Infarct-related Ventricular Tachycardia Research Articles

Novel systematic processing of cardiac magnetic resonance imaging identifies target regions associated with infarct-related ventricular tachycardia

Abstract Background and Aims There is lack of agreement on late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging processing for guiding ventricular tachycardia (VT) ablation. We aim at developing and validating a systematic processing approach on LGE-CMR images to identify VT corridors that contain critical VT isthmus sites. Methods Translational study including 18 pigs with established myocardial infarction and inducible VT undergoing in vivo characterization of the anatomical and functional myocardial substrate associated with VT maintenance. Clinical validation was conducted in a multicenter series of 33 patients with ischemic cardiomyopathy undergoing VT ablation. Three-dimensional CMR-LGE images were processed using systematic scanning of 15 signal intensity (SI) cut-off ranges to obtain surface visualization of all potential VT corridors. Analysis and comparisons of imaging and electrophysiological data were performed in individuals with full electrophysiological characterization of the isthmus sites of at least one VT morphology. Results In both the experimental pig model and patients undergoing VT ablation, all the electrophysiologically-defined isthmus sites (n=11 and n=19, respectively) showed overlapping regions with CMR-based potential VT corridors. Such imaging-based VT corridors were less specific than electrophysiologically-guided ablation lesions at critical isthmus sites. However, an optimized strategy using the 7 most relevant SI cut-off ranges among patients showed an increase in specificity compared to using 15 SI cut-off ranges (70% vs 62%, respectively), without diminishing the capability to detect VT isthmus sites (sensitivity 100%). Conclusions Systematic imaging processing of LGE-CMR sequences using several SI cut-off ranges may improve and standardize procedure planning to identify VT isthmus sites.

Novel systematic processing of cardiac magnetic resonance imaging identifies target regions associated with infarct-related ventricular tachycardia

Abstract Introduction In the clinic, complete characterization of reentrant ventricular tachycardia (VT) circuits using classical electrophysiological criteria and state-of-the-art high density mapping during VT is complex, and often cannot be completed because of hemodynamic instability. This common limitation has motivated the implementation of mapping strategies during sinus rhythm or ventricular pacing aiming to identify scar regions associated with VT isthmuses or potential arrhythmogenicity. Complementary imaging-based strategies including advanced analyses of scar tissue characteristics have been also proposed for procedure planning and identification of potential arrhythmogenic regions. However, the most recent expert consensus report on catheter ablation of ventricular arrhythmia highlights the lack of agreement on the preferable signal intensity (SI) cut-off values for assessment of tissue heterogeneity and scar areas on late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) images. The latter makes LGE-CMR imaging processing highly operator-dependent and potentially sensitive to selection bias. Purpose We aimed at developing and validating a systematic processing approach on LGE-CMR images to identify potential VT corridors that may include protected isthmuses associated with VT maintenance. Methods Translational study including 18 pigs with established myocardial infarction and inducible VT undergoing in vivo characterization of the anatomical and functional myocardial substrate associated with VT maintenance. Clinical validation was conducted in a multicenter series of 33 patients with ischemic cardiomyopathy undergoing VT ablation. Three-dimensional CMR-LGE images were processed using systematic scanning of 15 signal intensity cut-off ranges to obtain surface visualization of all potential VT corridors. Analysis and comparisons of imaging and electrophysiological data were performed in individuals with full electrophysiological characterization of the isthmus sites of at least one VT morphology. Results In both the experimental pig model and patients undergoing VT ablation, all the electrophysiologically-defined isthmus sites (n=11 and n=19, respectively) showed overlapping regions with CMR-based potential VT corridors. Such imaging-based VT corridors were less specific than electrophysiologically-guided ablation lesions at functionally relevant isthmus sites (Figure). However, in patients, decreasing from 15 to 7 the number of signal intensity cut-off ranges for systematic imaging processing significantly reduced the area of imaging-based potential VT corridors, without diminishing the capability to detect functionally relevant VT isthmus sites. Conclusions Systematic processing of 3D LGE-CMR images provides unbiased identification of imaging based potential VT corridors that contain functionally relevant protected isthmus sites.

