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Aims Left bundle branch area pacing (LBBAP) is a promising method for delivering cardiac resynchronization therapy (CRT), but its relative physiological effectiveness compared with His bundle pacing (HBP) is unknown. We conducted a within-patient comparison of HBP, LBBAP, and biventricular pacing (BVP). Methods and results Patients referred for CRT were recruited. We assessed electrical response using non-invasive mapping, and acute haemodynamic response using a high-precision haemodynamic protocol. Nineteen patients were recruited: 14 male, mean LVEF of 30%. Twelve had time for BVP measurements. All three modalities reduced total ventricular activation time (TVAT), (ΔTVATHBP -43 ± 14 ms and ΔTVATLBBAP −35 ± 20 ms vs. ΔTVATBVP −19 ± 30 ms, P = 0.03 and P = 0.1, respectively). HBP produced a significantly greater reduction in TVAT compared with LBBAP in all 19 patients (−46 ± 15 ms, −36 ± 17 ms, P = 0.03). His bundle pacing and LBBAP reduced left ventricular activation time (LVAT) more than BVP (ΔLVATHBP −43 ± 16 ms, P < 0.01 vs. BVP, ΔLVATLBBAP −45 ± 17 ms, P < 0.01 vs. BVP, ΔLVATBVP −13 ± 36 ms), with no difference between HBP and LBBAP (P = 0.65). Acute systolic blood pressure was increased by all three modalities. In the 12 with BVP, greater improvement was seen with HBP and LBBAP (6.4 ± 3.8 mmHg BVP, 8.1 ± 3.8 mmHg HBP, P = 0.02 vs. BVP and 8.4 ± 8.2 mmHg for LBBAP, P = 0.3 vs. BVP), with no difference between HBP and LBBAP (P = 0.8). Conclusion HBP delivered better ventricular resynchronization than LBBAP because right ventricular activation was slower during LBBAP. But LBBAP was not inferior to HBP with respect to LV electrical resynchronization and acute haemodynamic response.

Background Ablation of autonomic ectopy-triggering ganglionated plexuses (ET-GP) has been used to treat paroxysmal atrial fibrillation (AF). It is not known if ET-GP localisation is reproducible between different stimulators or whether ET-GP can be mapped and ablated in persistent AF. We tested the reproducibility of the left atrial ET-GP location using different high-frequency high-output stimulators in AF. In addition, we tested the feasibility of identifying ET-GP locations in persistent atrial fibrillation. Methods Nine patients undergoing clinically-indicated paroxysmal AF ablation received pacing-synchronised high-frequency stimulation (HFS), delivered in SR during the left atrial refractory period, to compare ET-GP localisation between a custom-built current-controlled stimulator (Tau20) and a voltage-controlled stimulator (Grass S88, SIU5). Two patients with persistent AF underwent cardioversion, left atrial ET-GP mapping with the Tau20 and ablation (Precision™, Tacticath™ [n = 1] or Carto™, SmartTouch™ [n = 1]). Pulmonary vein isolation (PVI) was not performed. Efficacy of ablation at ET-GP sites alone without PVI was assessed at 1 year. Results The mean output to identify ET-GP was 34 mA (n = 5). Reproducibility of response to synchronised HFS was 100% (Tau20 vs Grass S88; [n = 16] [kappa = 1, SE = 0.00, 95% CI 1 to 1)][Tau20 v Tau20; [n = 13] [kappa = 1, SE = 0, 95% CI 1 to 1]). Two patients with persistent AF had 10 and 7 ET-GP sites identified requiring 6 and 3 min of radiofrequency ablation respectively to abolish ET-GP response. Both patients were free from AF for > 365 days without anti-arrhythmics. Conclusions ET-GP sites are identified at the same location by different stimulators. ET-GP ablation alone was able to prevent AF recurrence in persistent AF, and further studies would be warranted.

A multivariate risk score model was proposed by Sieira et al in 2017 for sudden death in Brugada syndrome; their validation in 150 patients was highly encouraging, with a C-index of 0.81; however, this score is yet to be validated by an independent group. A total of 192 records of patients with Brugada syndrome were collected from 2 centers in the United Kingdom and retrospectively scored according to a score model by Sieira et al. Data were compiled summatively over follow-up to mimic regular risk re-evaluation as per current guidelines. Sudden cardiac death survivor data were considered perievent to ascertain the utility of the score before cardiac arrest. Scores were compared with actual outcomes. Sensitivity in our cohort was 22.7%, specificity was 57.6%, and C-index was 0.58. In conclusion, up to 75% of cardiac arrest survivors in this cohort would not have been offered a defibrillator if evaluated before their event. This casts doubt on the utility of the score model for primary prevention of sudden death. Inherent issues with modern risk scoring strategies decrease the likelihood of success even in robustly designed tools such as the Sieira score model.

IntroductionLeft bundle branch pacing (LBBP) can deliver physiological left ventricular activation, but typically at the cost of delayed right ventricular (RV) activation. A proposed solution is to advance RV activation through anodal capture, but there is uncertainty regarding the mechanism by which early RV activation is achieved (capture of right bundle or RV myocardial capture) and it is not known whether this produces hemodynamic benefit.MethodsWe recruited patients with LBBP leads in whom anodal capture eliminated the terminal R wave in lead V1.Ventricular activation pattern, timing and high precision acute hemodynamic response were studied during LBBP with and without anodal capture.ResultsWe recruited 21 patients, mean age 67 years, 14 were males. We measured ECG timings and hemodynamics in all patients and in 15 we also performed non-invasive mapping. Ventricular epicardial propagation maps demonstrated that right ventricular septal myocardial capture, rather than right bundle capture, was the mechanism for earlier RV activation. With anodal capture, QRS duration was shorter (116 ± 12ms versus 129 ± 14ms, p < 0.01), and total ventricular activation time was shorter (83 ± 18ms versus 90 ± 15ms, p = 0.01). This required higher outputs (3.6 ± 1.9V versus 0.6 ± 0.2V, p ConclusionLeft bundle pacing with anodal capture advances right ventricular activation as a result of stimulation of the RV septal myocardium. However, this requires higher outputs and did not improve acute hemodynamics. Aiming for anodal capture may therefore not be necessary.

BACKGROUND: Accurately determining arrhythmia mechanism from a 12-lead electrocardiogram (ECG) of supraventricular tachycardia can be challenging. We hypothesized a convolutional neural network (CNN) can be trained to classify atrioventricular re-entrant tachycardia (AVRT) vs atrioventricular nodal re-entrant tachycardia (AVNRT) from the 12-lead ECG, when using findings from the invasive electrophysiology (EP) study as the gold standard. METHODS: We trained a CNN on data from 124 patients undergoing EP studies with a final diagnosis of AVRT or AVNRT. A total of 4962 5-second 12-lead ECG segments were used for training. Each case was labeled AVRT or AVNRT based on the findings of the EP study. The model performance was evaluated against a hold-out test set of 31 patients and compared to an existing manual algorithm. RESULTS: The model had an accuracy of 77.4% in distinguishing between AVRT and AVNRT. The area under the receiver operating characteristic curve was 0.80. In comparison, the existing manual algorithm achieved an accuracy of 67.7% on the same test set. Saliency mapping demonstrated the network used the expected sections of the ECGs for diagnoses; these were the QRS complexes that may contain retrograde P waves. CONCLUSION: We describe the first neural network trained to differentiate AVRT from AVNRT. Accurate diagnosis of arrhythmia mechanism from a 12-lead ECG could aid preprocedural counseling, consent, and procedure planning. The current accuracy from our neural network is modest but may be improved with a larger training dataset.

