Insights into the mechanism of atrial tachycardia with over two types of reentrant circuits: the important role of the convertibility of functional conduction block regions in maintaining multiple reentrant circuit pathways

Background: Multiple atrial tachycardias (ATs) in one patient usually require more complex ablation procedures. Despite the superior accuracy and understanding of conduction features provided by high-resolution mapping, Multiple ATs are still associated with high recurrence rates, and other mechanisms may play a role. Therefore, we aimed to uncover the substrates maintaining these multiple reentrant circuits and the probable mechanisms for the high occurrence of arrhythmia. Methods: Mapping via the Carto system was carried out in 8 patients with more than two types of reentrant circuits during ablation. Functional conduction block (FCB) regions were marked and further analyzed. Results: Twenty sustained ATs were mapped in the 8 patients. Five of these patients exhibited a potential FCB region that changed between different ATs. The potentials of these regions converted between double potentials (DPs), fractionated potentials (FPs) and normal potential due to the different ATs. The FCB regions were the main obstacles and the center of the reentrant circuit in 8 of 14 ATs, and in the other ATs, these regions played a role in reorganizing the conduction pathway. In the activation mapping, the FCB areas were never the target ablation site. Conclusion: The potential FCB region is common in ATs with more than two types of reentrant circuits, especially in scar-related localized reentry. The convertibility of FCB regions provide one of the critical substrates in maintaining multiple ATs. The changefulness of this substrate may be one of the important causes of the high recurrence of related ATs

Risk factors and effective ablation strategy in patients presenting with left atrial flutter with no previous ablation for atrial fibrillation

Background A typical left atrial flutter (LAFL) may occur as a proarrhythmic complication of ablation for atrial fibrillation (AF). Objective We evaluated the risk factors and the best ablation strategy for LAFL in patients with no prior AF ablation. Methods Consecutive patients undergoing first catheter ablation for AFL with no prior procedure for AF were included in this prospective analysis. Based on the ablation strategy, patients were divided into, Group 1: PVI+ Flutter ablation (ablation of re-entry circuits) and Group 2: PVI+ Non-PV trigger ablation (targeting areas of focal activity as triggers). 3-D mapping of the LA was performed during tachycardia to identify the reentrant circuit. PV isolation was performed in all patients. In group 1, ablation line was chosen to transect the area critical for the circuit (roof and mitral line). In group 2, ectopic beats arising from extra-PV foci detected by isoproterenol challenge were ablated. Off-drug success rate was assessed in all. Results A total of 92 and 90 patients were included in group 1 and 2 respectively. Baseline characteristics are provided in table 1. Pre-existent LA scar was detected in 91.3% and 90% of patients in group 1 and 2 respectively. At 2 years of follow-up, 11/92 (12%) from group 1 and 60/90 (66.7%) from group 2 remained arrhythmia-free off-drugs (p<0.001). In the multivariate analysis, PVI +flutter ablation was detected to be associated with significantly high risk of recurrence [HR: 3.92 (95% CI: 2.52–6.1, p<0.001)] Conclusion In this series of patients presenting with LAFL with no earlier AF ablations, pre-existent left atrial scar was detected in majority of cases and PVI+ non-PV trigger ablation provided significantly better success rate than PVI+ flutter ablation. Funding Acknowledgement Type of funding source: None

Modulating the Infarcted Ventricle’s Refractoriness with an Epicardial Biomaterial

Patients diagnosed with heart failure with reduced ejection fraction (HFrEF) are at increased risk of monomorphic ventricular tachycardia (VT) and ventricular fibrillation. The presence of myocardial fibrosis provides both anatomical and functional barriers that promote arrhythmias in these patients. Propagation of VT in a reentrant circuit depends on the presence of excitable myocardium and the refractoriness of the circuit. We hypothesize that myocardial refractoriness can be modulated surgically in a model of HFrEF, leading to decreased susceptibility to VT.Male Sprague-Dawley rats were infarcted via permanent left coronary artery ligation. At 3 weeks post-infarction, engineered grafts composed of human dermal fibroblasts cultured into a polyglactin-910 biomaterial were implanted onto the epicardium to cover the area of infarction. Three weeks post-graft treatment, all rats underwent a terminal electrophysiologic study to compare monophasic action potential electroanatomic maps and susceptibility to inducible monomorphic VT.HFrEF rats (n=29) demonstrated a longer (p=0.0191) ventricular effective refractory period (ERP) and a greater (p=0.0394) VT inducibility compared with sham (n=7). HFrEF rats treated with the graft (n=12) exhibited no change in capture threshold (p=0.3220), but had a longer ventricular ERP (p=0.0029) compared with HFrEF. No statistically significant change in VT incidence was found between HFrEF rats treated with the graft and untreated HFrEF rats (p=0.0834).Surgical deployment of a fibroblast-containing biomaterial in a rodent ischemic cardiomyopathy model prolonged ventricular ERP as measured by programmed electrical stimulation. This hypothesis-generating study warrants additional studies to further characterize the antiarrhythmic or proarrhythmic effects of this novel surgical therapy.