Single-beat mapping during programmed ventricular stimulation identifies infarct-related ventricular tachycardia isthmus sites

Abstract Introduction Complete characterization of reentrant ventricular tachycardia (VT) circuits using classical electrophysiological criteria and high-density mapping during VT is complex. Often, VT episodes cannot be fully characterized because of hemodynamic instability during the mapping procedure. This common limitation has motivated the implementation of mapping strategies during sinus rhythm or ventricular pacing aiming to identify scar regions associated with VT isthmuses or potential arrhythmogenicity. However, these strategies still require time-consuming catheter-based mapping. Purpose We aimed to develop and validate a single-beat mapping strategy during programmed ventricular stimulation (PVS) to identify scar regions associated with VT isthmus sites. We hypothesize that protected VT isthmuses within scar regions are characterized by larger activation time dispersion than surrounding scar areas not related to critical isthmus sites. Methods Experimental study including 16 pigs with established myocardial infarction (MI) in the anterior wall. Ten-to-twelve weeks after MI, pigs underwent left ventricular characterization using 3D late-gadolinium enhancement cardiac magnetic resonance imaging, and further invasive electroanatomical mapping to obtain high-density sequential activation maps during ventricular pacing and VT. High-density maps were compared with single-beat maps using a 64-pole basket catheter positioned in the left ventricle. After VT induction, high-density activation maps in well-tolerated VT episodes were used to identify VT isthmus sites. Simultaneous activation data from the 64-pole basket catheter were also obtained during PVS and VT. Off-line analysis was performed to: (i) validate single-beat activation maps during the baseline drive pacing cycle length (S1), and (ii) identify basket-catheter electrodes with the larger local activation time-dispersion score (LAT-DS) during PVS including up to 4 coupled extrastimuli (S2, S3, S4, S5) (Figure 1). LAT-DS was defined as the normalized product of the LAT of each electrode and the activation dispersion among its neighboring electrodes. Results Basket-catheter based single-beat activation maps during S1 pacing showed high correlation values with high-density sequential activation maps (N=16. R²=0.91). In 7 pigs, the VT isthmus site was fully characterized using high-density activation maps. During any of the coupled extrastimuli of the PVS protocol, basket catheter electrodes colocalizing with documented VT isthmus sites on high-density maps showed higher LAT-DS values compared to surrounding electrodes located on scar or healthy regions. Conversely, LAT values alone could not differentiate scar regions relevant for VT maintenance during PVS protocol (Figure 2). Conclusions Sixty-four pole single-beat activation maps during PVS identify left ventricular scar areas with higher than surrounding LAT-DS values that are associated with VT isthmus sites.Figure 1.Experimental modelFigure 2.A-Example. B-C-Full results

ForCEPSS—A framework for cardiac electrophysiology simulations standardization

Background and Objective:Simulation of cardiac electrophysiology (CEP) is an important research tool that is increasingly being adopted in industrial and clinical applications. Typical workflows for CEP simulation consist of a sequence of processing stages starting with building an anatomical model and then calibrating its electrophysiological properties to match observable data. While the calibration stages are common and generalizable, most CEP studies re-implement these steps in complex and highly variable workflows. This lack of standardization renders the execution of computational CEP studies in an efficient, robust, and reproducible manner a significant challenge. Here, we propose ForCEPSS as an efficient and robust, yet flexible, software framework for standardizing CEP simulation studies. Methods and Results:Key processing stages of CEP simulation studies are identified and implemented in a standardized workflow that builds on openCARP11https://opencarp.org/. Plank et al. (2021) and the Python-based carputils22https://git.opencarp.org/openCARP/carputils. framework. Stages include (i) the definition and initialization of action potential phenotypes, (ii) the tissue scale calibration of conduction properties, (iii) the functional initialization to approximate a limit cycle corresponding to the dynamic reference state according to an experimental protocol, and, (iv) the execution of the CEP study where the electrophysiological response to a perturbation of the limit cycle is probed. As an exemplar application, we employ ForCEPSS to prepare a CEP study according to the Virtual Arrhythmia Risk Prediction protocol used for investigating the arrhythmogenic risk of developing infarct-related ventricular tachycardia (VT) in ischemic cardiomyopathy patients. We demonstrate that ForCEPSS enables a fully automated execution of all stages of this complex protocol. Conclusion:ForCEPSS offers a novel comprehensive, standardized, and automated CEP simulation workflow. The high degree of automation accelerates the execution of CEP simulation studies, reduces errors, improves robustness, and makes CEP studies reproducible. Verification of simulation studies within the CEP modeling community is thus possible. As such, ForCEPSS makes an important contribution towards increasing transparency, standardization, and reproducibility of in silico CEP experiments.

