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The Brugada pattern manifests as a spontaneous variability of the electrocardiographic marker, suggesting a variability of the underlying electrical substrate.The purpose of this study was to investigate the response of the epicardial substrate of Brugada syndrome (BrS) to programmed ventricular stimulation and to Na blocker infusion.We investigated 6 patients (all male; mean age 54 ± 14 years) with BrS and recurrent ventricular fibrillation. Five had no type 1 BrS electrocardiogram pattern at admission. They underwent combined epicardial-endocardial mapping using multielectrode catheters. Changes in epicardial electrograms were evaluated during single endocardial extrastimulation and after low-dose ajmaline infusion (0.5 mg/kg in 5 minutes).All patients had a region in the anterior epicardial right ventricle with prolonged multicomponent electrograms. Single extrastimulation prolonged late epicardial components by 59 ± 31 ms and in 4 patients abolished epicardial components at some sites, without reactivation by surrounding activated sites. These localized blocks occurred at an initial coupling interval of 335 ± 58 ms and then expanded to other sites, being observed in up to 40% of epicardial sites. Ajmaline infusion prolonged electrogram duration in all and produced localized blocks in 62% of sites in the same patients as during extrastimulation. Epicardial conduction recovery after ajmaline occurred intermittently and at discontinuous sites and produced beat-to-beat changes in local repolarization, resulting in an area of marked electrical disparity. These changes were consistent with models based on microstructural alterations under critical propagation conditions.In BrS, localized functional conduction blocks occur at multiple epicardial sites and with variable patterns, without being reactivated from the surrounding sites.

INTRODUCTION: Microstructural abnormalities at the epicardium of the right ventricular outflow tract (RVOT) may provide the arrhythmia substrate in Brugada syndrome (BrS). Endocardial unipolar electroanatomical mapping allows the identification of epicardial abnormalities. We evaluated the clinical implications of an abnormal endocardial substrate as perceived by high-density electroanatomical mapping (HDEAM) in patients with BrS. METHODS: Fourteen high-risk BrS patients with aborted sudden cardiac death (SCD) (12 males, mean age: 41.9 ± 11.8 years) underwent combined endocardial-epicardial HDEAM of the right ventricle/RVOT, while 40 asymptomatic patients (33 males, mean age: 42 ± 10.7 years) underwent endocardial HDEAM. Based on combined endocardial-epicardial procedures, endocardial HDEAM was considered abnormal in the presence of low voltage areas (LVAs) more than 1 cm2 with bipolar signals less than 1 mV and unipolar signals less than 5.3 mV. Programmed ventricular stimulation (PVS) was performed in all patients. RESULTS: The endocardial unipolar LVAs were colocalized with epicardial bipolar LVAs (p = .0027). Patients with aborted SCD exhibited significantly wider endocardial unipolar (p

Background Purkinje ectopics (PurkEs) are major triggers of idiopathic ventricular fibrillation (VF). Identifying clinical factors associated with specific PurkE characteristics could yield insights into the mechanisms of Purkinje-mediated arrhythmogenicity. Objective The purpose of this study was to examine the associations of clinical, environmental, and genetic factors with PurkE origin in patients with PurkE-initiated idiopathic VF. Methods Consecutive patients with PurkE-initiated idiopathic VF from 4 arrhythmia referral centers were included. We evaluated demographic characteristics, medical history, clinical circumstances associated with index VF events, and electrophysiological characteristics of PurkEs. An electrophysiology study was performed in most patients to confirm the Purkinje origin. Results Eighty-three patients were included (mean age 38 ± 14 years; 44 [53%] women), of whom 32 had a history of syncope. Forty-four patients had VF at rest. PurkEs originated from the right ventricle (RV) in 41 patients (49%), from the left ventricle (LV) in 36 (44%), and from both ventricles in 6 (7%). Seasonal and circadian distributions of VF episodes were similar according to PurkE origin. The clinical characteristics of patients with RV vs LV PurkE origins were similar, except for sex. RV PurkEs were more frequent in men than in women (76% vs 24%), whereas LV and biventricular PurkEs were more frequent in women (81% vs 19% and 83% vs 17%, respectively) (P Conclusion PurkEs triggering idiopathic VF originate dominantly from the RV in men and from the LV or both ventricles in women, adding to other sex-related arrhythmias such as Brugada syndrome or long QT syndrome. Sex-based factors influencing Purkinje arrhythmogenicity warrant investigation.

Introduction Ventricular fibrillation (VF) is the main mechanism of sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). The origin of VF and the success of catheter ablation to eliminate recurrent episodes in this population are poorly understood. Methods and results From 2010 to 2014, five patients with HCM (age 21 ± 9 years, three female) underwent invasive electrophysiological studies and ablation at our center after resuscitation from recurrent (9 ± 7) episodes of VF. Ventricular premature beats (VPBs), seen to initiate VF in certain cases, were recorded noninvasively before the ablation procedure. Postprocedural computed tomography (CT) was performed to correlate ablation sites with myocardial hypertrophy in three patients. Outcomes were assessed by clinical follow-up and implantable cardioverter-defibrillator interrogations. VPB triggers were localized invasively to the distal left Purkinje conduction system (left posterior fascicle [2], left anterior fascicle [1], and both fascicles [2]). All targeted VF triggers were successfully eliminated by radiofrequency ablation in the left ventricle. Among patients with postablation CT imaging, 93 ± 12% of ablation sites corresponded to hypertrophied segments. Over 50 ± 38 months, four of five patients were free from primary VF without antiarrhythmic drug therapy. One patient who had 13 episodes of VF before ablation had a single recurrence. Conclusion In our study of patients with HCM and recurrent VF, VF was not initiated from the myocardium but rather from Purkinje arborization. These sources colocalized with the hypertrophic substrate, suggesting electromechanical interaction. Focal ablation at these sites was associated with a marked reduction in VF burden.

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

Background Localized staining due to venule injury is attributable to ethanol infusion into the vein of Marshall (Et-VOM). Objective The purpose of this study was to investigate adverse outcomes of localized staining during Et-VOM in patients undergoing ablation for atrial fibrillation. Methods Two hundred four patients (age 64 ± 10 years; 153 male) were sorted based on the aspect of localized staining. Staining of atrial myocardium that spread uniformly along the VOM vascular tree following selective VOM venography was considered normal, in contrast to predominantly localized staining that spread concentrically from a focal point due to vascular injury. Outcomes between the 2 groups were compared. Results Localized staining was observed in 27% of patients. No patients developed clinically significant pericardial effusions during Et-VOM; however, 7 patients developed pericardial effusions on the first postprocedural day (3.6% in patients with vs 3.4% in patients without localized staining). No significant difference was found in achievement of acute mitral isthmus (MI) block (96% vs 98%) and size of the endocardial low-voltage area (8.5 ± 4.1 cm2 vs 9.3 ± 5.3 cm2) in patients with and without localized staining, respectively. Long-term follow-up was not impacted by localized staining. Freedom from recurrent atrial tachyarrhythmias (66% vs 76%) and durability of MI block (57% vs 54%) were not significantly different with and without localized staining. There were no cases of rehospitalization for pericarditis, chronic pericardial effusion, or heart failure. Conclusion In our study, localized staining was frequent but was not associated with clinically relevant impact or disadvantages.

