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Bipolar voltage is widely used to characterize the atrial substrate but has been poorly validated, particularly during clinical tachycardias.The purpose of this study was to evaluate the diagnostic performance of voltage thresholds for identifying regions of slow conduction during reentrant atrial tachycardias (ATs).Thirty bipolar voltage and activation maps created during reentrant ATs were analyzed to (1) examine the relationship between voltage amplitude and conduction velocity (CV), (2) measure the diagnostic ability of voltage thresholds to predict CV, and (3) identify determinants of AT circuit dimensions. Voltage amplitude was categorized as "normal" (0.50 mV), "abnormal" (0.05-0.50 mV), or "scar" (0.05 mV); slow conduction was defined as30 cm/s.A total of 266,457 corresponding voltage and CV data points were included for analysis. Voltage and CV were moderately correlated (r = 0.407; P.001). Bipolar voltage predicted regions of slow conduction with an area under the receiver operating characteristic curve of 0.733 (95% confidence interval 0.731-0.735). A threshold of 0.50 mV had 91% sensitivity and 35% specificity for identifying slow conduction, whereas 0.05 mV had 36% sensitivity and 87% specificity, with an optimal voltage threshold of 0.15 mV. Analyses restricted to the AT circuits identified weaker associations between voltage and CV and an optimal voltage threshold of 0.25 mV.Widely used bipolar voltage amplitude thresholds to define "abnormal" and "scar" tissue in the atria are, respectively, sensitive and specific for identifying regions of slow conduction during reentrant ATs. However, overall, the association of voltage with CV is modest. No clinical predictors of AT circuit dimensions were identified.

Beyond pulmonary vein (PV) isolation, anatomic isthmus transection is an adjunctive strategy for persistent atrial fibrillation. Data on the durability of multiple lines of block remain scarce.The purpose of this study was to evaluate the impact of gaps within such a lesion set.We followed 291 consecutive patients who underwent (1) vein of Marshall ethanol infusion, (2) PV isolation, and (3) mitral, cavotricuspid, and dome isthmus transection. Dome transection relied on 2 distinct strategies over time: a single roof line with touch-ups applied in case of gap demonstrated by conventional maneuvers (first leg), and an alternative floor line if the roof line exhibited a gap during high-density mapping with careful electrogram reannotation (second leg).Twelve-month sinus rhythm maintenance was 70% after 1 procedure and 94% after 1 or 2 procedures. Event-free survival after the first procedure was lower in case of residual gaps within the lesion set (log-rank, P = .004). Delayed gaps were found in 94% of a second procedure performed in the 69 patients relapsing despite a complete lesion set with PV gaps increasing the risk of recurrence of atrial fibrillation (67% vs 34%; P = .02) and anatomic isthmus gaps supporting a majority of atrial tachycardias (60%). Between the first leg and the second leg, a significant decrease was found in roof lines considered blocked during the first procedure (99% vs 78%; P.001) and in delayed dome gaps observed during a second procedure (68% vs 43%; P = .05).Gaps are arrhythmogenic and can be reduced by optimized ablation and assessment of lines of block. Closing these gaps improves sinus rhythm maintenance.

An understanding of normal atrial activation during sinus rhythm can inform catheter ablation strategies to avoid deleterious impacts of ablation lesions on atrial conduction and mechanics.The purpose of this study was to describe how the sinus node impulse originates, propagates, and collides in right and left atria with normal voltage.Fifty consecutive patients undergoing catheter ablation of atrial fibrillation with endocardial atrial voltage0.5 mV during high-density 3-dimensional mapping were studied.Sinus node exits varied among patients along a lateral oblique arc extending from the anterior aspect of the superior vena cava (SVC) to the mid-posterior wall of the right atrium (RA). Conduction slowing or block at one of the smooth components that faces the crista terminalis was observed in 54% of cases, including complete block at the SVC musculature and systemic venous sinus in 6% of cases. Depending on these 2 key features of RA activation, interatrial conduction was mediated by the Bachmann bundle (64%) and posterior bundles (54%), with an overlap of the resulting left atrial breakthrough location. Wavefront collision was consistently observed at 3 sites: the septal aspect of the cavotricuspid isthmus, and the lower aspects of the dome and of the mitral isthmus.During sinus rhythm, atrial activation occurs via distinct sequences mediated by a complex interaction of anatomic factors.

