Body Surface Mapping Research Articles

Body surface mapping of P-waves in sinus rhythm to predict recurrence following cardioversion for atrial fibrillation.

Direct current cardioversion (DCCV) is used as elective and emergency rhythm control for atrial fibrillation (AF). We aimed to explore the role of P-wave parameters measured during sinus rhythm using body surface mapping (BSM) in predicting successful DCCV for persistent atrial fibrillation (persAF) at 12 months. This case-control study included 56 males >18 years old who underwent DCCV for persAF. P-wave parameter collection after DCCV for AF was done using 128 unipolar leads. A band-pass filter of 1-50 Hz was utilised. Corrected P-wave duration (PWDc), P-wave amplitude, and P-wave dispersion were measured to predict 12-month outcomes and time of recurrence. The mean age was 64 ± 4 years, and 23 patients (44%) were on amiodarone. The 12-month success rate was 44% (n = 23), while the rest reverted to AF after 2.6 ± 0.4 months. The parameters were comparable between successful and failed DCCV in the entire cohort and patients not on amiodarone. In patients on amiodarone, patients with failed arms had higher PWDc than those with successful arms (188 vs. 150 ms, P = 0.04). Receiver operator characteristic curve analysis for PWDc in the amiodarone cohort showed an area under the curve (AUC) of 0.75 and P = 0.049. A recurrence cut-off >161 ms had a sensitivity of 69% and a specificity of 100%, with a hazard ratio of 10.7, P = 0.004. The parameters were not predictive of the time of recurrence. In patients on amiodarone, increased PWDc measured using BSM was associated with higher AF recurrence at 12 months following DCCV for persAF.

Comparison of the clinical efficacy of body surface mapping plus wire-guided localization and body surface mapping plus methylene blue-guided localization in occult breast lesions

Comparison of the clinical efficacy of body surface mapping plus wire-guided localization and body surface mapping plus methylene blue-guided localization in occult breast lesions

Significance of left posterior extension of early repolarization in patients with J-wave syndrome

J waves in the inferior or lateral leads are characteristic electrocardiographic (ECG) changes in patients with early repolarizationsyndrome (ERS). However, the presence of J waves in the left posterior region has not yet been evaluated. The purpose of this study was to clarify the significance of J waves in the posterior left ventricle using leads V7-V9 and a body surface mapping (BSM) system. Forty patients diagnosed with ERS were included. All patients exhibited J waves in either the contiguous inferior, lateral, or posterior leads. We evaluated the incidence of J waves in the inferolateral and posterior leads using a 15-lead ECG with synthesized V7-V9 and an 87-lead BSM. Additionally, we assessed the arrhythmogenicity of the posterior regions based on the morphology ofthe premature ventricular complexes (PVCs) associated with ventricularfibrillation (VF). J waves were observed in the lateral, inferior, and posterior leads of 26 (65%), 31 (78%), and 39 (97%) patients, respectively. J waves were found only in the posterior leads of 5 patients. BSM was evaluated in 9 patients, all of whom exhibited a positive area on the posterior region. PVCs associated with VF were recorded in 5 patients. Among patients with inferolateral and posterior J waves, all except 1 patient who displayed left bundle branch block morphology showed PVCs originating from the posterior left ventricular region. Posterior J waves are common in ERS patients. This abnormality can be detected using leads V7-V9 and the BSM system and may be associated with arrhythmogenesis.

Significant Delayed Activation on the Right Ventricular Outflow Tract Represents Complete Right Bundle-Branch Block Pattern in Brugada Syndrome.

Background The appearance of complete right bundle-branch block (CRBBB) in Brugada syndrome (BrS) is associated with an increased risk of ventricular fibrillation. The pathophysiological mechanism of CRBBB in patients with BrS has not been well established. We aimed to clarify the significance of a conduction delay zone associated with arrhythmias on CRBBB using body surface mapping in patients with BrS. Methods and Results Body surface mapping was recorded in 11 patients with BrS and 8 control patients both with CRBBB. CRBBB in control patients was transiently exhibited by unintentional catheter manipulation (proximal RBBB). Ventricular activation time maps were constructed for both of the groups. We divided the anterior chest into 4 areas (inferolateral right ventricle [RV], RV outflow tract [RVOT], intraventricular septum, and left ventricle) and compared activation patterns between the 2 groups. Excitation propagated to the RV from the left ventricle through the intraventricular septum with activation delay in the entire RV in the control group (proximal RBBB pattern). In 7 patients with BrS, excitation propagated from the inferolateral RV to the RVOT with significant regional activation delay. The remaining 4 patients with BrS showed a proximal RBBB pattern with the RVOT activation delay. The ventricular activation time in the inferolateral RV was significantly shorter in patients with BrS without a proximal RBBB pattern than in control patients. Conclusions The CRBBB morphology in patients with BrS consisted of 2 mechanisms: (1) significantly delayed conduction in the RVOT and (2) proximal RBBB with RVOT conduction delay. Significant RVOT conduction delay without proximal RBBB resulted in CRBBB morphology in patients with BrS.