Beyond pulmonary vein isolation, the two main additional strategies: Cox-Maze procedure or targeting of electrical signatures (focal bursts, rotational activities, meandering wavelets), remain controversial. High-density mapping of these arrhythmias has demonstrated firstly that a patchy lesion set is highly proarrhythmogenic, favoring macro-re-entry through conduction slowing and providing pivots for localized re-entry. Secondly, discrete anatomical structures such as the Vein or Ligament of Marshall (VOM/LOM) and the coronary sinus (CS) have epicardial muscular bundles that are more frequently involved in re-entry than previously thought. The Marshall Bundle can be ablated at any point along its course from the mid-to-distal coronary sinus to the left atrial appendage. If necessary, the VOM may be directly ablated using ethanol infusion to eliminate PV contributions and produce conduction block across the mistral isthmus. Ethanol ablation of the VOM, supplemented with RF ablation, may be more effective in producing conduction block at the mitral isthmus than repeat RF ablation alone.

Background Beyond pulmonary vein isolation (PVI), the optimal ablation strategy for persistent atrial fibrillation (AF) remains poorly defined. Objective The purpose of this study was to examine a novel comprehensive ablation strategy (Marshall bundle elimination, Pulmonary vein isolation, and Line completion for ANatomical ablation of persistent atrial fibrillation [Marshall-PLAN]) strictly based on anatomical considerations. Methods Left atrial (LA) sites were sequentially targeted as follows: (1) coronary sinus and vein of Marshall (CS-VOM) musculature; (2) PVI; and (3) anatomical isthmuses (mitral, roof, and cavotricuspid isthmus [CTI]). The primary endpoint was 12-month freedom from AF/atrial tachycardia (AT). Results Seventy-five consecutive patients were included (age 61 ± 9 years; 10 women; AF duration 9 ± 11 months; mean LA volume 197 ± 43 mL). VOM ethanol infusion was completed in 69 patients (92%). The full Marshall-PLAN lesion set (VOM, PVI, mitral, roof, and CTI with block) was successfully completed in 68 patients (91%). At 12 months, 54 of 75 patients (72%) were free from AF/AT after a single procedure (no antiarrhythmic drugs) in the overall cohort. In the subset of patients with a complete Marshall-PLAN lesion set (n = 68), the single procedure success rate was 79%. After 1 or 2 procedures, 67 of 75 patients (89%) remained free from AF/AT (no antiarrhythmic drugs). After 1 or 2 procedures, VOM ethanol infusion was complete in 72 of 75 patients (96%). Conclusion A novel ablation strategy that systematically targets anatomical atrial structures (VOM ethanol infusion, PVI, and prespecified linear lesions) is feasible, safe, and associated with a high rate of freedom from arrhythmia recurrence at 12 months in patients with persistent AF.

Recent data of electrophysiological mapping in patients with Brugada syndrome (BrS) suggest that the presence of an abnormal arrhythmogenic substrate in the epicardial right ventricular outflow tract is responsible for ST-segment elevation and ventricular fibrillation (VF). Complete elimination of the epicardial abnormal potentials normalizes Brugada-pattern electrocardiogram and suppresses VF recurrence. We herein report the first case of BrS in which an injection of adenosine unmasked dormant conduction in the epicardial RVOT after the disappearance of the epicardial potentials.

Background Ultralow temperature cyroablation (ULTC) is designed to create focal, linear, and circumferential lesions. The aim of this study was to assess the safety, efficacy, and durability of atrial and ventricular ULTC lesions in preclinical large animal models. Methods and results The ULTC system uses nitrogen near its liquid-vapor critical point to cool 11-cm ablation catheters. The catheter can be shaped to specific anatomies using pre-shaped stylets. ULTC was used in 11 swine and four sheep to create atrial (pulmonary vein isolation and linear ablation) and ventricular lesions. Acute and 90-day success were evaluated by intracardiac mapping and histologic examination. Cryoadherence was observed during all ULTC applications, ensuring catheter stability at target locations. Local electrograms were completely eliminated immediately after the first single-shot ULTC application in 49 of 53 (92.5%) atrial and in 31 of 32 (96.9%) ventricular applications. Lesion depth as measured on histology preparations was 1.96 ± 0.8 mm in atrial and 5.61 ± 2.2 mm in ventricular lesions. In all animals, voltage maps and histology demonstrated transmural and durable lesions without gaps, surrounded by intact collagen fibers without injury to surrounding tissues. Transient coronary spasm could be provoked with endocardial ULTC in the left ventricle in close proximity to a coronary artery. Conclusions ULTC created effective and efficient atrial and ventricular lesions in vivo without procedural complications in two large animal models. ULTC lesions were transmural, contiguous, and durable over 3 months.

Brugada syndrome (BrS) is a sudden cardiac death syndrome characterized by a coved-type electrocardiogram (ECG). Different disorders, such as ischemia, can emulate a Brugada-pattern ECG (Brugada phenocopy). We report herein, the first case of surgical epicardial electrophysiological mapping in a successfully resuscitated patient with an anomalous aortic origin of the coronary artery (AAOCA) associated with a coved-type ECG. It was debatable whether the coved-type ECG and the abnormal arrhythmogenic substrate in the epicardial right ventricular outflow tract were derived from BrS or from repetitive ischemia due to AAOCA; however, the epicardial electrophysiological mapping helped in deciding the treatment strategy. This article is protected by copyright. All rights reserved.

Aims An incomplete understanding of the mechanism of atrial tachycardia (AT) is a major determinant of ablation failure. We systematically evaluated the mechanisms of AT using ultra-high-resolution mapping in a large cohort of patients. Methods and results We included 107 consecutive patients (mean age: 65.7 ± 9.2 years, males: 81 patients) with documented endocardial gap-related AT after left atrial ablation for persistent atrial fibrillation (AF). We analysed the mechanism of 134 AT (94 macro-re-entries and 40 localized re-entries) using high-resolution activation mapping in combination with high-density voltage and entrainment mapping. Voltage in the conducting channels may be extremely low, even Conclusion High-resolution activation mapping in combination with high-density voltage and entrainment mapping is the ideal strategy to delineate the critical part of the circuit in endocardial gap-related re-entrant AT after AF ablation.

Background: Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease, and sudden cardiac death represents an important mode of death in these patients. Data evaluating the implantable cardioverter defibrillator (ICD) in this patient population remain scarce. Methods: A Nationwide French Registry including all patients with tetralogy of Fallot with an ICD was initiated in 2010 by the French Institute of Health and Medical Research. The primary time to event end point was the time from ICD implantation to first appropriate ICD therapy. Secondary outcomes included ICD-related complications, heart transplantation, and death. Clinical events were centrally adjudicated by a blinded committee. Results: A total of 165 patients (mean age, 42.2±13.3 years, 70.1% males) were included from 40 centers, including 104 (63.0%) in secondary prevention. During a median (interquartile range) follow-up of 6.8 (2.5–11.4) years, 78 (47.3%) patients received at least 1 appropriate ICD therapy. The annual incidence of the primary outcome was 10.5% (7.1% and 12.5% in primary and secondary prevention, respectively; P =0.03). Overall, 71 (43.0%) patients presented with at least 1 ICD complication, including inappropriate shocks in 42 (25.5%) patients and lead dysfunction in 36 (21.8%) patients. Among 61 (37.0%) patients in primary prevention, the annual rate of appropriate ICD therapies was 4.1%, 5.3%, 9.5%, and 13.3% in patients with, respectively, 0, 1, 2, or ≥3 guidelines-recommended risk factors. QRS fragmentation was the only independent predictor of appropriate ICD therapies (hazard ratio, 3.47 [95% CI, 1.19–10.11]), and its integration in a model with current criteria increased the 5-year time-dependent area under the curve from 0.68 to 0.81 ( P =0.006). Patients with congestive heart failure or reduced left ventricular ejection fraction had a higher risk of nonarrhythmic death or heart transplantation (hazard ratio, 11.01 [95% CI, 2.96–40.95]). Conclusions: Patients with tetralogy of Fallot and an ICD experience high rates of appropriate therapies, including those implanted in primary prevention. The considerable long-term burden of ICD-related complications, however, underlines the need for careful candidate selection. A combination of easy-to-use criteria including QRS fragmentation might improve risk stratification. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03837574.

