Postinfarction Ventricular Tachycardia Research Articles

Dynamic voltage mapping of the ventricular tachycardia substrate

Abstract Background Substrate mapping techniques that predict ventricular tachycardia (VT) isthmus components in sinus or paced rhythm are necessary as mapping during VT is often not possible. Voltage maps lack accuracy in differentiating scar, traditionally displayed as tissue <0.50mV, from bordering arrhythmogenic substrate. We developed a practical technique aiming to improve the utility of a voltage map during VT ablation, termed ‘Dynamic Voltage Mapping’ (DVM). Methods Consecutive patients with post-infarct VT at our centre underwent left ventricle (LV) voltage mapping (mean 4762 points) with Carto3 v.7® and a PentaRay®, or Ensite X® and a HD Grid mapping catheter. Both mapping systems offer algorithms that allow substrate activation maps to be superimposed and analysed on the surface of a voltage display (i.e. Carto Ripple Maps, or Ensite X activation vectors). DVM is a process that sequentially adjusts the voltage display to highlight scar tissue in areas devoid of Ripple bars, or in areas where activation vectors point in multiple unfathomable directions (‘vector disarray’). This approach is summarised in Figures 1 & 2 and was retrospectively performed in all cases. This alternative scar voltage limit was termed the ‘DVM scar threshold’ (mV). Tissue below this threshold was termed ‘DVM-scar’, and tissue immediately surrounding (up to 0.5mV) was termed "DVM-Borderzone (BZ)". Results Twenty-five patients (mean age 64.4±11.0 years, 88% male, LV ejection fraction 31.8±6.9%, 16.4±8.5 years since infarct) were studied (n=15 Carto; n=10 EnSite). Across all cases, the mean shell area with voltage <0.50 mV was 36.8±20.3 cm2. The mean DVM scar threshold was 0.24±0.07 mV (Carto: 0.22±0.07 mV [range 0.12–0.35 mV]; EnSite: 0.26±0.08 [range 0.18–0.50 mV]). The mean DVM-scar area was 18.4±14.3 cm2, significantly smaller than the traditional 0.50mV value (p=0.0002). In the 8 patients where stable VT was mapped, the VT isthmus sites co-located within the DVM-BZ in all cases, exemplified in the figures. Pace-mapping at the DVM-BZ matched the remaining unmappable VT morphologies. Ablation lesions were retrospectively superimposed onto the DVM map and generally co-located within the DVM-BZ. No ablation was delivered in tissues >0.5mV. At median follow-up of 8.8 months, VT burden significantly reduced (median 3 episodes in 3-months pre vs. 0 post; p<0.001), with 76% of patients VT-free. Conclusion DVM appears to improve the delineation of the post-infarct VT substrate, and is feasible using two commercially-available mapping systems. The mean voltage threshold that differentiated DVM-Scar from BZ tissue was significantly lower than the traditional 0.50 mV scar definition, at 0.24mV, though ranged widely, suggesting that scar thresholds require individualised substrate definition. Targeted ablation of DVM-BZ may be effective at reducing future VT, though requires prospective validation.Figure 1Figure 2

Predicting postinfarct ventricular tachycardia by integrating cardiac MRI and advanced computational reentrant pathway analysis