Body surface mapping to detect STT-wave changes during invasive coronary function testing

Drugs belonging to diverse therapeutic classes can prolong myocardial refractoriness or slow conduction. These drugs may be effective and well-tolerated, but the risk of sudden cardiac death from torsades de pointes (TdP) remains a major concern. The corrected QT interval has significant limitations when used for risk stratification. Measurement of global electrical heterogeneity (GEH) could help identify the substrate vulnerable to drug-induced ventricular arrhythmias.The purpose of this study was to improve risk stratification for drug-induced TdP by measuring GEH on the electrocardiogram (ECG).We analyzed ECG data from a case-control study of patients with a history of drug-induced TdP as well as age- and sex-matched controls. Vectorcardiograms were constructed from ECGs. GEH was measured via the spatial ventricular gradient (SVG) vector (magnitude, azimuth, and elevation). Log odds coefficients for TdP were estimated using multivariable logistic regression.Among 17 cases (47% male; age 58.9 ± 12.5 years) and 17 controls (29% male; age 61.0 ± 12.2 years), 34 ECGs were analyzed. SVG azimuth was significantly different between cases and controls (3.4 vs 22.0 degrees, respectively; P = 0.02). After adjusting for sex and QTc interval, odds of TdP increased by a factor of 3.2 for each 1 SD change in SVG azimuth from the control group mean (95% confidence interval 1.07–9.14; P = .04). QTc was not significant in the multivariable analysis (P = .20).SVG azimuth is correlated with a history of drug-induced TdP independent of QTc. GEH measurement may help identify patients at high risk for drug-induced arrhythmias.

Epicardial conduction abnormalities in patients with Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) and mutation positive healthy family members - A study using electrocardiographic imaging.

The diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC) in early stages is challenging. The aim of this study was therefore to investigate whether electrocardiographic imaging (ECGI) can detect epicardial conduction changes in ARVC patients and healthy mutation-carriers (M-carriers). Twelve ARVC patients, 20 M-carriers and 8 controls underwent 12-lead ECG, signal-averaged ECG, 2-dimensional echocardiography, 24-hours Holter monitoring and ECGI (body surface mapping and computer tomography with offline analysis of reconstructed epicardial signals). Total and Right Ventricular Activation Time (tVAT and RVAT respectively), area of Ventricular Activation during the terminal 20 milliseconds (aVAte20) and the activation patterns were compared between groups. In ARVC patients the locations of aVAte20 were scattered or limited to smaller parts of the right ventricle (RV) versus in controls, in whom aVAte20 was confined to right ventricular outflow tract (RVOT) and left ventricle (LV) base (+/- RV base). ARVC patients had smaller aVAte20 (35cm2 vs 87cm2, p<0.05), longer tVAT (99msec vs 58msec, p<0.05) and longer RVAT (66msec vs 43msec, p<0.05) versus controls. In 10 M-carriers (50%), the locations of aVAte20 were also eccentric. This sub-group presented smaller aVAte20 (53cm2 vs 87cm2, p = 0.009), longer RVAT (55msec vs 48msec, p = 0.043), but similar tVAT (65msec vs 60msec, p = 0.529) compared with the M-carriers with normal activation pattern. ECGI can detect epicardial conduction abnormalities in ARVC patients. Moreover, the observation of localized delayed RV epicardial conduction in M-carriers suggests an early stage of ARVC and may be a useful diagnostic marker enhancing an early detection of the disease.