Aims The precise localization of manifest posteroseptal accessory pathways (APs) often poses diagnostic challenges considering that a small area may encompass AP that may be ablated from the right or left endocardium, or epicardially within the coronary sinus (CS). We sought to explore whether the QRS transition pattern in the precordial lead may help to discriminate the necessary ablation approach. Methods and results Consecutive patients who underwent a successful ablation of a single manifest AP over a 5-year period were included. Standard 12-lead electrocardiograms were reviewed. A total of 273 patients were identified. Mean age was 31 ± 15 years and 62% were male. Of the 110 identified posteroseptal AP, 64 were ablated from the right endocardium, 33 from the left endocardium, and 13 inside the CS. While a normal precordial QRS transition was most often observed, a subset of 33 patients presented an atypical ‘double transition’ pattern which specifically identified right endocardial AP. The combination of a q wave in V1 with a proportion of the positive QRS component in V1 V3, predicted a right endocardial AP with a 100% specificity. In case of a positive QRS sum in V2, this ‘double transition’ pattern predicted a posteroseptal right endocardial AP with 99.5% specificity and 44% sensitivity. The positive predictive value was 97%. The only false positive was a midseptal AP. In the case of a negative or isoelectric QRS sum in V2, APs were located more laterally on the tricuspid annulus. Conclusion The combination of a q wave in V1 with a double QRS transition pattern in the precordial leads is highly specific of a right endocardial AP and rules out the need for CS or left-sided mapping.

Background Data on the optimal location of the ECG leads for the diagnosis of drug-induced long QT syndrome (diLQTS) with Torsades de Pointes (TdP) are lacking. Methods We systematically reviewed the literature for ECGs of patients with diLQTS and subsequent TdP. We assessed T-wave morphology in each lead and measured the longest QT interval in the limb and chest leads in a standardized fashion. Results Of 84 patients, 61.9% were female and mean age was 58.8 years. QTc was significantly longer in chest versus limb leads (mean (standard deviation) 671 (102) vs 655 (97) ms, p=0.02). Using only limb leads for QT interpretation, 18 (21.4%) ECGs were non-interpretable: 10 (11.9%) due to too flat T-waves, 7 (8.3%) due to frequent, early PVCs and 1 (1.2%) due to too low ECG recording quality. In the chest leads, ECGs were non-interpretable in 9 (10.7%) patients: 6 (7.1%) due to frequent, early PVCs, 1 (1.2%) due to insufficient ECG quality, 2 (2.4%) due to missing chest leads but none due to too flat T-waves. The most common T-wave morphologies in the limb leads were flat (51.0%), broad (14.3%) and late peaking (12.6%) T-waves. Corresponding chest lead morphologies were inverted (35.5%), flat (19.6%) and biphasic (15.2%) T-waves. Conclusions Our results indicate that QT evaluation by limb leads only underestimates the incidence of diLQTS experiencing TdP and favors the screening using both limb and chest lead ECG. This article is protected by copyright. All rights reserved.

Objectives This study systematically evaluated mechanisms of atrial tachycardia (AT) by using ultra-high-resolution mapping in a large cohort of patients. Background An incomplete understanding of the mechanism of AT is a major determinant of ablation failure. Methods Consecutive patients with ≥1 AT (excluding cavotricuspid isthmus–dependent flutter) were included. Mapping was performed with a 64-pole mapping catheter. The AT mechanism was defined based on activation mapping and confirmed by entrainment in selected cases. Results A total of 132 patients were included (60 ± 12 years; 31 [23%] female; 111 [84%] previous atrial fibrillation [AF] ablation; 5 [4%] previous left atriotomy). One hundred four (94%) of the 111 post–AF ablation AT patients had substrate-based ablation during the index AF ablation. A total of 214 ATs were mapped, with complete definition of the AT mechanism in 206 (96%). A total of 129 (60%) had anatomic macro re-entry (circuit diameter 44.2 ± 9.6 mm), 57 (27%) had scar-related localized re-entry (circuit diameter 25.8 ± 12.2 mm), and 20 (9%) had focal AT. Fifty-eight (45%) patients had multiple ATs (27 [20%] dual-loop re-entry; 60 [43%] sequential AT) with complex and highly variable transitions between AT circuits. A total of 116 (90%) of 129 macro re-entrant ATs, 56 (98%) of 57 localized AT, and 20 (100%) of 20 focal ATs terminated after radiofrequency ablation. After a mean follow-up of 13 ± 9 months, 57 (46%) patients experienced recurrence of AT. Conclusions Among patients with AT in the context of previous atrial interventions, particularly post–AF ablation patients, multiple complex AT circuits are common. Despite complete delineation of arrhythmia circuits using ultra-high-resolution mapping and high acute ablation success rates, long-term freedom from AT is modest.

Aims We hypothesized that an epicardial approach using ethanol infusion in the vein of Marshall (EIVOM) may improve the result of ablation for perimitral flutter (PMF). Methods and results We studied 103 consecutive patients with PMF undergoing high-resolution mapping. The first 71 were treated with radiofrequency (RF) ablation alone (RF-group), and the next 32 underwent EIVOM followed by RF on the endocardial and epicardial mitral isthmus (EIVOM/RF-group). Contact force was not measured during ablation. Acute and 1-year outcomes were compared. Flutter termination rates were similar between the RF-group (63/71, 88.7%) and EIVOM/RF-group (31/32, 96.8%, P = 0.27). Atrial tachycardia (AT) terminated with EIVOM alone in 22/32 (68.6%) in the EIVOM/RF-group. Bidirectional block of mitral isthmus was always achieved in the EIVOM/RF-group, but significantly less frequently achieved in the RF-group (62/71, 87.3%; P = 0.05). Median RF duration for AT termination/conversion was shorter [0 (0–6) s in the EIVOM/RF-group than 312 (55–610) s in the RF-group, P Conclusion Ethanol infusion in the vein of Marshall may reduce RF duration required for PMF termination as well as for mitral isthmus block without severe complications, and the mid-term outcome may be improved by this approach.

Idiopathic ventricular fibrillation is diagnosed in patients who survived a ventricular fibrillation episode without any identifiable structural or electrical cause after extensive investigations. It is a common cause of sudden death in young adults. The study reviews the diagnostic value of systematic investigations and the new insights provided by detailed electrophysiological mapping. Recent studies have shown the high incidence of microstructural cardiomyopathic areas, which act as the substrate of ventricular fibrillation re-entries. These subclinical alterations require high-density endo- and epicardial mapping to be identified using electrogram criteria. Small areas are involved and located individually in various sites (mostly epicardial). Their characteristics suggest a variety of genetic or acquired pathological processes affecting cellular connectivity or tissue structure, such as cardiomyopathies, myocarditis, or fatty infiltration. Purkinje abnormalities manifesting as triggering ectopy or providing a substrate for re-entry represent a second important cause. The documentation of ephemeral Purkinje ectopy requires continuous electrocardiography monitoring for diagnosis. A variety of diseases affecting Purkinje cell function or conduction are potentially at play in their pathogenesis. Comprehensive investigations can therefore allow the great majority of idiopathic ventricular fibrillation to ultimately receive diagnoses of a cardiac disease, likely underlain by a mosaic of pathologies. Precise phenotypic characterization has significant implications for interpretation of genetic variants, the risk assessment, and individual therapy. Future improvements in imaging or electrophysiological methods may hopefully allow the identification of the subjects at risk and the development of primary prevention strategies., Highlights • VF can be unexplained despite extensive investigations, notably in the young. • The use of high-density electrophysiological mapping detects causes in the great majority of victims. • Microstructural cardiomyopathies are the main causes, likely underlain by multiple pathological processes. • The phenotypic characterization of substrate is critical to develop therapy and interpret genetic results., Central Illustration

