Impact of filter configurations on bipolar EGMs: An optimal filter setting for identifying VT substrates.

BACKGROUND: The impact of filtering on bipolar electrograms (EGMs) has not been systematically examined. We tried to clarify the optimal filter configuration for ventricular tachycardia (VT) ablation. METHODS: Fifteen patients with VT were included. Eight different filter configurations were prospectively created for the distal bipoles of the ablation catheter: 1.0-250, 10-250, 100-250, 30-50, 30-100, 30-250, 30-500, and 30-1000 Hz. Pre-ablation stable EGMs with good contact (contact force > 10 g) were analyzed. Baseline fluctuation, baseline noise, bipolar peak-to-peak voltage, and presence of local abnormal ventricular activity (LAVA) were compared between different filter configurations. RESULTS: In total, 2276 EGMs with multiple bipolar configurations in 246 sites in scar and border areas were analyzed. Baseline fluctuation was only observed in the high-pass filter of (HPF) ≤ 10 Hz (p < .001). Noise level was lowest at 30-50 Hz (0.018 [0.012-0.029] mV), increased as the low-pass filter (LPF) extended, and was highest at 30-1000 Hz (0.047 [0.041-0.061] mV) (p < .001). Conversely, the HPF did not affect the noise level at ≤30 Hz. As the HPF extended to 100 Hz, bipolar voltages significantly decreased (p < .001), but were not affected when the LPF was extended to ≥100 Hz. LAVAs were most frequently detected at 30-250 Hz (207/246; 84.2%) and 30-500 Hz (208/246; 84.6%), followed by 30-1000 Hz (205/246; 83.3%), but frequently missed at LPF ≤ 100 Hz or HPF ≤ 10 Hz (p < .001). A 50-Hz notch-filter reduced the bipolar voltage by 43.9% and LAVA-detection by 34.5% (p < .0001). CONCLUSION: Bipolar EGMs are strongly affected by filter settings in scar/border areas. In all, 30-250 or 30-500 Hz may be the best configuration, minimizing the baseline fluctuation, baseline noise, and detecting LAVAs. Not applying the 50-Hz notch filter may be beneficial to avoid missing VT substrate.

Electrophysiological study prior to planned pulmonary valve replacement in patients with repaired tetralogy of Fallot.

AIM: Ventricular arrhythmias (VAs) are the most common cause of death in patients with repaired Tetralogy of Fallot (rTOF). However, risk stratifying remains challenging. We examined outcomes following programmed ventricular stimulation (PVS) with or without subsequent ablation in patients with rTOF planned for pulmonary valve replacement (PVR). METHODS: We included all consecutive patients with rTOF referred to our institution from 2010 to 2018 aged ≥18 years for PVR. Right ventricular (RV) voltage maps were acquired and PVS was performed from two different sites at baseline, and if non-inducible under isoproterenol. Catheter and/or surgical ablation was performed when patients were inducible or when slow conduction was present in anatomical isthmuses (AIs). Postablation PVS was undertaken to guide implantable cardioverter-defibrillator (ICD) implantation. RESULTS: Seventy-seven patients (36.2 ± 14.3 years old, 71% male) were included. Eighteen were inducible. In 28 patients (17 inducible, 11 non-inducible but with slow conduction) ablation was performed. Five had catheter ablation, surgical cryoablation in 9, both techniques in 14. ICDs were implanted in five patients. During a follow-up of 74 ± 40 months, no sudden cardiac death occurred. Three patients experienced sustained VAs, all were inducible during the initial EP study. Two of them had an ICD (low ejection fraction for one and important risk factor for arrhythmia for the second). No VAs were reported in the non-inducible group (p < .001). CONCLUSION: Preoperative EPS can help identifying patients with rTOF at risk for VAs, providing an opportunity for targeted ablation and may improve decision-making regarding ICD implantation.