PO-05-037 EFFICACY AND CLINICAL CHARACTERISTICS OF AVERT-VT: ABLATION AT VIRTUAL-HEART PREDICTED VT

We have previously demonstrated the feasibility of virtual-heart simulations in determining noninvasively the optimal infarct-related ventricular tachycardia (VT) ablation targets and guiding the clinical ablation. We are now proceeding with AVERT-VT, an FDA-approved study for ten prospective patients. To develop the end-to-end personalized computational modeling prediction pipeline enabling AVERT-VT and to assess the corresponding clinical characteristics of the predicted virtual-heart ablation targets. We developed a comprehensive end-to-end computational pipeline enabling AVERT-VT (Fig). 3D LGE-MRI scans with 1.5x1.5mm in-plane spatial resolution and slice thickness <2mm were used to reconstruct the 3D left ventricular (LV) model incorporating deep scar, border (gray) zone, and non-infarcted tissue. In silico rapid pacing from 7 LV regions were performed to induce VTs. The optimal ablation targets were determined by thorough analyses of the wavefront propagation of the induced in silico VTs. A linear ablation connecting a VT ablation target to a transmural deep scar region, the basal region, or the other VT target was performed to eliminate the potential VT pathway formed by the target ablation. Potential emergent VTs in the post-ablation substrate were investigated by repeating the VT induction pacing protocol. This process was iterated until complete VT non-inducibility was achieved. The initial and repeat ablation targets, linear ablations, as well as the LV, right ventricle, infarct area, aortic arch, and left and right coronary cusp geometries, were exported as an ablation strategy plan compatible with the clinical mapping system. The figure presents results from one patient in the clinical study. The ablation plan was successfully imported and co-registered to the patient’s heart. The extent of the model infarct corresponded to the bipolar low-voltage regions. Abnormal electrograms were observed at the proposed targets. 2 VTs were observed during the procedure. Areas of latest activation in sinus rhythm and best pace maps, with a long stimulus to QRS, were found at 2 of the proposed targets. One of the seven proposed targets was not ablated due to the proximity to the left sided His potential. The patient was not inducible of any VT at the end of the procedure. AVERT-VT proposed targets corresponded to abnormal electrograms, and ablating at the targets led to VT non-inducibility.

Pulsed Field Ablation of Left Ventricular Myocardium in a Swine Infarct Model.

Pulsed field ablation (PFA) leads to cell death by irreversible electroporation. There are limited data about PFA lesion characteristics in the ventricle, particularly in the presence of myocardial scar. This study sought to evaluate the lesion characteristics of PFA and radiofrequency energy (RFA) in healthy and infarcted left ventricular (LV) myocardium in swine. Swine (n=10) underwent either: 1) 120-minute left anterior descending coronary artery balloon occlusion myocardial infarction and survived for 6 to 8weeks (n=8); or 2) served as healthy control subjects (n=2). PFA or RFA was delivered to the LV endocardium in regions of healthy myocardium or scar identified with electroanatomical mapping. Bipolar, biphasic PFA was delivered for 2.5 seconds× 4 applications/site using 2 different catheters: linear quadripolar (FOCAL) or multispline 8-pole catheter (BASKET). Gross and histologic measurements of lesion size were performed. In the PFA group, 21 lesions were delivered to healthy LV and 20 to areas of scar. Overall, there was no significant difference in lesion depth between catheter groups (FOCAL linear vs BASKET; P = 0.740), whereas lesion width was greater for BASKET (10.6 ± 2.4mm vs 13.3 ± 3.3mm; P = 0.007). In myocardial scar, lesion depth was not significantly different between PFA catheters (P = 0.235). However, lesion depth for PFA was greater than for RFA (PFAvs RFA; 6.1 ± 1.7mm vs 3.8 ± 1.7mm; P = 0.005). PFA allows rapid, safe, and effective ablation of surviving islands of myocardium within and around infarcted LV substrate. This technology holds promise for treating infarct-related ventricular tachycardia in humans.

