Postinfarction Ventricular Tachycardia Research Articles

Correlation of exit sites of inducible ventricular tachycardia post-ST elevation myocardial infarction on electrophysiology study, with region of infarct.

Ventricular arrhythmia (VA) is the most common cause of sudden cardiac death post-ST elevation myocardial infarction (STEMI). Ventricular tachycardia (VT) may be inducible in electrophysiology studies (EPS) early (<40 days) post-STEMI. Whether it originates from the infarct site remains unknown. We examined the correlation between inducible VT and infarct location post-STEMI. To investigate the correlation between inducible VT and infarct location post-STEMI. We retrospectively analysed 46 patients from 2005 to 2017 with STEMI who underwent early programmed ventricular stimulation through EPS (>48 h post-STEMI and <40 days from admission). Gated heart pool scans were used to visualise infarct scar regions, and VT exit sites were derived from induction 12-lead electrocardiography. Patients were followed up for primary outcomes of recurrent VA and all-cause mortality. Forty-six patients were included for analysis, with 50 uniquely induced VT exit sites. Mean left ventricular ejection fraction was 30 ± 8.7% and 22% had impaired right ventricular ejection fraction. Mean time from presentation to EPS was 16 ± 31.3 days. Of the induced VT, 44 (88%) were from within scar and scar-border regions, whereas 6 (12%) of the induced VT were found to be remote to imaging-derived scar. Over a median follow-up period of 75 months, 6 (13%) patients died, and 7 (15%) patients had recurrent VA. No deaths occurred in patients with remote VT. The majority of early inducible post-infarct VT arises from acute myocardial scar; however, a small portion arises from sites remote from scars with a possible focal aetiology.

An automated near-real time computational method for induction and treatment of scar-related ventricular tachycardias.

Catheter ablation is currently the only curative treatment for scar-related ventricular tachycardias (VTs). However, not only are ablation procedures long, with relatively high risk, but success rates are punitively low, with frequent VT recurrence. Personalized in-silico approaches have the opportunity to address these limitations. However, state-of-the-art reaction diffusion (R-D) simulations of VT induction and subsequent circuits used for in-silico ablation target identification require long execution times, along with vast computational resources, which are incompatible with the clinical workflow. Here, we present the Virtual Induction and Treatment of Arrhythmias (VITA), a novel, rapid and fully automated computational approach that uses reaction-Eikonal methodology to induce VT and identify subsequent ablation targets. The rationale for VITA is based on finding isosurfaces associated with an activation wavefront that splits in the ventricles due to the presence of an isolated isthmus of conduction within the scar; once identified, each isthmus may be assessed for their vulnerability to sustain a reentrant circuit, and the corresponding exit site automatically identified for potential ablation targeting. VITA was tested on a virtual cohort of 7 post-infarcted porcine hearts and the results compared to R-D simulations. Using only a standard desktop machine, VITA could detect all scar-related VTs, simulating activation time maps and ECGs (for clinical comparison) as well as computing ablation targets in 48 minutes. The comparable VTs probed by the R-D simulations took 68.5 hours on 256 cores of high-performance computing infrastructure. The set of lesions computed by VITA was shown to render the ventricular model VT-free. VITA could be used in near real-time as a complementary modality aiding in clinical decision-making in the treatment of post-infarction VTs.

Repolarization Heterogeneity in Human Post-Infarct Ventricular Tachycardia.

Slow conduction, caused by fibrosis between surviving myocytes and connexin remodeling, is an important prerequisite for post-infarction ventricular tachycardia (VT); however, slow conduction is present throughout the infarct whereas VT circuits are finite in number and discrete. In a porcine model of VT, re-entrant circuits occur at region of significant repolarization heterogeneity caused by up-regulation of potassium channel β-subunits KCNE3 (increasing repolarization current) and KCNE4 (decreasing repolarization current), causing heterogeneous action potential durations. This study was designed to determine whether re-entrant circuits in human post-infarction VT are associated with repolarization heterogeneity. In 6 patients, left ventricular mapping was performed during induced VT to identify sites within the VT circuit. Subsequently, unipolar mapping (3.5-mm tip ablation catheter) was performed to characterize activation-recovery intervals (ARIs), which are surrogates for local action potential durations, at sites documented within the VT circuit isthmus (IN) compared to sites within the infarct scar but outside of the VT circuit (OUT). ARIs were significantly shorter in the IN compared with the OUT sites (420.2 ± 79.3 ms vs 462 ± 52.8ms; P=0.01). In all patients. sites that were associated with the circuit always had shorter ARI values than did those sampled from OUT regions. VT circuit sites in human post-infarct VT are associated with repolarization heterogeneity, similar to what was previously reported in a porcine model. This suggests the possibility of a common mechanism between humans and the porcine model of post-infarct VT, and that development of ablation strategies or small molecule or genetic therapies to restore normal repolarization kinetics may be antiarrhythmic.