BackgroundImplantable cardiac defibrillator (ICD) implantation can protect against sudden cardiac death after myocardial infarction. However, improved risk stratification for device requirement is still needed. ObjectiveThe purpose of this study was to improve assessment of postinfarct ventricular electropathology and prediction of appropriate ICD therapy by combining late gadolinium enhancement (LGE) and advanced computational modeling. MethodsADAS 3D LV (ADAS LV Medical, Barcelona, Spain) and custom-made software were used to generate 3-dimensional patient-specific ventricular models in a prospective cohort of patients with a myocardial infarction (N = 40) having undergone LGE imaging before ICD implantation. Corridor metrics and 3-dimensional surface features were computed from LGE images. The Virtual Induction and Treatment of Arrhythmias (VITA) framework was applied to patient-specific models to comprehensively probe the vulnerability of the scar substrate to sustaining reentrant circuits. Imaging and VITA metrics, related to the numbers of induced ventricular tachycardias and their corresponding round trip times (RTTs), were compared with ICD therapy during follow-up. ResultsPatients with an event (n = 17) had a larger interface between healthy myocardium and scar and higher VITA metrics. Cox regression analysis demonstrated a significant independent association with an event: interface (hazard ratio [HR] 2.79; 95% confidence interval [CI] 1.44–5.44; P < .01), unique ventricular tachycardias (HR 1.67; 95% CI 1.04–2.68; P = .03), mean RTT (HR 2.14; 95% CI 1.11–4.12; P = .02), and maximum RTT (HR 2.13; 95% CI 1.19–3.81; P = .01). ConclusionA detailed quantitative analysis of LGE-based scar maps, combined with advanced computational modeling, can accurately predict ICD therapy and could facilitate the early identification of high-risk patients in addition to left ventricular ejection fraction.

Delineating postinfarct ventricular tachycardia substrate with dynamic voltage mapping in areas of omnipolar vector disarray

BackgroundDefining post-infarct ventricular arrhythmic substrate is challenging with voltage mapping alone, though may be improved in combination with an activation map. Omnipolar Technology on the EnSite X system displays activation as vectors that can be superimposed onto a voltage map. ObjectiveTo optimise voltage map settings during ventricular tachycardia (VT) ablation, adjusting them dynamically using Omnipolar vectors. MethodsConsecutive patients undergoing substrate mapping were retrospectively studied. We categorised Omni-vectors as “uniform” when pointing in one direction, or in “disarray” when pointing in multiple directions. We superimposed vectors onto voltage maps coloured purple in tissue >1.5mV, and the voltage settings were adjusted so uniform vectors appeared within purple voltages, a process termed “Dynamic Voltage Mapping” (DVM). Vectors in disarray appeared within red-blue lower voltages. Results17 substrate maps were studied in 14 patients (mean age 63±13 years; mean LVEF 35±6%, median 4 (IQR 2-8.5) recent VT episodes). The DVM mean voltage threshold that differentiated tissue supporting uniform vectors from disarray was 0.27mV, ranging between patients from 0.18-0.50mV, with good inter-observer agreement (median difference: 0.00mV). We found that VT isthmus components, as well as sites of latest activation, isochronal crowding, and excellent pace-maps co-located with tissue along the DVM borderzone surrounding areas of disarray. ConclusionDynamic Voltage Mapping, guided by areas of Omnipolar vector disarray, allows for individualised post-infarct ventricular substrate characterisation. Tissue bordering areas of disarray may harbour greater arrhythmogenic potential.

Mechanism of Ventricular Tachycardia Occurring in Chronic Myocardial Infarction Scar.

Cardiac arrest is the leading cause of death in the more economically developed countries. Ventricular tachycardia associated with myocardial infarct is a prominent cause of cardiac arrest. Ventricular arrhythmias occur in 3 phases of infarction: during the ischemic event, during the healing phase, and after the scar matures. Mechanisms of arrhythmias in these phases are distinct. This review focuses on arrhythmia mechanisms for ventricular tachycardia in mature myocardial scar. Available data have shown that postinfarct ventricular tachycardia is a reentrant arrhythmia occurring in circuits found in the surviving myocardial strands that traverse the scar. Electrical conduction follows a zigzag course through that area. Conduction velocity is impaired by decreased gap junction density and impaired myocyte excitability. Enhanced sympathetic tone decreases action potential duration and increases sarcoplasmic reticular calcium leak and triggered activity. These elements of the ventricular tachycardia mechanism are found diffusely throughout scar. A distinct myocyte repolarization pattern is unique to the ventricular tachycardia circuit, setting up conditions for classical reentry. Our understanding of ventricular tachycardia mechanisms continues to evolve as new data become available. The ultimate use of this information would be the development of novel diagnostics and therapeutics to reliably identify at-risk patients and prevent their ventricular arrhythmias.