Deep Learning-Driven Real-Time Liver Tumor Localization via Optical Surface Imaging and Biomechanical Modeling

<h3>Purpose/Objective(s)</h3> To track liver tumors in real time via a deep learning-based framework, by exploring patient-specific correlations between patients' body surface maps and internal anatomical motion. <h3>Materials/Methods</h3> Real-time liver tumor localization was achieved via deformable registration-based motion estimation, in a two-step framework: (a) liver boundary motion estimation via deep features learnt from optical body surface imaging; and (b) intra-liver motion propagation via deep learning-based biomechanical modeling from liver boundary motion. In step (a), a patient-specific, fully-connected convolutional neural network (SurfCNN) predicts the motion of nodes residing on the boundary of a patient-specific reference liver mesh, by extracting saliency features from curvature entropy maps derived out of real-time optical body surface images. Subsequently, step (b) uses the liver boundary motion solved in (a) to infer intra-liver tumor motion, using a U-Net-style model (UNet-Bio) inspired by biomechanical modeling via finite element analysis (FEA). The cascaded framework was evaluated using a dataset of 8 liver cancer patients from our institute. Each patient had a 10-phase, contrast-enhanced 4D-CT set with liver and liver tumor contoured. To generate sufficient motion variations to train and test the patient-specific SurfCNN model, we augmented the dataset of each patient by simulating varying real-time motion patterns and magnitudes. The augmentation was achieved via a principal component analysis-based statistical model, expanding the nine inter-phase deformation-vector-fields (DVFs) of each 4D-CT into 1,728 different motion states including both rigid and deformable motion. Optical surface imaging was simulated from each motion state via extracted body surface maps, while corresponding liver boundary motion was derived via the augmented DVFs to supervise the training of SurfCNN. UNet-Bio, on the other hand, could be trained as a population-based model using supervisions from intra-liver DVFs solved by FEA-based biomechanical modeling. The liver tumor localization accuracy was assessed through Dice similarity coefficient (DSC), Hausdorff distance (HD), and center-of-mass-error (COME), by comparing the augmentation DVF-propagated ‘ground-truth' liver tumor volumes against ones deformed by the cascaded framework. <h3>Results</h3> Tested using 576 unseen scenarios for each patient case, the cascaded SurfCNN and UNet-Bio scheme can localize liver tumors to 0.791(mean) ± 0.141 (s.d.) in DSC, 3.6 ± 1.9 mm in HD, and 2.3 ± 1.7 mm in COME. In comparison, the prior reference image without deformable registration yielded 0.534 ± 0.277 in DSC, 8.3 ± 6.1 mm in HD and 6.8 ± 5.8 mm in COME. The whole model inference time was less than 100 milliseconds, satisfying the temporal constraints of real-time imaging. <h3>Conclusion</h3> The deep learning-based framework allows accurate 3D liver tumor tracking in real-time via non-ionizing, marker-less, and high frame-rate optical surface imaging.

Bariatric surgery reverses ventricular repolarisation heterogeneity in obesity: mechanistic insights into fat-related arrhythmic risk

Abstract Background Obesity is a growing global health problem that confers higher risks of atrial arrhythmias and sudden cardiac death. Despite this, the proarrhythmic substrate in obesity and its reversibility with weight loss has not been studied in-depth. Purpose To characterise the proarrhythmic substrate in obese patients, and its reversibility with bariatric surgery, using electrocardiographic imaging (ECGi). Methods ECGi was performed in 16 obese patients pre-bariatric surgery (PreSurg; mean age 43±12 years, 13 female) and 16 age- and sex-matched non-obese (lean) individuals (42±11 years). 12 of the 16 obese patients also underwent ECGi after bariatric surgery (PostSurg). Over 2000 atrial and ventricular epicardial electrograms were computed using high density body surface mapping (256-lead ECG) and heart-torso geometries from cardiac magnetic resonance imaging, by solving the inverse problem of electrocardiography. Local atrial and ventricular epicardial activation times (AT) were calculated as the steepest downslope of their respective activation complexes, and local ventricular repolarisation times (RT) as the steepest upslope of the T-wave. Atrial activation gradients (ATG) and ventricular repolarisation gradients (RTG) were calculated as the maximum difference within 10 mm radius divided by the corresponding distance. Results Body mass index was greater in PreSurg vs lean (46.7±5.5 vs 22.8±2.6 kg/m2, p&amp;lt;0.0001) and decreased with surgery (PostSurg 36.8±6.5 kg/m2, p&amp;lt;0.0001). Epicardial adipose tissue (EAT) was greater in PreSurg vs lean (83±56 vs 28±13 ml, p&amp;lt;0.0001) and decreased post-surgery (PostSurg 69±45 ml, p=0.0010). Total atrial AT was prolonged in PreSurg vs lean (62±15 vs 46±12 ms, p=0.0028), which persisted post-surgery (PostSurg 67±15 ms, p=0.86). Atrial ATG were also greater in PreSurg vs lean (26±11 vs 14±8 ms, p=0.0007) and did not change with weight loss (PostSurg 25±12, p=0.44). Ventricular RTG were greater in PreSurg vs lean (26±11 vs 15±7 ms/mm, p=0.0024) and decreased with weight loss (PostSurg 19±8, p=0.0009). Ventricular RTG were similar between PostSurg and lean (p=0.20). EAT from lean and PreSurg individuals correlated with atrial ATG (r=0.36, p=0.044) and ventricular RTG (r=0.54, p=0.0014). Ventricular AT were similar between lean (31±6 ms), PreSurg (34±5 ms) and PostSurg (35±9 ms); all p&amp;gt;0.05. Conclusion Steep ventricular repolarisation gradients and prolonged atrial activation contribute to the proarrhythmic substrate in obesity. Ventricular repolarisation gradients correlate with epicardial adiposity and both regress post-bariatric surgery. By contrast, atrial activation remains prolonged after weight loss. These results provide mechanistic insights into obesity-related arrhythmic risks and their reversibility with weight loss following bariatric surgery. Funding Acknowledgement Type of funding sources: Other. Main funding source(s): British Heart FoundationNational Institute for Health Research (NIHR) Imperial Biomedical Research Centre (BRC).