PO-709-07 THE IMPACT OF MULTI-DIRECTIONAL PACING ON THE DISTRIBUTION OF LATE SIGNAL ACTIVATION, ACTIVATION SLOWING AND REPOLARIZATION GRADIENTS IN RELATION TO VENTRICULAR TACHYCARDIA IN A PORCINE INFARCT MODEL

In ventricular tachycardia (VT) ablation electrograms with late or decremental activation properties have emerged as a target in substrate ablation, and spatial dispersion of repolarization has been shown to correlate with areas of late potentials and critical VT sites. Multi-directional pacing has been demonstrated to reveal a greater area of activation slowing in infarct related VT. The optimal strategy to identify key sites of arrhythmogenesis substrate mapping is not established.

CA-534-01 PULSED FIELD ABLATION COMPARED TO RADIOFREQUENCY ABLATION OF LEFT VENTRICULAR MYOCARDIUM IN A SWINE INFARCT MODEL

There is limited data on use of pulsed field ablation (PFA) in the left ventricle (LV), particularly in the presence of myocardial scar To evaluate the lesion characteristics of PFA and radiofrequency energy (RFA) in healthy and infarcted LV myocardium 10 swine were included: 8 underwent 120min LAD balloon occlusion myocardial infarction and were survived for 6-8 weeks; 2 were healthy controls. PFA and standard RFA was delivered to the LV endocardium in healthy myocardium or scar identified with electroanatomic mapping. Bipolar, biphasic PFA was delivered at 1800 to 2000V for 2.5secs x 4 applications/site using 2 different catheters: linear quadripolar (LINEAR) or multi-spline 8-pole catheter (BASKET). Irrigated RF energy was delivered from 35W-50W to achieve >10 ohm impedance drop. Detailed histologic measurements of ablation depth were performed. In the PFA group, 21 lesions were delivered to healthy LV and 20 to scar, all without complications. There was no significant difference in histologic lesion depth in healthy myocardium or scar between LINEAR vs. BASKET PFA catheters (Figure A). In the RF group, 19 lesions were delivered to healthy LV and 8 to scar. Maximal lesion depth for PFA and RFA were similar in healthy tissue, however lesion depth was greater for PFA than RFA in scar (Figure B, 6.1±1.7 vs 3.8±1.7 mm; P=0.005). There was no vascular injury observed with PFA, however RFA led to adventitial edema and thrombosis. PFA allows rapid, safe and effective ablation of surviving islands of myocardium within infarcted LV substrate. Lesion depth in myocardial scar is greater for PFA than RFA. This technology holds promise for treating infarct-related ventricular tachycardia in humans.

B-AB03-03 PULSED FIELD ABLATION OF LEFT VENTRICULAR MYOCARDIUM IN A SWINE INFARCT MODEL

Pulsed field ablation (PFA) leads to cell death by irreversible electroporation. However, there is limited data about lesion characteristics in ventricular myocardium in the presence of myocardial scar. To evaluate the lesion characteristics of PFA in healthy and infarcted left ventricular (LV) myocardium. Swine (n=6) underwent 120min LAD balloon occlusion myocardial infarction (MI) and were survived 6-8 weeks. PFA was delivered to the LV endocardium of 1) healthy myocardium or 2) MI identified with electroanatomic mapping. Bipolar, biphasic PFA was delivered for 2.5secs x 4 applications/site (10secs total) using 2 different catheters: a linear quadripolar (FOCAL, 2000-2100V) or multi-spline 8-pole catheter (BASKET, 1800V) (FARAPULSE, Menlo Park, CA) (Figure). After sectioning, gross lesions were identified, measured using calipers and tissue stained for histology. 21 lesions were delivered to healthy LV and 20 to areas with MI, all without complications. Overall, there was no significant difference in lesion depth between groups (FOCAL vs. BASKET; depth: 5.6 ±1.1 mm vs. 5.5 ± 1.1 mm, P=0.740), while lesion width was greater for BASKET (10.6 ± 2.4 mm vs. 13.3 ± 3.3 mm, P=0.007). In regions of MI, histology showed ablation of surviving myocardium both within and epicardial to scar; lesion depth in MI was not significantly different between catheters (5.6 ± 1.5 mm vs. 4.6 ± 0.9 mm; P=0.235). PFA allows rapid, safe, and effective ablation of surviving islands of myocardium within and around infarcted LV substrate. This technology holds promise for treating infarct-related ventricular tachycardia in humans.

