Abstract Background/Introduction Conduction system pacing (CSP), encompassing His bundle pacing (HBP) and left bundle branch area pacing (LBBAP), has gained prominence in treating bradycardia and heart failure in recent years. Despite its increasing utilization, data on real-world adoption of CSP are limited. Purpose The C-SING study aimed at assessing patient characteristics, implant success, procedural details, and safety of CSP when performed in routine clinical practice. Methods Periprocedural data from 27 experienced CSP centers across Italy were collected on patients undergoing CSP implantation for various indications between January 2021 and January 2024. Results The study comprised 1,317 patients (median age 78 years [interquartile range, 71-83], male 66.2%). Leading indications included atrioventricular (AV) block (40.8%), sinus node dysfunction (12.1%), atrial fibrillation with bradycardia (9.7%), AV node ablation (9.5%), and heart failure (12.5%). Pacemakers were implanted in 77.3% of patients, cardiac resynchronization devices in 21.7%, and implantable cardioverter-defibrillators in 1.0%. Stylet-driven and lumenless CSP leads were utilized in 64.7% and 35.3% of procedures, respectively. Final 12-lead ECG assessment revealed LBBAP capture in 88.7% patients, HBP in 8.4% (selective 4.2%, non-selective 4.2%), and no CSP capture in 3.0%, resulting in a 97.0% CSP lead implantation success rate. In patients with LBBAP, predominant capture types were left bundle branch pacing (19.6%), left posterior fascicular pacing (19.2%), and left septal fascicular pacing (14.8%). Comparing HBP to LBBAP, the latter showed shorter procedural time (60 minutes [45-80] vs. 70 minutes [60-95], p=0.003), but similar fluoroscopy time (6.0 minutes [3.3-10.8] vs. 6.1 minutes [4-10], p=0.735). Paced QRS duration was longer in LBBAP (118 ms [105-130]) compared to HBP (110 ms [101-122], p<0.001). LBBAP showed lower capture thresholds (0.6 V [0.5-0.9] @0.4 ms vs. 0.8 V [0.5-1.5] @1.0 ms, p<0.001) and higher R-wave sensing (10.7 mV [8-16] vs. 4.5 mV [2.4-9.9], p<0.001). The rate of periprocedural complications was higher in patients with LBBAP than HBP (7.3% vs. 1.8%, p=0.03), with the most frequent events being intraprocedural perforation into the left ventricular cavity during lead screwing (2.6%) and CSP lead dislodgment before hospital discharge (1.4%). These occurrences necessitated lead repositioning without additional complications. Conclusion CSP demonstrated feasibility as a primary pacing strategy for various indications in a real-world, multicenter setting. LBBAP, more frequently used than HBP, exhibited shorter procedural time and superior acute electrical parameters. LBBAP revealed a higher rate of minor procedural complications than HBP. Further investigations, supported by additional long-term outcome data, are essential to comprehensively assess CSP performance.

Abstract Background Transmural voltage gradient in RVOT induces ECG–phenotype in Brugada syndrome(BrS). Moreover,RVOT depolarization abnormalities have been described as contributors to BrS phenotype and arrhythmogenesis. Purpose To investigate the effect of ajmaline administration on J–elevation of RVOT unipolar signals in BrS patients. Moreover,we wanted to assess whether ajmaline–induced unipolar J–point elevation variations induced local depolarization abnormalities. Methods 21 BrS patients with spontaneous type–1 ECG pattern were enrolled. Due to the absence of BrS ECG pattern at the study, patients underwent RV endocardial mapping with the CARTO3 system, before (PRE) and after (POST) ajmaline administration. The data were exported from CARTO and converted into Matlab format using OpenEP. J–elevation for each point was calculated as the amplitude of the unipolar signal at J wave with respect to baseline. Activation time (AT) of each point was defined as the difference between local depolarization (minimum dV/dt of the unipolar signal) and surface ECG depolarization(time of the minimum signal on V2). With an automatic algorithm, corresponding PRE and POST points were selected. The difference between POST and PRE of each parameter was calculated to obtain the differential values delta–J and delta–AT. Differential values were then interpolated on the mesh of each subject to obtain 3D maps. The deltaJ map was divided into four intervals based on quartiles. We then selected a ROI ‘IN‘ on a region with the greatest deltaJ variation, and a second ROI ‘OUT‘ on the zone of lowest variation. The same ROIs were applied to the deltaAT map. The mean value of the respective differential parameters was extracted in each ROI. Results Greatest delta–J values were found in the RVOT/anterior wall. delta–J in the ROI ‘IN‘ was greater than in the ROI ‘OUT‘ (1.68 [1.11–2.28] vs 0.56 [0.38–0.93] mV, p<0.001). delta–AT in the ROI ‘IN’ was greater than in the ROI ‘OUT’ (27.96 [20.39–44.89] vs 7.62 [4.24–16.69] ms, p<0.001). A good correlation was found between delta–J and delta–AT, considering the data for the two ROIs together (Spearman R coefficient=0.71, p<0.001). Conclusions: Our study shows that the repolarization gradient, evaluated by localized delta–J increase in RVOT, justifies BrS ECG phenotype and local depolarization abnormalities. A strong correlation was present in these RVOT areas between J–elevation variation and slow conducting zones.

