Substrate modification or ventricular tachycardia induction, mapping, and ablation as the first step? A randomized study

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1 Substrate modification or ventricular tachycardia induction, mapping, and ablation as the first step? A randomized study Juan Fernández-Armenta, MD, PhD,* Diego Penela, MD,* Juan Acosta, MD,* David Andreu, MSc, PhD,* Reinder Evertz, MD,* Mario Cabrera, MD, PhD,* Viatcheslav Korshunov, MD, PhD,* Francesca Vassanelli, MD, PhD,* Mikel Martínez, MD,* Eduard Guasch, MD, PhD,* Elena Arbelo, MD, PhD,* Jose María Tolosana, MD, PhD,* Lluis Mont, MD, PhD,* Antonio Berruezo, MD, PhD* From the * Arrhythmia Section, Cardiology Department, Thorax Institute, Hospital Clínic, Universitat de Barcelona, Barcelona, Spain, and IDIBAPS (Institut d Investigació Agustí Pi i Sunyer), Barcelona, Spain. BACKGROUND The role and optimal sequence of ventricular tachycardia (VT) induction, mapping, and ablation when combined with substrate modification is unclear. OBJECTIVE The purpose of this study was to test the benefits of starting the scar-related VT ablation procedure with substrate modification vs the standard protocol of VT induction, mapping, and ablation as the first step. METHODS Forty-eight consecutive patients with structural heart disease and clinical VTs were randomized to simplified substrate ablation procedure with scar dechanneling as the first step (group 1, n ¼ 24) or standard procedure with VT induction, mapping, and ablation followed by scar dechanneling (group 2, n ¼ 24). Procedure and fluoroscopy times, the need for external cardioversion, acute results, and VT recurrence during follow-up were compared between groups. RESULTS Thirty-seven patients had ischemic cardiomyopathy, 10 nonischemic cardiomyopathy, and 1 arrhythmogenic cardiomyopathy. Before substrate ablation, 32 VTs were induced and targeted for ablation in 23 patients of group 2. Procedure time (209 ± 70 minutes vs 262 ± 63 minutes; P ¼.009), fluoroscopy time (14 ± 6 minutes vs 21± 9 minutes; P ¼.005), and electrical cardioversion (25% vs 54%; P ¼.039) were lower in group 1. After substrate ablation, 16 patients (66%) of group 1 and 12 patients (50%) of group 2 were noninducible (P ¼.242). End-procedure success (after residual inducible VT ablation) was achieved in 87.5% and 70.8% of patients, respectively (P ¼.155). There were no differences in VT recurrence rate between groups during a mean follow-up of 22 ± 14 months (log rank, P ¼.557). CONCLUSION VT induction and mapping before substrate ablation prolongs the procedure, radiation exposure, and the need for electrical cardioversion without improving acute results and longterm ablation outcomes. KEYWORDS Ventricular tachycardia; Catheter ablation; Substrate ablation; Myocardial infarction; Nonischemic cardiomyopathy (Heart Rhythm 2016;13: ) I 2016 Heart Rhythm Society. All rights reserved. Introduction Monomorphic ventricular tachycardia (VT) in patients with structural heart disease is almost always due to scarrelated reentry. 1,2 Conventional catheter ablation has been mainly based on activation, entrainment, and pace-mapping techniques. However, noninducibility and hemodynamic intolerance of VTs limits this approach. 3 Dr Andreu is an employee of Biosense Webster. This study was supported in part by a grant (no. PI11/02049) from Instituto de Salud Carlos III, Ministry of Science and Innovation, Madrid, Spain, and El Fondo Europeo de Desarrollo Regional (FEDER), European Union. Address reprint requests and correspondence: Dr Antonio Berruezo, Arrhythmia Section, Cardiology Department, Thorax Institute, Hospital Clinic, C/ Villarroel 170, Barcelona, Catalonia, Spain. address: berruezo@clinic.ub.es. Substrate mapping allows identification of potential VT isthmuses during stable rhythm (sinus or paced) regardless of their inducibility and hemodynamic tolerance. 4 6 There is no consensus about the best substrate modification technique and the most appropriate target for ablation, and the results remain suboptimal. 7 9 One recent randomized trial has shown that an extensive substrate-based ablation is superior to clinical and stable VT ablation. 10 Despite the widespread use of mapping techniques for arrhythmogenic substrate characterization, the induction and mapping of clinical and nonclinical VTs is still considered the initial step in any VT ablation procedure, 5 but may unnecessarily prolong the procedure and increase its complexity. Procedure time has been associated with increased hospital mortality. 11 The purpose of the present study was to test the possible benefits of starting the VT ablation procedure with substrate /$-see front matter B 2016 Heart Rhythm Society. All rights reserved.