Virtual induction and treatment of arrhythmias (VITA): a fast automated computational tool to induce scar-related tachycardia and identify ablation targets

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): British Heart Foundation, Wellcome Trust Background Catheter ablation therapy of post-infarction ventricular tachycardia (VT) is often a lengthy procedure, with a high risk profile, and VT recurrence remains common. While computational modeling may aid pre-procedure planning and target identification, state-of-the-art reaction diffusion (R-D) simulations require access to high performance computing facilities, making them incompatible with clinical workflows. Purpose To present the Virtual Induction and Treatment of Arrhythmias (VITA), a novel, fast and fully automated computational tool to induce VT and identify subsequent ablation targets. Methods VITA employs multisite pacing to automatically find split activation wavefronts associated with the presence of channel isthmuses of viable myocytes within the inexcitable scar. The algorithm probes for all possible associated reentrant pathways and refines these to obtain a set of unique circuits sustaining potential clinical VTs. VT sustenance is assessed by comparing the electrical wavelength with the anatomical circuit path length. Corresponding exit sites of susceptible circuits are automatically identified, and a minimal lesion set constructed for ablation targeting. VITA also allows for rapid simulation of ECGs for clinical comparison. A summary of the VITA is shown in the Figure. VITA was tested on a virtual cohort of 7 post-infarcted porcine hearts and results compared to R-D simulations. Results Using only a desktop computer, VITA successfully identified all possible scar-related VT circuits and optimal ablation targets in just 48mins (per model), compared to 68.5hrs using a high-performance computer required by the R-D approach. Furthermore, VITA consistently identified more VTs associated with intra-scar circuits than R-D (Figure C). Conclusion VITA provides the first near real-time computational tool to aid treatment of post-infarction VTs.

Ventricular tachycardia targeted in the aortic sinuses of Valsalva in patients with prior myocardial infarction.

Ventricular tachycardia (VT) in structurally normal hearts or nonischemic cardiomyopathy can originate from the aortic sinuses of Valsalva (SoV). It is unknown whether VT can originate from the SoVs in patients with prior myocardial infarction (MI). To evaluate the prevalence, arrhythmogenic substrate, and ablation outcomes of postinfarction VT originating from the SoVs. Among 217 consecutive patients with postinfarction VT undergoing ablation, we identified 13 (6%) patients who had ≥1 VT mapped in a SoV. Control groups of 13 patients with idiopathic SoV VT and 13 postinfarction patients without SoV VT were included. In the study group, 17 VTs were mapped in a SoV (right n = 5, left-right commissure n = 6, left n = 6). SoV VT target sites had low bipolar voltage during sinus rhythm [median 0.42 (IQR: 0.16-0.53) mV] which was significantly lower than target sites in patients with idiopathic SoV VTs [median 1.02 (IQR: 0.89-1.52) mV; p < .001]. An area of endocardial low voltage was found below the aortic valve in all patients with postinfarction SoV VTs compared to 9 (69%) of the patients in the postinfarction control group without SoV VT (p = .02). Morphology characteristics of postinfarction SoV VTs differed from idiopathic SoV VTs. None of the postinfarction SoV VTs were inducible after ablation and none recurred after a median follow-up of 14 months. In patients with prior MI, VT can be targeted in an aortic SoV. The SoVs should be routinely investigated in postinfarction patients with inferior axis VT and an area of low voltage below the aortic valve.

Late gadolinium enhancement cardiac magnetic resonance imaging of ablation lesions after postinfarction ventricular tachycardia ablation: Implications for ventricular tachycardia recurrence.

Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging distinguishes between intrinsic postinfarction scar and radiofrequency ablation lesion related scar (dark core lesions [DCLs]) in patients with prior ventricular tachycardia (VT) ablation procedures. To combine LGE-CMR and electroanatomic mapping data to describe the relationship between DCLs and recurrent VT among patients undergoing repeat ablations for postinfarction VT. Consecutive patients with repeat ablation for postinfarct VT with LGE-CMR before the repeat procedures were studied. Prior ablation procedures and implantable cardiac defibrillator electrograms were analyzed to determine new versus previously documented VT. DCLs were identified on preprocedure LGE-CMR and registered to electroanatomic maps. A control group of patients undergoing repeat ablation procedures without imaging was included. Nineteen study patients and 14 control patients were followed for 2.6 (1.6-5.6) years (31 [94%] men, age 65.8 ± 8.4 years, ejection fraction 24.7 ± 10.3, p > 0.10 for all). DCLs corresponded to unexcitable tissue during repeat procedures (area 22.4 ± 15.1 vs. 22.9 ± 16.8 cm3 , correlation coefficient = .93). Most VT target sites (39/50 [78%]) were in close proximity (<1 cm) to DCLs. Most DCL related VTs 32/39 (82%) were new VTs. Patients with LGE-CMR imaging incorporated into their ablation procedures had improved 24-month survival from VT (64% vs. 38%, log rank p < 0.02). LGE-MRI can identify prior ablation lesions corresponding to nonexcitable tissue during repeat ablation procedures for postinfarction VT. VT target sites are often located in close proximity to the DCL area that may function as a fixed border for reentry circuits. Registration of DCL from prior ablation may facilitate repeat ablation procedures.

Structure and function of the ventricular tachycardia isthmus.

Catheter ablation of postinfarction reentrant ventricular tachycardia (VT) has received renewed interest owing to the increased availability of high-resolution electroanatomic mapping systems that can describe the VT circuits in greater detail, and the emergence and need to target noninvasive external beam radioablation. These recent advancements provide optimism for improving the clinical outcome of VT ablation in patients with postinfarction and potentially other scar-related VTs. The combination of analyses gleaned from studies in swine and canine models of postinfarction reentrant VT, and in human studies, suggests the existence of common electroanatomic properties for reentrant VT circuits. Characterizing these properties may be useful for increasing the specificity of substrate mapping techniques and for noninvasive identification to guide ablation. Herein, we describe properties of reentrant VT circuits that may assist in elucidating the mechanisms of onset and maintenance, as well as a means to localize and delineate optimal catheter ablation targets.

Abstract 13947: Catheter-Induced Ectopy During Ventricular Electroanatomical Mapping: Simply Annoying or Potentially Useful?

Background: During ventricular catheter mapping to guide catheter ablation of scar-related ventricular tachycardia (VT), creating an electroanatomical map can be frustrated by catheter-induced ventricular ectopy. However, we observed anecdotally that catheter-induced ventricular ectopy may unmask local abnormal ventricular activities (LAVA). The aim of this study was to compare LAVA characteristics between catheter-induced ventricular ectopy and intrinsic ventricular conduction in post-infarction patients undergoing electroanatomic mapping. Methods: We performed a retrospective review of electroanatomical maps from 136 consecutive post-infarction VT patients who had undergone mapping using a contact force-sensing catheter (Thermocool STSF &amp; CARTO, Biosense Webster Inc). Patients who had any diagnostic catheters inside the ventricular were excluded. From 8 patients, 1154 discrete points were screened during sinus rhythm or right atrial pacing, and 443 points were identified to have ectopic and intrinsic beats - confirmed to be colocalized using show-catheter functionality. Results: Among 443 points, LAVA were identified in 151 points - either during catheter-induced ectopy or intrinsic rhythm. The interval from onset of QRS to ventricular electrogram (EGM) were measured: ectopy revealed negative values compared to intrinsic rhythm (-43.5 (-65.5, 0) vs 18.5 (0, 35.0), P&lt;0.001). Catheter-induced ectopy had significantly longer EGM duration (206.0ms (161.0, 285.0) vs 140.0 (123.8, 168.3), P&lt;0.001) and smaller EGM amplitude (0.59mV (0.34, 0.82) vs 0.66 (0.36, 1.06), P=0.003) compared to intrinsic rhythm. For 77 of 151 (51.0%) points, LAVA potentials were unmasked only during catheter-induced ectopy. Conclusions: During mapping of infarcted ventricles, catheter-induced ectopy offers potential insights into the underlying tissue, warranting further investigation as a guide to VT ablation.