Abstract Background Catheter ablation with radiofrequency in persistent atrial fibrillation (PeAF) has limited success and a significant proportion of patients requires redo ablation. Several trials showed that addition of vein of Marshall ethanol infusion (Vom-EI) to catheter ablation, compared with catheter ablation alone, increases the possibilities of remaining free of AF. No data are available about the effect on VoM-EI in Pe-AF patients that undergo a redo ablation. Purpose We evaluated acute impact on lesion formation post-VoM-EI and the mitral line block validation after a methodical approach including VoM-EI and check of pulmonary vein isolation (PVI), roof-line, mitral line (ML) and cavo-tricuspid isthmus line in a population of PeAF patients undergone redo ablation. We aimed also the results of a short follow-up. Methods Consecutive patients undergoing redo ablation for PeAF were enrolled. All patients underwent check of PVI, left atrium (LA) roofline and cavotricuspid isthmus line and, if necessary, ablation was completed. In all patients, after a detailed electroanatomical map of the LA (filter at 0.05-0.5 mV if the patient was in sinus rhythm or 0.05-0.3 mV in the case of AF), we proceeded with the VoM-ETHO. LA map was thus repeated to assess the extension of the newly-formed low voltage area (LVA). According to the newly-formed LVAs, the validation of mitral line was obtained by the evidence of bidirectional block. In presence of conduction through the mitral line also after endocardial revision, we proceeded to mapping and ablating in the CS epicardial gaps in the "anchored wall" or in the "free-wall"of the great cardiac vein (GCV). Results Twenty consecutive patients (64±8 years and 65% male) undergone redo ablation for AF with VoM-EI were included in this study. All patients underwent PVI in the previous procedure but only in 11 roof line has been performed. In twenty patients (52%) reconnection of PV was observed (12/20 in right superior pulmonary vein). In 4/11 roof line was not complete. The medium value of basal LA-LVAs was 3.38土5.27 cmq and the newly-formed LVAs after the VoM-EI procedure was 9.21土5.63 cmq. All patients achieved bidirectional block validated across ML: in 8/20 after epicardial gaps ablations into the anchored wall of GCV and in 6/20 after epicardial gaps ablation in the free wall of GCV. The ML procedural time was 18.82土12.79 minutes. The number of radiofrequency irrigation was 20.11土10.56. No major complications occurred. Five patients had VOM dissection without consequences. During a short follow-up period (6土5 months), only one patient had AF recurrences after the blanking period of one month. Conclusions VoM ethanol ablation added to PVI and linear lesions in the context of a methodical and anatomical approach during redo ablation of PeAF patients seems to have promising results and to be safe. Longer follow-up is needed to understand the role of this technique in redo ablation.

Abstract Background Cardiac amyloidosis (CA) is a highly prevalent cause of congestive heart failure. It often requires cardiac pacing due atrioventricular conduction (AV) system disorders, often with cardiac resynchronization (CRT) to prevent development/deterioration of left ventricular (LV) dysfunction. Left bundle branch area pacing (LBBAP) is an emerging alternative to CRT, offering a strict physiological LV activation and very limited use of iodinated contrast. The feasibility of LBBAP in CA is considered limited due to the presence of septal pseudohypertrophy which theoretically limits left-sided conduction system engagement. Purpose To evaluate the feasibility and effectiveness of LBBAP in cardiac amyloidosis. Methods Consecutive patients with CA (both light-chain -AL- or wild-type transtiretin -wtATTr) with a pacing indication for AV conduction disorders were enrolled. Patients underwent baseline echocardiographic examination. LBBAP was achieved by means of stylet-driven leads advanced transeptally (right ventricle (RV) to LV) via dedicated delivery systems, with continuous monitoring of 12-lead electrocardiographic morphology and impedance until a typical QRS morphology in V1 was obtained (usually rSr’ or Sr’). Standard measures for left bundle (LB) capture were used (stimulus to peak R in V6 – S-RV6, V6-V1 interpeak interval, presence of transition in these measures during threshold testing, presence of fascicular signal during spontaneous QRS). Results Between January 2022 and June 2023, among 63 patients undergoing LBBAP, 7 patients (11%) had CA, 2 AL (28%) and 5 (72%) wtATTR. Patients were prevalently old (78±7 y) males (6, 85%); LV mean septal thickness was 17±2 mm (min 16, max 20 mm) and mean LV ejection fraction (LVEF) was 45±6%. Indications were PR prolongation in 3, bradycardic atrial fibrillation and LB branch block (LBBB) in 2, primary LBBB in 1 and chronic RV pacing in 1. Baseline QRS duration was 145±47 ms (QRS<120 ms: 97±15 ms, QRS>120 ms: 182±13 ms). LBBAP success was 100%. Fascicular electrograms were observed in ¾ of patients without LBBB; S-RV6 interval was 74 ±11 ms (³70 ms in 3), RV6-RV1 interpeak interval was 47±9 ms (³ 30 ms in 6 patients). DQRS in baseline broad QRS was -52 ms and +32 ms in narrow. No complications were observed. Over a short follow up of 6 months, an increase in average LVEF was observed (LVEF at 6 months: 51±3%, p<0.05). Conclusions In patients with CA, LBBAP is easily achievable with stylet-driven systems with frequent selective engagement of conduction system. QRS narrowing in baseline broad QRS is significant while QRS broadening in baseline narrow QRS is limited. Early results regarding follow-up of surrogate endpoint such as LVEF are promising.