Background No study to date has used high-density mapping to investigate the relationship between prior radiofrequency (RF) lesions for persistent atrial fibrillation (PsAF) ablation and subsequent atrial tachycardias (ATs). Methods From 41 consecutive patients who underwent AT ablation at a second procedure using an ultrahigh-density mapping system, 22 patients (38 ATs) were included as they also had complete maps with a multipolar catheter and three-dimensional (3D) mapping system at the time of the first PsAF ablation procedure. We, therefore, compared voltage maps from the first AF ablation procedure to those from the subsequent AT ablation procedure, as well as the lesion sets used for AF ablation vs the activation patterns in AT during the second procedure. Results In the 38 ATs, 211 of 285 analyzed atrial areas displayed low voltage area (LVA) (74%). Eighteen percent (38/211) existed before the index ablation for AF while 82% (173/211) were newly identified as LVA during the second procedure. Ninety-nine percent (172/173) of the newly developed LVA colocalized with RF lesions delivered for PsAF. Of the 38 ATs, 89.5% (34/38) AT circuits were associated with newly developed LVA due to RF lesions whilst 10.5% (4/38) AT circuits were associated with pre-existing LVA observed at the index procedure. No AT circuit was completely independent from index RF lesions in this series. Conclusions Analysis of detailed 3D electroanatomical mapping demonstrates that most ATs after PsAF ablation are involving LVAs due to index RF lesions.

BACKGROUND: The mechanisms by which sodium channel blockade and high-rate pacing modify electrogram (EGM) substrates of Brugada syndrome (BrS) have not been elucidated. OBJECTIVE: The purpose of this study was to determine the effect of ajmaline and high pacing rate on the BrS substrates. METHODS: Thirty-two patients with BrS (mean age 40 ± 12 years) and frequent ventricular fibrillation episodes underwent right ventricular outflow tract substrate electroanatomical and electrocardiographic imaging (ECGI) mapping before and after ajmaline administration and during high-rate atrial pacing. In 4 patients, epicardial mapping was performed using open thoracotomy with targeted biopsies. RESULTS: Ajmaline increased the activation time delay in the substrate (33%; P = .002), ST-segment elevation in the right precordial leads (74%; P < .0001), and the area of delayed activation (170%; P < .0001), coinciding with the increased substrate size (75%; P < .0001). High atrial pacing rate increased the abnormal EGM duration at the right ventricular outflow tract areas from 112 ± 48 to 143 ± 66 ms (P = .003) and produced intermittent conduction block and/or excitation failure at the substrate sites, especially after ajmaline administration. Biopsies from the 4 patients with thoracotomy showed epicardial fibrosis where EGMs were normal at baseline but became fractionated after ajmaline administration. In some areas, local activation was absent and unipolar EGMs had a monophasic morphology resembling the shape of the action potential. CONCLUSION: Sodium current reduction with ajmaline severely compromises impulse conduction at the BrS fibrotic substrates by producing fractionated EGMs, conduction block, or excitation failure, leading to the Brugada ECG pattern and favoring ventricular fibrillation genesis.

Background: Sole pulmonary vein (PV) isolation by ablation therapy prevents atrial fibrillation (AF) in patients with short episodes of AF and without comorbidities. Since incomplete PV isolation can be curative, we tested the hypothesis that the PV in the absence of remodeling and comorbidities contains structural and functional properties that are proarrhythmic for AF initiation by reentry.Methods: We performed percutaneous transvenous in vivo endocardial electrophysiological studies and quantitative histological analysis of PV from healthy sheep.Results: The proximal PV contained more myocytes than the distal PV and a higher percentage of collagen and fat tissue relative to myocytes than the left atrium. Local fractionated electrograms occurred in both the distal and proximal PVs, but a large local activation (>0.75 mV) was more often present in the proximal PV than in the distal PV (86 vs. 50% of electrograms, respectively, p = 0.017). Atrial arrhythmias (run of premature atrial complexes) occurred more often following the premature stimulation in the proximal PV than in the distal PV (p = 0.004). The diastolic stimulation threshold was higher in the proximal PV than in the distal PV (0.7 [0.3] vs. 0.4 [0.2] mA, (median [interquartile range]), p = 0.004). The refractory period was shorter in the proximal PV than in the distal PV (170 [50] vs. 248 [52] ms, p < 0.001). A linear relation existed between the gradient in refractoriness (distal-proximal) and atrial arrhythmia inducibility in the proximal PV.Conclusion: The structural and functional properties of the native atrial-PV junction differ from those of the distal PV. Atrial arrhythmias in the absence of arrhythmia-induced remodeling are caused by reentry in the atrial-PV junction. Ablative treatment of early paroxysmal AF, rather than complete isolation of focal arrhythmia, may be limited to inhibition of reentry.

Introduction Human atria comprise distinct layers. One layer can bypass another, and lead to a downstream centrifugal propagation at their interface. We sought to characterize anatomical substrates, electrophysiological properties, and ablation outcomes of "pseudo-focal" atrial tachycardias (ATs), defined as macroreentrant ATs mimicking focal ATs. Methods and results We retrospectively analyzed left atrial ATs showing centrifugal propagation with post-pacing intervals (PPIs) after entrainment pacing suggestive of a macroreentrant mechanism. A total of 22 patients had pseudo-focal ATs consisting of 15 perimitral and 7 roof-dependent flutters. A low-voltage area was consistently found at the collision site and co-localized with distinct anatomical structures like the: (1) coronary sinus-great cardiac vein bundle (27%); (2) vein of Marshall bundle (18%); (3) Bachmann bundle (27%); (4) septopulmonary bundle (18%); and (5) fossa ovalis (9%). The mean missing tachycardia cycle length (TCL) was 65 ± 31 ms (22%) on the endocardial activation map. PPI was 0 [0-15] ms and 0 [0-21] ms longer than TCL at the breakthrough site and the opposite site, respectively. While feasible in 21 pseudo-focal ATs (95%), termination was better achieved by blocking the anatomical isthmus than ablating the breakthrough site [20/21 (95%) vs. 1/5 (20%); p Conclusion Perimitral and roof-dependent flutters with centrifugal propagation are favored by a low-voltage area located at well-identified anatomical structures. Comprehensive entrainment pacing maneuvers are crucial to distinguish pseudo-focal ATs from true focal ATs. Blocking the anatomical isthmus is a better therapeutic option than ablating the breakthrough site. This article is protected by copyright. All rights reserved.

Background: Because stretch of the atrial myocardium is proarrhythmic for atrial fibrillation (AF) and a left lateral body position increases atrial dimensions in humans, we hypothesized that left lateral recumbence is a frequent AF-triggering body position in AF patients.Methods: We performed a questionnaire study of symptomatic paroxysmal AF (episodes of AF < 1 week) patients scheduled for a first AF ablation therapy at Catharina Hospital, Eindhoven, the Netherlands and at University Hospital, Bordeaux, France.Results: Ninety-four symptomatic paroxysmal AF patients were included [mean age 61 ± 11 years, median AF history of 29(48) months, 31% were females]. Twenty-two percent of patients reported a specific body position as a trigger of their AF symptoms. The triggering body position was left lateral position in 57% of cases, supine position in 33%, right lateral position in 10%, and prone position in 5% (p = 0.003 overall difference in prevalence). Patients with positional AF had a higher body mass index compared to patients without nocturnal/positional AF [28.7(4.2) and 25.4(5.2) kg/m2, respectively, p = 0.025], but otherwise resembled these patients.Conclusion: Body position, and the left lateral position, in particular, is a common trigger of AF in symptomatic AF patients. Moreover, positional AF is associated with overweight. Understanding of the underlying mechanisms of positional AF can contribute to AF treatment and prevention.