Postinfarct ventricular tachycardia substrate: Characterization and ablation of conduction channels using ripple mapping.

Conduction channels have been demonstrated within the postinfarct scar and seem to be co-located with the isthmus of ventricular tachycardia (VT). Mapping the local scar potentials (SPs) that define the conduction channels is often hindered by large far-field electrograms generated by healthy myocardium. The purpose of this study was to map conduction channel using ripple mapping to categorize SPs temporally and anatomically. We tested the hypothesis that ablation of early SPs would eliminate the latest SPs without direct ablation. Ripple maps of postinfarct scar were collected using the PentaRay (Biosense Webster) during normal rhythm. Maps were reviewed in reverse, and clusters of SPs were color-coded on the geometry, by timing, into early, intermediate, late, and terminal. Ablation was delivered sequentially from clusters of early SPs, checking for loss of terminal SPs as the endpoint. The protocol was performed in 11 patients. Mean mapping time was 65 ± 23 minutes, and a mean 3050 ± 1839 points was collected. SP timing ranged from 98.1 ± 60.5 ms to 214.8 ± 89.8 ms post QRS peak. Earliest SPs were present at the border, occupying 16.4% of scar, whereas latest SPs occupied 4.8% at the opposing border or core. Analysis took 15 ± 10 minutes to locate channels and identify ablation targets. It was possible to eliminate latest SPs in all patients without direct ablation (mean ablation time 16.3 ± 11.1 minutes). No VT recurrence was recorded (mean follow-up 10.1 ± 7.4 months). Conduction channels can be located using ripple mapping to analyze SPs. Ablation at channel entrances can eliminate the latest SPs and is associated with good medium-term results.

High density intramural mapping of post-infarct premature ventricular contractions and ventricular tachycardia.

Spontaneous ventricular premature contractions (PVCs) and ventricular tachycardia (VT) in the acute post infarct milieu is assumed to be due to automaticity. However, the mechanism has not been studied with intramural mapping. To study the mechanism of spontaneous PVCs with high density intramural mapping in a canine model, and to test the hypothesis that post-infarct PVCs and VT are due to re-entry rather than automaticity. In 15 anesthetized dogs, using 768 intramural unipolar electrograms, simultaneous recordings were made. After 20 min of stabilization, recordings were made during the first 10 min of ischemia, and activation maps of individual beats were constructed. Acute ischemia was produced by clamping the left anterior descending coronary artery proximal to the first diagonal branch. In all experiments ST-T alternans was present. Spontaneous ventricular beats occurred in five of 15 dogs where the earliest ectopic activity was manifested in the endocardium, well within the ischemic zone. From there, activity spread rapidly along the subendocardium, with endo-to epicardial spread along the non-ischemic myocardium. Epicardial breakthrough always occurred at the border of the ischemic myocardium. In three dogs, delayed potentials were observed, which were earliest at the ischemic epicardium and extended transmurally with increasing delay towards the endocardium, where they culminated in a premature beat. A similar sequence was observed in VT that followed. Graded responses that occur with each sinus beat intramurally, when able to propagate from epicardium to endocardium are the mechanism of PVCs and VT in post-infarct myocardium.

B-PO05-116 RIPPLE-VT STUDY: MULTICENTRE, PROSPECTIVE EVALUATION OF CONDUCTION CHANNEL ENTRANCE ABLATION IN ISCHEMIC VENTRICULAR TACHYCARDIA WITH LATEST SCAR POTENTIAL ELIMINATION WITHOUT DIRECT ABLATION AS AN ENDPOINT

