importantly, with the opposite sign. As a result, zones with the highest ECG-AC values are displayed in red and those with lower ECG-AC values are color coded in yellow, then green, then blue, and finally purple for areas showing the lowest ECG-AC values (Figure 1). This newly generated, colorcoded map was given the name “pace-mapping [PM] map.”
Step 3: LV electroanatomic mapping during VT After the clinical VT was reinduced, the LV was remapped (“remap” function on CARTO XP) during the tachycardia to acquire an activation time VT map according to a previously published technique.6 In brief, EGMs recorded within the VT isthmus always show (early, mid, or late) diastolic potentials. VT isthmus boundaries correspond to either an anatomic obstacle (e.g., mitral valve) or a line of functional conduction block (LOB), which is characterized by a line of adjacent sites showing double-potential EGMs, with one the two components at a given site being an (early, mid, or late) diastolic potential and the other one being coincident with the QRS complex. One side of this LOB corresponds to the VT isthmus and the other side to an outer loop. The mapping procedure was terminated when a sufficient density of points was achieved to allow characterization of the VT circuit and precise delineation of its protected isthmus
boundaries. The resulting reentrant circuit was considered to be the spatially shortest route of unidirectional activation encompassing a full range of mapped activation times and returning to the site of earliest activation. Conventional mapping, including entrainment maneuvers, was not systematically performed after induction of the clinical VT because such maneuvers could result in either interruption of the VT or its transformation into another morphology. Characteristics of each VT isthmus (boundary definition, length, and width) were defined, and, for purposes of analysis, the area including each VT isthmus was subsequently compartmentalized into eight separate segments (Figure 2). Point-by-point RF ablation was performed during VT using a Stockert-Cordis RF generator, Stockert GmbH, Freiburg, Germany, (irrigation flow rate 17 mL/min, temperaturecontrolled mode with 451C target temperature and maximum 35-W power delivered), to transect the VT isthmus. The procedural end-point was ablation of all clinically welltolerated VTs. Successful ablation was defined as the inability to reinduce any VT (except polymorphic VT/ventricular fibrillation or monomorphic VT with a rate 4270/min). Partial success was defined as the inability to reinduce the index clinical VT but with inducibility of a nonclinical monomorphic VT with a rate r270/min at the end of procedure.
Management after ablation After ablation, patients were monitored for 72 hours by telemetry. Transthoracic echocardiography was performed within 2 days after ablation. Patients then were discharged
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Heart Rhythm, Vol 11, No 2, February 2014 difference was the two VT morphologies were a reversal of the depolarization wavefront propagation along the isthmus. Dimensions of the isthmuses were variable, with a mean length of 31 ⫾ 12 mm (range 21–59 mm), mean width of 27 ⫾ 11 mm (range 15–47 mm), and mean isthmus surface of 9.7 ⫾ 7.6 cm² (range 3–28 cm²). VT isthmuses were always fully located within an area with low (o1.5 mV) SR EGM voltages.
Ablation results
Figure 2 Eight different segments within and around a ventricular tachycardia (VT) isthmus. Note that the lateral and outer zones are 10-mm areas, whereas the dimensions of the exit and entrance zones depend on the isthmus width (IW).
and followed on an outpatient basis by clinical evaluation and 24-hour Holter recordings performed regularly. When available, the ICD Holter function was permanently activated. Post hoc analysis Both PM and VT activation maps were superimposed on the main screen of the CARTO XP system, thus allowing allocation of any point on any PM to a given compartment on the superimposed VT map. The correlation between a PM and its corresponding VT map then could be analyzed.
RF energy was applied for a mean of 9.8 ⫾ 8.9 minutes (range 4–33 minutes) to transect the critical VT isthmuses. Mean procedure time was 208 ⫾ 62 minutes (range 135–300 minutes), and mean fluoroscopy time was 10 ⫾ 8 minutes (range 4–32 minutes). VT stopped during RF energy application in all patients. The procedure was successful in eight patients, and a partial success was obtained in the remaining two patients. No perior postprocedural complications were observed. During mean follow-up of 65 ⫾ 6 months, four patients died (all with an ICD). The cause of death was heart failure in three patients and undetermined in one patient. VT recurrences were observed in three patients (all with an ICD, including one patient who died of heart failure).
Correlation between VT maps and PMs
All VTs exhibited a double-loop figure-of-eight reentrant circuit with two loops rotating in opposite directions around barriers delineating an isthmus. The approximately parallel barriers consisted of at least one functional LOB, with the second barrier being either another functional LOB (n ¼ 7) or the mitral valve annulus (n ¼ 3) as an anatomic barrier.
Considering the position of the PMs points in relation to their corresponding VT circuits, 43 PM points were in the isthmus zone (20 points in the entrance part of the isthmus and 23 points in the exit part of the isthmus), 92 points at the exit area, 85 points at the entrance area, 51 points at the lateral zones, 81 points at the outer exit zone, and 53 points at the outer entrance zone (Figures 3 and 4). The best mean average percentages of correlation between pace-mapping and VT morphology were found in the exit zone (89% ⫾ 8%) and in the exit part of the isthmus (84% ⫾ 7%), whereas the worst average mean correlation percentages were found in the outer entrance zone (23% ⫾ 28%), in the entrance zone (39% ⫾ 34%), and in the entrance part of the isthmus (32% ⫾ 26%). Within the isthmus zone, the mean average percentage of correlation was 59% ⫾ 32%, with a broad range of values (–31% to 99%) according to the location of the pacing site within the VT isthmus. Pacing sites close to the isthmus exit showed percentage of correlation values similar to those observed in the exit zone, whereas pacing sites close to isthmus entrance showed percentage of correlation values similar to those recorded in the entrance zone. A cutoff value 482% for the percentage of correlation best defined the exit site of VT circuits (sensitivity 82%, specificity 87%, predictive positive value 65%, negative predictive value 94%).