Abstract Background The vein of Marshall (VOM) is a promising therapeutic target for the atrial fibrillation (AF) treatment, fitting perfectly with the "Coumel triangle" as it contains triggers of focal activities and stable reentries, autonomic parasympathetic and sympathetic connection and it represents substrate for perimitral flutters. Lateral mitral line (ML) represents a fundamental part of the anatomical ablation setup for the treatment of AF but its bidirectional block is very difficult to achieve by endocardial ablations. Ethanol infusion into the VoM (VOM-EI) has demonstrated high effectiveness in facilitating ML block. Newly-formed bipolar lesion after VOM-EI is considered an index of effectiveness of the alcoholization procedure. Voltage analysis assessment after VOM-EI in predicting ML block is poorly investigated. Purpose To compare unipolar and bipolar low-voltage areas (LVAs) along VOM trajectory after VOM-EI, and their role in predicting ML block. Methods We enrolled 59 patients undergoing catheter ablation for persistent AF or mitral isthmus dependent atrial flutter. We performed first a high-density voltage map of the left atrium. After VOM-EI, a LA remap was performed. The area width difference was obtained and defined as ∆LVA (see Figure 1). Normal Bipolar voltage cutoffs were 0.50 mV in case of sinus rhythm or 0.29 mV in case of AF. Unipolar cutoffs were respectively 2.7 mV in sinus rhythm and 1.1 mV in AF. The anatomical lesions set, after VOM-EI, included wide antral PVI, linear lesion for dome and ML isthmus following the newly-formed lesion after the VOM-EI. Systematic lines block validation was performed. ML block was defined after coronary sinus electrograms sequence inversion (septal-to-lateral) during left atrial appendage pacing. In case of residual conduction gaps, RF applications into the coronary sinus-great cardiac vein were done to target residual epicardial gaps. Ablation time to obtain ML block (AblTime) was obtained. Results In our group, 56/59 patients (94.5%) achieved mitral isthmus block. Bipolar and unipolar low voltage areas after VOM-EI were 9.9 ± 6.9 cm2 and 12.2 ± 5.9 cm2 respectively. Bipolar ∆LVAs were significantly lower compared with unipolar ∆LVA (8.2 ± 6.5 cm2 vs 9.4 ± 6.0 cm2; p= 0.03). A strong linear correlation between AblTime and bipolar ∆LVA (R: 0.76) and a significant correlation between AblTime and unipolar ∆LVA (R: 0.6) were found (Figure 2). Patients that required coronary sinus applications to reach ML block (13/59, 22%), presented lower ∆LVAs at logistic regression both at bipolar (p<0.01) and unipolar (p=0.03) analysis. Conclusions Unipolar and bipolar voltage analysis along the mitral isthmus trajectory predicts ML block achievement, with VOM-EI inducing wider unipolar LVAs than bipolar LVAs. Furthermore, wider unipolar and bipolar LVAs post VOM-EI are linked to a shorter AblTime and an increased probability of avoiding the need to target epicardial gaps via the CS musculature.LVA along VOM territory after VOM EI∆LVAs linear correlation with AblTime

Abstract Introduction Adults with repaired tetralogy of Fallot (rToF) are prone to develop ventricular tachycardia (VT) in adulthood, due to reentry related to slowly conducting anatomical isthmuses (SCAI). Pulmonary valve replacement (PVR) in patients without history of VT, may lead to obliteration of unrecognized SCAI with subsequent catheter ablation failure; electrophysiologic study is thus recommended before PVR. A systematic evaluation of the topology of SCAI in this population is, however, scant. Methods Consecutive rToF patients undergoing PVR with native right ventricular outflow tract were studied with pre-PVR EPS. Electroanatomical mapping with systematic evaluation of all possible anatomical isthmuses (AI) with pacemapping, activation mapping in sinus/paced rhythm and bipolar voltage mapping was performed (AI1: anterior scar/patch to tricuspid annulus; AI2: anterior scar to pulmonary annulus; AI3: pulmonary annulus to ventricular septal defect – VSD- patch; AI4: VSD to tricuspid annulus). Conduction velocity (CV) across all documented AI was calculated (ratio between the distance among the nearest point with bipolar voltage >1.5 mV and their difference in activation timing). Ventricular programmed stimulation was performed at 2 sites (apex and outflow tract) with drive train ad 600/400 ms, up to three extrastimuli until refractoriness or induction, during baseline and isoproterenol infusion. Radiofrequency