Objectives A new electroanatomic mapping system (Rhythmia, Boston Scientific, Marlborough, Massachusetts) using a 64-electrode mapping basket is now available; we systematically assessed its use in complex congenital heart disease (CHD). Background The incidence of atrial arrhythmias post-surgery for CHD is high. Catheter ablation has emerged as an effective treatment, but is hampered by limitations in the mapping system’s ability to accurately define the tachycardia circuit. Methods Mapping and ablation data of 61 patients with CHD (35 males, age 45 ± 14 years) from 8 tertiary centers were reviewed. Results Causes were as follows: Transposition of Great Arteries (atrial switch) (n = 7); univentricular physiology (Fontans) (n = 8); Tetralogy of Fallot (n = 10); atrial septal defect (ASD) repair (n = 15); tricuspid valve (TV) anomalies (n = 10); and other (n = 11). The total number of atrial arrhythmias was 86. Circuits were predominantly around the tricuspid valve (n = 37), atriotomy scar (n = 10), or ASD patch (n = 4). Although the majority of peri-tricuspid circuits were cavo-tricuspid-isthmus dependent (n = 30), they could follow a complex route between the annulus and septal resection, ASD patch, coronary sinus, or atriotomy. Immediate ablation success was achieved in all but 2 cases; with follow-up of 12 ± 8 months, 7 patients had recurrence. Conclusions We demonstrate the feasibility of the basket catheter for mapping complex CHD arrhythmias, including with transbaffle and transhepatic access. Although the circuits often involve predictable anatomic landmarks, the precise critical isthmus is often difficult to predict empirically. Ultra–high-density mapping enables elucidation of circuits in this complex anatomy and allows successful treatment at the isthmus with a minimal lesion set.

Idiopathic ventricular fibrillation and J-wave syndromes are causes of sudden cardiac death (SCD) without any identified structural cardiac disease after extensive investigations. Recent data show that high-density electrophysiological mapping may ultimately offer diagnoses of subclinical diseases in most patients including those termed "unexplained" SCD. Three major conditions can underlie the occurrence of SCD: (1) localized depolarization abnormalities (due to microstructural myocardial alteration), (2) Purkinje abnormalities manifesting as triggering ectopy and inducible reentry; or (3) repolarization heterogeneities. Each condition may result from a spectrum of pathophysiologic processes with implications for individual therapy.

A novel "LUMIPOINT" software in the Rhythmia system (Boston Scientific) displays a histogram of activated area over the entire atrial tachycardia (AT) cycle length (CL) with a normalized score.The purpose of this study was to examine whether the pattern of this global activation histogram (GAH) identified reentrant vs focal AT and whether a decrease in atrial activation area, shown as valleys in the GAH, identifies isthmuses.One hundred eight activation maps of ATs (17 focal, 57 macroreentrant, 21 localized, 13 multiple loop) in 67 patients were reviewed retrospectively with the LUMIPOINT software. The ACTIVATION SEARCH feature highlighted the activated area in a given time period irrespective of the activation map. A 30-ms unit time interval was set, and the GAH patterns and electrophysiological properties of highlighted areas were examined.Focal ATs systematically displayed a plateau with GAH-Score0.1 for at least 30% of the CL. Most reentrant ATs (90/91 [98.9%]) lacked this plateau and displayed activity covering the entire CL, with 2 [1-2] GAH-Valleys per tachycardia. Each GAH-Valley highlighted 1 [1-2] areas in the map. Among 264 highlighted areas, 198 (75.0%) represented slow conduction, 19 (7.2%) lines of block, 27 (10.2%) wavefront collision, 3 (1.1%) unknown, and 17 (6.4%) absence of activation in focal ATs. Practical ablation sites all matched one of the highlighted areas based on GAH-Valleys, and they corresponded better with areas highlighted by GAH-Score ≤0.2 (P.0001).GAH shows focal vs reentrant mechanisms at first glance. Decrease in activated areas (displayed by GAH-Valleys) is mostly due to slow conduction and highlights areas of special interest, with 100% sensitivity for isthmus identification.

Background Atrial tachycardias (ATs) are often seen in the context of atrial fibrillation (AF) ablation. Objectives To evaluate the role of the Marshall bundle (MB) network in left atrial (LA) ATs using high-density 3-dimensional mapping. Methods A total of 199 ATs were mapped in 140 patients (112 male, mean age: 61.8 years); 133 (66.8%) were macroreentrant and 66 (33.2%) were scar-related reentry circuits. MB-dependent ATs were suggested by activation mapping analysis and confirmed with entrainment along the circuit. Results The MB network participated in 60 (30.2%) reentrant ATs: 31 perimitral ATs (PMATs) and 29 localized reentry circuits. Of 60 MB-related ATs, 49 (81.6%) terminated with radiofrequency (RF) ablation: 44 (73.3%) at the MB-LA junction and 5 (8.3%) at the MB-coronary sinus (CS) junction, while 9 (15%) terminated after 2.5–5 cc of ethanol infusion inside the vein of Marshall (VOM). Of the 31 PMATs, 17 (54.8%) terminated at the MB-LA junction, 5 (16.1%) at the MB-CS junction, and 7 (22.6%) with ethanol infusion. Of the 29 localized reentry circuits using the MB, 27 (93.1%) terminated at the MB-LA junction, none at the MB-CS junction, and 2 (6.9%) after ethanol infusion. Recurrences were mostly observed after RF ablation (18 of 37 patients, 49%) compared to ethanol infusion (1 of 9 patients, 11%) (P = .06). Conclusions MB reentrant ATs accounted for up to 30.2% of the left ATs after AF ablation. Ablation of the MB-LA or CS-MB connections or ethanol infusion inside the VOM is required to treat these arrhythmias.

Objectives This study sought to identify atrial tachycardia (AT) demonstrating atrial activation duration (AAD) lasting longer than the length of the tachycardia cycle (TCL); to assess AT prevalence; and to evaluate the mechanisms and characteristics associated with these AT episodes by using the Rhythmia system (Boston Scientific, Marlborough, Massachusetts). Background Ultra-high-density mapping allows very accurate characterization of mechanisms involved in AT. Some complex patterns may involve AAD which is longer than the tachycardia cycle length (TCL) which makes maps difficult to interpret. Prevalence and characteristics of such ATs are unknown. Methods A cohort of 100 consecutive patients undergoing ablation of 125 right (n = 21) or left (n = 104) ATs using ultra-high-density mapping were retrospectively included. Offline calculation of right or left AAD was compared to TCL. Results Mean TCL was 293 ± 65 ms, and mean AAD was 291 ± 74 ms (p = NS). AT mechanisms were macro-re-entry in 74 cases (59%), localized re-entry in 27 cases (22%), and focal AT in 21 cases (17%) (types were mixed in 3 cases). Fifteen ATs (12%) had AADs that were longer than the TCL (71 ± 45 ms longer, from 10 to 150 ms). TCL was equal to the AAD in 97 ATs (78%), whereas 13 ATs (10%) had AAD shorter than the TCL (focal AT in each case). There were no differences between right and left atria for prevalence of ATs with AADs that were longer than the TCLs. There were significant differences in AT mechanisms according to the AAD-to-TCL ratio (p Conclusions ATs with AAD lasting longer than the TCL were present in approximately 10% of the ATs referred for ablation, mostly in ATs caused by localized re-entry. Ultra-high-density mapping allows detection of these complex patterns of activation.