Excessive prolongation of PR interval impairs coupling of AV contraction, which reduces left ventricular pre-load and stroke volume, and worsens symptoms. His-bundle pacing allows AV-delay shortening while maintaining normal ventricular activation. HOPE-HF evaluated whether AV-optimized His pacing is preferable to no-pacing, in double-blind cross-over fashion, in patients with heart failure, left ventricular ejection fraction (LVEF) ≤40%, PR interval ≥200ms and either QRS ≤140ms or right BBB.Patients had atrial and His-bundle leads implanted (and an ICD lead if clinically indicated) and were randomized, to 6-months of pacing and 6-months of no-pacing utilizing a cross-over design. The primary outcome was peak oxygen uptake during symptom-limited exercise. Quality of life, LVEF and patients' holistic symptomatic preference between arms were secondary outcomes. 167 patients were randomized: 90% men, 69±10 years, QRS duration 124±26ms, PR interval 249±59ms, LVEF 33±9%. Neither peak VOHis-bundle pacing did not increase peak oxygen uptake but, under double-blind conditions, significantly improved quality of life and was symptomatically preferred by the clear majority of patients. Ventricular pacing delivered via the His bundle did not adversely impact ventricular function during the 6 months. This article is protected by copyright. All rights reserved.

Purpose Left atrial (LA) rapid AF activity has been shown to co-localise with areas of successful atrial fibrillation termination by catheter ablation. We describe a technique that identifies rapid and regular activity. Methods Eight-second AF electrograms were recorded from LA regions during ablation for psAF. Local activation was annotated manually on bipolar signals and where these were of poor quality, we inspected unipolar signals. Dominant cycle length (DCL) was calculated from annotation pairs representing a single activation interval, using a probability density function (PDF) with kernel density estimation. Cumulative annotation duration compared to total segment length defined electrogram quality. DCL results were compared to dominant frequency (DF) and averaging. Results In total 507 8 s AF segments were analysed from 7 patients. Spearman’s correlation coefficient was 0.758 between independent annotators (P P P P Conclusion DCL identifies rapid atrial activity that may represent psAF drivers. This study uses DCL as a tool to evaluate the dynamic, patient specific properties of psAF by identifying rapid and regular activity. If automated, this technique could rapidly identify areas for ablation in psAF.

OBJECTIVES: This first-in-human feasibility study was undertaken to translate the novel low-voltage MultiPulse Therapy (MPT) (Cardialen, Inc., Minneapolis, Minnesota), which was previously been shown to be effective in preclinical studies in terminating atrial fibrillation (AF), into clinical use. BACKGROUND: Current treatment options for AF, the most common arrhythmia in clinical practice, have limited success. Previous attempts at treating AF by using implantable devices have been limited by the painful nature of high-voltage shocks. METHODS: Forty-two patients undergoing AF ablation were recruited at 6 investigational centers worldwide. Before ablation, electrode catheters were placed in the coronary sinus, right and/or left atrium, for recording and stimulation. After the induction of AF, MPT, which consists of up to a 3-stage sequence of far- and near-field stimulation pulses of varied amplitude, duration, and interpulse timing, was delivered via temporary intracardiac leads. MPT parameters and delivery methods were iteratively optimized. RESULTS: In the 14 patients from the efficacy phase, MPT terminated 37 of 52 (71%) of AF episodes, with the lowest median energy of 0.36 J (interquartile range [IQR]: 0.14 to 1.21 J) and voltage of 42.5 V (IQR: 25 to 75 V). Overall, 38% of AF terminations occurred within 2 seconds of MPT delivery (p

Objectives The authors reviewed 3-dimensional electroanatomic maps of perimitral flutter to identify scar-related isthmuses and determine their effectiveness as ablation sites. Background Perimitral flutter is usually treated by linear ablation between the left lower pulmonary vein and mitral annulus. Conduction block can be difficult to achieve, and recurrences are common. Methods Patients undergoing atrial tachycardia ablation using CARTO3 (Biosense Webster Inc., Irvine, California) were screened from 4 centers. Patients with confirmed perimitral flutter were reviewed for the presence of scar-related isthmuses by using CARTO3 with the ConfiDense and Ripple Mapping modules. Results Confirmed perimitral flutter was identified in 28 patients (age 65.2 ± 8.1 years), of whom 26 patients had prior atrial fibrillation ablation. Scar-related isthmus ablation was performed in 12 of 28 patients. Perimitral flutter was terminated in all following correct identification of a scar-related isthmus using ripple mapping. The mean scar voltage threshold was 0.11 ± 0.05 mV. The mean width of scar-related isthmuses was 8.9 ± 3.5 mm with a conduction speed of 31.8 ± 5.5 cm/s compared to that of normal left atrium of 71.2 ± 21.5 cm/s (p < 0.0001). Empirical, anatomic ablation was performed in 16 of 28, with termination in 10 of 16 (63%; p = 0.027). Significantly less ablation was required for critical isthmus ablation compared to empirical linear lesions (11.4 ± 5.3 min vs. 26.2 ± 17.1 min; p = 0.0004). All 16 cases of anatomic ablation were reviewed with ripple mapping, and 63% had scar-related isthmus. Conclusions Perimitral flutter is usually easy to diagnose but can be difficult to ablate. Ripple mapping is highly effective at locating the critical isthmus maintaining the tachycardia and avoiding anatomic ablation lines. This approach has a higher termination rate with less radiofrequency ablation required.

Aims Accurately determining atrial arrhythmia mechanisms from a 12-lead electrocardiogram (ECG) can be challenging. Given the high success rate of cavotricuspid isthmus (CTI) ablation, identification of CTI-dependent typical atrial flutter (AFL) is important for treatment decisions and procedure planning. We sought to train a convolutional neural network (CNN) to classify CTI-dependent AFL vs. non-CTI dependent atrial tachycardia (AT), using data from the invasive electrophysiology (EP) study as the gold standard. Methods and results We trained a CNN on data from 231 patients undergoing EP studies for atrial tachyarrhythmia. A total of 13 500 five-second 12-lead ECG segments were used for training. Each case was labelled CTI-dependent AFL or non-CTI-dependent AT based on the findings of the EP study. The model performance was evaluated against a test set of 57 patients. A survey of electrophysiologists in Europe was undertaken on the same 57 ECGs. The model had an accuracy of 86% (95% CI 0.77–0.95) compared to median expert electrophysiologist accuracy of 79% (range 70–84%). In the two thirds of test set cases (38/57) where both the model and electrophysiologist consensus were in agreement, the prediction accuracy was 100%. Saliency mapping demonstrated atrial activation was the most important segment of the ECG for determining model output. Conclusion We describe the first CNN trained to differentiate CTI-dependent AFL from other AT using the ECG. Our model matched and complemented expert electrophysiologist performance. Automated artificial intelligence-enhanced ECG analysis could help guide treatment decisions and plan ablation procedures for patients with organized atrial arrhythmias.