2 1590 modification vs the standard protocol of VT induction, mapping, and ablation as the first step in patients with scar-related VTs. 12,13 Methods Patient population Forty-eight consecutive patients undergoing scar-related VT ablation in 1 center were included. Inclusion criteria were the presence of structural heart disease, defined as prior myocardial infarction, ventricular dilatation/systolic dysfunction, evidence of ventricular scar on contrast enhanced cardiac magnetic resonance (ce-cmr) or arrhythmogenic right ventricular dysplasia (ARVD), and symptomatic episode of sustained monomorphic VT (SMVT). Patients were randomized (in a 1:1 ratio) to a simplified ablation procedure with substrate modification as the first step (group 1, n = 24) or to a standard procedure with VT induction, mapping, and ablation followed by substrate modification (group 2, n = 24). All patients provided written informed consent to participate. The local ethics committee approved this study. Heart Rhythm, Vol 13, No 8, August 2016 Procedural approaches The procedural protocol flowchart is shown in Figure 1. In group 1 patients, the first step was substrate mapping. In group 2 patients, the procedure started with a programmed RV stimulation from the RV apex with 3 basal cycle lengths (600, 500, and 430 ms); up to 3 extra ventricular stimuli (up to 200 ms or ventricular refractory period) were used for VT induction. The protocol was followed until the end or stopped when clinical VT was induced. No antiarrhythmic drugs were used during the induction protocol. Antiarrhythmic drugs were discontinued in patients who were receiving intravenous infusion. The induced VT was considered the clinical VT on the basis of a comparison of 12-lead electrocardiographic morphologies and of cycle lengths (o20 ms) and/or intracardiac electrogram morphologies. Induced VTs were targeted with activation/entrainment mapping or pace mapping, depending on their hemodynamic tolerance. Preprocedural evaluation Preprocedural transthoracic echocardiography was performed to exclude intracavitary thrombus and to calculate systolic function. Transoesophageal echocardiography was performed in patients with atrial fibrillation history to rule out the presence of left atrial thrombus. Ce-CMR (in the absence of contraindications) or computed tomography was performed to characterize myocardial scars and to merge 3- dimensional reconstructions with the electroanatomic maps. Procedure techniques The procedure was performed under conscious sedation. A tetrapolar diagnostic catheter was positioned at the right ventricular (RV) apex. A 3.5-mm-tip open-irrigated ablation catheter (ThermoCool, NaviStar, Biosense Webster, Inc., Diamond Bar, CA) was used for mapping and ablation. A steerable sheath (Agilis, St. Jude Medical, Inc., St. Paul, MN) facilitated mapping through a transseptal access. A temperature control of 45ºC, a power limit of 50 W, and an irrigation rate of ml/min were used (40 W and 17 ml/min at the epicardium). The transseptal approach was used (except in ARVD) for left ventricular (LV) endocardial mapping (BRK needle, Medtronic, Inc., Minneapolis, MN). After transseptal access, heparin was administered intravenously to maintain an activated clotting time of 4300 seconds. The CARTO system (Biosense Webster, Inc.) or the EnSite NavX system (St. Jude Medical, Inc.) was used for substrate mapping. Epicardial mapping criteria were as follows: (1) underlying disease with a high probability of having epicardial substrate (ARVD or Chagas disease), (2) epicardial hyperenhancement on ce-cmr, (3) endocardial mapping not identifying endocardial scar, (4) electrocardiogram of clinical or induced VT, suggesting an epicardial origin, and (5) after previous endocardial ablation failure. Figure 1 Study workflow. Patients were randomized to starting the VT ablation procedure with substrate modification (group 1) or the standard protocol of VT induction, mapping, and ablation as the first step. CC ¼ conducting channel; Epi ¼ epicardial; SMVT ¼ sustained monomorphic ventricular tachycardia; VT ¼ ventricular tachycardia.