AimsAtrial fibrosis contributes to arrhythmogenesis in atrial fibrillation and can be detected by MRI or electrophysiological mapping. The current study compares the spatial correlation between delayed enhancement (DE) areas to low-voltage areas (LVAs) and to arrhythmogenic areas with spatio-temporal dispersion (ST-Disp) or continuous activity (CA) in atrial fibrillation (AF).Methods and resultsSixteen patients with persistent AF (nine long-standing) underwent DE-magnetic resonance imaging (1.25 mm × 1.25 mm × 2.5 mm) prior to pulmonary vein isolation. Left atrial (LA) voltage mapping was acquired in AF and the regional activation patterns of 7680 AF wavelets were analysed. Sites with ST-Disp or CA were characterized (voltage, duration) and their spatial relationship to DE areas and LVAs 0.5 mV). Spatio-temporal dispersion and CA more frequently co-localized with LVAs than with DE areas (78% vs. 63%, P = 0.02). Regional bipolar voltage of ST-Disp vs. CA was 0.64 ± 0.47 mV vs. 0.58 ± 0.51 mV. All 28 ST-Disp and 56 CA areas contained electrograms with prolonged duration (115 ± 14 ms) displaying low voltage (0.34 ± 0.11 mV).ConclusionA small portion of DE areas and LVAs harbour the arrhythmogenic areas displaying ST-Disp or CA. Most arrhythmogenic activities co-localized with LVAs, while there was less co-localization with DE areas. There is an important mismatch between DE areas and LVAs which needs to be considered when used as target for catheter ablation.

Background: Ventricular fibrillation (VF) storm after myocardial infarction (MI) is a life-threatening condition that necessitates multiple defibrillations. Catheter ablation is a potentially effective treatment strategy for VF storm refractory to optimal medical treatment. However, its impact on patient survival has not been verified in a large population. Methods: We conducted a multicenter, retrospective observational study involving consecutive patients who underwent catheter ablation of post-MI refractory VF storm without preceding monomorphic ventricular tachycardia. The target of ablation was the Purkinje-related ventricular extrasystoles triggering VF. The primary outcome was in-hospital and long-term mortalities. Univariate logistic regression and Cox proportional-hazards analysis were used to evaluate clinical characteristics associated with in-hospital and long-term mortalities, respectively. Results: One hundred ten patients were enrolled (age, 65±11years; 92 men; left ventricular ejection fraction, 31±10%). VF storm occurred at the acute phase of MI (4.5±2.5 days after the onset of MI during the index hospitalization for MI) in 43 patients (39%), the subacute phase (>1 week) in 48 (44%), and the remote phase (>6 months) in 19 (17%). The focal triggers were found to originate from the scar border zone in 88 patients (80%). During in-hospital stay after ablation, VF storm subsided in 92 patients (84%). Overall, 30 (27%) in-hospital deaths occurred. The duration from the VF occurrence to the ablation procedure was associated with in-hospital mortality (odds ratio for each 1-day increase, 1.11 [95% CI, 1.03–1.20]; P =0.008). During follow-up after discharge from hospital, only 1 patient developed recurrent VF storm. However, 29 patients (36%) died, with a median survival time of 2.2 years (interquartile range, 1.2–5.5 years). Long-term mortality was associated with left ventricular ejection fraction P =0.014), New York Heart Association class ≥III (hazard ratio, 2.68 [95% CI, 1.16–6.19]; P =0.021), a history of atrial fibrillation (hazard ratio, 3.89 [95% CI, 1.42–10.67]; P =0.008), and chronic kidney disease (hazard ratio, 2.74 [95% CI, 1.15–6.49]; P =0.023). Conclusions: In patients with MI presenting with focally triggered VF storm, catheter ablation of culprit triggers is lifesaving and appears to be associated with short- and long-term freedom from recurrent VF storm. Mortality over the long-term follow-up is associated with the severity of underlying cardiovascular disease and comorbidities in this specific patient population.

INTRODUCTION The epinephrine challenge has been proposed to improve the diagnosis of congenital long QT syndrome (LQTS). The aim of the study was to evaluate the diagnostic reliability of the epinephrine provocative test for LQTS diagnosis, taking into consideration intra- and interobserver variability in the interpretation of the test. METHODS AND RESULTS A retrospective analysis of 79 consecutive epinephrine provocative tests was conducted. Epinephrine was administered following a standardized protocol at two doses: 0.05 and 0.10 µg kg-1 min-1 . Electrocardiograms were blindly read twice by three different operators at ≥1-week interval. QT and RR intervals were collected at rest and at each dose, as well as final operator interpretation of the test. There was a high interobserver reproducibility of corrected QT measurements with an intraclass correlation (ICC) of 0.74 (95% confidence interval, 0.66-0.80) but a low interobserver reproducibility on the final interpretation with a κ of 0.31. Intraobserver reproducibility of corrected QT was very good (ICC 0.93; 0.91-0.95), but still resulted in an only moderate intraobserver reproducibility in the final diagnosis (κ of 0.47). Perceived certainty of at least 1 reading by 2 operators (N = 62 tests) increased interobserver reproducibility compared with baseline (κ = 0.43). CONCLUSION Inter- and intraobserver agreement in the interpretation of the epinephrine provocation test for LQTS is poor to modest. Complexity in interpretation varies from one case to the next. The low reliability of this test encourages a reconsideration of its importance in the clinical management of patients with suspected LQTS.

Background Ablation of complex atrial tachycardias (ATs) is difficult. Objective The purpose of this study was to elucidate a mechanism underlying the behavior of ATs during ablation and to create an algorithm to predict it. Methods An algorithm predicting termination/conversion of AT and the second AT circuit associated with the ablation site was developed from 52 index reentrant AT high-resolution activation maps in 45 patients (retrospective phase). First, the wavefront collision site was identified. Then, the N or N-1 beat was defined for each collision associated with the ablation site. When the AT involved wavefront collision solely between N-1/N-1 (N/N) beats, the AT would terminate during ablation. Conversely, when the AT included wavefront collision between N/N-1 beats, the index AT would convert to a second AT. The algorithm was then prospectively tested in 172 patients with 194 ATs (127 anatomic macroreentrant ATs [AMATs], 44 non-AMATs, 23 multiple-loop ATs). Results Accuracy in predicting AT termination/conversion and the second AT circuit was 95.9% overall, 96.1% in AMATs, 95.5% in non-AMATs, and 95.7% in multiple-loop ATs. Median (25th–75th percentile) absolute variation between predicted and actually observed cycle length of the second AT was 6 (4–9) ms. Prediction failure occurred in 8 ATs; either the second AT used an unmapped chamber or structure in the index map (n = 7) or a line of block was misinterpreted as very slow conduction in the index map (n = 1). Conclusion A simple mechanism underlies the behavior of ATs during ablation, even in complex ATs. With a simple algorithm using high-resolution mapping, AT termination/conversion and the second AT circuit and cycle length may be predicted from the index activation map.

In the context of structural heart disease, ventricular tachycardia (VT) is related to surviving fibres in incomplete scar. New technologies which allow electroanatomic mapping at higher density and with smaller, more closely spaced electrodes have allowed new insights into the characteristics of VT circuits. VT isthmuses are complex structures, with multiple entrances, exits and dead ends of activation. The isthmus is frequently defined by regions of functional block and several VT circuits can be possible in a VT “critical zone”. In this review, we discuss these new insights and how they may improve VT ablation strategies, as well as discussing emerging technologies which may further develop our understanding.