Characteristics of critical VT isthmuses
VT isthmus definition using PM
Using the activation maps during VT, one and only one VT isthmus was identified in each patient. In one patient, a second VT morphology was mapped during the procedure. Both VTs were sharing the same protected isthmus; the only
Visual inspection of the PMs gave important information about the VT isthmus location (Figures 3 and 4). A gradual and progressive decrease in the percentage of correlation values was noticed (with the corresponding colors changing
Results Mapping A complete VT map (mean VT cycle length 431 ⫾ 73ms, range 330–540 ms) with its corresponding PM was available for each of the 10 patients. The mean number of points acquired during PM was 41 ⫾ 11 (range 22–56), and the mean number of points acquired during VT mapping was of 163 ⫾ 61 (range 87–276). Total mapping time (including both PM and VT map) ranged from 49 to 118 minutes (average 75 ⫾ 23 minutes).
Characteristics of VT circuits
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Figure 3 Example of a three-dimensional reconstruction (CARTO pictures in the right anterior oblique projection) of a ventricular tachycardia (VT) circuit (left) and the corresponding pace-mapping map (middle, right) in a patient with an anterior wall myocardial infarction. The VT circuit is located at the left ventricular septum. A poor pace-mapping match zone is found 30 mm from the best pace-mapping matching sites at the isthmus entrance (middle). Arrows joining these two areas (right) have the same orientation as the VT isthmus.
from red to orange, yellow, green, and so forth) when moving from the exit zone to the outer exit zone and even further away from the VT circuit along a given axial direction. Looking at the 10% step isochronal PMs, isochronal zones could be relatively narrow (3–10 mm, as in Figure 3) or broad (up to 20 mm, as shown in Figure 4). Along the rotating double loops of the VT circuits, the percentage of correlation decreased as well, with the highest values at the exit zone and the lowest values at the entrance zone or just at the isthmus entrance. When following the isochronal color-coded sequence on the PM, a figure-of-eight picture, resembling the VT activation time mapping (Figure 4), can be observed. Linking the best to the poorest pace-mapping zone found in its vicinity (10–30 mm depending on VT isthmus length) defines the orientation of the VT isthmus.
Discussion Our study evaluated the value of pace-mapping during SR to localize the critical isthmus of postinfarct mappable VTs with definition of isthmuses boundaries identified by detailed activation mapping and displayed on an electroanatomic mapping system. The study shows that pace-mapping best matches the VT morphology in the region of the VT isthmus exit zone and at the exit part of the VT isthmus (average percentage of QRS correlation 89% ⫾ 8% and 84% ⫾ 7%, respectively). This confirms that pace-mapping during SR is helpful in identifying the exit zone of the isthmus as well as the exit part of the isthmus. Surprisingly, pace-mapping was neither sensitive nor specific for identification of the isthmus entrance part or isthmus entrance zone, with average percentages of QRS correlation
Figure 4 Example of a three-dimensional reconstruction (same patient and same projection as in Figure 1) showing (from left to right) the voltage map during sinus rhythm, the pace-mapping (PM) map (10% step isochrones), and the ventricular tachycardia (VT) circuit located at the apex with an upper exit (20-ms step isochrones). Arrows following the isochronal color-coded sequence on the PM (middle) depict a figure-of-eight that resembles the VT activation time mapping (right).
180 only 32% ⫾ 26% within the VT isthmus entrance part and 39% ⫾ 34% in the entrance zone of the isthmus. Importantly, the orientation of the isthmus of a reentrant postinfarct VT circuit may be recognized using pace-mapping, with identification of two zones consistent with the exit (area with pace-mapping showing a good correlation with the 12-lead ECG during VT) and the entrance (area with pace-mapping showing a poor correlation with the 12-lead ECG during VT) of the VT circuit. A distance of 10 to 30 mm consistently separated the VT entrance from the VT exit and corresponded to the isthmus zone. In the isthmus zone, pace-mapping showed a good correlation with the 12-lead ECG during VT at sites close to the isthmus exit and, in contrast, showed a poor correlation with the 12-lead ECG during VT at sites close to the isthmus entrance. Once the VT isthmus orientation is determined, RF lesions can be appropriately deployed to transect this isthmus. During the last 4 years, our road map to localize the VT isthmus using pace-mapping has first identified the exit zone (or the exit part of the isthmus). Then pace-mapping was performed centrifugally around these good pace-mapping sites to find sites close by (10–15 mm) with poor pace-mapping correlation that correspond to the VT isthmus entrance. When the PMs were generated, we expected to observe a centrifugal pattern, with points at the exit zone of the isthmus showing the best percentage QRS match, with the percentages of correlation gradually and homogenously decreasing when moving away in all directions from the best pacemapping zone. The results of our study invalidated this assumption. Indeed, within the isthmus zone, a poor correlation with VT morphology during pace-mapping was observed when pacing close to the isthmus entrance, whereas a good correlation was shown when pacing close to the isthmus exit. This is completely different compared to what is seen during VT entrainment where concealed entrainment (12-lead ECG identical during pacing and VT) can be observed all along VT isthmus, at both exit and entrance sites but with a different stimulus to QRS interval.7,16,17 