catheter ablation (RFCA) was performed in all patients with inducible VT and/or SCAI, aiming at conduction block across the SCAI validated with differential pacing. Results Between May 2023 and November 2023, 10 patients with rToF and 1 double outlet right ventricle were studied (73% males, age 46±10 years; 54% with a previous shunt, 46% with a previous transannular patch, 27% pulmonary valvotomy and infundibular boring; median age at surgery 4 years, interquartile range 3-6). EPS was positive for inducible VT in 4 patients (mean cycle length 297 ms, 3 with left bundle branch morphology and 1 right bundle branch morphology, all inferior axis) and polymorphic VT in 1. AI1 was present in 5 patients, AI2 in 5, AI3 in 7, AI 4 in 2. At least 1 SCAI was present in 7 patients (64%), 2 SCAI in 3 patients (43% of patients with SCAI; in every patient SCAI3+SCAI2 in 2 and SCAI 4 in 1 patient). There were no SCAI1; there were 3 SCAI 2 (mean CV 0.43 m/s), 4 SCAI 3 (mean CV 0.3 m/s), 1 SCAI 4 (CV 0.4 m/s). RFCA was performed in 8 patients; acute success was achieved in all patients, achieving bidirectional conduction block across treated SCAI and non-inducibility of VT. Conclusions SCAI are often present in rToF candidate to PVR and without clinical history of spontaneous VT, involving prevalently SCAI3 and SCAI2. Inducible VT is not sufficient as a marker of arrhythmic risk and SCAI should be better sought for. RFCA of SCAI with bidirectional conduction block is acutely highly efficacious.

Abstract Catheter ablation in persistent atrial fibrillation (PeAF) has limited success. Strategies beyond pulmonary veins isolation failed to demonstrate improvement of long-term rhythm maintenance. The vein of Marshall (VoM) is a promising therapeutic target because it contains triggers and autonomic parasympathetic and sympathetic activity implicated in arrhythmogenesis of AF. Moreover, as the VoM colocalizes with the trajectory of the "mitral isthmus", alcohol infusion into the vein facilitates bidirectional block across the line eliminating protected epicardial connections (1,2). Purpose We evaluated acute impact on lesion formation post-VOM-ETHO and the mitral line block validation after an approach including VOM-ETHO, pulmonary vein isolation (PVI), roof-line, mitral line (ML) and cavo-tricuspid isthmus line in a population of PeAF patients (Figure 1). We aimed also to report procedural outcomes after a short follow-up period. Methods After a detailed electroanatomical map of the left atrium (LA) (filter at 0.05-0.5 mV if the patient was in sinus rhythm or 0.05-0.3 mV in the case of AF), we thus proceeded with the VoM-ETHO using the technique previously described (3,4). LA map was thus repeated to assess the extension of the newly-formed low voltage area (LVA). According to the newly-formed LVAs, mitral isthmus ablation was completed endocardially. PVI, roof-line and cavo-tricuspid isthmus line were performed to complete the ablation setting. Bidirectional block across line was then validated during pacing from left atrial appendage. In case of persistence of conduction through the mitral line due to epicardial gaps, additional ablations were applied in the "anchored wall" or in the "free-wall" of the great cardiac vein (GCV). Results Twenty-one PeAF patients (67±6 years; 67% male) underwent ablation. The medium value of basal LA-LVAs was 3.1±63.8 cmq and the newly-formed LVAs after the VoM-ETHO procedure was 12.35±67.28 cmq. All patients had bidirectional block validated across the roof-line. Bidirectional block of the ML was achieved in 19/21 patients: in 12/21 patients after endocardial line only and in 9/21 after epicardial gaps ablations into the coronary sinus. The ML procedural time was 11.3±65.9 minutes. No major complications occurred. One patient had mild pericardial effusion due to VoM perforation with a spontaneous resolution. After a short follow-up period (6±63 months), no relapse of AF was observed in 19/21 (90%) patients. 12/21 patients were free from antiarrhythmic drugs (AADs). Interestingly, recurrences happened in patients in whom bidirectional block of the mitral line was not achieved. Conclusions VoM ethanol ablation added to PVI and linear lesions in the context of a methodical and anatomical approach seems to have promising results in PeAF patients. This strategy seems to be safe and reproducible. A favourable outcome depended on the interventional setting completion and the procedural end-points validation is crucial.