Detailed analysis of tachycardia cycle length aids diagnosis of the mechanism and location of atrial tachycardias.

AIMS: Although the mechanism of an atrial tachycardia (AT) can usually be elucidated using modern high-resolution mapping systems, it would be helpful if the AT mechanism and circuit could be predicted before initiating mapping. OBJECTIVE: We examined if the information gathered from the cycle length (CL) of the tachycardia can help predict the AT-mechanism and its localization. METHODS: One hundred and thirty-eight activation maps of ATs including eight focal-ATs, 94 macroreentrant-ATs, and 36 localized-ATs in 95 patients were retrospectively reviewed. Maximal CL (MCL) and minimal CL (mCL) over a minute period were measured via a decapolar catheter in the coronary sinus. CL-variation and beat-by-beat CL-alternation were examined. Additionally, the CL-respiration correlation was analysed by the RhythmiaTM system. : Both MCL and mCL were significantly shorter in macroreentrant-ATs [MCL = 288 (253-348) ms, P = 0.0001; mCL = 283 (243-341) ms, P = 0.0012], and also shorter in localized-ATs [MCL = 314 (261-349) ms, P = 0.0016; mCL = 295 (248-340) ms, P = 0.0047] compared to focal-ATs [MCL = 506 (421-555) ms, mCL = 427 (347-508) ms]. An absolute CL-variation (MCL-mCL) < 24 ms significantly differentiated re-entrant ATs from focal-ATs with a sensitivity = 96.9%, specificity = 100%, positive predictive value (PPV) = 100%, and negative predictive value (NPV) = 66.7%. The beat-by-beat CL-alternation was observed in 10/138 (7.2%), all of which showed the re-entrant mechanism, meaning that beat-by-beat CL-alternation was the strong sign of re-entrant mechanism (PPV = 100%). Although the CL-respiration correlation was observed in 28/138 (20.3%) of ATs, this was predominantly in right-atrium (RA)-ATs (24/41, 85.7%), rather than left atrium (LA)-ATs (4/97, 4.1%). A positive CL-respiration correlation highly predicted RA-ATs (PPV = 85.7%), and negative CL-respiration correlation probably suggested LA-ATs (NPV = 84.5%). CONCLUSION: Detailed analysis of the tachycardia CL helps predict the AT-mechanism and the active AT chamber before an initial mapping.

Purkinje network and myocardial substrate at the onset of human ventricular fibrillation: implications for catheter ablation.

AIMS: Mapping data of human ventricular fibrillation (VF) are limited. We performed detailed mapping of the activities underlying the onset of VF and targeted ablation in patients with structural cardiac abnormalities. METHODS AND RESULTS: We evaluated 54 patients (50 ± 16 years) with VF in the setting of ischaemic (n = 15), hypertrophic (n = 8) or dilated cardiomyopathy (n = 12), or Brugada syndrome (n = 19). Ventricular fibrillation was mapped using body-surface mapping to identify driver (reentrant and focal) areas and invasive Purkinje mapping. Purkinje drivers were defined as Purkinje activities faster than the local ventricular rate. Structural substrate was delineated by electrogram criteria and by imaging. Catheter ablation was performed in 41 patients with recurrent VF. Sixty-one episodes of spontaneous (n = 10) or induced (n = 51) VF were mapped. Ventricular fibrillation was organized for the initial 5.0 ± 3.4 s, exhibiting large wavefronts with similar cycle lengths (CLs) across both ventricles (197 ± 23 vs. 196 ± 22 ms, P = 0.9). Most drivers (81%) originated from areas associated with the structural substrate. The Purkinje system was implicated as a trigger or driver in 43% of patients with cardiomyopathy. The transition to disorganized VF was associated with the acceleration of initial reentrant activities (CL shortening from 187 ± 17 to 175 ± 20 ms, P < 0.001), then spatial dissemination of drivers. Purkinje and substrate ablation resulted in the reduction of VF recurrences from a pre-procedural median of seven episodes [interquartile range (IQR) 4-16] to 0 episode (IQR 0-2) (P < 0.001) at 56 ± 30 months. CONCLUSIONS: The onset of human VF is sustained by activities originating from Purkinje and structural substrate, before spreading throughout the ventricles to establish disorganized VF. Targeted ablation results in effective reduction of VF burden. KEY QUESTION: The initial phase of human ventricular fibrillation (VF) is critical as it involves the primary activities leading to sustained VF and arrhythmic sudden death. The origin of such activities is unknown. KEY FINDING: Body-surface mapping shows that most drivers (≈80%) during the initial VF phase originate from electrophysiologically defined structural substrates. Repetitive Purkinje activities can be elicited by programmed stimulation and are implicated as drivers in 37% of cardiomyopathy patients. TAKE-HOME MESSAGE: The onset of human VF is mostly associated with activities from the Purkinje network and structural substrate, before spreading throughout the ventricles to establish sustained VF. Targeted ablation reduces or eliminates VF recurrence.