Activation mapping using noninvasive electrocardiographic imaging (ECGi) has recently been used to describe the physiology of different cardiac abnormalities. These descriptions differ from prior invasive studies, and both methods have not been thoroughly confronted in a clinical setting.The goal of the present study was to provide validation of noninvasive activation mapping in a clinical setting through direct confrontation with invasive epicardial contact measures.Fifty-nine maps were obtained in 55 patients and aligned on a common geometry. Nearest-neighbor interpolation was used to avoid map smoothing. Quantitative comparison was performed by computing between-map correlation coefficients and absolute activation time errors.The mean activation time error was 20.4 ± 8.6 ms, and the between-map correlation was poor (0.03 ± 0.43). The results suggested high interpatient variability (correlation -0.68 to 0.82), wide QRS patterns, and paced rhythms demonstrating significantly better mean correlation (0.68 ± 0.17). Errors were greater in scarred regions (21.9 ± 10.8 ms vs 17.5 ± 6.7 ms; P.01). Fewer epicardial breakthroughs were imaged using noninvasive mapping (1.3 ± 0.5 vs 2.3 ± 0.7; P.01). Primary breakthrough locations were imaged 75.7 ± 38.1 mm apart. Lines of conduction block (jumps of ≥50 ms between contiguous points) due to structural anomalies were recorded in 27 of 59 contact maps and were not visualized at these same sites noninvasively. Instead, artificial lines appeared in 33 of 59 noninvasive maps in regions of reduced bipolar voltage amplitudes (P = .03). An in silico model confirms these artificial constructs.Overall, agreement of ECGi activation mapping and contact mapping is poor and heterogeneous. The between-map correlation is good for wide QRS patterns. Lines of block and epicardial breakthrough sites imaged using ECGi are inaccurate. Further work is required to improve the accuracy of the technique.

Catheter ablation for ventricular tachycardia (VT) has been increasingly used over the past two decades in patients with structural heart disease (SHD). In these individuals, a substrate mapping strategy is being more commonly applied to identify targets for VT ablation, which has been shown to be more effective versus targeting mappable VTs alone. There are a number of substrate mapping methods in existence that aim to explore potential VT isthmuses, although their success rates vary. Most of the reported electrogram-based mapping studies have been performed with ablation catheters; meanwhile, the use of multipolar mapping catheters with smaller electrodes and closer interelectrode spacing has emerged, which allows for an assessment of detailed near-field abnormal electrograms at a higher resolution. Another recent advancement has occurred in the use of imaging techniques in VT ablation, particularly in refining the substrate. The goal of this paper is to review the key developments and limitations of current mapping strategies of substrate-based VT ablation and their outcomes. In addition, we briefly summarize the role of cardiac imaging in delineating VT substrate.

Successful mapping and ablation of ventricular tachycardias remains a challenging clinical task. Whereas conventional entrainment and activation mapping was for many years the gold standard to identify reentrant circuits in ischaemic ventricular tachycardia ablation procedures, substrate mapping has become the cornerstone of ventricular tachycardia ablation. In the last decade, technology has dramatically improved. In parallel to high-density automated mapping, cardiac imaging and image integration tools are increasingly used to assess the structural ventricular tachycardia substrate. The aim of this review is to describe the technologies underlying these new mapping systems and to discuss their possible role in providing new insights into identification and visualization of reentrant tachycardia mechanisms.

Ventricular fibrillation (VF) is a common and life-threatening arrhythmia resulting in sudden cardiac death (SCD). Due to the inherent challenges of mapping VF in humans, the underlying mechanisms that initiate and sustain this common arrhythmia are still poorly understood. In high-risk patients and survivors of SCD, implantable cardioverter defibrillators (ICD) play a central role in treating VF episodes, however, ICDs do not prevent VF recurrences and patients remain at risk of electrical storm and multiple shocks that are often refractory to escalation of medical therapy. More recently, the utility of catheter ablation (CA) has extended to the treatment of VF storms. This review will focus on updates in elucidating the mechanism of VF leading into the role and indication of CA as a treatment strategy.

Introduction: Human atria comprise distinct epicardial layers, which can bypass endocardial layers and lead to downstream centrifugal propagation at the “epi-endo” connection. We sought to characterize anatomical substrates, electrophysiological properties, and ablation outcomes of “pseudo-focal” atrial tachycardias (ATs), defined as macroreentrant ATs mimicking focal ATs. Methods and Results: We retrospectively analyzed ATs showing centrifugal propagation with post-pacing intervals (PPIs) after entrainment pacing suggestive of a macroreentry. A total of 26 patients had pseudo-focal ATs consisting of 15 perimitral, 7 roof-dependent, and 5 cavotricuspid isthmus (CTI)-dependent flutters. A low-voltage area was consistently found at the collision site and co-localized with epicardial layers like the: (1) coronary sinus-great cardiac vein bundle (22%); (2) vein of Marshall bundle (15%); (3) Bachmann bundle (22%); (4) septopulmonary bundle (15%); (5) fossa ovalis (7%); and (6) low right atrium (19%). The mean missing tachycardia cycle length (TCL) was 67 ± 29 ms (22%) on the endocardial activation map. PPI was 9 [0-15] ms and 10 [0-20] ms longer than TCL at the breakthrough site and the opposite site, respectively. While feasible in 25 pseudo-focal ATs (93%), termination was better achieved by blocking the anatomical isthmus than ablating the breakthrough site [24/26 (92%) vs. 1/6 (17%); p < 0.001]. Conclusion: Perimitral, roof-dependent, and CTI-dependent flutters with centrifugal propagation are favored by a low-voltage area located at well-identified epicardial bundles. Comprehensive entrainment pacing maneuvers are crucial to distinguish pseudo-focal ATs from true focal ATs. Blocking the anatomical isthmus is a better therapeutic option than ablating the breakthrough site.

Background Mitral isthmus gaps have been ascribed to an epicardial musculature anatomically related to the great cardiac vein (GCV) and the vein of Marshall (VOM). Their lumen offers an access for radiofrequency application or ethanol infusion, respectively. Objective The purpose of this study was to evaluate the frequency of mitral isthmus gaps accessible via the GCV lumen, to assess their location around the GCV circumference, and to propose an efficient ablation strategy when present. Methods One hundred consecutive patients underwent VOM ethanol infusion (step 1) and endocardial linear ablation from the mitral annulus to the left inferior pulmonary vein (step 2). In cases of mitral isthmus gap, endovascular ablation of the GCV anchored wall facing the left atrium was systematically performed (step 3), while the opposite GCV free wall was targeted in case of block failure only (step 4). Results After VOM ethanol infusion and endocardial ablation, mitral isthmus block occurred in 51 patients (51%). Pacing maneuvers and activation sequences demonstrated an epicardial gap via the VOM in 2 patients (2%) and via the GCV in 47 patients (47%). In the latter case, block was achieved at the GCV anchored wall in 42 patients (89%) and the GCV free wall in 5 patients (11%). Global success rate of mitral isthmus block was 98%. No tamponade occurred. Conclusion With the advent of VOM ethanol infusion, residual mitral isthmus gaps are mostly eliminated within the first centimeter of the GCV. Thorough mapping of the entire circumference of the GCV wall can help identify these epicardial gaps.