The optimal strategy after a failed ablation for persistent atrial fibrillation (perAF) is unknown. This study evaluated the value of an anatomically guided strategy using a systematic set of linear lesions with adjunctive ethanol infusion into the vein of Marshall (Et-VOM) in patients referred for second perAF ablation procedures.Patients with perAF who underwent a second procedure were grouped according to the two strategies. The first strategy was an anatomically guided approach using systematic linear ablation with adjunctive Et-VOM, with bidirectional blocks at the posterior mitral isthmus (MI), roof, and cavotricuspid isthmus (CTI) as the procedural endpoint (Group I). The second one was an electrophysiology-guided strategy, with atrial tachyarrhythmia termination as the procedural endpoint (Group II). Arrhythmia behavior during the procedure guided the ablation strategy. Groups I and II consisted of 96 patients (65 ± 9 years; 71 men) and 102 patients (63 ± 10 years; 83 men), respectively. Baseline characteristics were comparable. In Group I, Et-VOM was successfully performed in 91/96 (95%), and procedural endpoint (bidirectional block across all three anatomical lines) was achieved in 89/96 (93%). In Group II, procedural endpoint (atrial tachyarrhythmia termination) was achieved in 80/102 (78%). One-year follow-up demonstrated Group I (21/96 [22%]) experienced less recurrence compared to Group II (38/102 [37%], Log-rank p = .01). This was driven by lower AT recurrence in Group I (Group I: 10/96 [10%] vs. Group II: 29/102 [28%]; p = .002).Anatomically guided strategy with adjunctive Et-VOM is superior to an electrophysiology-guided strategy for second procedures in patients with perAF at 1-year follow-up.

Introduction Electrogram (EGM) fractionation is often associated with diseased atrial tissue; however, mechanisms for fractionation occurring above an established threshold of 0.5 mV have never been characterized. We sought to investigate during sinus rhythm (SR) the mechanisms underlying bipolar EGM fractionation with high-density mapping in patients with atrial fibrillation (AF). Methods Forty-five patients undergoing AF ablation (73% paroxysmal, 27% persistent) were mapped at high density (18562 +/- 2551 points) during SR (Rhythmia). Only bipolar EGMs with voltages above 0.5 mV were considered for analysis. When fractionation (> 40 ms and >4 deflections) was detected, we classified the mechanisms as slow conduction, wave-front collision, or a pivot point. The relationship between EGM duration and amplitude, and tissue anisotropy and slow conduction, was then studied using a computational model. Results Of the 45 left atria analyzed, 133 sites of EGM fragmentation were identified with voltages above 0.5 mV. The most frequent mechanism (64%) was slow conduction (velocity 0.45 m/s +/- 0.2) with mean EGM voltage of 1.1 +/- 0.5 mV and duration of 54.9 +/- 9.4 ms. Wavefront collision was the second most frequent (19%), characterized by higher voltage (1.6 +/- 0.9 mV) and shorter duration (51.3 +/- 11.3 ms). Pivot points (9%) were associated with the highest degree of fractionation with 70.7 +/- 6.6 ms and 1.8 +/- 1 mV. In 10 sites (8%) fractionation was unexplained. The EGM duration was significantly different among the 3 mechanisms (p = .0351). Conclusion In patients with a history of AF, EGM fractionation can occur at amplitudes > 0.5 mV when in SR in areas often considered not to be diseased tissue. The main mechanism of EGM fractionation is slow conduction, followed by wavefront collision and pivot sites.

Detailed effects of electrode size on electrograms (EGMs) have not been systematically examined.We aimed to elucidate the effect of electrode size on EGMs and investigate an optimal configuration of electrode size and interelectrode spacing for gap detection and far-field reduction.This study included 8 sheep in which probes with different electrode size and interelectrode spacing were epicardially placed on healthy, fatty, and lesion tissues for measurements. Between 3 electrode sizes (0.1 mm/0.2 mm/0.5 mm) with 3 mm spacing. As indices of capability in gap detection and far-field reduction, in different electrode sizes (0.1 mm/0.2 mm/0.5 mm) and interelectrode spacing (0.1 mm/0.2 mm/0.3 mm/0.5 mm/3 mm) and the optimized electrode size and interelectrode spacing were determined. Compared between PentaRay and the optimal probe determined in study 2.Study 1 demonstrated that unipolar voltage and the duration of EGMs increased as the electrode size increased in any tissue (P.001). Bipolar EGMs had the same tendency in healthy/fat tissues, but not in lesions. Study 2 showed that significantly higher gap to lesion volume ratio and healthy to fat tissue voltage ratio were provided by a smaller electrode (0.2 mm or 0.3 mm electrode) and smaller spacing (0.1 mm spacing), but 0.3 mm electrode/0.1 mm spacing provided a larger bipolar voltage (P.05). Study 3 demonstrated that 0.3 mm electrode/0.1 mm spacing provided less deflection with more discrete EGMs (P .0001) with longer and more reproducible AF cycle length (P .0001) compared to PentaRay.Electrode size affects both unipolar and bipolar EGMs. Catheters with microelectrodes and very small interelectrode spacing may be superior in gap detection and far-field reduction. Importantly, this electrode configuration could dramatically reduce artifactual complex fractionated atrial electrograms and may open a new era for AF mapping.