Dynamic electrophysiological mechanism in patients with long-standing persistent atrial fibrillation.

BackgroundImproved understanding of the mechanisms that sustain persistent and long-standing persistent atrial fibrillation (LSpAF) is essential for providing better ablation solutions. The findings of traditional catheter-based electrophysiological studies can be impacted by the sedation required for these procedures. This is not required in non-invasive body-surface mapping (ECGI). ECGI allows for multiple mappings in the same patient at different times. This would expose potential electrophysiological changes over time, such as the location and stability of extra-pulmonary vein drivers and activation patterns in sustained AF.Materials and methodsIn this electrophysiological study, 10 open-heart surgery candidates with LSpAF, without previous ablation procedures (6 male, median age 73 years), were mapped on two occasions with a median interval of 11 days (IQR: 8–19) between mappings. Bi-atrial epicardial activation sequences were acquired using ECGI (CardioInsight™, Minneapolis, MN, United States).ResultsBi-atrial electrophysiological abnormalities were documented in all 20 mappings. Interestingly, the anatomic location of focal and rotor activities changed between the mappings in all patients [100% showed changes, 95%CI (69.2–100%), p < 0.001]. Neither AF driver type nor their number varied significantly between the mappings in any patient (median total number of focal activities 8 (IQR: 1–16) versus 6 (IQR: 2–12), p = 0.68; median total number of rotor activities 48 (IQR: 44–67) versus 55 (IQR: 44–61), p = 0.30). However, individual zones showed a high number of quantitative changes (increase/decrease) of driver activity. Most changes of focal activity were found in the left atrial appendage, the region of the left lower pulmonary vein and the right atrial appendage. Most changes in rotor activity were found also at the left lower pulmonary vein region, the upper half of the right atrium and the right atrial appendage.ConclusionThis clinical study documented that driver location and activation patterns in patients with LSpAF changes constantly. Furthermore, bi-atrial pathophysiology was demonstrated, which underscores the importance of treating both atria in LSpAF and the significant role that arrhythmogenic drivers outside the pulmonary veins seem to have in maintaining this complex arrhythmia.

Assessment of electrical dyssynchrony in cardiac resynchronization therapy: 12-lead electrocardiogram vs. 96-lead body surface map.