Impact of augmented-reality improvement in ablation catheter navigation as assessed by virtual-heart simulations of ventricular tachycardia ablation

BackgroundRecently, an augmented reality (AR) solution allows the physician to place the ablation catheter at the designated lesion site more accurately during cardiac electrophysiology studies. The improvement in navigation accuracy may positively affect ventricular tachycardia (VT) ablation termination, however assessment of this in the clinic would be difficult. Novel personalized virtual heart technology enables non-invasive identification of optimal lesion targets for infarct-related VT. This study aims to evaluate the potential impact of such catheter navigation accuracy improvement in virtual VT ablations. Methods2 MRI-based virtual hearts with 2 in silico induced VTs (VT 1, VT 2) were included. VTs were terminated with virtual “ground truth” endocardial ablation lesions. 106 navigation error values that were previously assessed in a clinical study evaluating the improvement of ablation catheter navigation accuracy guided with AR (53 with, 53 without) were used to displace the “ground truth” ablation targets. The corresponding ablations were simulated based on these errors and VT termination for each simulation was assessed. ResultsIn 54 VT 1 ablation simulations, smaller error with AR significantly resulted in more VT termination (25) compared to the error without AR (16) (P < 0.01). In 52 VT 2 ablation simulations, no significant difference was observed from error with (11) and without AR (13) (P = 0.58). The substrate characteristic may impact the effect of improved accuracy to an improved VT termination. ConclusionVirtual heart shows that the increased catheter navigation accuracy provided by AR guidance can affect the VT termination.

Arrhythmia exacerbation after post-infarction ventricular tachycardia ablation: prevalence and prognostic significance.

Catheter ablation is an effective treatment for post-infarction ventricular tachycardia (VT). However, some patients may experience a worsened arrhythmia phenotype after ablation. We aimed to determine the prevalence and prognostic impact of arrhythmia exacerbation (AE) after post-infarction VT ablation. A total of 1187 consecutive patients (93% men, median age 68 years, median ejection fraction 30%) who underwent post-infarction VT ablation at six centres were included. Arrhythmia exacerbation was defined as post-ablation VT storm or incessant VT in patients without prior similar events. During follow-up (median 717 days), 426 (36%) patients experienced VT recurrence. Events qualifying as AE occurred in 67 patients (6%). Median times to VT recurrence with and without AE were 238 [interquartile range (IQR) 35-640] days and 135 (IQR 22-521) days, respectively (P = 0.25). Almost half of the patients (46%) who experienced AE experienced it within 6 months of the index procedure. Patients with AE had had longer ablation times during the ablation procedures compared to the rest of the patients (median 42 vs. 34 min, P = 0.02). Among patients with VT recurrence, the risk of death or heart transplantation was significantly higher in patients with than without AE (hazard ratio 1.99, 95% CI 1.28-3.10; P = 0.002) after adjusting for age, gender, ejection fraction, cardiac resynchronization therapy, post-ablation non-inducibility, and post-ablation amiodarone use. Arrhythmia exacerbation after ablation of infarct-related VT is infrequent but is independently associated with an adverse long-term outcome among patients who experience a VT recurrence. The mechanisms and mitigation strategies of AE after catheter ablation require further investigation.

Ablation of Reentry-Vulnerable Zones Determined by Left Ventricular Activation From Multiple Directions: A Novel Approach for Ventricular Tachycardia Ablation: A Multicenter Study (PHYSIO-VT).

The optimal method to identify the arrhythmogenic substrate of scar-related ventricular tachycardia (VT) is unknown. Sites of activation slowing during sinus rhythm (SR) often colocalize with the VT circuit. However, the utility and limitations of such approach for guiding ablation are unknown. We conducted a multicenter study in patients with infarct-related VT. The left ventricular (LV) was mapped during activation from 3 directions: SR (or atrial pacing), right ventricular, and LV pacing at 600 ms. Ablation was applied selectively to the cumulative area of slow activation, defined as the sum of all regions with activation times of ≥40 ms per 10 mm. Hemodynamically tolerated VTs were mapped with activation or entrainment. The primary outcome was a composite of appropriate implanted cardioverter-defibrillator therapies and cardiovascular death. In 85 patients, the LV was mapped during activation from 2.4±0.6 directions. The direction of LV activation influenced the location and magnitude of activation slowing. The spatial overlap of activation slowing between SR and right ventricular pacing was 84.2±7.1%, between SR and LV pacing was 61.4±8.8%, and between right ventricular and LV pacing was 71.3±9.6% (P<0.05 between all comparisons). Mapping during SR identified only 66.2±8.2% of the entire area of activation slowing and 58% critical isthmus sites. Activation from other directions by right ventricular and LV stimulation unmasked an additional 33% of slowly conducting zones and 25% critical isthmus sites. The area of maximal activation slowing often corresponded to the site where the wavefront first interacted with the infarct. During a follow-up period of 3.6 years, the primary end point occurred in 14 out of 85 (16.5%) patients. The spatial distribution of activation slowing is dependent on the direction of LV activation with the area of maximal slowing corresponding to the site where the wavefront first interacts with the infarct. This data may have implications for VT substrate mapping strategies.

