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Funding Acknowledgements Type of funding sources: Other. Main funding source(s): The department of cardiology from Leiden University Medical Center receives unrestricted grants from Edwards Lifesciences, Biotronik, Medtronik, Boston Scientific and BioSense Webster. MS was supported by the Research Fellowship of the European Society of Cardiology 2017/2018. Background The current golden standard to accurately delineate scar potentially related to ventricular tachycardia relies on electroanatomical voltage mapping. Endocardial unipolar voltage (UV) mapping is increasingly used to detect intramural or subepicardial non-ischemic scars. 3D mapping systems determine and display the largest peak-to-peak amplitude of the electrogram within the window-of interest usually set from the QRS onset, but cannot not identify far-field electrograms or artifacts. Purpose To evaluate the influence of manual adjustment of the window-of-interest on the amplitude of endocardial and epicardial right ventricular (RV) unipolar electrograms. Methods Patients who underwent ablation of a RV scar-related VT with combined endo- and epicardial RV mapping were included. Endo- and epicardial points were reviewed with special interest towards the unipolar signal. In case a far-field, ST-segment elevation/depression or artifact was present, the window-of-interest was adjusted and the corresponding unipolar amplitude was collected. Results Thirty-three patients were included (age 50 ± 14years and 79% male). The underlying aetiology was definite arrhythmogenic right ventricular cardiomyopathy (ARVC; n = 17), athlete’s right ventricular outflow tract scar in (n = 9), cardiac sarcoidosis in (n = 3), scar of unknown origin (n = 2), borderline ARVC (n = 1) or myocarditis (n = 1). In total, 4225 endocardial points and 1960 epicardial points were re-analyzed. In 2987 (71%) endocardial points and 689 (65%) epicardial points the window-of-interest needed to be adjusted. Reason for this adjustment was ‘inclusion of far-field’ in 1380 (33%) endocardial- and 700 (36%) epicardial points; ‘inclusion of ST-segment elevation/depression’ in 1246 (29%) endocardial- and 316 (16%) epicardial points; RV-pacing artefact in 266 (6%) endocardial- and 116 (6%) epicardial points; and miscellaneous (e.g. unstable baseline or ablation point with artifact) in 95 (2%) endocardial- and 139 (7%) epicardial points (Figure). The median difference between the ‘automatically generated’ UV and the ‘adjusted’ UV was 0.81mV (IQR: 0.40-1.39) for the endocardial points and 0.54mV (IQR: 0.27-0.98) for the epicardial points. In 320 (8%) endocardial points the UV was changed from >5.5mV to 4.4 to 3.8mV to Conclusion In the majority of endocardial and epicardial points the window-of-interest for unipolar voltage mapping needs to be adjusted to exclude far-field signal or ST-segment elevation/depression contributing to the automatically determined amplitude. Unadjusted unipolar voltage mapping underestimates low UV regions. RV-pacing generates a large unipolar far-field signal, which can obscure the local unipolar near-field signal. Accordingly, RV UV mapping during RV pacing should be used with caution. Abstract Figure. The pitfalls of UV mapping of the RV

Funding Acknowledgements Type of funding sources: None. Background Patients with dilated cardiomyopathy (DCM) and ventricular tachyarrhythmias (VT) are at risk for heart failure (HF) death. Global left ventricular endocardial voltage may reflect the amount of excitable viable myocardium and identify patients at risk for rapid progression to end-stage HF. Aim To determine if volume-weighted endocardial voltage, as a surrogate for the total excitable viable myocardium, predicts mortality in patients with DCM and VT. Methods Consecutive patients with DCM, who underwent high-density endocardial voltage mapping for VT or PVC ablation (2012-2018), were included. Mapping data were transferred from CARTO to ParaView after excluding valve areas. The volume-weighted UV and BV (vwUV, vwBW) were calculated by mathematically integrating the UV and BV over the whole LV (thereby correcting for mapping density heterogeneity) divided by the endocardial LV surface area and corrected for LV wall thickness determined by echocardiography. The prognostic values of vwUV and vwBV for cardiac function and cardiac death were evaluated. Results One hundred three patients (VT, n = 83 and PVC, n = 20; age, 57 ± 14yrs; LVEF, 39 ± 13%; [likely] pathogenic genetic variants 33 [32%]; amiodarone use 36 [35%]) were included. VwUV and vwBV were 9.94 ± 3.42 and 4.70 ± 1.46. During a median follow-up of 24 months, cardiac mortality was 18% (end-stage HF 16/19, the median time to death 5.7 months). Patients who died had a significantly lower vwUV and vwBV (vwUV 5.62 ± 0.93 vs. 10.91 ± 3.10, P 5% and transition to HFrEF) occurred in 22% and was strongly related with a low vwUV (6.65 ± 1.15 vs. 10.08 ± 2.92, P = 0.02, Figure B left). Furthermore, in patients with HFrEF, a significant LVEF improvement (defined as an EF increase >5% and transition to HFmrEF) was noted in 32% and was correlated with a high vwUV (11.68 ± 2.70 vs. 8.62 ± 2.69, P = 0.002, Figure B right). Conclusion VwUV is a newly proposed surrogate for the amount of LV viable myocardium, available from routine endocardial mapping and an excellent parameter to identify patients with DCM at high risk for rapid progression to HF-related death. Abstract Figure. vwUV and outcomes