When pacing within the isthmus, the wavefront propagates in two opposite directions: orthodromically and antidromically with respect to isthmus depolarization sequence during VT. The activation wavefront significantly contributes to generate some portion of the QRS complex on the 12lead only when “leaving” the protected isthmus. During VT entrainment, the collision between the antidromic (N) paced wavefront with the previous (N-1) orthodromic wavefront prevents any change in QRS morphology whatever the pacing site along the VT isthmus. This is different when pacing during SR because there is no preexisting orthodromic wavefront propagating along the VT isthmus. As a consequence, when pacing during SR at the entrance of the VT isthmus, the wavefront will spread out from the pacing site to depolarize the adjacent myocardium in the opposite direction of the VT wavefront, creating a dramatic difference in QRS morphology compared to the VT morphology. Several authors have evaluated the feasibility of VT ablation in SR in patients with structural heart disease.7,8 In the study by Marchlinski et al,7 which included patients with ischemic and
Heart Rhythm, Vol 11, No 2, February 2014 nonischemic cardiomyopathy presenting nonmappable VT, successful VT control was achieved by drawing RF lines through sites with the best visual correlation of morphology between the QRS in VT and pace-map. The lines were drawn connecting the endocardial areas with the lowest voltage (o0.5 mV) to areas with normal voltage or to anatomic boundaries. Brunckhorst et al16 first proposed a method to identify VT circuit isthmuses during SR using pace-mapping and an electroanatomic mapping system. Pace-mapping was used to locate the exit zone (i.e., sites with good correlation with 12-lead ECG recorded during VT) while conduction delays during pace-mapping (regions with stimulus-to-QRS delays Z40ms) were associated with reentry target sites. Of great interest, the authors noted that marked mismatches between the paced QRS morphology compared to that of VT were common in the target ablation zone. In particular, pacing sites with a long stimulus-to-QRS interval and a complete mismatch compared to VT morphology could very well be located within the protected isthmus area. This finding is consistent with the present study and suggests that such sites were located at the VT isthmus entrance zone in the midisthmus with preferential conduction toward the entrance side within the VT isthmus.
Study limitations For methodologic rigor in truly defining the critical circuit, we limited our study to only patients for whom ablation across the isthmus prevented reinduction. Therefore, our study population consisted of only 10 patients. However, this is a very small number from which to make inferences regarding sensitivity and specificity cutoff values for defining VT exit and VT isthmus exit parts. Pacing threshold may be high in scar areas, resulting in larger size of the virtual bipolar pacing electrode with myocardial tissue capture at a remote site leading to significant changes in QRS morphology.18 To overcome this issue, pacing threshold was checked at each pacing site to set the stimulus strength to twice threshold. Many other parameters may affect QRS morphology, such as pacing rate, unipolar or bipolar configuration of stimulation, and size of the electrode used for pace-mapping.19,20 Pacing rate was adjusted to that of the clinical VT. A very high pacing threshold in the scar region might cause a lack of points within the isthmus because of the presence of unexcitable tissue under the catheter electrodes. In some patients, 41 VT morphology was induced and mapped. Because the Bard software does not allow simultaneous comparison of multiple QRS morphologies, we only correlated the most frequently induced VT during the PM acquisition to avoid a significant increase in procedure time during this investigation. Although we have applied our findings in patients with poorly tolerated VTs to our daily practice since 2007 (Figure 5), this study only included well-tolerated mappable VTs. Additional study is required to validate the findings in patients with unmappable VT and nonischemic cardiomyopathies.
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Figure 5 Example of a deductive reconstruction (only based upon pace-maps [PMs]) of a ventricular tachycardia (VT) reentrant circuit in a patient with a poorly tolerated VT. A: Twelve-lead ECG of the clinical VT induced during electrophysiologic study. B: PM (14% step isochrones) of the three-dimensional reconstructed LV (posterior view). Yellow tags represent PM sites. The percentage of matching between the 12-lead ECG during VT and that during PM ranges from 97% to –7%. C: Twelve-lead ECGs recorded during PM at two different left ventricular sites 15 mm apart (red and blue asterisks in B). D: VT circuit reconstruction (perimitral circuit) with isthmus boundaries corresponding to the mitral valve and an hypothesized line of conduction block.
Conclusion This study confirms that pace-mapping during SR with a good QRS match to VT is helpful in identifying the exit zone of the VT isthmus. More importantly, by pacing more extensively into the depths of the low-voltage region, one can identify a transition to a poorer matching pace-map with the poorest match between the 12-lead ECG recorded in VT and that obtained during pace-mapping at the VT isthmus entrance. By quantifying the degree of QRS match, one can use the colorcoded sequence (from best to poorest matching sites) on the PMs to identify the course of the VT isthmus and facilitate targeted ablation. Prospective VT ablation studies with large cohorts of patients should compare this technique to identify and target postinfarct VT isthmuses with other substrate-based approaches, especially in patients with poorly tolerated VTs.