221Evaluating the ability of different substrate mapping techniques to identify scar-related ventricular tachycardia circuits using computational modelling

Funding Acknowledgements National Institute for Health Research; British Heart Foundation; and The Wellcome Trust and Engineering and Physical Sciences Research Council. Background Accurate identification of targets for catheter ablation therapy of ventricular tachycardias (VTs) in the postinfarction heart remains a significant challenge. Identification of such targets often requires VT-induction to delineate the entry/exit points of the reentrant circuit sustaining the VT. However, inducibility may not be possible due to hemodynamic instability. In this scenario, substrate ablation strategies can still be performed to uncover the arrhythmogenic substrate during sinus or paced rhythm. However, substrate mapping may fail to accurately delineate the reentrant circuit resulting in VT recurrence after the procedure. Purpose To use computer simulations to compare the ability of different electroanatomical maps constructed following typical substrate ablation strategies to identify the VT exit site. Methods An image-based computational model of the porcine post-infarction left ventricle was constructed to simulate VT and paced rhythm. Electroanatomical maps were constructed based on the following features extracted from electrograms computed on the endocardial surface: activation time (AT), bipolar electrogram amplitude, signal fractionation and the reentry vulnerability index (RVI - a metric combining activation and repolarization timings to identify tissue susceptibility to reentry). Potential ablation targets during substrate mapping were compared for: highest 5% AT gradient; lowest 5% bipolar signal amplitudes; areas with fragmented signals (more than one peak); and lowest 5% RVI. The minimum distance, d, between the manually identified VT exit site and the targets was measured. Results The RVI performed better than the other metrics at detecting the VT exit site (see Figure). The minimum distance between sites of lowest RVI and the exit site was 3.2mm compared to 13.1mm and 15.9mm in traditional AT and voltage maps, respectively. As the scar was not transmural, parameters derived from all electrograms (including those located on dense scar regions) were used to construct the electroanatomical maps. This improved the performance of the RVI significantly, making it more specific than the other metrics as can be seen in the Figure. Conclusions Among all metrics investigated here, the RVI identified the vulnerable region closest to VT exit site. This finding suggests that activation-repolarization metrics may improve the detection of pro-arrhythmic regions without having to induce VT. Moreover, the RVI may be particularly well suited for detecting vulnerable regions within non-transmural scars. Abstract Figure. VT and Substrate Mapping

Idiopathic Left Ventricular Tachycardia Originating in the Left Posterior Fascicle

Ventricular tachycardias originating from the Purkinje system are the most common type of idiopathic left ventricular tachycardia. The majority if not all of the reentrant circuit involved in this type of tachycardia is formed by the Purkinje fibres of the left bundle branch, particularly the left posterior fascicle. In general, slowly conducting Purkinje fibres (P1) form the antegrade limb, and normally conducting Purkinje fibres (P2) form the retrograde limb of the reentrant circuit of the ventricular tachycardia originating from the left posterior fascicle. Elimination of the critical Purkinje elements in the reentrant circuit is the route to successful ablation. While the reentrant circuit identified by activation mapping provides the roadmap to ablation targets, comparing the difference in the His-ventricular interval during sinus rhythm and tachycardia also helps to identify the critical site in the reentrant circuit.