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.

Introduction: Ultra-high-density mapping for ventricular tachycardia (VT) is increasingly used. However, manual annotation of local abnormal ventricular activities (LAVAs) is challenging in this setting. Therefore, we assessed the accuracy of the automatic annotation of LAVAs with the Lumipoint algorithm of the Rhythmia system (Boston Scientific). Methods and Results: One hundred consecutive patients undergoing catheter ablation of scar-related VT were studied. Areas with LAVAs and ablation sites were manually annotated during the procedure and compared with automatically annotated areas using the Lumipoint features for detecting late potentials (LP), fragmented potentials (FP), and double potentials (DP). The accuracy of each automatic annotation feature was assessed by re-evaluating local potentials within automatically annotated areas. Automatically annotated areas matched with manually annotated areas in 64 cases (64%), identified an area with LAVAs missed during manual annotation in 15 cases (15%), and did not highlight areas identified with manual annotation in 18 cases (18%). Automatic FP annotation accurately detected LAVAs regardless of the cardiac rhythm or scar location; automatic LP annotation accurately detected LAVAs in sinus rhythm, but was affected by the scar location during ventricular pacing; automatic DP annotation was not affected by the mapping rhythm, but its accuracy was suboptimal when the scar was located on the right ventricle or epicardium. Conclusion: The Lumipoint algorithm was as/more accurate than manual annotation in 79% of patients. FP annotation detected LAVAs most accurately regardless of mapping rhythm and scar location. The accuracy of LP and DP annotations varied depending on mapping rhythm or scar location.

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.

Introduction Cardioneuroablation (CNA) is a technique used to modulate cardiac parasympathetic tone in patients with sino-atrial (SA) and atrio-ventricular (AV) vagally mediated syncope. We describe the case of a patient who developed AV block after a first procedure of CNA, requiring a second procedure. Case presentation A 47-Year-old man presented with recurrent syncope (daily episodes) associated with high vagal tone conditions. An ECG monitoring showed frequent episodes of sinus bradycardia and sinus arrest, with pauses up to 17 seconds. AV node conduction impairment was never identified. A CNA procedure targeting the right superior and posterior ganglionated plexi (GPs), both from the left and right atrium, was performed with acute success. The subsequent night, repetitive episodes of AV block with normal sinus rate were observed. A second procedure was performed targeting the posteromedial left GP. Follow-up at 4 months showed no recurrent syncopal event and no bradyarrhythmia episode on the implantable loop recorder. Conclusion This case report demonstrates that ablation limited to the right superior and posterior GPs may not be enough for neurocardiogenic syncope and a more systematic approach, extending the ablation to the posteromedial left GP, should be considered.

Background: Fifty-watt radiofrequency applications have proven to be safe and efficient for pulmonary vein isolation (PVI). However, as PV reconnection still occurs and ablation catheter instability significantly contributes to suboptimal lesion formation, a new ablation catheter capable of delivering 90 W for 4 seconds only has been developed with the aim of improving PVI outcomes. In this setting, we sought to determine whether 90 W applications create transmural lesions without collateral damage experimentally and whether they can safely improve PVI procedures clinically compared with 50 W settings. Methods: Experimentally, individual lesions were created in vivo in the right atrium of 6 swine with 90 W-4 seconds applications using the SmartTouch-SF catheter in a power-controlled mode (3 animals) or the QDOT-MICRO catheter in a temperature-controlled mode (3 animals). Clinically, PVI was performed in a homogenous population of 150 consecutive paroxysmal atrial fibrillation patients using CARTO and the QDOT-MICRO catheter in a temperature-controlled mode (75 patients 50 W-ablation index-guided and 75 patients 90 W-4 seconds). Results: Mostly, (94.9%) experimental lesions were transmural in the thin-walled right atrium of swine. However, collateral damage was observed with both catheters in 17.9% of lesions. Clinically, 90 W procedures had a lower first-pass PVI rate (49% versus 81%, P −4 ) and a higher acute PV reconnection rate (21% versus 5%, P =0.004) than 50 W procedures, whereas total procedural duration (62 versus 66 minutes, P =0.09), 1-year sinus rhythm maintenance (88% versus 90%, P =0.6) and safety (1 tamponade per group) were similar in both groups. Conclusions: Experimentally, using the QDOT-MICRO catheter, 90 W-4 seconds lesions are mostly transmural in the thin-walled right atrium of swine (median depth 1.87 mm) with a moderate lesion diameter of 6.62 mm but retain the potential for collateral damage. Clinically, 90 W-4 seconds applications are associated with a lower first-pass PVI rate and a higher acute PV reconnection rate than 50 W applications but similar safety outcomes and effectiveness at 1 year.