Catheter ablation for ventricular tachycardia after myocardial infarction: meta-analysis of randomised controlled trials

Abstract Background The prognostic impact of ventricular tachycardia (VT) catheter ablation is an important outstanding research question. Purpose We undertook a reconstructed individual patient data meta-analysis of randomised controlled trials comparing ablation to medical therapy in patients developing VT after myocardial infarction (MI). Methods We systematically identified all trials comparing catheter ablation to medical therapy in patients with VT and prior MI. The pre-specified primary endpoint was all-cause mortality assessed using reconstructed individual patient data obtained by digitisation of published Kaplan-Meier curves and subsequent construction of Cox proportional hazards regression models. Pre-specified secondary endpoints included trial-level assessment by random effects meta-analysis of all-cause mortality, VT recurrence, defibrillator shocks and all-cause hospitalisations. Meta-regression was performed to evaluate the effect of VT mapping in addition to substrate modification. Sensitivity analyses were performed depending on the proportion of patients with prior MI included. (PROSPERO ID CRD42023390799) Results Eight trials, recruiting a total of 874 patients, were included. 430 patients were randomised to catheter ablation and 444 to medical therapy. Catheter ablation reduced all-cause mortality compared to medical therapy when synthesising reconstructed individual patient data (hazard ratio 0.57, 95% confidence interval (CI) 0.38 to 0.85, p=0.007), but not in trial-level analysis (relative risk 0.91, 95%CI 0.67 to 1.23, p=0.53, I2=0%). Catheter ablation significantly reduced VT recurrence, defibrillator shocks and hospitalisations compared to medical therapy. Sensitivity analyses were consistent with the primary analyses. Conclusion In patients with post-infarct ventricular tachycardia, catheter ablation reduces mortality.

Evaluation of the Patients with Post-infarction Ventricular Tachycardia and Programmed Ventricular Stimulation

Evaluation of the Patients with Post-infarction Ventricular Tachycardia and Programmed Ventricular Stimulation

Efficient Patient-Specific Simulations of Ventricular Tachycardia Based on Computed Tomography-Defined Wall Thickness Heterogeneity

BackgroundElectrophysiological mapping of ventricular tachycardia (VT) is tedious and poorly reproducible. Substrate analysis on imaging cannot explicitly display VT circuits. ObjectivesThis study sought to introduce a computed tomography–based model personalization approach, allowing for the simulation of postinfarction VT in a clinically compatible time frame. MethodsIn 10 patients (age 65 ± 11 years, 9 male) referred for post-VT ablation, computed tomography–derived wall thickness maps were registered to 25 electroanatomical maps (sinus rhythm, paced, and VT). The relationship between wall thickness and electrophysiological characteristics (activation-recovery interval) was analyzed. Wall thickness was then employed to parameterize a fast and tractable organ-scale wave propagation model. Pacing protocols were simulated from multiple sites to test VT induction in silico. In silico VTs were compared to VT circuits mapped clinically. ResultsClinically, 6 different VTs could be induced with detailed maps in 9 patients. The proposed model allowed for fast simulation (median: 6 min/pacing site). Simulations of steady pacing (600 milliseconds) from 100 different sites/patient never triggered any arrhythmia. Applying S1-S2 or S1-S2-S3 induction schemes allowed for the induction of in silico VTs in the 9 of 10 patients who were clinically inducible. The patient who was not inducible clinically was also noninducible in silico. A total of 42 different VTs were simulated (4.2 ± 2 per patient). Six in silico VTs matched a VT circuit mapped clinically. ConclusionsThe proposed framework allows for personalized simulations in a matter of hours. In 6 of 9 patients, simulations show re-entrant patterns matching intracardiac recordings.

Arrhythmogenic Vulnerability of Reentrant Pathways in Post-Infarct Ventricular Tachycardia Assessed by Advanced Computational Modelling.

Arrhythmogenic Vulnerability of Reentrant Pathways in Post-Infarct Ventricular Tachycardia Assessed by Advanced Computational Modelling.