Background Left bundle area pacing is growing in use both for bradycardia pacing and cardiac resynchronization, but implants are not always successful. We prospectively studied consecutive patients to determine whether septal scar contributes to implant failure. Methods Patients scheduled for left bundle area pacing, using the 3830 Selectsecure lead were prospectively enrolled. All patients underwent standardized scar assessment by cardiac MRI with late gadolinium enhancement imaging. Scar burden was quantified as the proportion of basal septal segments showing late enhancement. Results 35 patients were recruited: 29 male, mean age 68 years, 10 with ischemic and 16 with dilated cardiomyopathy. Pacing indication was bradycardia in 26% and cardiac resynchronization in 74%. In 5/35 (14%) it was not possible to advance the lead through the ventricular septum. Basal septal late gadolinium enhancement was significantly more extensive in these patients (median 67%, IQR 58-69.5) compared to the other 30 (median 10%, IQR 0-20, p = 0.0006). There was no significant correlation between the paced QRS duration achieved and the extent of basal septal scar (r = 0.06, P = 0.75). Conclusions Failure to deliver a lead to the left bundle area is strongly associated with a (very) high burden of scar in the basal septum. Once the lead is delivered, however, the electrical response is independent of scar burden. This suggests that it would be worth developing delivery tools to tackle scarred basal septa, because if the lead could be delivered the electrical capture might still achieve a narrow QRS.

Background His bundle pacing (HBP) can be achieved in 2 ways: selective HBP (S-HBP), where the His bundle is captured alone, and nonselective HBP (NS-HBP), where local myocardium is also captured, resulting a pre-excited electrocardiogram appearance. Objective We assessed the impact of this ventricular pre-excitation on left and right ventricular dyssynchrony. Methods We recruited patients who displayed both S-HBP and NS-HBP. We performed noninvasive epicardial electrical mapping for left and right ventricular activation time (LVAT and RVAT) and pattern. Results Twenty patients were recruited. In the primary analysis, the mean within-patient change in LVAT from S-HBP to NS-HBP was -5.5 ms (95% confidence interval: -0.6 to -10.4, noninferiority P < .0001). NS-HBP did not prolong RVAT (4.3 ms, -4.0 to 12.8, P = .296) but did prolong QRS duration (QRSd, 22.1 ms, 11.8 to 32.4, P = .0003). In patients with narrow intrinsic QRS (n = 6), NS-HBP preserved LVAT (-2.9 ms, -9.7 to 4.0, P = .331) but prolonged QRS duration (31.4 ms, 22.0 to 40.7, P = .0003) and mean RVAT (16.8 ms, -5.3 to 38.9, P = .108) compared to S-HBP. Activation pattern of the left ventricular surface was unchanged between S-HBP and NS-HBP, but NS-HBP produced early basal right ventricular activation that was not seen in S-HBP. Conclusion Compared to S-HBP, local myocardial capture during NS-HBP produces pre-excitation of the basal right ventricle resulting in QRS duration prolongation. However, NS-HBP preserves the left ventricular activation time and pattern of S-HBP. Left ventricular dyssynchrony is not an important factor when choosing between S-HBP and NS-HBP in most patients., Graphical abstract

Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): British Heart Foundation Background; Left bundle area pacing is a novel technique that provides direct stimulation of cardiac conduction tissue in order to deliver physiological ventricular activation. The approach for left bundle area pacing is transseptal lead implantation, where the lead is advanced from the right ventricular side of the septum to the left ventricular side to capture the proximal left bundle. Observational data suggests that whilst this is a safe and feasible method, implant success rate is not 100%, and appears to be lower in patients with a cardiac resynchronization therapy (CRT) indication rather than a bradycardia indication for pacing. The mechanisms for failure to advance the lead through the ventricular septum are not well understood. Purpose; We used pre-procedural CMR to determine whether there are features which can help identify patients where lead implantation may be challenging. We assessed whether the extent and location of septal late gadolinium enhancement identified patients in whom left bundle area pacing will be challenging. We hypothesized that the presence of extensive scar in the septum impedes advancing the lead to the left ventricular septum and prevents capture of the left bundle. Methods; Patients underwent cardiac MRI including motion corrected free-breathing late gadolinium enhancement imaging1 before implantation. Scar was quantified using the full height half maximum method and expressed as the overall proportion of myocardial mass in the basal anteroseptal and basal inferoseptal segments, as shown in Figure 1. Left bundle area pacing was then attempted in patients with a CRT indication for pacing. We compared the extent of septal scar between patients in whom left bundle area pacing was achieved and those where there was failure to advance the lead deep into the septum. Results; 12 patients (11 male, 1 female), with average age 72 (IQR 63 to 78) and LVEF 30% (IQR 26 to 33) were studied. There was failure to advance the lead deep into the septum in 4 patients. There was a significantly higher basal septal scar burden in those patients where there was failure to advance the left bundle lead compared to those in which left bundle capture was achieved as shown in Figure 2 (median 55% and 5% respectively, p-value 0.02 by Wilcoxon signed rank test). Conclusion; The presence and extent of late gadolinium enhancement in the basal septum appears to be an important determinant of successful implantation of left bundle pacing lead using current implant technology. This may be because extensive septal scar prevents advancement of the pacing lead through the septum. Cardiac MRI before left bundle area pacing is likely to be useful in procedural planning.

Background: Atrial fibrillation (AF) and ventricular fibrillation (VF) are complex heart rhythm disorders and may be sustained by distinct electrophysiological mechanisms. Disorganised self-perpetuating multiple-wavelets and organised rotational drivers (RDs) localising to specific areas are both possible mechanisms by which fibrillation is sustained. Determining the underlying mechanisms of fibrillation may be helpful in tailoring treatment strategies. We investigated whether global fibrillation organisation, a surrogate for fibrillation mechanism, can be determined from electrocardiograms (ECGs) using band-power (BP) feature analysis and machine learning.Methods: In this study, we proposed a novel ECG classification framework to differentiate fibrillation organisation levels. BP features were derived from surface ECGs and fed to a linear discriminant analysis classifier to predict fibrillation organisation level. Two datasets, single-channel ECGs of rat VF (n = 9) and 12-lead ECGs of human AF (n = 17), were used for model evaluation in a leave-one-out (LOO) manner.Results: The proposed method correctly predicted the organisation level from rat VF ECG with the sensitivity of 75%, specificity of 80%, and accuracy of 78%, and from clinical AF ECG with the sensitivity of 80%, specificity of 92%, and accuracy of 88%.Conclusion: Our proposed method can distinguish between AF/VF of different global organisation levels non-invasively from the ECG alone. This may aid in patient selection and guiding mechanism-directed tailored treatment strategies.

Background: The mechanisms underlying atrial fibrillation (AF) remain controversial. We developed Representation of Electrical Tracking or Origin-Mapping to characterize activation wavefronts by direction and uniformity, accumulating data as an orbital plot and analyzed as frequency histograms. We applied this technique to patients undergoing AF ablation to determine if AF activation is random. Methods: Patients undergoing persistent AF ablation were recruited, and an AFocusII was positioned at multiple left atrial locations and kept steady for 1 minute to collect electrograms. The AFocusII was returned to the original site and position after >10 minutes for a repeat 1-minute data collection. Data were exported to custom Representation of Electrical Tracking or Origin-Mapping software, and 30 seconds consecutive time windows at each location were studied using frequency histograms of wavefronts. R50 (the range in degrees containing 50% of the total activation) was used as a method to enable statistical comparisons of activation patterns. Electrogram characterization into categories of complex fractionated atrial electrograms by Ensite Precision was subjected to similar analysis. Results: Consecutive 30 seconds segments were studied at 161 locations in 18 pts. Mean overlap between frequency histograms was 79.5%±7.7 (95% CI, 78.3–80.7). Nine patients underwent delayed mapping at the same location, and mean overlap between the first 30 seconds and >10 minute interval was 73%±11.8 and 71.9%±13.6 for consecutive 30-second segments. Stability was confirmed using R50 (Bland-Altman mean difference: 0.87°; limits of agreement: −34.0 to 36.0; r =0.005; P =0.95). A greater variance in R50 was observed between different locations within a patient than the variance within the same locations (intraclass correlation=0.765; P P r =0.36, P Conclusions: There appears to be preferential activation patterns during persistent AF indicating spatiotemporal stability. This has important implication to our mechanistic understanding of persistent AF.

Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): British Heart Foundation Background Cardiac resynchronization therapy delivered via biventricular pacing is thought to improve haemodynamic function through resynchronization of ventricular activation. Biventricular pacing also improves ventricular filling by shortening atrioventricular delay. Quantifying the relative contributions of these two mechanisms requires atrioventricular delay to be altered while left bundle branch block is preserved. This occurs when the His bundle is paced at an output below the left bundle branch block correction threshold. Purpose We performed His bundle pacing with preservation of left bundle branch block to measure the relative contributions of atrioventricular delay shortening and ventricular resynchronisation to the overall haemodynamic benefit of biventricular pacing. Methods Patients with left bundle branch block referred for conventional cardiac resynchronization therapy with biventricular pacing were recruited. Using a high precision, beat-by-beat systolic blood pressure assessment protocol, we assessed the haemodynamic effects of biventricular pacing and temporary His bundle pacing with left bundle branch block preservation at a full range of atrioventricular delays. We used non-invasive epicardial mapping (ECGI) to assess left ventricular activation time. Left bundle branch block preservation was defined as Results In 19 patients, His bundle pacing with preservation of left bundle branch block produced a peak systolic blood pressure improvement of 5.1mmHg (95% confidence interval: 2.2 to 8.0, p = 0.0013) compared to AAI pacing. In 16 of these patients, biventricular pacing was performed and produced a peak systolic blood pressure improvement of 7.1mmHg (3.8 to 10.4, p Conclusion Biventricular pacing in left bundle branch block improves haemodynamic function through ventricular resynchronization and shortening of atrioventricular delay. The majority of benefit appears to be produced by atrioventricular delay shortening. When left bundle branch block is not corrected, His bundle pacing may still produce considerable haemodynamic improvement through this mechanism. Abstract Figure.

Background Conduction channels have been demonstrated within the postinfarct scar and seem to be co-located with the isthmus of ventricular tachycardia (VT). Mapping the local scar potentials (SPs) that define the conduction channels is often hindered by large far-field electrograms generated by healthy myocardium. Objective The purpose of this study was to map conduction channel using ripple mapping to categorize SPs temporally and anatomically. We tested the hypothesis that ablation of early SPs would eliminate the latest SPs without direct ablation. Methods Ripple maps of postinfarct scar were collected using the PentaRay (Biosense Webster) during normal rhythm. Maps were reviewed in reverse, and clusters of SPs were color-coded on the geometry, by timing, into early, intermediate, late, and terminal. Ablation was delivered sequentially from clusters of early SPs, checking for loss of terminal SPs as the endpoint. Results The protocol was performed in 11 patients. Mean mapping time was 65 ± 23 minutes, and a mean 3050 ± 1839 points was collected. SP timing ranged from 98.1 ± 60.5 ms to 214.8 ± 89.8 ms post QRS peak. Earliest SPs were present at the border, occupying 16.4% of scar, whereas latest SPs occupied 4.8% at the opposing border or core. Analysis took 15 ± 10 minutes to locate channels and identify ablation targets. It was possible to eliminate latest SPs in all patients without direct ablation (mean ablation time 16.3 ± 11.1 minutes). No VT recurrence was recorded (mean follow-up 10.1 ± 7.4 months). Conclusion Conduction channels can be located using ripple mapping to analyze SPs. Ablation at channel entrances can eliminate the latest SPs and is associated with good medium-term results.

Funding Acknowledgements Type of funding sources: Other. Main funding source(s): BRAVO trial: BHF SP/10/002/28189, FS/10/038, FS/11/92/29122, FS/13/44/30291) National Institute for Health Research Imperial Biomedical Research Centre. HOPE-HF trial: British Heart Foundation (CS/15/3/31405, FS/13/44/30291, FS/15/53/31615, FS/14/27/30752, FS/10/038). Introduction The optimal atrioventricular (AV) delay for implantable cardiac devices can be derived by echocardiography or beat-by-beat blood pressure measurements. However, both of these approaches are labour intensive and neither could be incorporated into an implantable cardiac device for frequent repeated optimisations. Laser Doppler perfusion monitoring (LDPM) measures blood flow through tissue. LDPM has been miniaturised ready to be incorporated into future implantable cardiac devices. Purpose We studied if LDPM is a clinically reliable alternative method to blood-pressure measurements to determine optimal AV delay. Methods Data from 58 patients undergoing 94 clinical AVD optimisations using LDPM and simultaneous non-invasive beat-by-beat blood pressure was obtained. The optimal AV delay for each method and for each optimisation was determined using a curve of haemodynamic response to switching from AAI (reference state) to DDD (test state) at a series of AV delays (40, 80, 120, 160, 200, 240 ms). We then compared the derived optimal AV delays between the two measurement approaches. We also assessed the impact of the paced heart-rate on agreement between laser Doppler and Blood-Pressure derived optimal AV delays. Results The AV delay derived using LDPM was not clinically significant different from that derived by blood pressure changes. The median difference was -9ms (IQR -26 to 7, p = 0.05). Variability between the two methods was low (median absolute deviation 17ms). Optimisations performed at higher heart-rates resulted in a non-significant smaller difference between the LDPM and blood-pressure derived AV delays (median absolute deviation 12 vs 22 ms, p = 0.11). Conclusions Optimal AVDs derived from non-invasive blood-pressure or laser Doppler perfusion methods are clinically equivalent. The addition of laser Doppler to future implantable cardiac devices may enable devices to dynamically and reliably optimise AV delays. Abstract Figure 1

Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): British Heart Foundation Background: His bundle pacing can be achieved in two ways selective His bundle pacing, where the His bundle is captured alone, and non-selective His bundle pacing, where local myocardium is also captured resulting a pre-excited ECG appearance. We assessed the impact of this ventricular pre-excitation on left and right ventricular dys-synchrony. Methods We recruited patients who displayed both selective and non-selective His bundle pacing. We performed non-invasive epicardial electrical mapping to determine left and right ventricular activation times and patterns. Results In the primary analysis (n = 20, all patients), non-selective His bundle pacing did not prolong LVAT compared to select His bundle pacing by a pre-specified non-inferiority margin of 10ms (LVAT prolongation: -5.5ms, 95% confidence interval (CI): -0.6 to -10.4, non-inferiority p In patients with narrow intrinsic QRS (n = 6), non-selective His bundle pacing preserved left ventricular activation time (-2.9ms, 95%CI: -9.7 to 4.0, p = 0.331) but prolonged QRS duration (31.4ms, 95%CI: 22.0 to 40.7, p = 0.0003) and mean right ventricular activation time (16.8ms, 95%CI: -5.3 to 38.9, p = 0.108) compared to selective His bundle pacing. Activation pattern of the left ventricular surface was unchanged between selective and non-selective His bundle pacing. Non-selective His bundle pacing produced early basal right ventricular activation, which was not observed with selective His bundle pacing. Conclusions Compared to selective His bundle pacing, local myocardial capture during non-selective His bundle pacing produces right ventricular pre-excitation resulting in prolongation of QRS duration. However, non-selective His bundle pacing preserves the left ventricular activation time and pattern of selective His bundle pacing. When choosing between selective and non-selective His bundle pacing, left ventricular dyssynchrony is not an important factor. Abstract Figure: Selective vs Non-Selective HBP