The standard deviation of activation time (SDAT) derived from body surface maps (BSMs) has been proposed as an optimal measure of electrical dyssynchrony in patients with cardiac resynchronization therapy (CRT). The goal of this study was two-fold: (i) to compare the values of SDAT in individual CRT patients with reconstructed myocardial metrics of depolarization heterogeneity using an inverse solution algorithm and (ii) to compare SDAT calculated from 96-lead BSM with a clinically easily applicable 12-lead electrocardiogram (ECG). Cardiac resynchronization therapy patients with sinus rhythm and left bundle branch block at baseline (n = 19, 58% males, age 60 ± 11 years, New York Heart Association Classes II and III, QRS 167 ± 16) were studied using a 96-lead BSM. The activation time (AT) was automatically detected for each ECG lead, and SDAT was calculated using either 96 leads or standard 12 leads. Standard deviation of activation time was assessed in sinus rhythm and during six different pacing modes, including atrial pacing, sequential left or right ventricular, and biventricular pacing. Changes in SDAT calculated both from BSM and from 12-lead ECG corresponded to changes in reconstructed myocardial ATs. A high degree of reliability was found between SDAT values obtained from 12-lead ECG and BSM for different pacing modes, and the intraclass correlation coefficient varied between 0.78 and 0.96 (P < 0.001). Standard deviation of activation time measurement from BSM correlated with reconstructed myocardial ATs, supporting its utility in the assessment of electrical dyssynchrony in CRT. Importantly, 12-lead ECG provided similar information as BSM. Further prospective studies are necessary to verify the clinical utility of SDAT from 12-lead ECG in larger patient cohorts, including those with ischaemic cardiomyopathy.

What Body Surface Mapping Has Taught Us About Ventricular Conduction Disease Implications for Cardiac Resynchronization Therapy and His Bundle Pacing

The degree and pattern of conduction disease seem determinant when assessing potential cardiac resynchronization therapy (CRT) candidates. In the present review, the authors discuss the available noninvasive techniques that can be used to acquire ventricular activation time maps. They describe what body surface mapping has taught us about left bundle branch block, right bundle branch block, intraventricular conduction delay, and right ventricular pacing and discuss the ability of derived parameters of electrical dyssynchrony to predict long-term clinical response to CRT or His bundle pacing.

Measurement of electrical dyssynchrony in CRT patients: 12-lead ECG versus 96-lead body surface map

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Grant agency AZV, Ministry of Health of the Czech Republic Background Quantification of electrical dyssynchrony would allow optimization of lead placement and timing in patients with CRT. The standard deviation of activation times (SDAT) derived from body surface maps (BSM) was proposed as a measure of electrical dyssynchrony in CRT patients. However, SDAT derived from standard 12-lead ECG would be clinically preferred. Objective To evaluate and compare the SDAT measured from BSM and 12-lead ECG for assessment of electrical resynchronization in patients with implanted CRT. Methods CRT patients with sinus rhythm and LBBB at baseline (n=19, 58% males; age 60±11 years; NYHA class II-III; QRS 160±29) were studied using 96-lead BSM. For each ECG lead, the activation time was automatically detected and SDAT was calculated using either 96 leads or standard 12 leads. Electrical dyssynchrony was assessed during native sinus rhythm and 6 different pacing modes (see figure). Results SDAT calculated from BSM and 12-lead ECG decreased during optimal BiV pacing as compared to sinus rhythm by 26% (p=0.006) and 30% (p=0.003), respectively. The two other BiV setups showed also a decrease in SDAT values. Importantly, a high degree of reliability was found between values of SDAT obtained from12-lead ECG and 96-lead BSM for different pacing modes, the intraclass correlation coefficient was 0.8 to 0.9 (95% CI 0.7 - 0.9, p&amp;lt;0.001). Conclusion SDAT assessment is considered an important metric of electrical dyssynchrony in CRT. Our results suggest that 12-lead ECG provides similar results as BSM and thus, allows simplification of the measurement. Further prospective studies are necessary to verify the clinical utility of SDAT from 12-lead ECG.

Body Surface Mapping system - a potential diagnostic tool for unmasking delayed right ventricular epicardial activation in ARVC patients and phenotype-negative gene-carriers

Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Selanders stiftelsen Background Life-threatening ventricular arrhythmias can occur at any stages of ARVC – the detection of early manifestations of the disease may have prognostic implications. Purpose The purpose was to explore the usefulness of a 252-leads noninvasive Body Surface Mapping (BSM) system for the detection of delayed epicardial activation in ARVC patients and phenotype-negative gene-carriers (GC). Methods Twelve patients with ARVC, 20 GC and 8 genotype and phenotype negative family members served as controls (C) were included. 12-lead ECG, signal-averaged-electrocardiogram, echocardiography, 252-lead BSM recordings and thoracic CT scan were performed in all subjects. The noninvasively reconstructed epicardial signals of the right ventricle (RV) were analysed using the Activation Time Editing tool of the BSM system. Local depolarisation was defined as the steepest negative dV/dt of the local epicardial signal. The time from the start of RV epicardial signals to the earliest local depolarisation (ELD) and to the latest local depolarisation (LLD), were measured for the whole RV and separately for the anterior free wall (AW) and inferior wall (IW). The duration of the activation, defined as LLD-ELD, was calculated for AW, IW and the whole RV. Results The ELDs was similar in all study groups whereas the LLD in the IW and whole RV was significantly longer among ARVC patients compared to C. Although the activation durations in the AW and IW did not differ between the groups, the activation duration of the whole RV was significantly longer in ARVC patients. A LLD cut off of 81ms in RV and an activation duration cut off of 49msec in RV discriminated ARVC patients from C with highest sensitivity and specificity. Based on these cut-offs, 35% of GC group had longer LLD times and 70 % had longer activation duration (figure 1). Conclusions ARVC patients as well as the majority of GC demonstrated prolonged LLD and/or activation duration times in RV compared to C, suggesting that the 252-leads noninvasive BSM system may be a useful tool for early detection of delayed RV epicardial activations. Larger studies are required to confirm our results.

Abnormal patterns of noninvasively reconstructed epicardial signals and right ventricle activations in patients with Arrhythmogenic Right Ventricular Cardiomyopathy and gene-carriers

Abstract Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Selanders stiftelsen Background ARVC primarily affects the epicardium resulting in electrical abnormalities and ventricular arrhythmias that can appear before its clinical correlate with structural changes, which is often hard to evaluate non-invasively. Purpose To evaluate whether a 252-leads Body Surface Mapping (BSM) system can reveal RV activation abnormalities by non-invasively reconstructed epicardial signals of the right ventricle (RV) in ARVC patients and non-affected gene-carriers (GC). Methods Twelve ARVC patients, 20 GC and 8 genotype-negative family members serving as controls (C) underwent 12-leads ECG, signal-average ECG, echocardiography and 10 minutes recording with a non-invasive 252-leads BSM System. A thoracic CT scan was required for the construction of anatomically adapted epicardial signals. The reconstructed epicardial signals were studied using the Activation Time Editing tool of the BSM system. The morphologies of QRS complexes and T waves in predefined areas, including anterior free wall (AW), apex, RV base, RV inferior wall (IW) and RVOT, were studied. The pattern of RV activation was also studied. Results In controls the QRS morphology showed a rS pattern in most RV regions except for in the RVOT showing a rSr’ pattern and the IW where the signals had either a rS or rSr’ morphology. The T waves were positive in all areas, except for in the RV basis and in the IW, where 6 and 3 controls, respectively, had negative/isoelectric T waves. The earliest activation of the RV occurred in the anterior paraseptal region in 7/8 C, while the latest activation occurred in RVOT in 7/8 C (figure 1). ARVC patients also more commonly had a rS pattern in all regions except for in the RVOT (rSr’ pattern) and IW (rS or rSr’ pattern), but had a higher variation in the QRS morphology. Fractionated signals were seen in 7/12 cases. The epicardial T waves were negative/ isoelectric in 11/12 cases. Even though the RV activation more commonly started in the anterior paraseptal region and ended at the RVOT, 58% of ARVC patients had different areas of earliest and/or latest activation (figure 1). GC had the same distribution of QRS morphology as in C, but up to 75% of the T waves were negative or isoelectric, particularly in the RV base and IW. Fractionated signals were seen in two cases. In 60% of GC the earliest and/or latest activation location differed from those see in C. Conclusions Using the 252-leads BSM system, distinct characteristics of reconstructed epicardial signals and RV activation patterns were detected in ARVC patients, distinguishing them from C. The observation that similar changes were observed in epicardial signals and activation patterns among GC suggest that the 252-leads BSM system may be useful as a non-invasive tool evaluating genetically predisposed subjects for early manifestations of the disease.

Endocardial and epicardial ECG imaging during sinus rhythm to detect local conduction delay in arrhythmogenic cardiomyopathy