Abstract Background Coved-type electrocardiographic (ECG) pattern of patients with Brugada syndrome (BrS) is secondary to action potential lengthening in the right ventricular outflow tract (RVOT) epicardium. This may be approximated by activation-recovery interval (ARI), a marker of local repolarization dispersion. Purpose Our aim was to examine epicardial repolarization dispersion by ARI in the RVOT in patients with BrS and its correlation with conduction slowing and Tpeak-Tend (Tpe) interval, a marker of altered repolarization on surface ECG previously associated with a higher arrhythmic risk in this setting. Methods 24 patients with coved-type BrS phenotype underwent an invasive electrophysiological evaluation with endocardial high-density 3D mapping and programmed ventricular stimulation (PVS). Mapping data was exported and converted into MatLab format using OpenEP. Paraview was used to select a region of interest (ROI) specifically comprising of sub-pulmonary RVOT and RV free wall. ARI was calculated for each point of the ROI using a semi-automated algorithm with the Wyatt method and corrected with the Bazett formula (ARIc). The values were then interpolated to create ARI maps. For each patient, we calculated the value of ARIc at 75% of the distribution (ARIcQ3) and mean ARI for the values in the interval above ARIcQ3 (meanARIcQ3); ARIcQ3 points were also used to create maps. Activation maps were used to determine right ventricular activation time (RVAT). Tpe intervals were calculated with the tangent method on V1, V2 and V3 of 20 low-noise sinus beats recorded during the procedure, and then corrected with the Bazzett formula. Results Out of 24 patients, 6 had inducible VT/ VF during PVS (PVS+) while 18 did not (PVS-). Average ARI, ARIc, ARIcQ3, and meanARIcQ3 were 291.4 ± 22.1 ms; 306.0 ± 27.3 ms; 335.1 ± 28.3 ms; 353.1 ± 30.3 ms, respectively. Average Tpe was 75.0 ± 7.3 ms, with a mean corrected Tpe of 79.0 ± 10 ms. Mean RVAT was 111.9 ± 30.7 ms. Zones with ARIcQ3 were all located into the anterior and subpulmonary RVOT. We found a correlation between ARIcQ3 and mean corrected Tpe (R=0.58, p=0.003), and between meanARIcQ3 and mean corrected Tpe (R=0.65, p<0.001). A good correlation was also found between ARIcQ3 and RVAT (R=0.5441, p=0.009), and meanARIcQ3 and RVAT (R=0.49, p=0.02). No significant differences were found between PVS+ and PVS- patients. Conclusions Our results show the presence of zones with long ARI within RVOT of BrS with type-1 phenotype, indicating marked local repolarization dispersion. Longer ARIs correlate with altered repolarization on surface ECG and with prolongation of local activation time. ARI mapping can help identify repolarization dispersion and should be evaluated in the setting of a multi-parametric risk assessment in BrS with spontaneous coved-type ECG.

Abstract Funding Acknowledgements Type of funding sources: None. Background Accentuation of the action potential notch in the epicardium causes the prolongation of the epicardial action potentials in the right ventricular outflow tract (RVOT) and is the basis for arrhythmogenesis in patients affected by Brugada syndrome (BrS). Activation-recovery interval (ARI) approximates the action potential duration and may be used to study repolarization dispersion in BrS. Purpose Our aim was to investigate repolarization dispersion within the RVOT in spontaneous coved-type ECG BrS patients and in controls, evaluating also the relation between repolarization dispersion and conduction abnormalities to better define the electro-anatomical substrate of the disease. Methods BrS probands (n=13) and control subjects (n=4) underwent endocardial mapping of RV with the CARTO 3 system. BrS patients were also studied with programmed ventricular stimulation (PVS). Data was exported from the CARTO system and converted into MatLab format using OpenEP. A specific region of interest (ROI) including the sub-pulmonary RVOT and entire RV free wall was then selected using Paraview. With an automated algorithm, we measured ARI and ARIc (corrected using the "Bazett formula") for each point of the ROI, which were then interpolated to obtain ARI maps. We also acquired right ventricular activation time (RVAT) and maps for the assessment of slow conduction zones. By dividing RVAT color scale in 5 ms steps (isoSteps), isochronal activation areas were identified in the ROI. Results Out of the 13 BrS subjects, 4 had VT or VF inducible during PVS (PVS+) while 9 did not (PVS-). One patient had appropriate ICD shocks during follow-up. BrS patients had higher mean ARI and ARIc compared to controls (288.5±22.2 vs 251.5±8.4 ms, p<0.001; 312.0±30.4 vs 281.8±10.3 ms, p=0.023). ARI was found to be higher in PVS+ than in PVS- patients (294.8±27.1 vs 285.8±20.1 ms, p=0.5), as well as ARIc (327.7±49.9 vs 304.6±16.4 ms, p=0.49) although these differences were not significant. BrS patients showed a longer RVAT (106.0±21.4 vs 74.5±5.5 ms, p=0.003), and increased zones of crowding, as expressed by isochronal steps (13.85±2.94 vs 9.25±1.26, p=0.01). Notably, a strong correlation was found between ARIc and RVAT (Pearson R coefficient = 0.83, p<0.05), independently from the results of PVS (PVS+ R=0.99, p=0.01; PVS- R=0.83, p=0.06). Conclusions We introduced a novel workflow for the electrical substrate characterisation of subjects with BrS phenotype. Our preliminary data show the presence of repolarization dispersion along with conduction slowing in the RVOT of BrS patients compared to controls. In our population, repolarization dispersion and impairment of RVOT conduction were strongly related especially in inducible BrS patients.