3 Fernández-Armenta et al Substrate Modification as the First Procedural Step 1591 Substrate mapping and ablation Using the ablation catheter a high-density substrate voltage map of the LV was obtained during stable sinus rhythm in 40 patients, during atrial fibrillation in 6 patients, and during RV pacing in 2 patients. Fill thresholds of 10 mm to fill the cavity and 8 mm to fill the low-voltage area were established. The RV endocardium, instead of LV, was mapped in patients with ARVD. Scar areas were identified using the standard voltage cutoff values for dense scar (o0.5 mv) and border zone (o1.5 mv). Unipolar maps were used to define areas of interest, particularly in patients with nonischemic cardiomyopathy. Electrograms with delayed components (E-DCs) were tagged and classified as entrance or inner conducting channel (CC) points, depending on the delayed component precocity during sinus rhythm. 12,13 Radiofrequency (RF) applications were directed to the CC-entrance points with a temperature control of 45ºC, a power limit of 50 W, and an irrigation rate of ml/min. Each discrete application was continued for seconds, depending on the elimination of the abnormal electrogram. After each RF application, the abolition/persistence of the CC was checked and, in a case of persistence, a new application was performed in the closest site with an E-DC with CC-entrance characteristics until the CC entrance was blocked. RF applications inside the scar core area were also delivered when the RF lesions at the CC entrance were not able to eliminate internal E-DCs. A remap focused on the scar area was obtained to prove the persistence of residual E-DCs, which were ablated with the same approach. A detailed description of the methodology used for substrate characterization and modification has been published elsewhere. 12 VT induction after substrate ablation All patients received a programmed RV apex stimulation with 3 basal cycle lengths (600, 500, and 430 ms); up to 3 extra ventricular stimuli decremented until refractoriness or 200 ms. The protocol was stopped when completed or when VT/VF (ventricular fibrillation) was induced. Induced monomorphic VTs were targeted by conventional mapping techniques (entrainment or pace mapping). After each VT ablation, inducibility was checked again using the same stimulation protocol. Procedural success Acute success was defined as noninducibility of any SMVT. The evidence of any sustained ventricular arrhythmia episode during follow-up (treated or not) was considered a recurrence. Patients were followed up at 1 month and every 6 months thereafter. Remote device monitoring was used when available. Implantable cardioverter-defibrillators (ICDs) were programmed for 3-zone detection: VT monitor ( beats/min), fast VT zone ( beats/min), and VF zone (4230 beats/min). Procedure time, fluoroscopy time, and the need for electrical cardioversion were registered. Any procedurerelated complication was recorded. Statistical analysis Values are expressed as number (percentage) or as mean ± SD for normally distributed data or median (interquartile range [IQR]) for nonnormally distributed data. The t test or Mann-Whitney U test was used to compare continuous variables with nonnormal distribution. We used the χ 2 test to compare proportions between the 2 groups, Kaplan-Meier analysis to estimate event rates, and the log-rank test for the follow-up comparison between groups. Results Patient sample During the study period, 122 ventricular arrhythmia ablation procedures (including sustained and nonsustained ventricular arrhythmias) were performed in 112 patients in our center. Of these patients, 57 had idiopathic VT or premature ventricular contractions/nonsustained VT and 55 fulfilled the study inclusion criteria. Four patients were not included because of incessant VT, 1 because of a redo procedure with exclusive epicardial mapping (surgical approach for pericardial adherences), and 2 patients refused to participate. Finally, 48 patients were enrolled in the study and were randomized in a 1:1 ratio (Figure 1). A median of 4 VT episodes was recorded before the procedure. All but 8 patients had an ICD. ICD implantation was performed after substrate ablation in 4 patients of group 1 and 9 patients of group 2. The baseline characteristics of the patient population are summarized in Table 1. VT induction Thirty-two VTs were