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Dutch Heart Foundation Introduction We recently optimized our ECG imaging (ECGi) method for the estimation of endo- and epicardial activation during sinus rhythm. In patients with arrhythmogenic cardiomyopathy, late gadolinium enhancement (LGE)-CMR can identify regional myocardial injury and the combination of structural and electrical information may provide valuable insight in disease progression and risk stratification. However, the effect of structural disease and local conduction delay on the ECGi estimation of ventricular activation has not been studied. Purpose Evaluate the relation between LGE-CMR and non-invasively estimated local conduction velocity (CV). Methods 8 pathogenic mutation carriers (PKP2/PLN) underwent LGE-CMR for clinical follow up and 67 lead body surface mapping. Subject specific triangulated surface heart/torso/lung meshes were created. ECGi activation sequences were used to determine local CV with the triangulation method. The LGE location was identified according to the AHA 17 segment model. Per segment, variation in CV was computed and local activation timing maps and CV maps were constructed. Results Isochronal crowding was observed in subjects in segments with LGE (figure, red boxes) and locally, conduction velocity decreased. Variation in conduction velocity per segment in subjects with extensive LGE presence (&amp;gt;9 segments) was higher 0.031±0.018 vs. 0.026±0.013 m/s/cm2 in subjects without. Conclusion Our preliminary results indicate the ability of the ECGi method to identify regions with higher variation in local CV. This increase in CV variability might be used to assess the vulnerability to cardiac arrhythmia. Analysis will be extended towards the RV and subsequently, more subjects will be included.

PO-714-02 RIGHT VENTRICULAR EPICARDIAL ACTIVATION DELAY IN ARRHYTHMOGENIC RIGHT VENTRICULAR CARDIOMYOPATHY PATIENTS AND GENE CARRIERS UNMASKED BY BODY SURFACE MAPPING SYSTEM

ARVC is afflicted by life-threatening ventricular arrhythmias even before the manifestations of right ventricular (RV) structural abnormalities. Therefore, an early diagnosis is crucial albeit still challenging. To investigate whether a 252-leads noninvasive Body Surface Mapping (BSM) system could detect epicardial conduction delays in ARVC patients and unaffected gene-carrying family members (GC). Twelve ARVC patients, 20 GC and 8 gene-negative family members serving as controls (C) underwent 12-lead ECG, signal-averaged-electrocardiogram (SAECG), echocardiography, 252-lead BSM recordings and thoracic CT scan. Reconstructed epicardial signals were analysed using the Activation Time Editing tool of the activation map. Local depolarisation was defined as the steepest negative dV/dt of the unipolar local epicardial signal. The time from the earliest start of RV epicardial activation to the earliest local depolarisation (ELD) and to the latest local depolarisation (LLD), respectively, were measured separately for the RV free wall (RFW), inferior wall (RIW) and the whole RV. The activation duration, defined as LLD-ELD, was calculated for RFW, RIW and the whole RV. The ELD was similar in all study groups whereas the LLD in the RFW and whole RV was significantly longer among ARVC patients compared to C, but similar in the RIW. Similarly, the activation durations in the RFW and whole RV were significantly longer in ARVC patients but did not differ in the RIW among the groups. A 43ms LLD cut off in the RV and 20 msec activation duration cut off in the RV discriminated ARVC patients from C with highest sensitivity and specificity. Based on these cut-offs, 40% of GC group had longer LLD times and 20 % had also longer activation duration (figure 1). ARVC patients demonstrated prolonged LLD and activation duration times in the RFW and whole RV compared to C. The finding that prolonged conductions could be demonstrated in the GC group as well suggest that the 252-leads noninvasive BSM system may be used as screening tool for the detection of early delays of the RV epicardial activation. Larger studies are required to confirm our results.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

PO-658-04 NON-INVASIVE ANATOMICAL LEAD LOCALIZATION IN CRT PATIENTS: BODY SURFACE POTENTIAL MAP VERSUS THE 12-LEAD ECG

Non-invasive, inverse ECG (iECG), estimating the cardiac activation from ECG signals, may be useful both to support CRT implant and optimization. However, most iECG strategies require a 32-250 electrode body surface map (BSM), limiting their clinical utility.

Ventricular Dyssynchrony and Pacing-induced Cardiomyopathy in Patients with Pacemakers, the Utility of Ultra-high-frequency ECG and Other Dyssynchrony Assessment Tools.

The majority of patients tolerate right ventricular pacing well; however, some patients manifest signs of heart failure after pacemaker implantation and develop pacing-induced cardiomyopathy. This is a consequence of non-physiological ventricular activation bypassing the conduction system. Ventricular dyssynchrony was identified as one of the main factors responsible for pacing-induced cardiomyopathy development. Currently, methods that would allow rapid and reliable ventricular dyssynchrony assessment, ideally during the implant procedure, are lacking. Paced QRS duration is an imperfect marker of dyssynchrony, and methods based on body surface mapping, electrocardiographic imaging or echocardiography are laborious and time-consuming, and can be difficult to use during the implantation procedure. However, the ventricular activation sequence can be readily displayed from the chest leads using an ultra-high-frequency ECG. It can be performed during the implantation procedure to visualise ventricular depolarisation and resultant ventricular dyssynchrony during pacing. This information can assist the electrophysiologist in selecting a pacing location that avoids dyssynchronous ventricular activation.