Abstract Introduction Adults with repaired tetralogy of Fallot (rToF) experience episodes of atrial tachycardia (AT) and radiofrequency catheter ablation (RFCA) is often required but systematic evaluation of the mechanisms and recurrences is lacking. Methods Between January 2013 and October 2021, 20 rToF patients with AT referred for catheter ablation were enrolled. Electrophysiologic study with 3D electroanatomic mapping with multi–electrode mapping catheters was done, with right atrial bipolar voltage and activation mapping of the AT. Three mechanisms were searched: intra–atrial re–entrant tachycardias (IART), focal (FAT), other. Critical isthmus (CI) for IART was identified with activation mapping. FATs were localized according to the earliest uni/bipolar signal. All induced AT were treated. RFCA was aimed at the earliest activation point for FAT and at the critical isthmus for IART, anchoring lesion to fixed obstacles (valve annuli or scar). Written informed consent was provided. Results Among 20 adult (age 46±14 years) and mainly females (n=11, 55%) enrolled pts, 36 AT were documented: 25 (70%) IART, 10 (27%) FAT and only 1 (3%) had a typical atrioventricular nodal reentrant tachycardia. Mean tachycardia cycle length was 307±95 ms. Two ATs were induced in 11 pts, 3 in 4 pts and 4 in 2 during index EPS. Among IART, cavo–tricuspid isthmus (CTI) was the prevalent CI (n=14, 60%), while incisional IART (IARTinc, atriotomy and superior and inferior vena cava orifices, SVC and IVC, respectively) was the second mechanism (n=9, 39%). In two pts, due to non–inducibility, a pre–emptive lesion set comprising in one case CTI and in the second case CTI+SVC–atriotomy–IVC line was performed. Among FAT, in 3 cases the AT was mapped in the coronary sinus, in two at the tricuspid annulus, other at the crista terminalis, right appendage base, posterolateral scar or between atriotomy and SVC. During a median follow–up of 23 months (interquartile range, 6–37) recurrence occurred in 8 pts (25% of pts, 22% of tachycardias). Pts with recurrences were younger (43±7 vs. 48±17 y, p=0.04); no differences were found according to critical isthmus location (4 CTI and 4 IARTinc, 50%, p=ns). Conclusions Among rToF pts with AT, IART is the prevalent mechanism and CTI is the prevalent CI; atriotomy scar, however, is involved in a substantial portion of the critical isthmuses of the IART; FAT location is much more variable. Long–term freedom from AT in this clinical setting is encouraging.