Funding Acknowledgements Type of funding sources: None. Background Atrial tachycardias (ATs) are often seen in the context of AF ablation. Objectives We evaluated the role of the Marshall bundle (MB) network in left atrial (LA) ATs using high-density high-spatial resolution 3D mapping. Methods 199 post-AF ablation LA tachycardias were mapped in 140 consecutive patients (112 (80%) males, mean age: 61.8 years); 133 (66.8%) were macro-reentrant and 66 (33.2%) were scar-related re-entry. MB-dependent perimitral AT (PMAT) was diagnosed where the difference between the post pacing interval and the tachycardia cycle length (PPI-TCL) was 20ms in areas bypassed by the VOM (the distal coronary sinus (CS), the posterior LA and the mitral isthmus). MB-related re-entry was diagnosed by PPI-TCL 20ms in the septal annulus. Typically, in MB-dependent localized re-entry, the earliest activation was found along the MB-LA endocardial connection or MB-CS epicardial connection. Results The MB network was found to participate in 60 (30.2%) re-entrant ATs, 31 PMATs and 29 localized re-entries. High-frequency multiphasic fragmented electrograms with long duration were often recorded endocardially or epicardially at the MB-LA or MB-CS connections. The amplitude and duration of these signals were 0.5 ± 0.79 mV and 65 ± 40 ms for MB-PMATs and 0.26 ± 0.28mV and 122 ± 67 ms for MB-localized re-entries. Unipolar EGMs at the site of endocardial-epicardial breakthrough had a rS pattern in all MB-related ATs. Of 60 MB-related ATs, 49 (81.6%) terminated with RF ablation, 44 (73.3%) at the MB-LA junction and 5 (8.3%) at the MB-CS junction, while 9 (15%) terminated after 2.5-5 cc of alcohol infusion inside the vein of Marshall (VOM). Of the 31 MB-related macroreentrant ATs, 17 (54.8%) terminated at the MB-LA junction, 5 (16.1%) at the MB-CS junction and 7 (22.6%) with alcohol infusion inside the VOM. Two macroreentries (6.5%) using the MB did not terminate with RF energy either endocardially at the MB-LA junction or epicardially at the MB-CS junction, and we were unable to identify or cannulate the VOM for ethanol infusion. Of the 29 localized re-entrant ATs using the MB, 27 (93.1%) terminated at the MB-LA junction, none terminated at the MB-CS junction and 2 (6.9%) terminated after alcohol infusion. After a mean follow up of 12 months, only 4 patients (6.7%) had AT recurrence. Conclusions MB re-entrant ATs accounted for up to 29% of the left ATs after AF ablation. Ablation of the MB-LA or CS-MB connections or alcohol infusion inside the VOM is required to treat these arrhythmias. Abstract Figure.

Little is known about persistent atrial fibrillation (AF) ablation in patients with cardiac laminopathy (CLMNA).We aimed to characterize atrial electrophysiological properties and to assess the long-term outcomes of persistent AF ablation in patients with CLMNA.All patients with CLMNA referred in our center for persistent AF ablation were retrospectively included. Left atrial (LA) volume, left atrial appendage (LAA) cycle length, interatrial conduction delay, and LA voltage amplitude were analyzed during the ablation procedure. Sinus rhythm maintenance and LA contractile function were assessed during long-term follow-up.From 2011 to 2020, 8 patients were included. The mean age was 47 ± 14 years, and 3 patients (38%) were women. The LA volume was 205.8 ± 43.7 mL; the LAA AF cycle length was 250.7 ± 85.6 ms; and the interatrial conduction delay was 296.5 ± 110.1 ms. Large low-voltage areas (50% of the LA surface;0.5 mV electrogram) were recorded in all 8 patients. Two patients had inadvertent LAA disconnection during ablation. All A waves recorded by pulsed Doppler in sinus rhythm were30 cm/s before and after AF ablation. Early arrhythmia recurrence was recorded in 7 patients (87%) (time to recurrence 4 ± 4 months; 1.5 procedures per patient). After a mean follow-up of 4.4 ± 3.2 years, 4 patients underwent implantable cardioverter-defibrillator therapy for life-threatening ventricular arrhythmia and 3 patients finally underwent heart transplantation.Patients with persistent AF afflicted by CLMNA exhibit severe LA impairment because of large low-voltage areas, prolonged conduction velocity, and reduced contractile function. Ablation procedures have a limited effect with a high recurrence rate.

Background Epicardial ablation is occasionally limited by coronary artery (CA) injuries or epicardial fat (EF). Objective The purpose of this study was to evaluate the anatomic obstacles that prevent ablation of epicardial abnormal potentials (EAPs) in patients with Brugada syndrome (BrS) and to investigate the feasibility of EAP elimination by endocardial right ventricular (RV) ablation. Methods This study included 16 BrS patients with previous ventricular fibrillation (VF), including 10 with an electrical storm. Data from multidetector computed tomography were assessed, and the proximity of the CA and EF was correlated with EAPs. Results EAPs were present in the epicardial RV outflow tract and RV inferior wall in all patients and 12 patients (75%), respectively. These EAPs were present within 5 mm of the main body and branches of the right CA in 14 patients (87.5%). However, only 1.4% ± 2.9% of the EAP area was covered with thick EF (≥8 mm). Partial EAP elimination by endocardial RV ablation was feasible in all 10 patients, with 53.3% successful endocardial RV radiofrequency applications for eliminating EAPs. After the procedure, VF remained inducible in 37.5% of the patients. During the 25.1 ± 29.1 months of follow-up, no patients experienced an electrical storm, and VF burden significantly decreased (median VF episodes before and after ablation: 7 and 0, respectively). Conclusion EAPs are near the CA in most BrS patients, thereby requiring caution during epicardial ablation, whereas EF is less of an issue. Endocardial ablation is feasible to eliminate some EAPs and may be combined with epicardial ablation.

Centrifugal activation is not always the origin of a focal atrial tachycardia (AT) ("true-focal"), but passive activation from the other structures ("pseudo-focal").We aimed to establish a method to differentiate true-focal from pseudo-focal.In 49 centrifugal activations in 35 patients with AT, 12-lead electrocardiogram, activation map, atrial global activation histogram (GAH), and local electrograms were analyzed. GAH demonstrates the relation between the activation area and timing through the cycle length, displayed with a normalized value, ranging from 0 (smallest activation area) to 1.0 (largest activation area).Of 30 centrifugal activations observed in the septal region, 6/30 (20.0%) were true-focal. The remaining 24/60 (80.0%) were pseudo-focal, of which 23 (95.8%) were from the opposite chamber. P-wave/flutter-wave duration200 ms discriminated true-focal from pseudo-focal (sensitivity 100%; specificity 54.5%; positive predictive value 33.3%; negative predictive value 100%). Multiple breakthrough ruled out the possibility of a true-focal AT. Other differentiating factors were an activation area within the initial 20 ms of5 mmCentrifugal activation is not necessarily due to a focal AT but passive activation. The activation map with GAH in addition to the 12-lead electrocardiogram and local electrograms enables an accurate differentiation.

Background: Achieving bidirectional mitral isthmus (MI) block using radiofrequency catheter ablation (RFCA) alone is challenging, and MI reconnection is common. Adjunctive vein of Marshall (VOM) ethanol infusion (VOM-Et) can facilitate acute MI block. However, little is known about its long-term success. This study sought to evaluate the impact of adjunctive VOM-Et on MI block achievement and durability compared with RFCA alone. Methods: Patients undergoing the first attempt of posterior MI ablation were grouped according to their MI block index strategy: adjunctive VOM-Et and RFCA alone. Rates of acute MI block and MI reconnection observed during repeat procedures were compared between the 2 groups. Results: The VOM-Et group consisted of 152 patients (63.8±9.4 years) undergoing adjunctive VOM-Et for MI block. The RFCA group consisted of 110 patients (60.9±9.2 years) undergoing MI ablation using RFCA alone. Acute MI block was more frequently achieved in the VOM-Et group (98.7% [150/152] versus 63.6% [70/110]; P P P P =0.008). Conclusions: Beyond facilitating acute MI block, VOM-Et is associated with greater lesion durability as evidenced by higher rates of MI block during repeat procedures.