Arrhythmogenic vulnerability of re-entrant pathways in post-infarct ventricular tachycardia assessed by advanced computational modelling.

Substrate assessment of scar-mediated ventricular tachycardia (VT) is frequently performed using late gadolinium enhancement (LGE) images. Although this provides structural information about critical pathways through the scar, assessing the vulnerability of these pathways for sustaining VT is not possible with imaging alone.This study evaluated the performance of a novel automated re-entrant pathway finding algorithm to non-invasively predict VT circuit and inducibility. Twenty post-infarct VT-ablation patients were included for retrospective analysis. Commercially available software (ADAS3D left ventricular) was used to generate scar maps from 2D-LGE images using the default 40-60 pixel-signal-intensity (PSI) threshold. In addition, algorithm sensitivity for altered thresholds was explored using PSI 45-55, 35-65, and 30-70. Simulations were performed on the Virtual Induction and Treatment of Arrhythmias (VITA) framework to identify potential sites of block and assess their vulnerability depending on the automatically computed round-trip-time (RTT). Metrics, indicative of substrate complexity, were correlated with VT-recurrence during follow-up. Total VTs (85 ± 43 vs. 42 ± 27) and unique VTs (9 ± 4 vs. 5 ± 4) were significantly higher in patients with- compared to patients without recurrence, and were predictive of recurrence with area under the curve of 0.820 and 0.770, respectively. VITA was robust to scar threshold variations with no significant impact on total and unique VTs, and mean RTT between the four models. Simulation metrics derived from PSI 45-55 model had the highest number of parameters predictive for post-ablation VT-recurrence. Advanced computational metrics can non-invasively and robustly assess VT substrate complexity, which may aid personalized clinical planning and decision-making in the treatment of post-infarction VT.

Site-specific prolongation of repolarization prevents postmyocardial infarction tachycardia.

Site-specific prolongation of repolarization prevents postmyocardial infarction tachycardia.

Lipomatous Metaplasia Facilitates Slow Conduction in Critical Ventricular Tachycardia Corridors Within Postinfarct Myocardium

BackgroundMyocardial lipomatous metaplasia (LM) has been reported to be associated with post-infarct ventricular tachycardia (VT) circuitry. ObjectivesThis study examined the association of scar versus LM composition with impulse conduction velocity (CV) in putative VT corridors that traverse the infarct zone in post-infarct patients. MethodsThe cohort included 31 post-infarct patients from the prospective INFINITY (Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy) study. Myocardial scar, border zone, and potential viable corridors were defined by late gadolinium enhancement cardiac magnetic resonance (LGE-CMR), and LM was defined by computed tomography. Images were registered to electroanatomic maps, and the CV at each electroanatomic map point was calculated as the mean CV between that point and 5 adjacent points along the activation wave front. ResultsRegions with LM exhibited lower CV than scar (median = 11.9 vs 13.5 cm/s; P < 0.001). Of 94 corridors computed from LGE-CMR and electrophysiologically confirmed to participate in VT circuitry, 93 traversed through or near LM. These critical corridors displayed slower CV (median 8.8 [IQR: 5.9-15.7] cm/s vs 39.2 [IQR: 28.1-58.5]) cm/s; P < 0.001) than 115 noncritical corridors distant from LM. Additionally, critical corridors demonstrated low-peripheral, high-center (mountain shaped, 23.3%) or mean low-level (46.7%) CV patterns compared with 115 noncritical corridors distant from LM that displayed high-peripheral, low-center (valley shaped, 19.1%) or mean high-level (60.9%) CV patterns. ConclusionsThe association of myocardial LM with VT circuitry is at least partially mediated by slowing nearby corridor CV thus facilitating an excitable gap that enables circuit re-entry.