Background His bundle pacing (HBP) is an alternative to biventricular pacing (BVP) for delivering cardiac resynchronisation therapy (CRT) in patients with heart failure and left bundle branch block (LBBB). It is not known whether ventricular activation times and patterns achieved by HBP are equivalent to intact conduction systems and not all patients with LBBB are resynchronised by HBP. Objective To compare activation times and patterns of His-CRT with BVP-CRT, LBBB and intact conduction systems. Methods In patients with LBBB, non-invasive epicardial mapping (ECGI) was performed during BVP and temporary HBP. Intrinsic activation was mapped in all subjects. Left ventricular activation times (LVAT) were measured and epicardial propagation mapping (EPM) was performed, to visualise epicardial wavefronts. Normal activation pattern and a normal LVAT range were determined from normal subjects. Results 45 patients were included, 24 with LBBB and LV impairment and 21 with normal 12-lead ECG and LV function. In 87.5% of patients with LBBB, His-CRT successfully shortened LVAT by ≥10ms. In 33.3%, His-CRT resulted in complete ventricular resynchronisation, with activation times and patterns indistinguishable from normal subjects. EPM identified propagation discontinuity artifacts in 83% of patients with LBBB. This was the best predictor of whether successful resynchronisation was achieved by HBP (logarithmic odds ratio (logOR) 2.19, 95% CI 0.07 to 4.31, p=0.04). Conclusion Non-invasive electrocardiographic mapping appears to identify patients whose LBBB can be resynchronized by HBP. In contrast to BVP, His-CRT may deliver the maximum potential ventricular resynchronization, returning activation times and patterns to those seen in normal hearts. This article is protected by copyright. All rights reserved.

Background Epicardial ganglionated plexuses (GP) have an important role in the pathogenesis of atrial fibrillation (AF). The relationship between anatomical, histological and functional effects of GP is not well known. We previously described atrioventricular (AV) dissociating GP (AVD-GP) locations. In this study, we hypothesised that ectopy triggering GP (ET-GP) are upstream triggers of atrial ectopy/AF and have different anatomical distribution to AVD-GP. Objectives We mapped and characterised ET-GP to understand their neural mechanism in AF and anatomical distribution in the left atrium (LA). Methods 26 patients with paroxysmal AF were recruited. All were paced in the LA with an ablation catheter. High frequency stimulation (HFS) was synchronised to each paced stimulus for delivery within the local atrial refractory period. HFS responses were tagged onto CARTO™ 3D LA geometry. All geometries were transformed onto one reference LA shell. A probability distribution atlas of ET-GP was created. This identified high/low ET-GP probability regions. Results 2302 sites were tested with HFS, identifying 579 (25%) ET-GP. 464 ET-GP were characterised, where 74 (16%) triggered ≥30s AF/AT. Median 97 (IQR 55) sites were tested, identifying 19 (20%) ET-GP per patient. >30% of ET-GP were in the roof, mid-anterior wall, around all PV ostia except in the right inferior PV (RIPV) in the posterior wall. Conclusion ET-GP can be identified by endocardial stimulation and their anatomical distribution, in contrast to AVD-GP, would be more likely to be affected by wide antral circumferential ablation. This may contribute to AF ablation outcomes., Highlights • ET-GP can be stimulated endocardially using high frequency stimulation within the local atrial refractory period. • ET-GP stimulation displays a wide range of responses from single ectopy to sustained AF and occasionally AV block. • ET-GP have distinct anatomical regions in patients with AF, and their distribution contrasts that of AV dissociating GP. • Most ET-GP are in the roof/PV ostia and inadvertently ablated during PVI. This may contribute to AF ablation success.

Funding Acknowledgements Research grant from Abbott Introduction We have recently described a novel evaluation of AF voltage which correlates better with MRI-DE defined scar than sinus rhythm voltage. We evaluated the clinical efficacy of additional voltage-based substrate modification in the Persistent AF patient cohort in a single centre case series. Methods 22 PsAF patients undergoing catheter ablation were recruited. Left atrial electroanatomical maps were created in AF before any ablation was performed in all patients. Mean peak to peak AF voltage mapping was undertaken using 8s segments of AF ( Results Of the 22 patients currently under follow up, 16 patients are more than 12 months after their initial procedure. 11/16 patients have had no recurrence and no patient is currently on anti-arrhythmic medication. Conclusion From our series, 69% of PsAF patients remain arrhythmia free at one year follow up post blanking period with a single procedure. Ablation of low voltage areas appears to infer incremental benefit in the Persistent AF population. Table 1 Mean Age, yrs 64 ± 9 Male 19 (86.3) Diabetes mellitus 1 (4.5) Hypertension 7 (31.8) TIA/CVA 2 (9) Left ventricular EF ≥55% 22 (100.0) LA size (diameter, according to British Society of Echocardiography Guidelines) Normal -Mild 12 (54.5) Moderate - Severe 10 (45.5) Mean AF duration, months 24.2 ± 20.8 Current antiarrhythmic strategy Amiodarone 3 (13.6) Sotalol 1 (4.5) Current anticoagulation Warfarin 3 (13.6) Direct oral anticoagulants 19 (86.3) Values are mean ± SD or N (%) or duration in months ± SD AF = atrial fibrillation; CVA= cerebrovascular accident; EF = ejection fraction; LA = left atrium; TIA = transient ischaemic attack. Baseline characteristics of patients (n = 22) Abstract Figure. Ablation sets and AF Voltage

Aims: A prolonged PR interval may adversely affect ventricular filling and therefore cardiac function. AV delay can be corrected using right-ventricular-pacing (RVP) but this induces ventricular dyssynchrony, itself harmful. Therefore, in intermittent heart-block, pacing-avoidance algorithms are often implemented. We tested His-bundle pacing (HBP) as an alternative. Methods: Out-patients with a long PR interval(>200ms) and intermittent need for ventricular pacing were recruited. We measured within patient differences in high-precision haemodynamics between AV-optimized RVP, and HBP, as well as a pacing-avoidance algorithm [Managed Ventricular Pacing (MVP)]. Results We recruited 18 patients. Mean left ventricular ejection fraction was 44.3±9%. Mean intrinsic PR interval was 266±42ms and QRS duration was 123±29ms. RVP lengthened QRS duration(+54 ms, 95%CI 42 to 67ms, p