Abstract Funding Acknowledgements Type of funding sources: None. Background Differential action potential duration shortening across the right ventricular (RV) myocardial wall is primarily responsible for the Brugada Syndrome (BrS) phenotype [1]. To date, data on electrical substrate characterization in humans with BrS phenotype is limited and risk evaluation is still controversial. Purpose We hypothesized that Uni-JEl mapping could be used as a marker of transmural voltage gradient dispersion resulting. Our aim was to evaluate Uni-JEl mapping in defining arrhythmogenic substrates in patients with BrS phenotype. Methods 12 patients were included in our analysis. 2 normal patients provided control data and 10 asymptomatic subjects with spontaneous type-1 BrS underwent 3D RV mapping (CARTO3 System, Biosense Webster). Among BrS patients we had 3 patients with arrhythmic events (aborted sudden death or appropriate ICD therapies) during follow-up (median 56, interquartile range: 46-74 months) and 7 patients without arrhythmic events. In the former group we had 1 patient with inducibility of VT/VF during EPS (EPS+) and 2 patients non-inducibles during EPS (EPS-), in the latter group we had 3 patients with EPS+ and 4 patients with EPS-. Electrophysiological data and signals were exported and OpenEP [2] was used to convert Carto proprietary data formats into Matlab format (Fig.1). Uni-JEl was calculated for each point map as the unipolar value at J point on surface electrocardiogram. Uni-JEl values were then interpolated in Paraview to create Uni-JEl maps, interpolating data points on the mesh cell (Fig.1). Finally, a region of interest (ROI) was selected and the calculation of mean Uni-JEI (MUni-JEI, as a measure of voltage gradient dispersion), interquartile range and range (intrqUni-JEI and ∆Uni-JEI, as markers of heterogeneity of dispersion) was performed. Results are shown as mean ± standard deviation for the group of BrS patients and the actual values for the two controls. Results BrS patients showed Muni-JEl, intrqUni-JEl and ∆Uni-JEI higher than controls (2.03 mV ± 0.31 mV vs 0,82 mV and 1,1 mV, 1.90 mV ± 0.82 mV vs 1,04 mV and 1,18 mV 6.26 mV ± 1.98 mV vs 3,54 mV and 4,01 mV, respectively). BrS patients with arrhythmic events during the follow-up showed higher intrqUni-JEl and the ∆Uni-JEI respect to BrS with EPS+ and without arrhythmic events during follow-up (2.31 mV ± 0.44 mV vs 0.78 mV ± 0.11 mV and 6.69 mV ± 2.27 mV vs 3.98 mV ± 0.31 mV). Figure 2 shows some examples of calculated Uni-JEl maps for each group under study. Conclusions In this work we introduced a novel workflow for the electrical substrate characterization of subjects with BrS phenotype. The results from our preliminary analysis indicate that a higher transmural voltage gradient dispersion and heterogeneity can be found in type-1 BrS with respect to normal subjects. Voltage gradient dispersion heterogeneity could be used to better recognize high risk BrS patients regardless of VT/VF inducibility during EPS.

Abstract Funding Acknowledgements Type of funding sources: None. Risk stratification in Brugada syndrome (BrS) is needed especially for the choice of an Implantable Cardiac Defibrillator (ICD). To date the predictive value of either clinical or conventional electrophysiological indexes in type 1 electrocardiographic pattern BrS is rather low. We aimed to evaluate the eventual prognostic significance of refractoriness heterogeneity of right ventricular outflow tract, an emergent relevant pathophysiological substrate, at electrophysiological study (EPS) in patients with BrS. From 5 centers 348 patients were retrospectively selected (age 44 ± 15 years, males 68%). Eighty-five (24%) patients had an ICD. EPS was proposed in patients with spontaneous type-1 ECG pattern regardless of symptoms, or in patients with drug-induced type-1 ECG pattern with symptoms (n = 174). The difference in the refractory period between the right ventricular outflow tract and the apex (ΔRPRVOT-apex) at EPS was evaluated as a prognostic factor. The optimal ΔRPRVOT-apex cutpoint for prognosis prediction was calculated through a P-spline hazard ratio analysis. Thus, ΔRPRVOT-apex was compared through different statistical analyses to other other clinical or conventional electrophysiological prognostic indexes previosly described in literature. During a 36-month median follow-up (range 6-228) 3 SCD and 10 appropriate ICD shocks (aborted SCD, aSCD) occurred. Fifty patients (29%) had a positive EPS (induction of sustained ventricular tachycardia, VT, or ventricular fibrillation, VF, during the procedure). At multivariable logistic analysis, only ΔRPRVOT-apex and late potentials remained independent predictors of a positive EPS. At Cox Proportional Hazard analysis, family history of SCD, history of syncope, VT/VF inducibility and a ΔRPRVOT-apex >60 ms were all univariate predictors of SCD/aSCD. At bivariate analysis, a ΔRPRVOT-apex >60 ms remained an independent predictor of SCD/aSCD even when adjusted the other univariate predictors. At C-Statistic analysis, the strongest predictive model was the one using ΔRPRVOT-apex >60 ms as covariate with a C-statistics (95% CI) of 0.72 (0.51-0.93). At Kaplan-Meyer curves, ΔRPRVOT-apex >60 ms was confirmed a strong predictor of SCD/aSCD and another very interesting observation was possible: patients with positive EPS, but a ΔRPRVOT-apex < 60 ms, had a similar risk to SCD/aSCD compared to patients with a negative EPS, while those with a positive EPS and a ΔRPRVOT-apex > 60 ms were found to be at a higher risk of events. Refractory period heterogeneity of the right ventricle defined as ΔRPRVOT-apex > 60 ms at EPS is a strong and independent predictor of SCD/aSCD in patients with BrS, beyond VT/VF inducibility at EPS and common clinical predictors. Abstract Figure.