The importance of the right ventricular insertion area for the functional substrate of ventricular tachycardia after myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: None. Background Conducting systematic annotation and ablation of evoked delayed potentials (EDP) in response to short coupled right ventricular extra-stimuli (RV-ES) has improved ablation outcome of post myocardial infarction (MI) ventricular tachycardia (VT). The reported short radiofrequency catheter ablation (RFCA) times suggests the presence of predilection areas for these functional substrates. Purpose To evaluate the electroanatomical characteristics and distribution of EDPs in post-MI patients referred for RFCA of VT. Methods Electroanatomical mapping (EAM) data of 48 post-MI patients (69 ± 9 years, 39 male, LV ejection fraction 36 ± 10%, anterior MI 20 [42%], inferior MI 28 [58%]), who underwent functional substrate mapping and ablation were analyzed. Pre-procedural cardiac CTs of 16 patients (8 anterior, 8 inferior MI) were integrated with EAM data. Infarct extension (defined as bipolar voltage [BV] &amp;lt;3.0mV, dense scar &amp;lt;0.5mV and scar borderzone [BZ] 0.5-3mV) and EDP location were determined based on the AHA 17-segment model of the left ventricle. Results RV-ES was performed during mapping at 2180 LV sites (median 46 per patient, range 8-81) and EDPs were observed at 631 (29%) sites. Patients had a median of 11 (range 1-37) EDP sites. Compared to no-EDP sites, EDP sites had lower BV (median 0.57 mV vs. 0.77 mV, P &amp;lt;0.001), longer duration (median 79 ms vs. 66 ms, P &amp;lt;0.001), and larger number of positive sharp deflections (median 6 vs. 5, P &amp;lt;0.001) during sinus rhythm. Of all EDP sites, 278 (44%), 286 (45%), 64 (10%), and 3 (1%) had BV of &amp;lt;0.5mV, ≥ 0.5mV and &amp;lt;1.5 mV, a BV of ≥1.5 mV and &amp;lt;3.0 mV, and a BV of &amp;gt;3.0 mV, respectively. In the 16 patients with CT image integration, a total of 124/272 segments showed EA scar with a median (IQR, range) of 8 (6-9, 4-12) segments per patient. Any EDP was identified in 71/124 (57%) of segments with EA scar. Of note, 73% of all EDPs in inferior MIs and 64% of all EDPs in anterior MI were located in 4 AHA segments, namely 3,4, 9,10 and 7,8,13,14, respectively, close to the inferior or anterior RV insertion. Such a cluster of EDP sites around the RV insertion was found in 6 (75%) patients with inferior MI and in 7 (88%) patients with anterior MI. Conclusion About 10% of EDPs are identified at sites with BV of ≥1.5mV and &amp;lt;3.0mV during sinus rhythm supporting the recently proposed BV threshold &amp;lt;3.0mV for post-MI scars. EDPs are frequently located near the RV insertion in both inferior MI and anterior MI suggesting a role of the RV insertion in the functional substrate of post-MI VT.

The effect of scar imaging quality on in-silico pace-mapping of post-infarction ventricular tachycardia