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8. 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. 9. Kottkamp H, Wetzel U, Schirdewahn P, et al. Catheter ablation of ventricular tachycardia in remote myocardial infarction: substrate description guiding placement of individual linear lesions targeting noninducibility. J Cardiovasc Electrophysiol 2003;14:675–681. 10. Arenal A, del Castillo S, Gonzalez-Torrecilla E, et al. 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. 11. Jaïs P, Maury P, Khairy P, et al. Elimination of local abnormal ventricular activities: a new end point for substrate modification in patients with scar-related ventricular tachycardia. Circulation 2012;125:2184–2196. 12. Ben-Haim SA, Osadchy D, Schuster I, Hayam G, Josephson ME. Nonfluoroscopic in vivo navigation and mapping technology. Nat Med 1996;2: 1393–1395. 13. Shpun S, Gepstein L, Hayam G, Ben-Haim SA. Guidance of radiofrequency endocardial ablation with real-time three-dimensional magnetic navigation system. Circulation 1997;96:2016–2021. 14. Wrobleski D, Houghtaling C, Josephson ME, Ruskin J, Reddy V. 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. 15. Callans JD, Ren J-F, Michele J, Marchlinski F, Dillon S. Electroanatomic left ventricular mapping in the porcine model of healed anterior myocardial infarction. Correlation with intracardiac echocardiography and pathological analysis. Circulation 1999;100:1744–1750. 16. Brunckhorst CB, Stevenson WG, Soejima K, et al. Relationship of slow conduction detected by pace-mapping to ventricular tachycardia re-entry circuit sites after infarction. J Am Coll Cardiol 2003;41:802–809. 17. Brunckhorst CB, Delacretaz E, Soejima K, Maisel WH. Friedman, Stevenson WG. Identification of the ventricular tachycardia isthmus after infarction by pace mapping. Circulation 2004;110:652–659. 18. Kadish AH, Childs K, Schmaltz S, Morady F. Differences in QRS configuration during unipolar pacing from adjacent sites: implications for the spatial resolution of pace-mapping. J Am Coll Cardiol 1991;17:143–1151. 19. Goyal R, Havey M, Daoud EG, et al. Effect of coupling interval and pacing cycle length on morphology of paced ventricular complexes. Implications for pace mapping. Circulation 1996;94:2843–2849. 20. Kadish AH, Schmaltz S, Morady F. A comparison of QRS complexes resulting from unipolar and bipolar pacing: implications for pace-mapping. Pacing Clin Electrophysiol 1991;14:823–832.
to scar border in the outer entrance zones (23% ⫾ 28%), in the entrance zones (39% ⫾ 34%), and in the entrance part of the isthmus (32% ⫾ 26%). The color-coded sequence (from the best to the poorest matching sites) on the PMs revealed figure-of-eight pictures matching the VT activation time maps and identifying VT isthmuses.
OBJECTIVE The purpose of this study was to assess pace-maps (PMs) to identify postinfarct VT isthmuses. We hypothesized that an abrupt change in paced QRS morphology may be used to identify a VT isthmus and be targeted for successful ablation.
CONCLUSION Pace-mapping is useful for unmasking VT isthmuses in patients with well-tolerated postinfarct endocardial reentrant VTs.
METHODS High-density 3D PMs were matched to the subsequent 3D endocardial reentrant VT activation mapping in 10 patients (8 men; age 70.7 ⫾ 10.8 years) who underwent successful postinfarct VT ablation. At each pacing site in a given patient, the 12-lead ECG recorded during pacing was compared to that of VT, with the resulting matching percentage (up to 100% for perfect matches) allocated to this point to generate color-coded PMs. RESULTS With respect to VT isthmuses, the best percentages of matching were found in the exit zones and isthmus exit part (89% ⫾ 8% and 84% ⫾ 7%, respectively) and the poorest adjacent
A reentrant mechanism1–3 explains most postinfarct ventricular tachycardias (VTs). The so-called “protected isthmus” of the reentrant circuit is the critical element for the maintenance of these VTs and, therefore, the target for ablation.4 Identifying such a protected isthmus can be performed either by a conventional electrophysiologic approach based on VT entrainment techniques or by electroanatomic activation mapping using a three-dimensional (3D) mapping system.4–6 However, such techniques cannot be used to define the protected VT isthmus in the presence of a poorly Drs. de Chillou, Andronache, Aliot, and Marchlinski have received lecture fees from Biosense Webster. Dr. Abdelaal is currently an employee of Biosense Webster. Address reprint requests and correspondence: Dr. Christian de Chillou, Département de Cardiologie, Hôpitaux de Brabois, 1, rue du Morvan, 54511 Vandœuvre lès Nancy, France. E-mail address: [email protected].
1547-5271/$-see front matter B 2014 Heart Rhythm Society. All rights reserved.
KEYWORDS Catheter ablation; Electroanatomic mapping; Electrophysiologic mapping; Ischemic cardiomyopathy; Pacemapping; Ventricular tachycardia ABBREVIATIONS 3D ¼ three-dimensional; ECG-AC ¼ ECG average correlation; EGM ¼ electrogram; ICD ¼ implantable cardioverterdefibrillator; LOB ¼ line of functional conduction block; LV ¼ left ventricle; PM ¼ pace-map; RF ¼ radiofrequency; SR ¼ sinus rhythm; VT ¼ ventricular tachycardia (Heart Rhythm 2014;11:175–181) I 2014 Heart Rhythm Society. All rights reserved.
tolerated unmappable VT. Several investigators have proposed a substrate-based approach that either relies on sinus rhythm (SR) scar definition using bipolar voltage and pacemapping to create linear lesions or targets electrograms (EGMs) showing late potentials (or fractionation).7–11 The techniques and response of pace-mapping during SR have been incompletely correlated with the actual definition of isthmus location and boundaries. We hypothesized that abrupt transitions in paced QRS morphology when pacing the endocardium of infarcted myocardium from one that matches VT to one that has little similarity should help identify VT isthmuses.
