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Introduction Implantable cardio-defibrillators (ICDs) have proven benefit in treating lethal ventricular arrhythmias and preventing sudden death (SD) in hypertrophic cardiomyopathy (HCM), making risk stratification essential. We retrospectively evaluate the effectiveness of the 2014 European Society of Cardiology (ESC) risk scoring system in our cohort of HCM patients. Methods We evaluated the ESC risk scoring system which employs mathematical and statistical modelling of 7 disease variables to predict SD risk over 5 years, with a recommendation for ICD implant if SD risk ≥6%. From our cohort of HCM patients previously evaluated at our centre, we retrospectively calculated the ESC 5 year SD risk score at point of implant and measured it against ICD outcome. Decision of ICD implant, prior to the introduction of the ESC scoring system, was based on clinical history and number of conventional risk markers as defined by the American College of Cardiology and Heart Association. Results 52 out of 199 HCM patients (mean age 51 ± 13 yrs) underwent ICD implantation for primary prevention, with 8 (15%) having appropriate therapy for sustained ventricular tachycardia/fibrillation (VT/VF) over an average follow up period of 6.2 ± 4.9 yrs. There was no difference in the ESC risk scores between patients with or without device therapy (4.79% ± 1.5 vs 5.37% ± 3.3, p = 0.68) (Table 1). 5 of 8 (62%) patients with appropriate therapies for VT/VF had scores ranging from 3.08–5.05% and would not have reached the threshold for an ICD recommendation. In two an ICD would not be recommended and may be considered in the other three. Conclusion The current ESC scoring system potentially leaves many high-risk patients unprotected or with ambiguous ICD implant guidance. Lowering the current threshold may improve accuracy.

Introduction Ventricular Tachycardia (VT) is a common cause of mortality post myocardial infarction. Any mortality benefit of an implantable cardiac defibrillator (ICD) may be offset by the significant morbidity caused by VT shocks from the device. The VT circuit is dependent upon channels of surviving myocardium within the infarct substrate. As VT is often poorly tolerated, ablation of characteristic electrograms (fractionated and late potentials) associated with these channels in sinus rhythm is preferred to reduce ICD therapies, though recurrence rates remain high. Ripple Mapping (RM) displays all electrogram components from each anatomical point as a dynamic bar that protrudes from its 3D location. We have described how RM might visualize “conducting channels” (RM-CCs) of these characteristic electrograms within the infarcted substrate in a retrospective series. In this study, we used RM prospectively (CARTO3v4™) to characterize the VT substrate to guide ablation. Methods Consecutive pts referred for VT ablation following episodes of sustained VT or ICD therapies post distant MI were included. High point density bipolar LV endocardial electrograms were collected in sinus rhythm or ventricular pacing within the infarct “scar” ( Results 15 consecutive pts (median age 68yrs, LVEF 30%) were studied (6 month pre-procedural ICD therapies: median 19 ATP events (IQR=4–93) and 1 shock (IQR=0–3)). Scar ( Conclusions RM identifies conducting channels within the post-infarct scar that might support re-entrant VT and can be used to guide substrate based ablation to reduce future ICD therapies.

Introduction The cardiac neural network comprises ganglionated plexi (GP) adjacent to each pulmonary vein (PV) which can trigger AV block and PV ectopy. We hypothesised that AV block in response to GP stimulation is mediated through the right lower GP (RLGP) and could be abolished by ablation of the RLGP, whereas a local PV ectopy response could be abolished by selective local GP ablation. Methods and Results 10 patients undergoing left atrial (LA) ablation with autonomic modification were recruited. Continuous HFS was delivered endocardially at presumed GP sites using a Grass Stimulator (20 Hz, 10 ms pulse duration, 10 V). GP sites with connections to the AV node (producing AV block) were marked on LA geometry. RLGP group (N=5) had RF ablation of RLGP and 2 of 15 sites remained positive (p Conclusions Our study shows that neural inputs from LA GPs act on the AV node via the RLGP “gateway” and if AV block is used to identify GP sites for autonomic modulation, intact connections via the RLGP are required. We propose using synchronised HFS to identify and ablate GP sites initiating ectopic firing from the PV, as it only requires intact local connections to the PV. PVI acutely prevents this ectopic activity, possibly by transecting neural inputs to the veins. However, reconnection of PVs is common and RF ablation of the GP site alone may prevent ectopic firing within PVs.