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Wellcome Trust and British Heart Foundation. Background In-silico pacing mapping is a technique which involves using an anatomically-personalised image-based computational model to generate a ‘virtual’ clinical pace map for enhanced pre-procedural ablation planning of post-infarction ventricular tachycardia (VT). Utilising, as it does, a direct clinical ECG (or implanted device) recording of the clinical VT in order to construct the map, it has a number of advantages over other computational methods which attempt to simulate patient-specific VTs to identify ablation targets. However, accurate model construction relies on adequate scar imaging data, which may not be available with current clinical cardiac MR (CMR) sequences. Purpose To investigate the impact of scar imaging quality on the ability of in-silico pace-mapping to determine the VT origin. Methods VTs were simulated in three post-infarction porcine heart models reconstructed from high resolution (1mm isotropic) contrast-enhanced CMR data. Visual analysis of the VT circuits was performed to identify the VT site of origin (exit site) in each case (as the gold standard). The ECG of each simulated VT was computed and used as input for the construction of the in-silico virtual pace-mapping approach. Prior to pace map construction, the scar anatomy was modified to represent three different levels of imaging resolution: high resolution scar mapping (default); low resolution scar (representing standing clinical CMR sequences), obtained by performing dilation and erosion in the scar to close all inner pathways; and, finally, no scar (cardiac anatomy only, representing CT-based reconstructions). In-silico pace-mapping was performed by pacing the heart in N = 1000 sites from randomly chosen locations, on both surfaces and intramurally, within close proximity (&amp;lt;5mm) from the infarct. ECG signals computed following each paced activation wavefront were compared to the VT ECG through correlation analysis to construct the virtual pace map. The distance d between the VT exit site and the pacing location with the strongest correlation was also computed. Results As can be seen in Figure 1, correlation between VT and paced ECGs was found to be strongest at pacing locations near the VT exit site in all models. Correlation coefficients were similar in value and distribution in models with high- (min: -0.49±0.27 and max: 0.92±0.05) and low-resolution scars (min: -0.46±0.29 and max: 0.93±0.05). While the correlation map in the absence of scar had smaller values when compared to the other two models (min: -0.50±0.24 and max: 0.71±0.09), the VT exit was still located near the pacing location with the strongest correlation: d = 9.47±2.83 (high-res), d = 6.63±6.35mm (low-res) and d = 18.60±7.10mm (no scar). Conclusion In-silico pace-mapping successfully detected the VT exit sites regardless the resolution of the scar. This finding suggest that the level of infarct anatomical detail has a minor effect on simulated paced activation to localize VT ablation.

Catheter Ablation for Ventricular Tachycardia After MI: A Reconstructed Individual Patient Data Meta-analysis of Randomised Controlled Trials.

The prognostic impact of ventricular tachycardia (VT) catheter ablation is an important outstanding research question. We undertook a reconstructed individual patient data meta-analysis of randomised controlled trials comparing ablation to medical therapy in patients developing VT after MI. We systematically identified all trials comparing catheter ablation to medical therapy in patients with VT and prior MI. The prespecified primary endpoint was reconstructed individual patient assessment of all-cause mortality. Prespecified secondary endpoints included trial-level assessment of all-cause mortality, VT recurrence or defibrillator shocks and all-cause hospitalisations. Prespecified subgroup analysis was performed for ablation approaches involving only substrate modification without VT activation mapping. Sensitivity analyses were performed depending on the proportion of patients with prior MI included. Eight trials, recruiting a total of 874 patients, were included. Of these 874 patients, 430 were randomised to catheter ablation and 444 were randomised to medical therapy. Catheter ablation reduced all-cause mortality compared with medical therapy when synthesising individual patient data (HR 0.63; 95% CI [0.41-0.96]; p=0.03), but not in trial-level analysis (RR 0.91; 95% CI [0.67-1.23]; p=0.53; I2=0%). Catheter ablation significantly reduced VT recurrence, defibrillator shocks and hospitalisations compared with medical therapy. Sensitivity analyses were consistent with the primary analyses. In patients with postinfarct VT, catheter ablation reduces mortality.

Lipomatous metaplasia prolongs repolarization and increases repolarization dispersion within post-infarct ventricular tachycardia circuit cites.

Post-infarct myocardium contains viable corridors traversing scar or lipomatous metaplasia (LM). Ventricular tachycardia (VT) circuitry has been separately reported to associate with corridors that traverse LM and with repolarization heterogeneity. We examined the association of corridor activation recovery interval (ARI) and ARI dispersion with surrounding tissue type. The cohort included 33 post-infarct patients from the prospective Intra-Myocardial Fat Deposition and Ventricular Tachycardia in Cardiomyopathy (INFINITY) study. We co-registered scar and corridors from late gadolinium enhanced magnetic resonance, and LM from computed tomography with intracardiac electrogram locations. Activation recovery interval was calculated during sinus or ventricular pacing, as the time interval from the minimum derivative within the QRS to the maximum derivative within the T-wave on unipolar electrograms. Regional ARI dispersion was defined as the standard deviation (SD) of ARI per AHA segment (ARISD). Lipomatous metaplasia exhibited higher ARI than scar [325 (interquartile range 270-392) vs. 313 (255-374), P < 0.001]. Corridors critical to VT re-entry were more likely to traverse through or near LM and displayed prolonged ARI compared with non-critical corridors [355 (319-397) vs. 302 (279-333) ms, P < 0.001]. ARISD was more closely associated with LM than with scar (likelihood ratio χ2 50 vs. 12, and 4.2-unit vs. 0.9-unit increase in 0.01*Log(ARISD) per 1 cm2 increase per AHA segment). Additionally, LM and scar exhibited interaction (P < 0.001) in their association with ARISD. Lipomatous metaplasia is closely associated with prolonged local action potential duration of corridors and ARI dispersion, which may facilitate the propensity of VT circuit re-entry.