induced in 23 of 24 patients randomized to arrhythmia induction and ablation before substrate modification (group 2). In 15 patients, 1 VT was induced and targeted for ablation and no repeated stimulation protocol was performed before substrate mapping. Two VTs were induced and targeted for ablation in 7 patients and 3 VTs in 1 patient (Figure 2). In group 1, sustained VT was mechanically induced during substrate mapping in 5 patients (20.8%). Four VTs were tolerated and abolished during tachycardia using activation/entrainment mapping. In the remaining patients, the VT was not tolerated; it finished with a burst and ablation was guided by pace mapping (Figure 2). Substrate-guided mapping ablation Preacquired cardiac imaging was integrated into the navigation system in 19 patients: ce-cmr in 10 patients (4 of group 1 and 6 of group 2) and computed tomographic scan in 9 patients (6 of group 1 and 3 of group 2). Endocardial electroanatomic maps (EAMs) during sinus rhythm were created with a mean of 497 ± 194 points, without differences between groups (P ¼.271). Epicardial mapping was performed in 15 patients (31%) (5 of group 1 and 10 of group 2; P ¼.119) with a mean of 565 ± 216 points, without differences between groups (P ¼.301). Epicardial-only mapping and ablation was performed in 2

4 1592 Heart Rhythm, Vol 13, No 8, August 2016 Table 1 Characteristic Baseline clinical characteristics of the patient population Group 1: Simplified substrate ablation (n ¼ 24) Group 2: VT induction plus substrate ablation (n ¼ 24) Age (y) 66 ± ± CAD 19 (79) 18 (75).731 Sex: male 24 (100) 23 (96).312 Hypertension 21 (88) 19 (79).439 Diabetes 5 (21) 4 (17).712 LVEF (%) 36 ± ± ICD 20 (83) 20 (83).241 AAD β-blockers 18 (75) 16 (77).525 Class I 0 2 (8).149 Class III 15 (63) 14 (58).768 Prior VT ablation 3 (13) 1 (4).296 No. of VT episodes per patient (range) 4 (1 60) 4 (1 12).706 AAD at last follow-up β-blockers 21 (88) 22 (92).128 Class I 0 0 Class III 10 (42) 9 (38).766 Arrhythmic storm 6 (25) 7 (31).677 Clinical VT-CL (ms) 358 ± ± Values are presented as mean ± SD or as n (%) unless specified otherwise. AAD ¼ antiarrhythmic drug; CAD ¼ coronary artery disease; CL ¼ cycle length; ICD ¼ implantable cardioverter-defibrillator; LVEF ¼ left ventricular ejection fraction; VT ¼ ventricular tachycardia. P patients, 1 from each group, because of previous endocardial ablation failure. Electrograms with double components were divided into entrance or inner CC points according to the relative delay of the local electrogram. All patients received at least 1 RF application in the low-voltage area (o0.5 mv). Findings from substrate mapping are summarized in Table 2. A mean of 18 ± 13 RF applications per patient were applied at the endocardium, without differences between groups. A new electroanatomic substrate map (remap) was created in 34 patients (71%) to document the complete elimination of the E-DCs. A mean of 578 ± 297 endocardial points were acquired for the remap. A median of 6.5 (IQR 4 10) RF applications were necessary to abolish a median of 9.5 (IQR 4 15) CC electrograms identified per patient in the remap, without differences between the 2 groups. Inducibility after substrate ablation and residual VT ablation Programmed ventricular stimulation (PVS) was performed after substrate ablation. SMVT was noninducible in 16 patients (66%) of group 1 and 12 patients (50%) of group 2(P ¼.242) (Figure 2). Twelve SMVTs were induced in 8 patients of group 1 (33%) and 13 SMVTs in 12 patients of group 2 (50%). No ablation was attempted in 3 SMVTs in each group. The remaining SMVTs were then mapped and targeted for ablation (53% guided by activation/entrainment mapping and the rest by pace mapping). Seven SMVTs (58%) in group 1 and 5 SMVTs (38%) in group 2 were successfully abolished (Figure 2). Figure 2 Flowchart of VT induction and ablation before and after substrate modification. * Mechanically induced VTs. SMVT ¼ sustained monomorphic ventricular tachycardia; VT ¼ ventricular tachycardia. Procedure results In group 2, VT induction and ablation attempt before substrate ablation, a higher procedure time (3.5 ± 1.2 hours vs 4.4 ± 1.1 hours; P ¼.009), and higher fluoroscopy time (14 ± 6 minutes vs 21 ± 9 minutes; P ¼.005) were necessary (Table 2). Moreover, patients of group 1 less frequently required electrical cardioversion for unstable VT (25% vs 54%; P ¼.039).