Background In patients with non-ischemic cardiomyopathy (NICM), non-inducibility after catheter ablation has been associated with lower VT recurrence rates. We hypothesized that induced VT pleomorphism (PL-VT) may be indicative for a complex VT substrate that might be associated with poor ablation outcome independently of non-inducibility at the end of the procedure. Methods Consecutive patients with left-dominant NICM undergoing VT ablation (2008–2018) were included. All patients underwent genetic screening. PL-VT was defined as occurrence of ≥1 morphologically distinct QRS lasting for ≥6 consecutive beats during the same induced VT episode. Complete acute success was defined as non-inducibility of any VT at the end of procedure. Results Eighty-five patients (56±15 yrs, LVEF 38±12%), inducible for 365 VTs (median 3/patient, IQR 1–6) were included. PL-VT was observed in 29 patients (34%). Patients with PL-VT had more often anteroseptal substrates, a higher number of induced VTs, and larger endocardial bipolar ( Figure 1 Conclusions Induced PL-VT was not associated with acute outcome but higher VT recurrence rate after catheter ablation in patients with NICM. Moreover, co-existence of PL-VT and persistent VT inducibility identifies patients at highest risk for VT recurrence whereas non-inducible patients without PL-VT have a favorable prognosis.

Veltmann C, Schimpf R, Steitner F, Hu D, Pfeiffer R, Borggrefe M, Wolpert C, Antzelevitch C. Electrocardiographic identification of SCN5A mutation carriers in a large European family. Europace Journal 2009, 11(Supplement 2), Abstract 34.Wijnmaalen AP, Van Der Geest RJ, Siebelink HJ, Kroft L, Bax JJ, Reiber JH, Schalij MJ, Zeppenfeld K. Integration of MRI derived 3D scar maps with electroanatomical mapping during catheter ablation of scar-related ventricular tachycardia late after myocardial infarction. Europace Journal 2009, 11(Supplement 2), Abstract 35.Algalarrondo VA, Dinanian SD, Juin CJ, Adams DA, Slama MS. Paroxystic AV block and prophylactic pacing in familial amyloid polyneuropathy. Europace Journal 2009, 11(Supplement 2), Abstract 36.# Electrocardiographic identification of SCN5A mutation carriers in a large European family {#article-title-2} Veltmann C, Schimpf R, Steitner F, Hu D, Pfeiffer R, Borggrefe M, Wolpert C, Antzelevitch C. Electrocardiographic identification of SCN5A mutation carriers in a large European family. Europace Journal 2009, 11(Supplement 2), Abstract 34.Wijnmaalen AP, Van Der Geest RJ, Siebelink HJ, Kroft L, Bax JJ, Reiber JH, Schalij MJ, Zeppenfeld K. Integration of MRI derived 3D scar maps with electroanatomical mapping during catheter ablation of scar-related ventricular tachycardia late after myocardial infarction. Europace Journal 2009, 11(Supplement 2), Abstract 35.Algalarrondo VA, Dinanian SD, Juin CJ, Adams DA, Slama MS. Paroxystic AV block and prophylactic pacing in familial amyloid polyneuropathy. Europace Journal 2009, 11(Supplement 2), Abstract 36.The loss-of-function SCN5A missense mutation E1784K leads to the Brugada and/or Long QT phenotype and to cardiac conduction disease. The aim of the present study was to perform a genotype-phenotype correlation in a large family with the E1784K mutation and to identify electrocardiographic markers capable of differentiating between mutation carriers and non-carriers. Methods: We screened a large 33-member European family. The work-up included the medical and family history (n=33), a baseline ECG (n=27), sodium blocker challenge (n=23) and genetic screening (n=27). Results: 27 members (28±15 years of age; 16 males, 11 females) were genotyped. In 17 of 27 patients (8 males, 9 females) a E1784K missense mutation was identified in SCN5A. Mutation carriers revealed significantly longer PR and QT intervals and QRS duration compared to non-carriers. (PQ: 195ms vs. 155ms, P 70ms or between 60ms and 70ms with ECG abnormalities) or in case of unexplained syncope. By using pacing systems wich preserve physiological AV conduction, our purpose was to estimate prevalence of AV block and pacing dependance for high risk FAP patients. Methods: In a cohort of 29 FAP patients with conduction disorders leading to prophylactic pacing, we studied AV conduction using the "AAI Safe R" system (ELA medical). Datas were collected by using the Holter memories of pacemakers. Results: Patients were 50±15 years old and were followed during 13.7±11.9 months after pace maker insertion (12080 days cumulated). Before pace maker insertion, ECG was normal in 23% of cases. Electrophysiologic study showed 118±12ms for AH interval and 62±6ms for HV interval. Average percentage of ventricular pacing was 15±25%and 31±34% for atrial pacing. If 58% of patients (17/29) had less than 5% needs of ventricular pacing, we noted AV blocks episods for all patients but three (90%). Frequency of AV conduction disorders was 356±514 events per month (epm) and was distributed in 17±56 epm for type III AV block, 288±483 epm for type II AV block, 39±61epm for type I AV block and 1±4 for pauses. Percentage of ventricular pacing was positively correlated to frequency of AV block (R = 0.9, P70ms, HV interval between 60ms and 70ms with ECG abnormalities or in case of unexplained syncope), prophylactic pacemaker insertion should be performed. Pacemaker features designed to promote spontaneous atrioventricular conduction allow a good AV conduction monitoring in FAP patients. Pre operative impairment of the nodal conduction is correlated to the rate of ventricular pacing with this stimulation mode.