Non-invasive localization of post-infarct ventricular tachycardia exit sites to guide ablation planning: a computational deep learning platform utilizing the 12-lead electrocardiogram and intracardiac electrograms from implanted devices.

Existing strategies that identify post-infarct ventricular tachycardia (VT) ablation target either employ invasive electrophysiological (EP) mapping or non-invasive modalities utilizing the electrocardiogram (ECG). Their success relies on localizing sites critical to the maintenance of the clinical arrhythmia, not always recorded on the 12-lead ECG. Targeting the clinical VT by utilizing electrograms (EGM) recordings stored in implanted devices may aid ablation planning, enhancing safety and speed and potentially reducing the need of VT induction. In this context, we aim to develop a non-invasive computational-deep learning (DL) platform to localize VT exit sites from surface ECGs and implanted device intracardiac EGMs. A library of ECGs and EGMs from simulated paced beats and representative post-infarct VTs was generated across five torso models. Traces were used to train DL algorithms to localize VT sites of earliest systolic activation; first tested on simulated data and then on a clinically induced VT to show applicability of our platform in clinical settings. Localization performance was estimated via localization errors (LEs) against known VT exit sites from simulations or clinical ablation targets. Surface ECGs successfully localized post-infarct VTs from simulated data with mean LE = 9.61 ± 2.61 mm across torsos. VT localization was successfully achieved from implanted device intracardiac EGMs with mean LE = 13.10 ± 2.36 mm. Finally, the clinically induced VT localization was in agreement with the clinical ablation volume. The proposed framework may be utilized for direct localization of post-infarct VTs from surface ECGs and/or implanted device EGMs, or in conjunction with efficient, patient-specific modelling, enhancing safety and speed of ablation planning.

Characterization of the right ventricular substrate participating in postinfarction ventricular tachycardia.

The right ventricle (RV) is uncommonly implicated in postinfarction ventricular tachycardia (VT). The prevalence and features of the RV substrate participating in postinfarction VT are undefined. The purpose of this study was to characterize critical right ventricular substrate (CRVS) involvement in patients with postinfarction VT. We retrospectively reviewed 1279 patients with postinfarction VT undergoing catheter ablation at our center from January 2000 through May 2020. Cases with CRVS defined by conclusive demonstration of participation in VT with activation, entrainment, and/or pacemapping during sinus rhythm were identified. CRVS was identified in 27 of 1279 patients (2.1%): age 65± 13 years, 96% male, median left ventricular (LV) ejection fraction 25%, and 93% with left bundle branch block (LBBB) morphology VT. CRVS was identified by RV activation and/or entrainment mapping (n = 19) or by the presence of low-voltage abnormal electrograms with excellent pacemap for the targeted VT and noninducibility after ablation (n = 8). VT termination during RV ablation occurred in 15 patients. After median follow-up of 20 months (interquartile range 9-53 months) and median of 2 procedures (interquartile range 1-3), 22 of 27 patients (80%) had no VT recurrence and 11 (41%) died. The RV contains critical substrate elements of postinfarction VT in at least 2.1% of cases. RV mapping should be considered in cases in which LV mapping fails to demonstrate adequate targets, particularly in patients with LBBB morphology VT.

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.