Funding Acknowledgements Our research group receives an educational grant from Abbott Inc. Introduction. Outcomes from catheter ablation of persistent AF (psAF) are not favourable. The two prevailing major directions to improve success are left atrial (LA) substrate ablation, and non pulmonary vein driver ablation. In LA substrate ablation guided by intracardiac voltage, there is debate on the most fitting mapping rhythm and the appropriate cut offs for low voltage zones (LVZ). Non pulmonary vein driver ablation requires extensive experience and relies on complex pattern recognition by the operator, introducing subjectivity, that may lead to reduced reproducibility. AF drivers have been shown to localise to LVZs. We propose an objective, patient-tailored method of identifying rapid activity within LVZs to locate drivers of psAF. Methods. Eleven patients (61 ± 10.8 years of age, 9 male) undergoing first time catheter ablation for psAF were included. 3D maps were collected with a double spiral 20 pole catheter, in non-cardiac triggered mode, recording 8s segments at each bipole. Mean AF voltage (AFV) a AF cycle length (AFCL) was calculated for each 8s segment using automated algorithms. Grades of rapid activity and low voltage were defined as the 10th 20th and 30th percentile of all collected points within a patient. Percentile-matched composite LVZ-ARA maps were created on a research platform. Results. Mean LVZ percentage of the total mapped area was 4.67 ± 2.4%, 13.95 ± 3.8%, 23.81 ± 5.7% for the 10th, 20th and 30th percentiles respectively (Table 1). Mean, percentile matched LVZ-ARA overlap area percentage of the total mapped area was 0.3 ± 0.25% (10th-10th), 0.86 ± 0.58 (20th-20th), 3.1 ± 1.9% (30th-30th). ARAs represented a small proportion of all LVZs. Location of overlap areas differed significantly between patients and were marked with colours. Multi-colour areas including purple represent LVZ, multi-colour areas excluding purple, show LVZ-ARA overlap (examples in Fig 1). Conclusion. Analysis of LVZ-ARA overlap by mean AFV and AFCL provides an objective method of identifying potential drivers that localise to LVZs. The identified overlap areas constituted small, occasionally disparate areas within the LVZ of the LA. By adjusting the AFCL and AFV percentiles, the overlap areas can be tailored at the operator’s discretion, maintaining reproducible, objective decision making, without the need for complex pattern recognition. If ablation is planned, established techniques can be used to target the overlap areas, such as homogenisation or transection and connection to anatomical or ablative non-conductive tissues. AFCL 10th AFCL 20th AFCL 30th AFV 10th AFV 20th AFV 30th All patients 128 ± 13 ms 144 ± 10 ms 150 ± 9 ms 0.15 ± 0.02 mV 0.19 ± 0.03 mV 0.24 ± 0.04 mV Mean values of percentile cut offs. AFCL: AF cycle length; AFV: AF voltage Abstract Figure. Fig 1

Funding Acknowledgements Our research group receives an educational grant from Abbott Inc. Introduction. There is evidence to suggest that structural remodelling in psAF potentially gives rise to areas of rapid cycle length activity that may act as driving mechanisms. We describe a new method to compare rapid activity (RA) in psAF prior to and after pulmonary vein isolation, in extended AF segments (EAFS). We focus on patterns of RA, based on the hypothesis that AF drivers are transient but recur in the same locations. Methods. Five patients (61 ± 8 years of age, 3 male) for catheter ablation of psAF were included. 3D maps were collected with a double spiral 20 pole catheter. In stable locations, pre and post PVI, 37s EAFS were recorded using 8s segments, automatically every 1s, creating a 7s overlap between segments. Dominant cycle length (DCL) was determined for every 8s segment by a fully automated algorithm. RA was defined as the rapidest 20th percentile for each patient. RA episodes consisted of continuous segments with rapid DCL (black lines in Fig 1) and terminated with a non-rapid segment (red lines on Fig 1). Episodes were truncated where overlap occurred (Box 1 and Box 2 in Fig 1). The pattern of RA was assessed by the number, cumulative duration and mean duration of RA episodes within an EAFS pre and post PVI. Results. Mean DCL of EAFS increased significantly in 4/5 patients after PVI, the number of EAFS with rapid activity showed a reduction in all patients. The percentage of new sites with RA post PVI was 27%. The number of sites that retained RA post PVI was 14 ± 11.3 (58.3%; Table 1). Of these, number and cumulative duration of RA did not change in 4/5 patients, and mean duration of RA remained stable in 5/5. Conclusion. An automated DCL algorithm shows that, in most cases, global AFCL prolongs significantly with PVI overall, but selected foci retain RA and RA patterns. These may represent active drivers, as their activity appears to be independent of their surroundings. Table 1 Patient ID Number of segments Mean AFCL ± SD of all segments Number of EAFS with rapid activity Pre-PVI Post-PVI P Pre-PVI Post-PVI New sites 1 145 135 ± 8.9 141 ± 9.8 Abstract Figure.

Aims A prolonged PR interval may adversely affect ventricular filling and, therefore, cardiac function. AV delay can be corrected using right ventricular pacing (RVP), but this induces ventricular dyssynchrony, itself harmful. Therefore, in intermittent heart block, pacing avoidance algorithms are often implemented. We tested His‐bundle pacing (HBP) as an alternative. Methods Outpatients with a long PR interval (>200 ms) and intermittent need for ventricular pacing were recruited. We measured within‐patient differences in high‐precision hemodynamics between AV‐optimized RVP and HBP, as well as a pacing avoidance algorithm (Managed Ventricular Pacing [MVP]). Results We recruited 18 patients. Mean left ventricular ejection fraction was 44.3 ± 9%. Mean intrinsic PR interval was 266 ± 42 ms and QRS duration was 123 ± 29 ms. RVP lengthened QRS duration (+54 ms, 95% CI 42–67 ms, p

Introduction A spontaneous type I electrocardiogram (ECG) pattern and/or unheralded syncope are conventionally used as risk markers for primary prevention of sudden cardiac arrest/death (SCA/SCD) in Brugada syndrome (BrS). In this study, we determine the prevalence of conventional and newer markers of risk in those with and without previous aborted SCA events. Methods All patients with BrS were identified at our institute. History of symptoms was obtained from medical tests or from interviews. Other markers of risk were also obtained, such as presence of (1) spontaneous type I pattern, (2) fractionated QRS (fQRS), (3) early repolarization (ER) pattern, (4) late potentials on signal‐averaged ECG (SAECG), and (5) response to programmed electrical stimulation. Results In 133 patients with Bars, 10 (7%) patients (mean age = 39 ± 11 years; nine males) were identified with a previous ventricular fibrillation/ventricular tachycardia episode (n = 8) or requiring cardio‐pulmonary resuscitation (n = 2). None of these patients had a prior history of syncope before their SCA event. Only two (20%) patients reported a history of palpitations or dizziness. None had apneic breathing and three (30%) patients had a family history of SCA. From their ECGs, a spontaneous pattern was only found in one (10%) of these patients. Further, 10% of patients had fQRS, 17% had late potentials on SAECG, 20% had deep S waves in lead I, and 10% had an ER pattern in the peripheral leads. No significant differences were observed in the non‐SCA group. Conclusion The majority of BrS patients with previous aborted SCA events did not have a spontaneous type I and/or prior history of syncope. Conventional and newer markers of risk appear to only have limited ability to predict SCA.