Methods Patients Of the 82 consecutive patients who underwent a postinfarct sustained VT ablation procedure in our institution between http://dx.doi.org/10.1016/j.hrthm.2013.10.042
176 2004 and 2007 (4-year period), 10 fulfilled the following criteria and were included in the present retrospective study: (1) presence of a monomorphic clinical VT documented by 12-lead ECG, which subsequently was inducible, sustained, and well tolerated during electrophysiologic study; (2) availability of SR 3D electroanatomic mapping of the left ventricle (LV) along with high-density pace-mapping; (3) performance of 3D activation mapping of the clinical VT confirming a reentrant mechanism and allowing precise definition of the critical isthmus boundaries; and (4) confirmation that radiofrequency (RF) catheter ablation lesions applied across the isthmus prevented induction of VT. All 10 patients (8 men, mean age 70.7 ⫾ 10.8 years) included in the study had a remote (19.2 ⫾ 5.6 years) myocardial infarction. Infarct locations were anterior (n = 4), inferior (n = 5), or anterior and inferior (n = 1). Mean LV ejection fraction was 0.37 ⫾ 0.14. Four patients were equipped with an implantable cardioverter-defibrillator (ICD) at the time of the ablation procedure, and another four underwent ICD placement after the ablation procedure.
Electrophysiologic study, mapping, and ablation Procedures were performed after informed consent was obtained. Systemic anticoagulation was achieved with heparin (initial bolus of 50 U/kg intravenous, followed by 1000– 2000 U/h) throughout the procedure. Sedation was obtained with 10 mg nalbuphine intravenous with incremental doses of 5 mg as necessary.
Step 1: Ventricular programmed electrical stimulation Endocardial signal and surface ECG were recorded using the BARD LabSystem PRO (CR Bard Inc, Lowell, MA). ICDs were programmed off during the procedure. In brief, a bipolar catheter was inserted via the femoral vein and positioned at the right ventricular apex. With this catheter, ventricular programmed electrical stimulation was used to induce VT, applying up to three extrastimuli during spontaneous rhythm and during paced rhythm (600-ms then 400-ms basic cycle length). Programmed electrical stimulation was delivered through an external stimulator (Micropace III EPS-320 Cardiac Stimulator 3.18, Micropace EP Inc, Sidney, Australia) with 2-ms pulse width at twice diastolic threshold. Failure to obtain the clinical VT promoted the same protocol in the right ventricular outflow tract. The clinical VT was eventually induced and sustained in all patients (see inclusion criteria). SR was restored by overdrive pacing after the original induction in order to pass on to the next stage.
Step 2: LV electroanatomic mapping and pace-mapping during SR The CARTO XP nonfluoroscopic electrophysiologic mapping and navigation system (Biosense Webster, Diamond Bar, CA) as well as the technique used for postinfarct VT mapping have been described previously.6,12,13 In brief, the
Heart Rhythm, Vol 11, No 2, February 2014 LV was approached in retrograde fashion via the aorta. Detailed endocardial bipolar SR mapping was performed in SR. The left atrioventricular junction (sites showing both an atrial and a ventricular EGM with an 1:1 amplitude ratio) was delineated. Infarct regions were identified, and more datapoints were acquired within and around these areas. Defining the area under more intense investigation relied on the usual clinical indicators, such as echocardiography, Q-wave topography, and VT morphology on 12-lead ECG as well as the presence of low (o1.5 mV) bipolar voltage EGMs.14,15 LV mapping was considered completed when the color-coded 3D shell showed no gap in both the infarct region (fill threshold set to 10) as well as the rest of the LV (fill threshold set to 20). Pace-mapping (10- to 15-second duration with 2-ms pulse width at twice diastolic threshold and maximum output of 25 mA) was performed at a pacing cycle length equal to that of the clinical VT at each site where a point was acquired during LV electroanatomic mapping within the area of interest (i.e., the scar region). Pacing threshold was repeatedly checked to set the stimulus strength at twice threshold. Each 12-lead ECG generated by pace-mapping was compared with that of the VT induced prior to mapping and confirmed based on 12-lead ECG comparison to represent the clinical VT. This comparison was done automatically by the data processing template matching software integrated into the Bard workstation. In brief, a reference QRS is selected on the 12-lead ECG obtained during the induced clinical VT and the one to be compared with the reference is selected on a pacemapping 12-lead ECG. The Bard software “slides” the reference over the incoming data until the best local match is found by using a correlation calculation. This calculation is repeated at multiple positions for each of the ECG leads. The position that yields the highest average correlation across all of the leads is the best local match. This position is marked, and the values for each lead are calculated and displayed along with an average correlation value for the entire ECG. As a result, an ECG average correlation (ECG-AC) value toward 99% to 100% means a perfect match between two 12-lead ECG morphologies, whereas an ECG-AC value toward zero (or even negative values) identifies a poor match between the two 12-lead ECG morphologies compared beforehand. For each lead-to-lead comparison, both the polarity and the amplitude of the QRS complexes play an important role as to the resulting value of the percentage of correlation calculated by the Bard software. Two QRS complexes with similar polarities and amplitude will have a positive percentage of correlation, up to 100%, which is the maximum possible value indicating a perfect match. In contrast, the percentage of correlation may have a negative value, down to –100%, which is the minimum possible value indicating the worst possible match, for example, in the case of similar amplitude but complete reversion of polarity (e.g., a “QS” and a “R” pattern) between the two QRS complexes. Because the CARTO XP system cannot integrate the ECG-AC values calculated by the Bard template matching software onto a 3D map, we took the effort to generate such
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Figure 1 Example of a pace-mapping (PM) map in a patient with an anterior wall myocardial infarction. The 12-lead ECG during ventricular tachycardia (VT) as well as four ECGs resulting from PM at four different sites (PM1 to PM4) are shown (left, right) with their location shown on the three-dimensional reconstruction (CARTO picture of the left ventricle in the left anterior oblique projection; middle). The percentage of correlation using the QRS matching algorithm is shown on each 12-lead ECG as well as the CARTO picture. Color-coding (from red to purple) relates to the percentage of matching between the 12lead ECG during VT and that during PM (from 99% to –46% in the examples shown).