Activation During Sinus Rhythm in Ventricles With Healed Infarction: Differentiation Between Arrhythmogenic and Nonarrhythmogenic Scar.

In infarct-related ventricular tachycardia (VT), the circuit often corresponds to a location characterized by activation slowing during sinus rhythm (SR). However, the relationship between activation slowing during SR and vulnerability for reentry and correlation to components of the VT circuit are unknown. This study examined the relationship between activation slowing during SR and vulnerability for reentry and correlated these areas with components of the circuit. In a porcine model of healed infarction, the spatial distribution of endocardial activation velocity was compared between SR and VT. Isthmus sites were defined using activation and entrainment mapping as areas exhibiting diastolic activity within the circuit while bystanders were defined as areas displaying diastolic activity outside the circuit. Of 15 swine, 9 had inducible VT (5.2±3.0 per animal) while in 6 swine VT could not be induced despite stimulation from 4 RV and LV sites at 2 drive trains with 6 extra-stimuli down to refractoriness. Infarcts with VT had a greater magnitude of activation slowing during SR. A minimal endocardial activation velocity cutoff ≤0.1 m/s differentiated inducible from noninducible infarctions (P=0.015). Regions of maximal endocardial slowing during SR corresponded to the VT isthmus (area under curve=0.84 95% CI, 0.78-0.90) while bystander sites exhibited near-normal activation during SR. VT circuits were complex with 41.7% exhibiting discontinuous propagation with intramural bridges of slow conduction and delayed quasi-simultaneous endocardial activation. Regions forming the VT isthmus borders had faster activation during SR while regions forming the inner isthmus were activated faster during VT. Endocardial activation slowing during SR may differentiate infarctions vulnerable for VT from those less vulnerable for VT. Sites of slow activation during SR correspond to sites forming the VT isthmus but not to bystander sites.

Modulating the Baseline Impedance: An Adjunctive Technique for Maximizing Radiofrequency Lesion Dimensions in Deep and Intramural Ventricular Substrate: An Adjunctive Technique for Maximizing Radiofrequency Lesion Dimensions in Deep and Intramural Ventricular Substrate.

Background Radiofrequency ablation of intramural ventricular substrate is often limited by insufficient tissue penetration despite high energy settings. As lesion dimensions have a direct and negative relationship to impedance, reducing the baseline impedance may increase the ablation effect on deep ventricular tissue. Methods This study included 16 patients with ventricular tachycardia or frequent ventricular premature complexes refractory to ablation with irrigated catheters. After a failed response to radiofrequency ablation, impedance was modulated by adding or repositioning return patches in an attempt to decrease the circuit impedance. Ablation was repeated at a similar location and power settings, and the effect on arrhythmia suppression and adverse effects were evaluated. Results Six patients with idiopathic ventricular premature complexes originating from the left ventricular summit (n=4) or papillary muscles (n=2), 6 patients with noninfarct related ventricular tachycardia and 4 patients with infarct-related ventricular tachycardia had unsuccessful response to radiofrequency ablation at critical sites (number of applications: 10.4±3.1, power: 42.3±2.9 W, duration: 55.3±25.5 seconds, impedance reduction: 14.6±3.5 Ω, low-ionic solution was used in 81.25%). Modulating the return patches resulted in reduced baseline impedance (111.7±8.2 versus 134.7±6.6 Ω, P<0.0001), increased current output (0.6±0.02 versus 0.56±0.02 Amp; P<0.0001) and greater impedance drop (16.8±3.0 Ω, P<0.001). Repeat ablation at similar locations had a successful effect in 12 out of 16 (75.0%) patients. During a follow-up duration of 13±5 months, 10 out of 12 (83.3%) patients remained free of arrhythmia recurrence. The frequency of steam pops was similar between the higher and lower baseline impedance settings (7.1 versus 8.2%; P=0.74). Conclusions In patients with deep ventricular substrate, reducing the baseline impedance is a simple, safe, and effective technique for increasing the effect of radiofrequency ablation. However, its combination with low-ionic solutions may increase the risk for steam pops and neurological events.