Recurrent implantable cardioverter-defibrillator (ICD) therapies for post-infarct ventricular tachycardia (VT) can cause significant morbidity. Substrate modification of the ventricular scar by targeting conduction channels has been proposed as a potential intervention. To prospectively assess ICD therapies after substrate modification using Ripple Mapping to locate and ablate channel entrances with loss of latest scar potentials without direct ablation as an endpoint. Patients with ICD therapies for post-infarct VT were prospectively recruited. High-density ventricular scar maps were collected using the Pentaray. Ripple Maps of the scar were viewed in reverse-play from the end of the T-wave to peak QRS to identify clusters of >3 Ripple bars. Ablation was delivered at clusters of earliest scar potentials and the Pentaray was used to monitor the effect on the latest scar potentials. Patients were followed up for a combined primary endpoint of ICD therapy, VT recurrence and mortality for 1 yr. Fifty patients (mean age 70.2±7.1 years, mean EF 32.9±9.5%) were enrolled from 5 centres. 24% had previous VT ablation and 48% were on amiodarone. There were 42.3±75.4 VT episode and 2.3±2.7 shock in the 12 months prior. High-density substrate maps (median points 2606 [2211 - 3254]) were collected. In 37pts (74%) the latest scar potentials were eliminated without direct ablation and 11pts (22%) required direct ablation of latest scar potentials as well. The protocol was not feasible in 1pt and abandoned in 1pt due to vascular complication. After ablation of channel entrances (n=37), VT was non-inducible in 91% (29 of 32 tested) and 30/35pts (86%) remained free of VT recurrence during median follow up of 6.5 [1.2 - 12.0] months. In pts where channel entrance ablation alone did not eliminate latest scar potentials (n=11), VT was non-inducible in 6/11 (55%) pts and 8/10pts (80%) remained free of VT over follow up of 4.6 [1.2 - 7.8] months. On an intention-to-treat basis, 40/50pts (80%) were free from the primary endpoint at a median 5.7 [1.8 - 12.0] months. 3pts died during follow up without VT recurrence. Ablation of conduction channel entrances using Ripple Mapping is feasible and has comparable outcomes to other techniques.

B-PO03-126 DELAYED ENHANCEMENT CARDIAC MAGNETIC RESONANCE IMAGING IDENTIFIES PRIOR ABLATION LESIONS AFTER POSTINFARCTION VENTRICULAR TACHYCARDIA ABLATION PROCEDURES: IMPLICATIONS FOR VT RECURRENCE

Ventricular tachycardia (VT) frequently recurs after radiofrequency catheter ablation for post-infarction VT. Delayed enhancement cardiac magnetic resonance (DE-CMR) imaging delineates between native postinfarction scarring and radiofrequency ablation lesions related scar and may be used to study the relationship between VT circuits and prior ablation lesions.

Metabolic Scar Assessment with18F-FDG PET: Correlation to Ischemic Ventricular Tachycardia Substrate and Successful Ablation Sites.

The functional and molecular imaging characteristics of ischemic ventricular tachycardia (VT) substrate are incompletely understood. Our objective was to compare regional 18F-FDG PET tracer uptake with detailed electroanatomic maps (EAMs) in a more extensive series of postinfarction VT patients to define the metabolic properties of VT substrate and successful ablation sites. Methods: Three-dimensional (3D) metabolic left ventricular reconstructions were created from perfusion-normalized 18F-FDG PET images in consecutive patients undergoing VT ablation. PET defects were classified as severe (defined as <50% uptake) or moderate (defined as 50%-70% uptake), as referenced to the maximal 17-segment uptake. Color-coded PET scar reconstructions were coregistered with corresponding high-resolution 3D EAMs, which were classified as indicating dense scarring (defined as voltage < 0.5 mV), normal myocardium (defined as voltage > 1.5 mV), or border zones (defined as voltage of 0.5-1.5 mV). Results: All 56 patients had ischemic cardiomyopathy (ejection fraction, 29% ± 12%). Severe PET defects were larger than dense scarring, at 63.0 ± 48.4 cm2 versus 13.8 ± 33.1 cm2 (P < 0.001). Similarly, moderate/severe PET defects (≤70%) were larger than areas with abnormal voltage (≤1.5 mV) measuring 105.1 ± 67.2 cm2 versus 56.2 ± 62.6 cm2 (P < 0.001). Analysis of bipolar voltage (23,389 mapping points) showed decreased voltage among severe PET defects (n = 10,364; 0.5 ± 0.3 mV) and moderate PET defects (n = 5,243; 1.5 ± 0.9 mV, P < 0.01), with normal voltage among normal PET areas (>70% uptake) (n = 7,782, 3.2 ± 1.3 mV, P < 0.001). Eighty-eight percent of VT channel or exit sites (n = 44) were metabolically abnormal (severe PET defect, 78%; moderate PET defect, 10%), whereas 12% (n = 6) were in PET-normal areas. Metabolic channels (n = 26) existed in 45% (n = 25) of patients, with an average length and width of 17.6 ± 12.5 mm and 10.3 ± 4.2 mm, respectively. Metabolic channels were oriented predominantly in the apex or base (86%), harboring VT channel or exit sites in 31%. Metabolic rapid-transition areas (>50% change in 18F-FDG tracer uptake/15 mm) were detected in 59% of cases (n = 33), colocalizing to VT channels or exit sites (15%) or near these sites (85%, 12.8 ± 8.5 mm). Metabolism-voltage mismatches in which there was a severe PET defect but voltage indicating normal myocardium were seen in 21% of patients (n = 12), 41% of whom were harboring VT channel or exit sites. Conclusion: Abnormal 18F-FDG uptake categories could be detected using incremental 3D step-up reconstructions. They predicted decreasing bipolar voltages and VT channel or exit sites in about 90% of cases. Additionally, functional imaging allowed detection of novel molecular tissue characteristics within the ischemic VT substrate such as metabolic channels, rapid-transition areas, and metabolism-voltage mismatches demonstrating intrasubstrate heterogeneity and providing possible targets for imaging-guided ablation.