maps using the CARTO LAT-map by changing the LAT value of each point acquired during SR by its corresponding ECG-AC value. To do so, the caliper marking the LAT was manually moved to a new LAT position whose value corresponds to the measured ECG-AC value but, importantly, with the opposite sign. As a result, zones with the highest ECG-AC values are displayed in red and those with lower ECG-AC values are color coded in yellow, then green, then blue, and finally purple for areas showing the lowest ECG-AC values (Figure 1). This newly generated, colorcoded map was given the name “pace-mapping [PM] map.”
Step 3: LV electroanatomic mapping during VT After the clinical VT was reinduced, the LV was remapped (“remap” function on CARTO XP) during the tachycardia to acquire an activation time VT map according to a previously published technique.6 In brief, EGMs recorded within the VT isthmus always show (early, mid, or late) diastolic potentials. VT isthmus boundaries correspond to either an anatomic obstacle (e.g., mitral valve) or a line of functional conduction block (LOB), which is characterized by a line of adjacent sites showing double-potential EGMs, with one the two components at a given site being an (early, mid, or late) diastolic potential and the other one being coincident with the QRS complex. One side of this LOB corresponds to the VT isthmus and the other side to an outer loop. The mapping procedure was terminated when a sufficient density of points was achieved to allow characterization of the VT circuit and precise delineation of its protected isthmus
boundaries. The resulting reentrant circuit was considered to be the spatially shortest route of unidirectional activation encompassing a full range of mapped activation times and returning to the site of earliest activation. Conventional mapping, including entrainment maneuvers, was not systematically performed after induction of the clinical VT because such maneuvers could result in either interruption of the VT or its transformation into another morphology. Characteristics of each VT isthmus (boundary definition, length, and width) were defined, and, for purposes of analysis, the area including each VT isthmus was subsequently compartmentalized into eight separate segments (Figure 2). Point-by-point RF ablation was performed during VT using a Stockert-Cordis RF generator, Stockert GmbH, Freiburg, Germany, (irrigation flow rate 17 mL/min, temperaturecontrolled mode with 451C target temperature and maximum 35-W power delivered), to transect the VT isthmus. The procedural end-point was ablation of all clinically welltolerated VTs. Successful ablation was defined as the inability to reinduce any VT (except polymorphic VT/ventricular fibrillation or monomorphic VT with a rate 4270/min). Partial success was defined as the inability to reinduce the index clinical VT but with inducibility of a nonclinical monomorphic VT with a rate r270/min at the end of procedure.
Management after ablation After ablation, patients were monitored for 72 hours by telemetry. Transthoracic echocardiography was performed within 2 days after ablation. Patients then were discharged
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Heart Rhythm, Vol 11, No 2, February 2014 difference was the two VT morphologies were a reversal of the depolarization wavefront propagation along the isthmus. Dimensions of the isthmuses were variable, with a mean length of 31 ⫾ 12 mm (range 21–59 mm), mean width of 27 ⫾ 11 mm (range 15–47 mm), and mean isthmus surface of 9.7 ⫾ 7.6 cm² (range 3–28 cm²). VT isthmuses were always fully located within an area with low (o1.5 mV) SR EGM voltages.
Ablation results
Figure 2 Eight different segments within and around a ventricular tachycardia (VT) isthmus. Note that the lateral and outer zones are 10-mm areas, whereas the dimensions of the exit and entrance zones depend on the isthmus width (IW).
and followed on an outpatient basis by clinical evaluation and 24-hour Holter recordings performed regularly. When available, the ICD Holter function was permanently activated. Post hoc analysis Both PM and VT activation maps were superimposed on the main screen of the CARTO XP system, thus allowing allocation of any point on any PM to a given compartment on the superimposed VT map. The correlation between a PM and its corresponding VT map then could be analyzed.
RF energy was applied for a mean of 9.8 ⫾ 8.9 minutes (range 4–33 minutes) to transect the critical VT isthmuses. Mean procedure time was 208 ⫾ 62 minutes (range 135–300 minutes), and mean fluoroscopy time was 10 ⫾ 8 minutes (range 4–32 minutes). VT stopped during RF energy application in all patients. The procedure was successful in eight patients, and a partial success was obtained in the remaining two patients. No perior postprocedural complications were observed. During mean follow-up of 65 ⫾ 6 months, four patients died (all with an ICD). The cause of death was heart failure in three patients and undetermined in one patient. VT recurrences were observed in three patients (all with an ICD, including one patient who died of heart failure).
Correlation between VT maps and PMs
All VTs exhibited a double-loop figure-of-eight reentrant circuit with two loops rotating in opposite directions around barriers delineating an isthmus. The approximately parallel barriers consisted of at least one functional LOB, with the second barrier being either another functional LOB (n ¼ 7) or the mitral valve annulus (n ¼ 3) as an anatomic barrier.