Personalized Cardiac Computational Models: From Clinical Data to Simulation of Infarct-Related Ventricular Tachycardia.

In the chronic stage of myocardial infarction, a significant number of patients develop life-threatening ventricular tachycardias (VT) due to the arrhythmogenic nature of the remodeled myocardium. Radiofrequency ablation (RFA) is a common procedure to isolate reentry pathways across the infarct scar that are responsible for VT. Unfortunately, this strategy show relatively low success rates; up to 50% of patients experience recurrent VT after the procedure. In the last decade, intensive research in the field of computational cardiac electrophysiology (EP) has demonstrated the ability of three-dimensional (3D) cardiac computational models to perform in-silico EP studies. However, the personalization and modeling of certain key components remain challenging, particularly in the case of the infarct border zone (BZ). In this study, we used a clinical dataset from a patient with a history of infarct-related VT to build an image-based 3D ventricular model aimed at computational simulation of cardiac EP, including detailed patient-specific cardiac anatomy and infarct scar geometry. We modeled the BZ in eight different ways by combining the presence or absence of electrical remodeling with four different levels of image-based patchy fibrosis (0, 10, 20, and 30%). A 3D torso model was also constructed to compute the ECG. Patient-specific sinus activation patterns were simulated and validated against the patient's ECG. Subsequently, the pacing protocol used to induce reentrant VTs in the EP laboratory was reproduced in-silico. The clinical VT was induced with different versions of the model and from different pacing points, thus identifying the slow conducting channel responsible for such VT. Finally, the real patient's ECG recorded during VT episodes was used to validate our simulation results and to assess different strategies to model the BZ. Our study showed that reduced conduction velocities and heterogeneity in action potential duration in the BZ are the main factors in promoting reentrant activity. Either electrical remodeling or fibrosis in a degree of at least 30% in the BZ were required to initiate VT. Moreover, this proof-of-concept study confirms the feasibility of developing 3D computational models for cardiac EP able to reproduce cardiac activation in sinus rhythm and during VT, using exclusively non-invasive clinical data.

Virtual heart guides cardiac ablation.

A computational model of the heart that finds the optimal ablation sites to treat infarct-related ventricular tachycardia eliminates the need for invasive electrical mapping.

Personalized virtual-heart technology for guiding the ablation of infarct-related ventricular tachycardia.

Ventricular tachycardia (VT), which can lead to sudden cardiac death, occurs frequently in patients with myocardial infarction. Catheter-based radiofrequency ablation of cardiac tissue has achieved only modest efficacy, owing to the inaccurate identification of ablation targets by current electrical mapping techniques, which can lead to extensive lesions and to a prolonged, poorly tolerated procedure. Here we show that personalized virtual-heart technology based on cardiac imaging and computational modelling can identify optimal infarct-related VT ablation targets in retrospective animal (5 swine) and human studies (21 patients) and in a prospective feasibility study (5 patients). We first assessed in retrospective studies (one of which included a proportion of clinical images with artifacts) the capability of the technology to determine the minimum-size ablation targets for eradicating all VTs. In the prospective study, VT sites predicted by the technology were targeted directly, without relying on prior electrical mapping. The approach could improve infarct-related VT ablation guidance, where accurate identification of patient-specific optimal targets could be achieved on a personalized virtual heart prior to the clinical procedure.

Role of 3-Dimensional Architecture of Scar and Surviving Tissue in Ventricular Tachycardia: Insights From High-Resolution Ex Vivo Porcine Models.