Different Expressions of Pericardial Fluid MicroRNAs in Patients With Arrhythmogenic Right Ventricular Cardiomyopathy and Ischemic Heart Disease Undergoing Ventricular Tachycardia Ablation.

Introduction: Pericardial fluid is enriched with biologically active molecules of cardiovascular origin including microRNAs. Investigation of the disease-specific extracellular microRNAs could shed light on the molecular processes underlying disease development. Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited heart disease characterized by life-threatening arrhythmias and progressive heart failure development. The current data about the association between microRNAs and ARVC development are limited.Methods and Results: We performed small RNA sequence analysis of microRNAs of pericardial fluid samples obtained during transcutaneous epicardial access for ventricular tachycardia (VT) ablation of six patients with definite ARVC and three post-infarction VT patients. Disease-associated microRNAs of pericardial fluid were identified. Five microRNAs (hsa-miR-1-3p, hsa-miR-21-5p, hsa-miR-122-5p, hsa-miR-206, and hsa-miR-3679-5p) were found to be differentially expressed between patients with ARVC and patients with post-infarction VT. Enrichment analysis of differentially expressed microRNAs revealed their close linkage to cardiac diseases.Conclusion: Our data extend the knowledge of pericardial fluid microRNA composition and highlight five pericardial fluid microRNAs potentially linked to ARVC pathogenesis. Further studies are required to confirm the use of pericardial fluid RNA sequencing in differential diagnosis of ARVC.

The prognostic value of J-wave pattern for recurrence of ventricular tachycardia after catheter ablation in patients with myocardial infarction.

BackgroundJ‐waves and fragmented QRS (fQRS) on surface ECGs have been associated with the occurrence of ventricular tachyarrhythmias. Whether these non‐invasive parameters can also predict ventricular tachycardia (VT) recurrence after radiofrequency catheter ablation (RFCA) is unknown. Of interest, patients with a wide QRS‐complex have been excluded from clinical studies on J‐waves, although a J‐wave like pattern has been described for wide QRS.MethodsWe retrospectively included 168 patients (67 ± 10 years; 146 men) who underwent RFCA of post‐infarct VT. J‐wave pattern were defined as J‐point elevation ≥ 0.1 mV in at least two leads irrespective of QRS width. fQRS was defined as various RSR` pattern in patients with narrow QRS and more than two R wave in those with wide QRS. The primary endpoint was VT recurrence after RFCA up to 24 months.ResultsJ‐wave pattern and fQRS were present in 27 and 28 patients, respectively. Overlap of J‐wave pattern and fQRS was observed in nine. During a median follow‐up of 20 (interquartile range 9–24) months, 46 (27%) patients had VT recurrence. Kaplan–Meier curves revealed that both J‐wave pattern and fQRS were associated with VT recurrence. Multivariate Cox regression analysis demonstrated that the presence of J‐wave pattern (hazard ratio [HR] 2.84; 95% confidence interval [CI] 1.45–5.58; P = .002) and greater number of induced VT (HR 1.29; 95% CI 1.15–1.45; P < .001) were the independent predictors of VT recurrence.ConclusionsA J‐wave pattern—but not fQRS—is independently associated with an increased risk of post‐infarct VT recurrence after RFCA irrespective of QRS width. This simple non‐invasive parameter may identify patients who require additional treatment.