5 Fernández-Armenta et al Substrate Modification as the First Procedural Step 1593 Table 2 Variable Procedure data Group 1: Simplified substrate ablation (n ¼ 24) Group 2 : VT induction plus substrate ablation (n ¼ 24) No. of map points 467 ± ± Endocardial scar area o1.5 mv (cm 2 ) 59 ± ± Epicardial scar area o1.5 mv (cm 2 ) * 114 ± ± No. of CC-EGs per patient 66 ± ± No. of CC entrance-egs per patient (range) 10 (7 20) 11 (6 21).725 Radiofrequency ablation time (min) 23 ± ± Electrical cardioversion 6 (25) 13 (54).039 Procedure time (min) 209 ± ± Fluoroscopy time (min) 14 ± 6 21 ± Incomplete substrate ablation 3 (12.5) 2 (8).637 SMVT inducible after substrate ablation 8 (33) 12 (50).242 Acute success 21 (87.5) 17 (71).115 Values are presented as mean ± SD or as n (%) unless specified otherwise. CC-EG ¼ conducting channel electrogram; CC entrance EG ¼ conducting channel entrance electrogram (the CC-EG with the shortest local activation time of the near-field); SMVT ¼ sustained monomorphic ventricular tachycardia. 15 patients with epicardial mapping. Sum of endocardial and epicardial CC-EGs. Noninducibility of any SMVT at the end of the procedure. P Acute procedure success after residual VT ablation was achieved in 87.5% of patients of group 1 and 70.8% of patients of group 2 (P ¼.155). In 9 patients (5 of group 1 and 4 of group 2), VF or pleomorphic/polymorphic VT was induced. After a mean follow-up of 22 ± 14 months, 10 patients (41.7%) of group 1 and 8 patients (33.3%) of group 2 had a VT recurrence, without differences between groups (log rank, P ¼.557) (Figure 3). Most of those patients (14 of 18 [78%]) showed new VTs that had not been observed before the first procedure. In group 1, the VT recurrence was treated by antitachycardia pacing in 6 patients (60%) and a shock was required in 1 patient (10%). In 3 patients (30%), the VT recurrence had a cycle length above the treatment window. In group 2, the VT recurrence was treated by antitachycardia pacing in 3 patients (38%) and a shock was required in 4 patients (50%). In 1 patient (13%), the VT had a cycle length exceeding the treatment window. Seven patients (39%) who had a VT recurrence underwent a second ablation procedure. The remaining patients were managed with oral antiarrhythmic treatment. Attempting VT induction and ablation before substrate modification did not improve long-term outcome (hazard ratio 0.980; 95% confidence interval ; P ¼.968). There were 2 cardiac deaths and 1 noncardiac death during follow-up. No sudden cardiac death occurred. Complications Four patients, all of them from group 2, presented acute complications related to the procedure. The sample size of the study does not permit any conclusions about procedural safety. Two patients had cardiac tamponade, 1 after epicardial ablation, solved by pericardiocentesis in the electrophysiology laboratory. Iatrogenic complete atrioventricular block was provoked during RF ablation in 1 patient with healed anterior myocardial infarction with septal involvement. One patient presented transient ischemic attack (dysarthria) after external cardioversion that resolved spontaneously in the electrophysiology laboratory. Figure 3 Kaplan-Meier curves for the recurrence of sustained monomorphic ventricular tachycardia. No significant differences were found between the 2 approaches (log rank, P ¼.557). VT ¼ ventricular tachycardia. Discussion Main findings This study shows that the routine practice of starting the VT ablation procedures with VT induction, mapping, and ablation attempt is unnecessary when substrate modification is planned. In this context, this standard protocol appears to prolong the procedure, radiation exposure, and the need for