Supplemental Digital Content is available in the text., Background: The mechanisms sustaining myocardial fibrillation remain disputed, partly due to a lack of mapping tools that can accurately identify the mechanism with low spatial resolution clinical recordings. Granger causality (GC) analysis, an econometric tool for quantifying causal relationships between complex time-series, was developed as a novel fibrillation mapping tool and adapted to low spatial resolution sequentially acquired data. Methods: Ventricular fibrillation (VF) optical mapping was performed in Langendorff-perfused Sprague-Dawley rat hearts (n=18), where novel algorithms were developed using GC-based analysis to (1) quantify causal dependence of neighboring signals and plot GC vectors, (2) quantify global organization with the causality pairing index, a measure of neighboring causal signal pairs, and (3) localize rotational drivers (RDs) by quantifying the circular interdependence of neighboring signals with the circular interdependence value. GC-based mapping tools were optimized for low spatial resolution from downsampled optical mapping data, validated against high-resolution phase analysis and further tested in previous VF optical mapping recordings of coronary perfused donor heart left ventricular wedge preparations (n=12), and adapted for sequentially acquired intracardiac electrograms during human persistent atrial fibrillation mapping (n=16). Results: Global VF organization quantified by causality pairing index showed a negative correlation at progressively lower resolutions (50% resolution: P=0.006, R2=0.38, 12.5% resolution, P=0.004, R2=0.41) with a phase analysis derived measure of disorganization, locations occupied by phase singularities. In organized VF with high causality pairing index values, GC vector mapping characterized dominant propagating patterns and localized stable RDs, with the circular interdependence value showing a significant difference in driver versus nondriver regions (0.91±0.05 versus 0.35±0.06, P=0.0002). These findings were further confirmed in human VF. In persistent atrial fibrillation, a positive correlation was found between the causality pairing index and presence of stable RDs (P=0.0005,R2=0.56). Fifty percent of patients had RDs, with a low incidence of 0.9±0.3 RDs per patient. Conclusions: GC-based fibrillation analysis can measure global fibrillation organization, characterize dominant propagating patterns, and map RDs using low spatial resolution sequentially acquired data.

INTRODUCTION: We hypothesized that very high density mapping of typical atrial flutter (AFL) would facilitate a more complete understanding of its circuit. Such very high density mapping was performed with the Rhythmia mapping system using its 64 electrode basket catheter. METHODS AND RESULTS: Data were acquired from 13 patients in AFL. Functional anatomy of the right atrium (RA) was readily identified during mapping including the Crista Terminalis and Eustachian ridge. The leading edge of the activation wavefront was identified without interruption and its conduction velocity (CV) calculated. CV was not different at the cavotricuspid isthmus (CTI) compared to the remainder of the RA (1.02 vs. 1.03 m/s, p = 0.93). The sawtooth pattern of the surface EKG flutter waves were compared to the position of the dominant wavefront. The downslope of the surface EKG flutter waves represented on average, 73% ± 9% of the total flutter cycle length. During the downslope the activation wavefront travelled significantly further than during the upslope (182 ± 21 ms vs. 68 ± 29 ms, p

Aims Rate adaptation of the action potential ensures spatial heterogeneities in conduction across the myocardium are minimized at different heart rates providing a protective mechanism against ventricular fibrillation (VF) and sudden cardiac death (SCD), which can be quantified by the ventricular conduction stability (V-CoS) test previously described. We tested the hypothesis that patients with a history of aborted SCD due to an underlying channelopathy or cardiomyopathy have a reduced capacity to maintain uniform activation following exercise. Methods and results Sixty individuals, with (n = 28) and without (n = 32) previous aborted-SCD event underwent electro-cardiographic imaging recordings following exercise treadmill test. These included 25 Brugada syndrome, 13 hypertrophic cardiomyopathy, 12 idiopathic VF, and 10 healthy controls. Data were inputted into the V-CoS programme to calculate a V-CoS score that indicate the percentage of ventricle that showed no significant change in ventricular activation, with a lower score indicating the development of greater conduction heterogeneity. The SCD group, compared to those without, had a lower median (interquartile range) V-CoS score at peak exertion [92.8% (89.8–96.3%) vs. 97.3% (94.9–99.1%); P Conclusion Data from this pilot study demonstrate the potential use of this technique in risk stratification for the inherited cardiac conditions.

Background Clinical identification of fibrillation drivers remains challenging in both atrial and ventricular fibrillation (VF). In this study, we developed novel tools using granger causality (GC) analysis for quantifying the causal relationship between neighbouring fibrillatory signals. We tested whether it was adaptable to low resolution, limited coverage and sequentially acquired data for quantifying global organisation of VF and mapping regions with stable rotational drivers (RDs). Methods Eighteen Sprague-Dawley rat hearts were perfused ex vivo for optical mapping studies. VF with differing degrees of organisation was induced with carbenoxolone (10–50μM, n=8), or prior maturation of patchy ventricular fibrosis (n=10) generated by ischaemia-reperfusion. After phase mapping, the data was downsampled to 25% of full resolution to develop validated GC-based tools. The causality pairing index (CPI), a global measure of organisation, quantified propagational effects between all neighboring signals. Low-resolution GC-vector maps localized areas harboring RDs and quantified the prevalence of RDs over time using a novel index called circular interdependence value (CIV). These GC-based tools were then adapted to analyze low-resolution multi-electrode electrograms of sixteen persistent-AF (psAF) patients presenting for a first ablation procedure. Results A spectrum of fibrillatory organisation and mechanisms in VF was observed. In rat VF there was a positive correlation between CPI and the number of stable RDs (R2=0.41, p=0.004), and CIV showed a significant difference in driver vs non-driver regions (0.91±0.05 vs 0.35±0.06, p=0.0002). Similarly, in psAF patients, there was a positive correlation between CPI and the number of stable RDs (R2=0.56, p≤0.001). GC vector mapping showed that 8/16 of patients had at least one RD area, and 8/16 had chaotic activity with no RDs. Conclusion Mechanisms of myocardial fibrillation occurs along a spectrum between organized activity with discrete areas harboring RDs and disorganised myocardial activation with no RDs. GC maps can be utilised for identifying regions localising RDs with sequential mapping in limited spatial resolution and coverage. In psAF GC-based analysis accurately identified specific fibrillatory mechanisms from low-resolution mapping. GC vector mapping holds potential for development with human fibrillation data as a mapping tool for driver guided ablation. Acknowledgement/Funding BHF Programme Grant PG/16/17/32069

Background: Ripple mapping (RM) is an alternative approach to activation mapping of atrial tachycardia (AT) that avoids electrogram annotation. We tested whether RM is superior to conventional annotation based local activation time (LAT) mapping for AT diagnosis in a randomized and multicenter study. Methods: Patients with AT were randomized to either RM or LAT mapping using the CARTO3v4 CONFIDENSE system. Operators determined the diagnosis using the assigned 3D mapping arm alone, before being permitted a single confirmatory entrainment manuever if needed. A planned ablation lesion set was defined. The primary end point was AT termination with delivery of the planned ablation lesion set. The inability to terminate AT with this first lesion set, the use of more than one entrainment manuever, or the need to crossover to the other mapping arm was defined as failure to achieve the primary end point. Results: One hundred five patients from 7 centers were recruited with 22 patients excluded due to premature AT termination, noninducibility or left atrial appendage thrombus. Eighty-three patients (pts; RM=42, LAT=41) completed mapping and ablation within the 2 groups of similar characteristics (RM versus LAT: prior ablation or cardiac surgery n=35 [83%] versus n=35 [85%], P =0.80). The primary end point occurred in 38/42 pts (90%) in the RM group and 29/41pts (71%) in the LAT group ( P =0.045). This was achieved without any entrainment in 31/42 pts (74%) with RM and 18/41 pts (44%) with LAT ( P =0.01). Of those patients who failed to achieve the primary end point, AT termination was achieved in 9/12 pts (75%) in the LAT group following crossover to RM with entrainment, but 0/4 pts (0%) in the RM group crossing over to LAT mapping with entrainment ( P =0.04). Conclusions: RM is superior to LAT mapping on the CARTO3v4 CONFIDENSE system in guiding ablation to terminate AT with the first lesion set and with reduced entrainment to assist diagnosis. Clinical Trials Registration: https://www.clinicaltrials.gov . Unique identifier: NCT02451995.