P2439Reconstructing electrocardiograms from computational models of infarcted ventricles to determine the location of myocardial infarct scars based on features of the signal

Myocardial infarction can cause ventricular tachycardia as a result of reentrant electrical activation waves propagating around the infarct scar. The tachycardia can be treated by radiofrequency catheter ablation which requires the cardiologist to deliver radiofrequency, via an intracardiac catheter, to ablate a specific site within the scar, disrupting the reentrant circuit, to terminate the arrhythmia. Therefore, determining the location of the scar is an important step in the procedure. MRI and CT scans can show the region of scar but are costly and are contraindicated in many cases. Cardiologists observe ECG recordings of the patient's tachycardia, looking at the gross characteristics of the signal to determine an approximate location of the scar. However, this technique assumes a recording of the patient's tachycardia is available, and is only able to suggest a gross region of the heart. In addition, the method is based on studies which have identified characteristic features of the ECG using intracardiac mapping to determine the location of the scar, which may be unreliable. This study aims to determine features of the ECG which may be able to predict the location of an infarct scar with more accuracy and specificity than current methods allow. The use of computational models ensures that the true location of the scar is known, unlike in previous studies. Moreover, we aim to determine whether there are any characteristics of resting state ECG which may indicate the location of an infarct scar. An anatomically accurate finite element model of rabbit ventricles in a conductive bath was utilised in order to simulate electrical activation waves and generate ECG signals, by reconstructing the extracellular potentials. Scar regions comprising of non-conducting scar surrounded by tissue with altered electrophysiological properties to represent the borderzone were incorporated into the ventricular model at varying locations across the myocardium. The models were stimulated using an S1S2 protocol to produce wave block and reentry. ECGs were reconstructed and the differences between models were observed. Results suggest that differences in timing and amplitude of the R wave on the ECG could be an indication of scar location. Changes in the repolarisation phase of the ECG were also apparent, suggesting more features which could determine the location of the scar. Importantly, characteristic features of the ECG could also be determined from resting state ECG, generated from models where scar was present but no reentry occurred. Utilising computational models of rabbit ventricles with scars incorporated at a variety of locations around the myocardium, we were able to determine a set of features from the ECG which may be of use in determining the location of an infarct scar. Future validation of this study using patient data could indicate that this methodology may be of use in predicting scar location in ablation procedures. Acknowledgement/Funding YH is funded by the MRC (MR/R024995/1). JT acknowledges the financial support of the EPSRC (EP/N014391/1) and the Wellcome Trust WT105618MA.

P1005Origin, distribution and timing of the slow pathway potentials recorded inside the Kock's triangle in Avnrt patients through High-density Mapping

Background Atrial activation during typical atrioventricular nodal reentrant tachycardia (AVNRT) exhibits anatomic variability and spatially heterogeneous propagation inside the Kock's Triangle (KT). The mechanism of the reentrant circuit has not been elucidated yet. Purpose To evaluate signal characteristics and find out the origin, distribution, and timing of the slow pathway (SP) potentials recorded in the KT. Methods The 3-D KT geometry was created during both sinus rhythm (SR) and tachycardia (TR) from the basket mapping catheter IntellaMap Orion and the Rhythmia Mapping System (Boston Scientific). The KT was divided into 8 regions moving from an antero-septal to postero-septal areas and bounded by tricuspid annulus (TA) anteriorly and tendon of Todaro (TT) posteriorly. Each area was characterized in terms of distribution and timing of Jackman (JP) and Haissaguerre (HP) potentials and signal amplitude. Results 20 consecutive successful SP ablation cases of AVNRT were included (mean RA acquired points = 6000±1100, 275±63 inside the KT; mean KT area=29±3mm2; mean mapping time=12±5 minutes). During SR, the site of earliest atrial activation within the KT was anterior in 80% of patients whereas a midseptal activation occurred less frequently (20%). The mid-septal regions bounded by TA anteriorly and TT posteriorly showed higher prevalence of JP as compared to antero-/mid-septal regions across TT both in SR and TR (77.4% vs 4.8% during SR, p<0.0001; 84.1% vs 0% during TR, p<0.0001, respectively). HPs seemed to have variable distribution across KT (50% of these potentials recorded in antero- to mid-septal regions across TT for SR, 52.3% for TR). The median signal voltage was 0.44 [0.2–0.9] mV during SR and 0.5 [0.22–0.895] mV during TR. The mid-septal region was the area of lowest voltage compared to other regions (0.2 [0.1–0.7] mV vs 0.5 [0.4–1.5] mV for SR, p<0.0001; 0.2 [0.15–0.6] mV vs 0.6 [0.4–1.5] mV for TR, p<0.0001, respectively). Conclusion JPs seem to be associated with low signal-amplitude areas whereas HPs seem to have variable distribution across KT. Although not perfectly known, the typical low-high-type double potential of JP might be therefore explained by wavefront collision in the lowest area of the KT. Acknowledgement/Funding None