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.

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.

Mitral isthmus (MI) ablation is commonly performed as an adjunct therapy to pulmonary isolation during the treatment for persistent atrial fibrillation. Confirmation of complete MI block is essential because an incomplete MI block may result in iatrogenic atrial tachycardia. However, there are several pitfalls in the diagnosis of an MI line block. We herein report a case of transient pause-dependent MI block during MI ablation. This article is protected by copyright. All rights reserved.

Systematic and quantitative descriptions of vein of Marshall (VOM)-induced tissue ablation are lacking. We sought to characterize the distribution of low voltage observed in the left atrium (LA) after VOM ethanol infusion.The distribution of ethanol-induced low voltage was evaluated by comparing high-density maps performed before and after VOM ethanol infusion in 114 patients referred for atrial fibrillation ablation. The two most frequently impacted segments were the inferior portion of the ridge (82.5%) and the first half of the mitral isthmus (pulmonary vein side) (92.1%). Low-voltage absence in these typical areas resulted from inadvertent ethanol infusion in the left atrial appendage vein (n = 3), initial VOM dissection (n = 3), or a "no branches" VOM morphology (n = 1). Visible anastomosis of the VOM with roof or posterior veins more frequently resulted in low-voltage extension beyond typical areas, toward the entire left antrum (19.0% vs. 1.9%, p = .0045) or the posterior LA (39.7% vs. 3.8%, p .001) but with a limited positive predictive value ranging from 29.4% to 43.5%. Ethanol-induced low voltage covered a median LA surface of 3.6% (1.9%-5.0%) and did not exceed 8% of the LA surface in 90% of patients.VOM ethanol infusion typically locates at the inferior ridge and the adjacent half of the mitral isthmus. Low-voltage extensions can be anticipated but not guaranteed by the presence of visible anastomosis of the VOM with roof or posterior veins.

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 Use of lesion metric indices is a proposed strategy to support pulmonary vein isolation procedures and these indices show good correlations with lesion sizes. The aim of this in silico study is to provide a detailed analysis of radiofrequency (RF) settings, including high-power short-duration (HPSD) settings, and resulting lesion metric indices. METHODS AND RESULTS A software program was designed which simulated virtual RF ablations. Lesion metric indices (Ablation index: AI, Lesion size index: LSI) were calculated based on underlying RF settings (contact force [CF], power, duration). In series of calculations, the applied settings were varied within defined ranges (CF: 1-80 g, power: 1-60 W, duration: 1-60 seconds). Overall, n = 388 000 virtual ablations were calculated. The resulting lesion metric indices were compared with each other and analyzed in relation to respective RF settings. Increasing contact force from 1 to 10 g resulted in a 4.4-fold LSI value, whilst increasing contact force from 10 to 20g resulted in a 1.5-fold value (P

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.

International audience; Pulsed field ablation (PFA), a non-thermal ablative modality, may show different effects on the myocardial tissue compared to thermal ablation. Thus, this study aimed to compare the left atrial (LA) structural and mechanical characteristics after PFA vs. thermal ablation.Cardiac magnetic resonance was performed pre-ablation, acutely (

A Wenckebach periodicity at the mitral isthmus lesion has rarely been reported. We described a case presenting conduction recovery with Wenckebach periodicity at the mitral isthmus lesion after achieving the posterior mitral isthmus block. These findings demonstrate an early reconnection of mitral isthmus lesion, and an arrhythmogenic substrate that can lead to development of reentrant tachycardia, that is, peri-mitral atrial flutter.

Evidence on sex differences in the pathophysiology and interventional treatment of ventricular arrhythmia in ischemic (ICM) or non-ischemic cardiomyopathies (NICM) is limited. However, women have different etiologies and types of structural heart disease due to sex differences in genetics, proteomics and sex hormones. These differences may influence ventricular electrophysiological parameters and may require different treatment strategies. Considering that women were consistently under-represented in all randomized-controlled trials on VT ablation, the applicability of the study results to female patients is not known. In this article, we review the current knowledge and gaps in evidence about sex differences in the epidemiology, pathophysiology and catheter ablation in patients with ventricular arrhythmias.

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.

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.