BACKGROUND Conventional mapping techniques during atrial fibrillation (AF) are difficult to apply because of cycle length irregularity. Mapping studies are usually restricted to short durations of AF in limited regions because of the laborious manual annotation of local activation time (LAT). The purpose of this study was to test an automated algorithm to map activation during AF, with comparable accuracy to manual annotation. METHODS Left atrial (LA) mapping was performed using a 20-pole double loop catheter (AFocusII) in 30-second data segments from 16 patients. The new algorithm (RETRO-Mapping) was designed to detect wavefront propagation between electrodes, and display activating wavefronts on a two-dimensional representation of the catheter. Activation patterns were validated against their bipolar electrograms and with isochronal maps. The mapping protocol was approved by the research ethics committee (13/LO1169 and 14/LO1367). RESULTS During AF, uniform wavefront activation direction (mean ± SD, degrees) from manually constructed isochronal maps was comparable to RETRO-Propagation Map (RETRO-PM) and RETRO-Automated Direction (RETRO-AD): 1 ± 6.9 for RETRO-PM; and 2 ± 6.6 for RETRO-AD. There was no significant difference in activation direction assigned to 1373 uniform wavefronts during AF when comparing RETRO-PM with RETRO-AD (Bland-Altman mean difference: -0.1 degrees; limits of agreement: -8.0 to 8.3; 95% CI -0.4 to 0.2; (r = 0.01) R2 =

Sudden cardiac death (SCD) is defined as unexpected death due to a cardiac disease, in a patient with or without known cardiac disease and which occurs within 1 hour from the appearance of the first clinical symptoms. The sudden cessation of cardiac activity leads to haemodynamic collapse, typically due to sustained ventricular tachyarrhythmias. The event is described as an aborted SCD (or sudden cardiac arrest) when an intervention (e.g. defibrillation) or spontaneous reversion restores circulation. The lack of uniformity with this definition complicates SCD statistics. By convention, the use of SCD to describe both fatal and non-fatal cardiac arrests persists. SCD continues to be a leading cause of death in Western countries, and accounts for 15%–20% of all natural deaths in adults in the US and Western Europe, and up to 50% of all cardiovascular deaths. In the US, estimates of SCDs from retrospective death certificate analyses range from 300 000 to 350 000 annually, giving an incidence of 0.1%–0.2% per year amongst the population above the age of 35 years. Event rates are said to be similar in Europe, although worldwide incidence is difficult to estimate and varies in accordance to the prevalence of CHD. The incidence of SCD increases with age and underlying cardiac disease. There is also a male preponderance, with men 2–3 times more likely to experience SCD than women, and this reflects the higher incidence of CHD in men.

Ventricular tachyarrhythmias are abnormal patterns of electrical activity arising from the ventricular tissue (myocardium and conduction tissue). Ventricular tachycardia (VT) is an abnormal rapid heart rhythm originating from the ventricles. The rhythm may arise from the ventricular myocardium and/or from the distal conduction system. The normal heart rate is usually regular, between 60 and 100 bpm, and there is synchronized atrial and ventricular contraction. In VT, the ventricles contract at a rate greater than 120 bpm and typically from 150 to 300 bpm, and are no longer coordinated with the atria. There is still organized contraction of the ventricles in VT, with discrete QRS complexes. It is a potentially life-threatening arrhythmia, with the risk of degenerating into ventricular fibrillation and resulting in sudden cardiac death. It is characterized by a broad-complex tachycardia on ECG.

Multifocal atrial tachycardia (MAT) is an atrial arrhythmia arising in the left or right atrium, or both, with multiple different P wave morphologies (at least three), with an atrial rate usually faster than 100 min−1. The atrial rhythm may be irregular; however, the defining difference between MAT and atrial fibrillation is the presence of a P wave prior to each QRS complex in MAT (but the absence of P waves in atrial fibrillation). MAT may be compared to sinus rhythm with very frequent polymorphic atrial ectopic beats, and in fact similar pathophysiologic mechanisms underlie both conditions; thus, differentiating one from the other may be difficult—the principle difference is the lack of a single dominant sinus pacemaker in MAT.

Atrioventricular (AV) re-entrant tachycardia (AVRT) is a type of supraventricular tachycardia, manifesting most commonly as a regular, narrow-QRS-complex tachycardia. It is usually a paroxysmal tachycardia, and is dependent upon the presence of an accessory electrical connection located between the atria and the ventricles (distinct and separate from the AV node–His–Purkinje system) and which is capable of atrioventricular (antegrade) or ventriculoatrial (retrograde) electrical conduction (or both). This pathway, together with the AV node–His–Purkinje system and the atrial and ventricular myocardia, forms a macro-re-entrant circuit which enables AVRT to occur.

Atrial flutter is the term given to one of the four types of supraventricular tachycardia; in it, atrial activation occurs as a consequence of a continuous ‘short circuit’: a defined and fixed anatomical route, resulting in a fairly uniform atrial rate, and uniform atrial flutter waves on the ECG. The ventricles are not a part of this arrhythmia circuit, and ventricular activation is variable, dependent on atrioventricular (AV) nodal conduction. Given that the atrial rate is essentially uniform (e.g. 300 min−1), ventricular activation tends to be regular (i.e. 150 min−1, 100 min−1, 75 min−1, etc., if the atrial rate is 300 mins−1), or regularly irregular if changes are occurring in the fraction of conducted impulses to the ventricles. When AV nodal conduction permits only 4:1 conduction or less, atrial flutter is usually obvious, but when ventricular rates are higher (150 min−1 or more) the flutter waves can be obscured by the QRS complexes, making diagnosis more difficult. Atrial flutter is of two types, typical and atypical. Typical atrial flutter is a right atrial tachycardia, with electrical activation proceeding around the tricuspid valve annulus. This arrhythmia is dependent on a zone of slow electrical conduction through the cavotricuspid isthmus (the tissue lying between the origin of the inferior vena cava and the posterior tricuspid valve). The resulting circuit can be either anticlockwise (activation proceeds up the inter-atrial septum, across the atrial roof, down the free wall, and then through the cavotricuspid isthmus to the basal septum) or clockwise (down the inter-atrial septum and around the circuit in the opposite direction). Anticlockwise typical atrial flutter is more common. Atypical atrial flutter refers to all other atrial flutters, and this includes other right atrial flutters (e.g. pericristal flutter), left atrial flutters, post-ablation or post-surgical flutters, and pulmonary vein flutters. The feature common to all types of flutter and which differentiates flutter from other types of supraventricular tachycardia is the presence of a macro-re-entrant anatomical circuit around which the electrical impulse travels continuously and repeatedly, thereby generating the flutter. Even though typical atrial flutter has a fairly obvious and specific appearance on the ECG, atypical flutters do not, and often it is only possible to differentiate atypical flutter from atrial tachycardias by invasive electrophysiology studies, as the ECG alone may be insufficient.

Sinus tachycardia is a condition of multiple different potential etiologies, characterized by an elevated rate of automaticity of the sinoatrial node, such that the heart rate is elevated. The exact point at which sinus tachycardia meets sinus rhythm is debatable; however, by convention, an upper rate of 100 min−1 is accepted for sinus rhythm; >100 min−1 denotes sinus tachycardia.