6 1594 external defibrillation without improving acute and longterm ablation results. Usefulness of VT mapping/ablation before substrate modification To our knowledge, this is the first study attempting to evaluate the utility of conventional SMVT mapping and ablation before substrate modification. Several techniques and targets have been proposed for substrate modification with satisfactory results. 6,14 16 Irrespective of the substrate ablation technique used, previous studies have performed PVS at the beginning of the procedure. Induced VTs were mapped and ablated with conventional mapping techniques depending on their hemodynamic tolerance We have previously published the results of substrate modification (using scar dechanneling) in a series of 101 patients with structural heart disease and VT, in whom PVS and VT mapping/ablation was not performed before substrate mapping/ablation. 12 We observed that more than half of the patients had no inducible VT after performing only substrate modification. In the remaining patients, standard techniques were used for ablation of the residual VT. Patients who were noninducible after substrate ablation alone had lower procedure requirements (time and radiation exposure) and better outcomes (lower probability of VT recurrence/sudden death: 16% vs 37%; P ¼.018). Although this could be interpreted to indicate that this subgroup of patients had a more accessible substrate, it also seemed to suggest that substrate ablation before the inducibility test could be enough to obtain satisfactory outcomes. In the present study, patients were randomly allocated to undergo VT induction and ablation attempt before substrate modification or to start the procedure with the scar dechanneling technique used for substrate ablation in the present study. The inducibility test and the subsequent VT mapping and ablation attempt before substrate modification did not contribute to the acute results of the procedure (noninducibility of 71% vs 87.5%) or follow-up (VT recurrences of 25% vs 29%) in group 2 and group 1, respectively. However, procedure time, radiation exposure, and percentage of patients needing an electrical cardioversion were higher in group 2. A decrease in the complexity of ablation procedures while maintaining effectiveness can decrease the risk of complications. A reduction in fluoroscopy time needed is desirable for the patient and the health care team. Recently, Yu et al 11 have shown that procedure time is an independent risk factor for hospital mortality. Similarly to what was observed in the aforementioned observational series, 12 in the present study 66% of group 1 became noninducible after substrate modification offered as the first step. Patients in this group did not experience any VT during the procedure. Performing substrate ablation in patients with structural heart disease (frequently with severe systolic dysfunction) during sinus rhythm all along the procedure is likely to reduce the risk of hemodynamic decompensation. Some studies have shown the utility of Heart Rhythm, Vol 13, No 8, August 2016 LV assist devices (ie, Impella, Abiomed Inc., Danvers, MA, USA) for scar-related VT ablation These devices permit mapping a great number of unstable VTs and greater duration of VT mapping maneuvers. However, mechanical circulatory support has not been shown to improve acute and follow-up results. 17 Importantly, these techniques are associated with an increased risk of complications. 17,18 In a multicenter observational study of VT ablation with a percutaneous LV assist device, 26% of patients had 1 major complications. 17 Future research is needed to improve our capacity to identify all potential VT isthmuses during stable rhythms, either invasively or noninvasively (with preprocedural cardiac imaging), rather than aiming to develop systems to prolong the time of VT mapping to locate those isthmuses by conventional mapping techniques. Substrate mapping and ablation approach The strategy used in the present study is the elimination/ isolation of the slow conducting zones by ablation at the CC entrances. 