An improved knowledge of the spatial organization of infarct structure and its contribution to ventricular tachycardia (VT) is important for designing optimal treatments. This study explores the relationship between the 3-dimensional structure of the healed infarct and the VT reentrant pathways in high-resolution models of infarcted porcine hearts. Structurally detailed models of infarcted ventricles were reconstructed from ex vivo late gadolinium enhancement and diffusion tensor magnetic resonance imaging data of 8 chronically infarcted porcine hearts at submillimeter resolution (0.25×0.25×0.5 mm3). To characterize the 3-dimensional structure of surviving tissue in the zone of infarct, a novel scar-mapped thickness metric was introduced. Further, using the ventricular models, electrophysiological simulations were conducted to determine and analyze the 3-dimensional VT pathways that were established in each of the complex infarct morphologies. The scar-mapped thickness metric revealed the heterogeneous organization of infarct and enabled us to systematically characterize the distribution of surviving tissue thickness in 8 hearts. Simulation results demonstrated the involvement of a subendocardial tissue layer of varying thickness in the majority of VT pathways. Importantly, they revealed that VT pathways are most frequently established within thin surviving tissue structures of thickness ≤2.2 mm (90th percentile) surrounding the scar. The combination of high-resolution imaging data and ventricular simulations revealed the 3-dimensional distribution of surviving tissue surrounding the scar and demonstrated its involvement in VT pathways. The new knowledge obtained in this study contributes toward a better understanding of infarct-related VT.

Thromboembolic prophylaxis protocol with warfarin after radiofrequency catheter ablation of infarct-related ventricular tachycardia.

Ablation in the left ventricle (LV) is associated with a risk of thromboembolism. There are limited data on the use of specific thromboembolic prophylaxis strategies postablation. We aimed to evaluate a thromboembolic prophylaxis protocol after ventricular tachycardia (VT) ablation. The index procedures of 217 patients undergoing ablation for infarct-related VT with open irrigated-tip catheters were included. Patients with large LV endocardial ablation area (>3cm between ablation lesions) were started on low-dose, slowly escalating unfractionated heparin (UFH) infusion 8hours after access hemostasis, followed by 3months of anticoagulation. Patients with less extensive ablation were treated only with antiplatelet agents postablation. Postablation bridging anticoagulation was used in 181 (83%) patients. Of them, 11 (6%) patients experienced bleeding events (1 required endovascular intervention) and 1 (0.6%) experienced lower extremity arterial embolism requiring vascular surgery. Systemic anticoagulation was prescribed in 190 (89%) of 214 patients discharged from the hospital (warfarin in 98%), while the rest received single- or dual-antiplatelet therapy alone. Patients treated with an anticoagulant had significantly longer radiofrequency time compared to patients treated with antiplatelet agents only. One (0.5%) of the patients treated with oral anticoagulation experienced major bleeding 2 weeks postablation. No thromboembolic events were documented in either the anticoagulation or the "antiplatelet only" group postdischarge. A slowly escalating bridging regimen of UFH, followed by 3months of oral anticoagulation, is associated with low thromboembolic and bleeding risks after infarct-related VT ablation. In the absence of extensive ablation, antiplatelet therapy alone is reasonable.

Prognostic Impact of the Timing of Recurrence of Infarct-Related Ventricular Tachycardia After Catheter Ablation.

Recurrence of ventricular tachycardia (VT) after ablation in patients with previous myocardial infarction is associated with adverse prognosis. However, the impact of the timing of VT recurrence on outcomes is unclear. We analyzed data from a multicenter collaborative database of patients who underwent catheter ablation for infarct-related VT. Multivariable Cox regression analyses investigated the effect of the timing of VT recurrence on the composite outcome of death or heart transplantation using VT recurrence as a time-varying covariate. A total of 1412 patients were included (92% men; age: 66.7±10.7 years), and 605 patients (42.8%) had a recurrence after median 116 days (188 [31.1%] within 1 month, 239 [39.5%] between 1 and 12 months, and 178 [29.4%] after 12 months). At median follow-up of 670 days, 375 patients (26.6%) experienced death or heart transplantation. The median time from recurrence to death or heart transplantation was 65 and 198.5 days in patients with recurrence ≤30 days and >30 days post ablation, respectively. The adjusted hazard ratio (95% confidence interval) for the effect of VT recurrence occurring immediately post ablation on death or heart transplantation was 3.45 (2.33-5.11) in reference to no recurrence. However, the magnitude of this effect decreased statistically significantly (P<0.001) as recurrence occurred later in the follow-up period. The respective risk estimates for VT recurrence at 30 days, 6 months, 1 year, and 2 years were 3.36 (2.29-4.93), 2.94 (2.09-4.14), 2.50 (1.85-3.37), and 1.81 (1.37-2.40). VT recurrence post ablation is associated with a mortality risk that is highest soon after the ablation and decreases gradually thereafter.