Moderated Posters (2)51global High Density Mapping of Re-Entry Vulnerability Index Indentifies Sites of Right Ventricular Arrhythmia Initiation in Brugada Syndrome and Arvc52the Role of Adenosine-Guided Pulmonary Vein Isolation in Patients Undergoing Atrial Fibrillation Ablation:an Updated Meta-Analysis53first Evident That T-Peak and Tpeak-Tend Correlate With Right to Left and Transmural Dynamic Dispersion of Repolarization in the Intact Human Heart54ripple Mapping Ventricular Scar to Characterize Channels Supporting Re-Entrant Tachycardia as a Guide to Ablation55long Term Durability of Pulmonary Vein Isolation: Insights From a Randomised Trial of Cryoballoon Versus Radiofrequency Ablation for a Combined Approach56a Single-Centre Experience of the Convergent Procedure for the Treatment of Long-Standing Persistent Atrial Fibrillation57moderate Sedation in the Cardiac Electrophysiology Laboratory: A Retrospective Analysis to Assess Safety58use of General Anaesthesia in Catheter Ablation of Persistent Af: Improved Outcome and Cost Effectiveness:

Introduction: Initiation of reentrant ventricular tachycardia (VT) involves complex interactions between activation and repolarization gradients. Recently, an algorithm has been developed to generate a spatial map (designated the “reentry vulnerability index”-RVI) from intervals between local activation times (AT) and repolarization times (RT) at all adjacent points over a multielectrode grid. The algorithm has been shown to accurately identify the region of a macro-reentrant circuit in two animal models (1). The aim of this study was to test the feasibility of RVI mapping in the right ventricle (RV) to aid ablation strategy of RV micro-reentrant arrhythmias. Methods: Patients with Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) (n = 9), Brugada Syndrome (BrS) (n = 6) and normal heart RV outflow tract (RVOT) VT (n = 6) underwent invasive electrophysiological studies. Unipolar electrograms were recorded from a non-contact array (St Jude Medical) placed in the RVOT and geometry created with the Ensite system. Recordings were made during a programmed electrical stimulation protocol consisting of a 600ms drive train and S2 extras. ATs and RTs were computed from the unipolar electrograms from a Matlab system using the Wyatt criteria (2) and the RVI calculated as previously described (1). The distance <it>Dmin</it> between the region of lowest RVI (lowest 5% of all RVI values) and the region of earliest activation during VT (sites that activate within 5 ms and 20 mm from the point of earliest activation) was computed for each patient. Results: The figure shows representative spatial distributions of AT, RT and RVI from patients with ARVC, BrS and normal heart VT. The region of lowest RVI, which represents sites of highest susceptibility to re-entry, co-localised with the earliest activation region during VT in the 4 patients with ARVC/BrS where VT was initiated. In the ARVC patients this corresponded with the location of RV scar as seen on MRI. In the 6 patients with normal heart focal RVOT VT, regions of lowest RVI did not co-localise with VT origin. The distance between the region of lowest RVI and the region of earliest activation during VT, <it>Dmin</it>, was significantly lower in BrS and ARVC than in normal heart VT (6.6 + /-8.7 vs 28.0 + /-10.8 mm, p = 0.038). In both ARVC patients <it>Dmin</it> = 0, indicating the region of lowest RVI overlapped with the region of earliest VT activation. <f><inline-fig> <link locator="euw26901"></inline-fig></f> Discussion: An algorithm based on relative local activation and repolarization times identifies localized regions of high susceptibility to conduction block and re-entry, with lowest RVI values localising VT origin of reentrant but not focal arrhythmias. This index could potentially be used to target ablation for micro-reentrant arrhythmias which are difficult to induce or are haemodynamically unstable, without the need for arrhythmia initiation. References 1. Child N et al. Heart Rhythm. 2015; 12: 1644–1653. 2. Wyatt RFBM and Evans AK. Am J Cardiol. 1981; 47:488.