1,7 This technique (scar dechanneling) was developed to minimize RF delivery, and so a median of 27 minutes of RF delivery was used. Using the same substrate ablation approach, Tung et al 20 required a median of 9.7 RF applications (60 seconds per application) to homogenize the scar in 21 patients with scar-related VT. In the VISTA trial, targeting all abnormal electrograms, 68 minutes of RF was reported (extensive substrate-based ablation). To date, no studies have compared different substrate ablation strategies in terms of efficacy, safety, and procedure requirements. Postsubstrate ablation inducibility Inducibility of VT after substrate ablation probably reflects the presence of VT circuits not mapped or not accessible to RF ablation. In the present study, 20 of 48 patients (42%) had any VT inducible after substrate ablation, 30% in the subgroup with simplified substrate ablation approach. Jaïs et al 15 reported that 30% of patients had inducible VTs after local abnormal ventricular activities (LAVA) ablation. Vergara et al 14 showed that 29% of patients remained inducible after late potential abolition, with significant differences between patients depending on complete and those depending on incomplete late potential abolition. Problem of scar-related VT ablation end point Inducibility testing is the most widely accepted tool to assess the results of VT ablation. 5 Recent cohort studies and metaanalysis have shown that noninducibility of any SMTV after infarct-related VT ablation is associated with better outcomes, including lower mortality. 21,22 Similar results have been observed in nonischemic cardiomyopathy. 23 The lack of an inducibility test before substrate ablation might limit the interpretation of PVS afterward, since the effect of ablation on the capacity to induce VT cannot be evaluated. However, it is reasonable to assume that nearly all patients would have an inducible VT before ablation, as they have had at least the clinical one. VT inducibility in patients with structural heart

7 Fernández-Armenta et al Substrate Modification as the First Procedural Step 1595 disease and documented VT is 490% (93.8% in a recent study involving 1011 patients referred for ablation). 22 In contrast, several studies using varied substrate ablation strategies have shown that the complete elimination of all identifiable potential VT isthmuses during sinus rhythm (local abnormal ventricular activities, dechanneling, and late potential abolition) improves substrate ablation outcomes. 12,15 Complete substrate elimination appears to be a desirable and recognizable end point of the scar-related VT ablation procedure with relevance for patient outcome. 14 Therefore, the combined end point of complete substrate elimination and noninducibility appears to be useful and does not require the verification of VT inducibility at the beginning of the procedure. Complications Four patients, all of them from group 2, suffered procedurerelated complications. The sample size of this study does not permit any conclusions about procedure safety. However, reducing procedure time, fluoroscopy time, and the need for electrical cardioversion would make it likely that the risk of complications could also be reduced by substrate modification before the VT induction and ablation attempt. Along this line, the only embolic event (transient ischemic attack) in the present study occurred immediately after a non toleratedinduced VT was terminated by electrical cardioversion. Study limitations This was a single-center study. Investigators were not blinded to participant allocation to procedure type. All patients included had monomorphic VT; therefore, our results cannot be extrapolated to patients with pleomorphic/polymorphic VT. The small sample size makes it difficult to extrapolate the results to all etiologies that may underlie a patient with scar-related VT. Conclusion VT induction, mapping, and ablation attempt before substrate ablation prolongs the procedure, radiation exposure, and the need for electrical cardioversion without improving acute and long-term outcomes. References 1. Andreu D, Ortiz-Perez JT, Boussy T, Fernandez-Armenta J, de Caralt TM, Perea RJ, Prat-Gonzalez S, Mont L, Brugada J, Berruezo A. Usefulness of contrast-enhanced cardiac magnetic resonance in identifying the ventricular arrhythmia substrate and the approach needed for ablation. Eur Heart J 2014;35: Pogwizd SM, McKenzie JP, Cain ME. Mechanisms underlying spontaneous and induced ventricular arrhythmias in patients with idiopathic dilated cardiomyopathy. Circulation 1998;98: Morady F, Harvey M, Kalbfleisch SJ, el-atassi R, Calkins H, Langberg JJ. Radiofrequency catheter ablation of ventricular tachycardia in patients with coronary artery disease. Circulation 1993;87: Marchlinski FE, Callans DJ, Gottlieb CD, Zado E. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation 2000;101: Aliot EM, Stevenson WG, Almendral-Garrote JM, et al. EHRA/HRA expert consensus on catheter ablation of ventricular arrhythmias. Heart Rhythm 2009;6: Arenal A, Glez-Torrecilla E, Ortiz M, Villacastin J, Fdez-Portales J, Sousa E, del Castillo S, Perez de Isla L, Jimenez J, Almendral J. Ablation of electrograms with an isolated, delayed component as treatment of unmappable monomorphic ventricular tachycardias in patients with structural heart disease. J Am Coll Cardiol 2003;41: Santangeli P, Marchlinski FE. Substrate mapping for unstable ventricular tachycardia. Heart Rhythm 2015;13: Stevenson WG, Wilber DJ, Natale A, et al. Irrigated radiofrequency catheter ablation guided by electroanatomic mapping for recurrent ventricular tachycardia after myocardial infarction: the multicenter thermocool ventricular tachycardia ablation trial. Circulation 2008;118: Berruezo A, Fernandez-Armenta J. Lines, circles, channels, and clouds: looking for the best design for substrate-guided ablation of ventricular tachycardia. Europace 2014;16: Di Biase L, Burkhardt JD, Lakkireddy D, et al. Ablation of stable VTs versus substrate ablation in ischemic cardiomyopathy: the VISTA randomized multicenter trial. J Am Coll Cardiol 2015;66: Yu R, Ma S, Tung R, et al. Catheter ablation of scar-based ventricular tachycardia: relationship of procedure duration to outcomes and hospital mortality. Heart Rhythm 2015;12: Berruezo A, Fernandez-Armenta J, Andreu D, et al. Scar dechanneling: new method for scar-related left ventricular tachycardia substrate ablation. Circ Arrhythm Electrophysiol 2015;8: Berruezo A, Fernandez-Armenta J, Mont L, Zeljko H, Andreu D, Herczku C, Boussy T, Tolosana JM, Arbelo E, Brugada J. Combined endocardial and epicardial catheter ablation in arrhythmogenic right ventricular dysplasia incorporating scar dechanneling technique. Circ Arrhythm Electrophysiol 2012;5: Vergara P, Trevisi N, Ricco A, Petracca F, Baratto F, Cireddu M, Bisceglia C, Maccabelli G, Della Bella P. Late potentials abolition as an additional technique for reduction of arrhythmia recurrence in scar related ventricular tachycardia ablation. J Cardiovasc Electrophysiol 2012;23: 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: Di Biase L, Santangeli P, Burkhardt DJ, et al. Endo-epicardial homogenization of the scar versus limited substrate ablation for the treatment of electrical storms in patients with ischemic cardiomyopathy. J Am Coll Cardiol 2012;60: Reddy YM, Chinitz L, Mansour M, et al. Percutaneous left ventricular assist devices in ventricular tachycardia ablation: a multicenter experience. Circ Arrhythm Electrophysiol 2014;7: Miller MA, Dukkipati SR, Chinitz JS, Koruth JS, Mittnacht AJ, Napolitano C, d Avila A, Reddy VY. Percutaneous hemodynamic support with Impella 2.5 during scar-related ventricular tachycardia ablation (PERMIT 1). Circ Arrhythm Electrophysiol 2013;6: Miller MA, Dukkipati SR, Mittnacht AJ, Chinitz JS, Belliveau L, Koruth JS, Gomes JA, d Avila A, Reddy VY. Activation and entrainment mapping of hemodynamically unstable ventricular tachycardia using a percutaneous left ventricular assist device. J Am Coll Cardiol 2011;58: Tung R, Mathuria NS, Nagel R, Mandapati R, Buch EF, Bradfield JS, Vaseghi M, Boyle NG, Shivkumar K. Impact of local ablation on interconnected channels within ventricular scar: Mechanistic implications for substrate modification. 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