Repolarization abnormalities unmasked with a 252‐lead BSM system in patients with ARVC and healthy gene carriers

Background: Diagnosing arrhythmogenic right ventricular cardiomyopathy (ARVC) at an early stage can be challenging even after ECG recording and a combination of several imaging techniques. The purpose of this study was to explore if a body surface mapping (BSM) system with 252‐leads could identify repolarization abnormalities and thereby diagnose early stages of ARVC.Methods: ARVC patients, gene carriers without signs of ARVC and controls underwent a 12‐lead resting ECG, signal‐averaged ECG, echocardiography, 24‐hours Holter monitoring, and BSM with electrocardiographic imaging (ECGI). All 252‐leads, divided into four quadrants of the vest, were analyzed regarding concordances between T wave polarity and QRS main vector.Results: Of 40 patients included there were 12 ARVC patients, 20 gene carriers, and 8 controls. The ARVC patients had two different repolarization patterns, one with more pronounced negative T waves at the lower left panel and another with mixed changes that clearly differed from the controls, all of whom had a normal 12 lead ECGs and consistent repolarization patterns on their BSM recordings. The patterns observed in ARVC patients were also present in 5/20 (25%) gene carriers, three of whom had normal resting ECG. A novel repolarization index successfully detected all ARVC patients and 88% of gene carriers with pathologic repolarization pattern.Conclusions: The finding that abnormal repolarization patterns could be unmasked by BSM in 25% of healthy gene carriers, suggests that it may potentially be a useful tool for identifying early manifestations of ARVC. Further and larger studies are warranted to assess its diagnostic accuracy.

Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation.

AimsMapping data of human ventricular fibrillation (VF) are limited. We performed detailed mapping of the activities underlying the onset of VF and targeted ablation in patients with structural cardiac abnormalities.Methods and resultsWe evaluated 54 patients (50 ± 16 years) with VF in the setting of ischaemic (n = 15), hypertrophic (n = 8) or dilated cardiomyopathy (n = 12), or Brugada syndrome (n = 19). Ventricular fibrillation was mapped using body-surface mapping to identify driver (reentrant and focal) areas and invasive Purkinje mapping. Purkinje drivers were defined as Purkinje activities faster than the local ventricular rate. Structural substrate was delineated by electrogram criteria and by imaging. Catheter ablation was performed in 41 patients with recurrent VF. Sixty-one episodes of spontaneous (n = 10) or induced (n = 51) VF were mapped. Ventricular fibrillation was organized for the initial 5.0 ± 3.4 s, exhibiting large wavefronts with similar cycle lengths (CLs) across both ventricles (197 ± 23 vs. 196 ± 22 ms, P = 0.9). Most drivers (81%) originated from areas associated with the structural substrate. The Purkinje system was implicated as a trigger or driver in 43% of patients with cardiomyopathy. The transition to disorganized VF was associated with the acceleration of initial reentrant activities (CL shortening from 187 ± 17 to 175 ± 20 ms, P < 0.001), then spatial dissemination of drivers. Purkinje and substrate ablation resulted in the reduction of VF recurrences from a pre-procedural median of seven episodes [interquartile range (IQR) 4–16] to 0 episode (IQR 0–2) (P < 0.001) at 56 ± 30 months.ConclusionsThe onset of human VF is sustained by activities originating from Purkinje and structural substrate, before spreading throughout the ventricles to establish disorganized VF. Targeted ablation results in effective reduction of VF burden.Key questionThe initial phase of human ventricular fibrillation (VF) is critical as it involves the primary activities leading to sustained VF and arrhythmic sudden death. The origin of such activities is unknown.Key findingBody-surface mapping shows that most drivers (≈80%) during the initial VF phase originate from electrophysiologically defined structural substrates. Repetitive Purkinje activities can be elicited by programmed stimulation and are implicated as drivers in 37% of cardiomyopathy patients.Take-home messageThe onset of human VF is mostly associated with activities from the Purkinje network and structural substrate, before spreading throughout the ventricles to establish sustained VF. Targeted ablation reduces or eliminates VF recurrence.