Considering the position of the PMs points in relation to their corresponding VT circuits, 43 PM points were in the isthmus zone (20 points in the entrance part of the isthmus and 23 points in the exit part of the isthmus), 92 points at the exit area, 85 points at the entrance area, 51 points at the lateral zones, 81 points at the outer exit zone, and 53 points at the outer entrance zone (Figures 3 and 4). The best mean average percentages of correlation between pace-mapping and VT morphology were found in the exit zone (89% ⫾ 8%) and in the exit part of the isthmus (84% ⫾ 7%), whereas the worst average mean correlation percentages were found in the outer entrance zone (23% ⫾ 28%), in the entrance zone (39% ⫾ 34%), and in the entrance part of the isthmus (32% ⫾ 26%). Within the isthmus zone, the mean average percentage of correlation was 59% ⫾ 32%, with a broad range of values (–31% to 99%) according to the location of the pacing site within the VT isthmus. Pacing sites close to the isthmus exit showed percentage of correlation values similar to those observed in the exit zone, whereas pacing sites close to isthmus entrance showed percentage of correlation values similar to those recorded in the entrance zone. A cutoff value 482% for the percentage of correlation best defined the exit site of VT circuits (sensitivity 82%, specificity 87%, predictive positive value 65%, negative predictive value 94%).
Characteristics of critical VT isthmuses
VT isthmus definition using PM
Using the activation maps during VT, one and only one VT isthmus was identified in each patient. In one patient, a second VT morphology was mapped during the procedure. Both VTs were sharing the same protected isthmus; the only
Visual inspection of the PMs gave important information about the VT isthmus location (Figures 3 and 4). A gradual and progressive decrease in the percentage of correlation values was noticed (with the corresponding colors changing
Results Mapping A complete VT map (mean VT cycle length 431 ⫾ 73ms, range 330–540 ms) with its corresponding PM was available for each of the 10 patients. The mean number of points acquired during PM was 41 ⫾ 11 (range 22–56), and the mean number of points acquired during VT mapping was of 163 ⫾ 61 (range 87–276). Total mapping time (including both PM and VT map) ranged from 49 to 118 minutes (average 75 ⫾ 23 minutes).
Characteristics of VT circuits
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Figure 3 Example of a three-dimensional reconstruction (CARTO pictures in the right anterior oblique projection) of a ventricular tachycardia (VT) circuit (left) and the corresponding pace-mapping map (middle, right) in a patient with an anterior wall myocardial infarction. The VT circuit is located at the left ventricular septum. A poor pace-mapping match zone is found 30 mm from the best pace-mapping matching sites at the isthmus entrance (middle). Arrows joining these two areas (right) have the same orientation as the VT isthmus.
from red to orange, yellow, green, and so forth) when moving from the exit zone to the outer exit zone and even further away from the VT circuit along a given axial direction. Looking at the 10% step isochronal PMs, isochronal zones could be relatively narrow (3–10 mm, as in Figure 3) or broad (up to 20 mm, as shown in Figure 4). Along the rotating double loops of the VT circuits, the percentage of correlation decreased as well, with the highest values at the exit zone and the lowest values at the entrance zone or just at the isthmus entrance. When following the isochronal color-coded sequence on the PM, a figure-of-eight picture, resembling the VT activation time mapping (Figure 4), can be observed. Linking the best to the poorest pace-mapping zone found in its vicinity (10–30 mm depending on VT isthmus length) defines the orientation of the VT isthmus.
Discussion Our study evaluated the value of pace-mapping during SR to localize the critical isthmus of postinfarct mappable VTs with definition of isthmuses boundaries identified by detailed activation mapping and displayed on an electroanatomic mapping system. The study shows that pace-mapping best matches the VT morphology in the region of the VT isthmus exit zone and at the exit part of the VT isthmus (average percentage of QRS correlation 89% ⫾ 8% and 84% ⫾ 7%, respectively). This confirms that pace-mapping during SR is helpful in identifying the exit zone of the isthmus as well as the exit part of the isthmus. Surprisingly, pace-mapping was neither sensitive nor specific for identification of the isthmus entrance part or isthmus entrance zone, with average percentages of QRS correlation
Figure 4 Example of a three-dimensional reconstruction (same patient and same projection as in Figure 1) showing (from left to right) the voltage map during sinus rhythm, the pace-mapping (PM) map (10% step isochrones), and the ventricular tachycardia (VT) circuit located at the apex with an upper exit (20-ms step isochrones). Arrows following the isochronal color-coded sequence on the PM (middle) depict a figure-of-eight that resembles the VT activation time mapping (right).