BackgroundIn non-ischaemic dilated cardiomyopathy (NIDCM), it is uncertain which late gadolinium enhancement (LGE) pattern, extent and location predict ventricular arrhythmias.MethodsWe analysed 183 NIDCM patients (73% men, median age 66 years) receiving an implantable cardioverter defibrillator (ICD) for primary prevention, undergoing cardiac magnetic resonance within 1 month before implantation. The primary endpoint was appropriate ICD shock, the secondary endpoint was a composite of appropriate ICD shock and cardiac death.ResultsLGE was found in 116 patients (63%), accounting for 9% of LV mass (5–13%). Over a 30-month follow-up (10–65), 20 patients (11%) experienced the primary and 30 patients (16%) the secondary endpoint. LGE presence, inferior wall LGE, diffuse (≥2 wall) LGE, the number of segments with LGE, the number of segments with 50–75% transmural LGE, and percent LGE mass were univariate predictors of both endpoints. Also septal LGE predicted the primary, and lateral LGE predicted the secondary endpoint. LGE limited to right ventricular insertion points did not predict any endpoint.Percent LGE mass had an area under the curve of 0.734 for the primary endpoint, with 13% as the best cut-off (55% sensitivity, 86% specificity, 32% PPV, 94% NPV), conferring a 7-fold higher risk compared to patients with no LGE or LGE <13%. Survival free from both endpoints was significantly worse for patients with LGE ≥13%.ConclusionsIn patients with NIDCM receiving a defibrillator for primary prevention, LGE presence and extent predicted appropriate ICD shock and cardiac mortality; also specific LGE patterns and locations predicted a worse prognosis.

Abstract Background Implantable cardioverter defibrillator (ICD) is recommended for patients with non-ischaemic heart failure (HF) and left ventricular ejection fraction (LVEF) ≤35%, although most patients will not experience any appropriate ICD intervention. We assessed if cardiovascular magnetic resonance (CMR) findings may predict benefit from ICD implantation. Methods and results We retrieved the data of all patients (n=183) with non-ischaemic HF receiving an ICD for primary prevention at our Institution, and undergoing CMR within 1 month before implantation. 183 patients were evaluated (men 73%, median age 66 years, LVEF 24%, N-terminal fraction of pro-B-type natriuretic peptide 1217 ng/L, atrial fibrillation, flutter or atrial ectopic rhythm 21%). They received single-chamber (n=21, 12%), dual-chamber (n=34, 19%), or cardiac resynchronization therapy devices (n=127, 69%); 1 patient (1%) received a subcutaneous defibrillator. Twenty patients (11%) experienced a shock for ventricular tachycardia or fibrillation (VT/VF) over 2.5 years (0.8–5.4), and 13 (7%) had an inappropriate shock over 2.7 years (0.9–5.4). Late gadolinium enhancement (LGE) was present in 146 patients (80%), but on average accounted for limited percentage of LV mass (4% [2–11%]). LGE mass independently predicted shocks for VT/VF (HR 2.13, 95% CI 1.02–4.47; p=0.045). LGE mass ≥14% (the best cut-off at receiver operating characteristics analysis) independently predicted shocks for VT/VF (HR 3.82, 95% CI 1.51–9.68; p=0.005). LGE mass <4% was the only univariate predictor of inappropriate shocks (HR 4.82, 95% CI 1.07–21.76; p=0.041). Conclusions Patients with non-ischaemic HF and LGE mass ≥14% benefit most from ICD, while those with LGE mass <4% display mainly inappropriate shocks.

In patients treated with CRT no data relative to the relationship between regional wall motion and perfusion and reverse remodelling of the left ventricle at short and medium term followup were available. To this aim, 36 heart failure patients were studied by G-SPECT before (T0), within 2 months (T1) and 6 months (T2) after CRT. A clinical followup was completed for 36 months. In 30/36 patients there was an improvement of NYHA Class at T1 that persisted at T2. G-SPECT showed significant improvement of perfusion at T1 in 92% of patients without further changes at T2. A reduction of LV volumes, an increase of EF and an improvement of regional wall motion and thickening were observed at T1 versus baseline, with only minor changes at T2. Moreover, baseline extension of perfusion defects was scarcely correlated with improvement after CRT. Finally, end diastolic volume, perfusion defect and diabetes mellitus were independent predictors of survival. The main effects of CRT on regional myocardial perfusion and wall motion are obtained within 2 months. Volume overload modulates recovery of ventricular function independently of reperfusion and, with extension of perfusion abnormalities and diabetes were independent predictors of survival during followup.