Factors associated with recurrent postinfarction ventricular tachycardia following ablation.

INTRODUCTION Ablation of ventricular tachycardia is the main therapy for patients with drug-refractory ventricular tachycardia (VT). Although evidence suggests that VT ablation could lower the incidence of recurrent VT, many cases still develop VT in follow-up. In this study, we performed a systematic review and meta-analysis to examine risk factors for recurrent VT in patients with postinfarction VT who underwent VT ablation. EVIDENCE ACQUISITION We comprehensively searched the databases of MEDLINE and EMBASE from inception to March 2020. Included studies were cohort studies, experimental trials, or randomized controlled trials that evaluate the risk of recurrent VT in postinfarction VT patients who underwent VT ablation. Data from each study were combined using random-effects. EVIDENCE SYNTHESIS Thirteen studies involving 1803 postinfarction patients who underwent VT ablation were included. Inducibility after the procedure (pooled HR=1.71, P<0.001), lower baseline left ventricular ejection fraction (LVEF) (pooled HR=0.98, P<0.001) and higher baseline New York Heart Association (NYHA) classification (pooled HR=1.34, P=0.003) were significantly associated with VT recurrence during the follow-up. There was no significant association between age, gender or diabetes mellitus and VT recurrence. CONCLUSIONS Our meta-analysis demonstrated that inducibility after the procedure, lower baseline LVEF and higher baseline NYHA classification were associated with an increased risk of VT recurrence in postinfarction VT patients who underwent VT ablation.

Assessing the ability of substrate mapping techniques to guide ventricular tachycardia ablation using computational modelling

BackgroundIdentification of targets for ablation of post-infarction ventricular tachycardias (VTs) remains challenging, often requiring arrhythmia induction to delineate the reentrant circuit. This carries a risk for the patient and may not be feasible. Substrate mapping has emerged as a safer strategy to uncover arrhythmogenic regions. However, VT recurrence remains common. GoalTo use computer simulations to assess the ability of different substrate mapping approaches to identify VT exit sites. MethodsA 3D computational model of the porcine post-infarction heart was constructed to simulate VT and paced rhythm. Electroanatomical maps were constructed based on endocardial electrogram features and the reentry vulnerability index (RVI - a metric combining activation (AT) and repolarization timings to identify tissue susceptibility to reentry). Since scar transmurality in our model was not homogeneous, parameters derived from all signals (including dense scar regions) were used in the analysis. Potential ablation targets obtained from each electroanatomical map during pacing were compared to the exit site detected during VT mapping. ResultsSimulation data showed that voltage cut-offs applied to bipolar electrograms could delineate the scar, but not the VT circuit. Electrogram fractionation had the highest correlation with scar transmurality. The RVI identified regions closest to VT exit site but was outperformed by AT gradients combined with voltage cut-offs. The performance of all metrics was affected by pacing location. ConclusionsSubstrate mapping could provide information about the infarct, but the directional dependency on activation should be considered. Activation-repolarization metrics have utility in safely identifying VT targets, even with non-transmural scars.

Magnetic Resonance Mapping of Catheter Ablation Lesions After Post-Infarction Ventricular Tachycardia Ablation

ObjectivesThis study sought to describe cardiac magnetic resonance (CMR) characteristics of ablation lesions within post-infarction scar. BackgroundChronic ablation lesions created during radiofrequency ablation of ventricular tachycardia (VT) in the setting of prior myocardial infarction have not been described in humans. MethodsSeventeen patients (15 men, ejection fraction 25 ± 8%, 66 ± 6 years of age) with CMR imaging prior to repeat ablation procedures for VT were studied. Electroanatomic maps from first-time procedures and subsequent CMR images were merged and retrospectively compared with electroanatomic maps from repeat procedures. ResultsThe delay between the index ablation procedure and the CMR study was 30 ± 29 months. Late gadolinium–enhanced CMR revealed a confluent nonenhancing subendocardial dark core within the infarct-related scar tissue in all patients. Intracardiac thrombi were ruled out by transthoracic and intracardiac echocardiography. These core lesions matched the distribution of prior ablation lesions, and corresponded to unexcitable areas at repeat procedures. ConclusionsAblation lesions can be detected by CMR after VT ablation in post-infarction patients and have a different appearance than scar tissue. These lesions can be observed many months after an initial ablation.