180 only 32% ⫾ 26% within the VT isthmus entrance part and 39% ⫾ 34% in the entrance zone of the isthmus. Importantly, the orientation of the isthmus of a reentrant postinfarct VT circuit may be recognized using pace-mapping, with identification of two zones consistent with the exit (area with pace-mapping showing a good correlation with the 12-lead ECG during VT) and the entrance (area with pace-mapping showing a poor correlation with the 12-lead ECG during VT) of the VT circuit. A distance of 10 to 30 mm consistently separated the VT entrance from the VT exit and corresponded to the isthmus zone. In the isthmus zone, pace-mapping showed a good correlation with the 12-lead ECG during VT at sites close to the isthmus exit and, in contrast, showed a poor correlation with the 12-lead ECG during VT at sites close to the isthmus entrance. Once the VT isthmus orientation is determined, RF lesions can be appropriately deployed to transect this isthmus. During the last 4 years, our road map to localize the VT isthmus using pace-mapping has first identified the exit zone (or the exit part of the isthmus). Then pace-mapping was performed centrifugally around these good pace-mapping sites to find sites close by (10–15 mm) with poor pace-mapping correlation that correspond to the VT isthmus entrance. When the PMs were generated, we expected to observe a centrifugal pattern, with points at the exit zone of the isthmus showing the best percentage QRS match, with the percentages of correlation gradually and homogenously decreasing when moving away in all directions from the best pacemapping zone. The results of our study invalidated this assumption. Indeed, within the isthmus zone, a poor correlation with VT morphology during pace-mapping was observed when pacing close to the isthmus entrance, whereas a good correlation was shown when pacing close to the isthmus exit. This is completely different compared to what is seen during VT entrainment where concealed entrainment (12-lead ECG identical during pacing and VT) can be observed all along VT isthmus, at both exit and entrance sites but with a different stimulus to QRS interval.7,16,17 When pacing within the isthmus, the wavefront propagates in two opposite directions: orthodromically and antidromically with respect to isthmus depolarization sequence during VT. The activation wavefront significantly contributes to generate some portion of the QRS complex on the 12lead only when “leaving” the protected isthmus. During VT entrainment, the collision between the antidromic (N) paced wavefront with the previous (N-1) orthodromic wavefront prevents any change in QRS morphology whatever the pacing site along the VT isthmus. This is different when pacing during SR because there is no preexisting orthodromic wavefront propagating along the VT isthmus. As a consequence, when pacing during SR at the entrance of the VT isthmus, the wavefront will spread out from the pacing site to depolarize the adjacent myocardium in the opposite direction of the VT wavefront, creating a dramatic difference in QRS morphology compared to the VT morphology. Several authors have evaluated the feasibility of VT ablation in SR in patients with structural heart disease.7,8 In the study by Marchlinski et al,7 which included patients with ischemic and
Heart Rhythm, Vol 11, No 2, February 2014 nonischemic cardiomyopathy presenting nonmappable VT, successful VT control was achieved by drawing RF lines through sites with the best visual correlation of morphology between the QRS in VT and pace-map. The lines were drawn connecting the endocardial areas with the lowest voltage (o0.5 mV) to areas with normal voltage or to anatomic boundaries. Brunckhorst et al16 first proposed a method to identify VT circuit isthmuses during SR using pace-mapping and an electroanatomic mapping system. Pace-mapping was used to locate the exit zone (i.e., sites with good correlation with 12-lead ECG recorded during VT) while conduction delays during pace-mapping (regions with stimulus-to-QRS delays Z40ms) were associated with reentry target sites. Of great interest, the authors noted that marked mismatches between the paced QRS morphology compared to that of VT were common in the target ablation zone. In particular, pacing sites with a long stimulus-to-QRS interval and a complete mismatch compared to VT morphology could very well be located within the protected isthmus area. This finding is consistent with the present study and suggests that such sites were located at the VT isthmus entrance zone in the midisthmus with preferential conduction toward the entrance side within the VT isthmus.
Study limitations For methodologic rigor in truly defining the critical circuit, we limited our study to only patients for whom ablation across the isthmus prevented reinduction. Therefore, our study population consisted of only 10 patients. However, this is a very small number from which to make inferences regarding sensitivity and specificity cutoff values for defining VT exit and VT isthmus exit parts. Pacing threshold may be high in scar areas, resulting in larger size of the virtual bipolar pacing electrode with myocardial tissue capture at a remote site leading to significant changes in QRS morphology.18 To overcome this issue, pacing threshold was checked at each pacing site to set the stimulus strength to twice threshold. Many other parameters may affect QRS morphology, such as pacing rate, unipolar or bipolar configuration of stimulation, and size of the electrode used for pace-mapping.19,20 Pacing rate was adjusted to that of the clinical VT. A very high pacing threshold in the scar region might cause a lack of points within the isthmus because of the presence of unexcitable tissue under the catheter electrodes. In some patients, 41 VT morphology was induced and mapped. Because the Bard software does not allow simultaneous comparison of multiple QRS morphologies, we only correlated the most frequently induced VT during the PM acquisition to avoid a significant increase in procedure time during this investigation. Although we have applied our findings in patients with poorly tolerated VTs to our daily practice since 2007 (Figure 5), this study only included well-tolerated mappable VTs. Additional study is required to validate the findings in patients with unmappable VT and nonischemic cardiomyopathies.
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Figure 5 Example of a deductive reconstruction (only based upon pace-maps [PMs]) of a ventricular tachycardia (VT) reentrant circuit in a patient with a poorly tolerated VT. A: Twelve-lead ECG of the clinical VT induced during electrophysiologic study. B: PM (14% step isochrones) of the three-dimensional reconstructed LV (posterior view). Yellow tags represent PM sites. The percentage of matching between the 12-lead ECG during VT and that during PM ranges from 97% to –7%. C: Twelve-lead ECGs recorded during PM at two different left ventricular sites 15 mm apart (red and blue asterisks in B). D: VT circuit reconstruction (perimitral circuit) with isthmus boundaries corresponding to the mitral valve and an hypothesized line of conduction block.
Conclusion This study confirms that pace-mapping during SR with a good QRS match to VT is helpful in identifying the exit zone of the VT isthmus. More importantly, by pacing more extensively into the depths of the low-voltage region, one can identify a transition to a poorer matching pace-map with the poorest match between the 12-lead ECG recorded in VT and that obtained during pace-mapping at the VT isthmus entrance. By quantifying the degree of QRS match, one can use the colorcoded sequence (from best to poorest matching sites) on the PMs to identify the course of the VT isthmus and facilitate targeted ablation. Prospective VT ablation studies with large cohorts of patients should compare this technique to identify and target postinfarct VT isthmuses with other substrate-based approaches, especially in patients with poorly tolerated VTs.
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