Epicardial voltage mapping in patients with postinfarction ventricular tachycardia: a pilot study

Introduction. Radiofrequency ablation (RFA) is an established treatment of post-myocardial infarction ventricular tachycardia (VT). Endocardial VT ablation can be insufficient for VT termination when the scar is intramural/epicardial.Purpose: to assess the extent of epicardial electrophysiological VT substrate in patients with remote myocardial infarction.Materials and methods. Thirteen patients with sustained postinfarction VT, who signed an informed consent, were included into the study. All patients underwent full clinical evaluation. Electroanatomical voltage bi- and unipolar mapping of endocardial and epicardial surfaces was performed. Maps were evaluated for the presence of low-voltage areas and local abnormal ventricular activity (LAVA). RFA was performed at LAVA sites. The end-point of the procedure was scar LAVA abolition and VT noninducibility (procedure success). VT recurrence was detected using an implantable cardioverter-defibrillator and/or ECG monitoring.Results. Epicardial access was successful in 12 patients. Epicardial access was performed at a first procedure in 7 patients, 4 patients had a history of previous endocardial ablation. Epicardial LAVA sites were detected in 9 patients. Endocardial and epicardial arrhythmogenic substrate localization coincided in 8 patients. One patient had only epicardial scar, 1 patient had only septal endocardial scar. In one patient LAVA sites had different localizations on epicardial and endocardial maps. Acute ablation success was noted in 12 patients.Conclusion. In our patient group transmural scar and epicardial electrophysiological arrhythmogenic substrate was detected in 82% of cases. Isolated endocardial ablation may be unsuccessful, in such cases epicardial mapping and ablation might be useful.

Abstract 14985: Presence of Repolarization Gradients Reverses Post-infarct Ventricular Tachycardia Exit and Entrance Sites in Personalized Digital Hearts

Introduction: Post-infarct ventricular tachycardias (VT) arise due to structural remodeling (scarring). Physiological repolarization gradients (apicobasal and transmural) exist in the human heart, but the effects on post-infarct VT dynamics are unknown. Hypothesis: We hypothesized that incorporation of repolarization gradients in personalized digital hearts of post-infarct patients impacts VT exit sites without altering the location of the VTs. Methods: 3D late-gadolinium enhanced CMR images were acquired from 7 post-infarct patients. Personalized image-based computational heart models (digital hearts) representing scar and infarct border zone distributions were constructed. Apicobasal (AB) and transmural (TM) repolarization gradients were incorporated using a validated method (Fig A). VTs were induced at baseline (no repolarization gradient) via rapid pacing in the right ventricular apex, using two pacing cycle lengths, mimicking non-invasive programmed stimulation. Pacing protocols that induced baseline VTs were repeated under AB and TM conditions. Results: Ten VTs were induced in baseline digital hearts. 8 AB VTs and 8 TM VTs were induced; the remaining 2 VTs for both AB and TM digital hearts could not be induced. 5/8 induced AB VTs had VT exit sites matching baseline VT exit sites; the remaining 3/8 AB VTs had reversed VT exit and entrance sites from the corresponding baseline VTs (Fig B, VT 1 &amp; 2). 4/8 induced TM VTs had exit sites that matched those at baseline; the remaining TM VTs had exit and entrance sites reversed from those of baseline VTs (Fig B, VT 1, 2 &amp; 3). All 8 AB VTs and 8 TM VTs had the same location as corresponding baseline VTs. Conclusion: AB and TM repolarization gradients can act to reverse VT entrance and exit sites without changing VT location. Thus, incorporation of physiological repolarization gradients into personalized digital hearts may not impact VT ablation targeting but may affect accurate prediction of VT exit or entrance sites.