Distribution of atrial low voltage induced by vein of Marshall ethanol infusion.

INTRODUCTION: 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. METHODS AND RESULTS: 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. CONCLUSION: 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.

Preoperative personalization of atrial fibrillation ablation strategy to prevent esophageal injury: Impact of changes in esophageal position.

INTRODUCTION: Due to changes in esophageal position, preoperative assessment of the esophageal location may not mitigate the risk of esophageal injury in catheter ablation for atrial fibrillation (AF). This study aimed to assess esophageal motion and its impact on AF ablation strategies. METHODS AND RESULTS: Ninety-seven AF patients underwent two computed tomography (CT) scans. The area at risk of esophageal injury (AAR) was defined as the left atrial surface ≤3 mm from the esophagus. On CT1, ablation lines were drawn blinded to the esophageal location to create three ablation sets: individual pulmonary vein isolation (PVI), wide antral circumferential ablation (WACA), and WACA with linear ablation (WACA + L). Thereafter, ablation lines for WACA and WACA + L were personalized to avoid the AAR. Rigid registration was performed to align CT1 onto CT2, and the relationship between ablation lines and the AAR on CT2 was analyzed. The esophagus moved by 3.6 [2.7 to 5.5] mm. The AAR on CT2 was 8.6 ± 3.3 cm2 , with 77% overlapping that on CT1. High body mass index was associated with the AAR mismatch (standardized ß 0.382, p < .001). Without personalization, AARs on ablation lines for individual PVI, WACA, and WACA + L were 0 [0-0.4], 0.8 [0.5-1.2], and 1.7 [1.2-2.0] cm2 . Despite the esophageal position change, the personalization of ablation lines for WACA and WACA + L reduced the AAR on lines to 0 [0-0.5] and 0.7 [0.3-1.0] cm2 (p < .001 for both). CONCLUSION: The personalization of ablation lines based on a preoperative CT reduced ablation to the AAR despite changes in esophageal position.

Strategy for repeat procedures in patients with persistent atrial fibrillation: Systematic linear ablation with adjunctive ethanol infusion into the vein of Marshall versus electrophysiology-guided ablation.

INTRODUCTION: 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. METHODS AND RESULTS: 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). CONCLUSION: 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.

Sex differences in ventricular arrhythmia: epidemiology, pathophysiology and catheter ablation.

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.

Electrogram fractionation during sinus rhythm occurs in normal voltage atrial tissue in patients with atrial fibrillation.

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.

Purkinje triggers of ventricular fibrillation in patients with hypertrophic cardiomyopathy.

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.

Accuracy of automatic abnormal potential annotation for substrate identification in scar-related ventricular tachycardia.

INTRODUCTION: Ultrahigh-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.

Characteristics of macroreentrant atrial tachycardias using an anatomical bypass: Pseudo-focal atrial tachycardia case series.

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 postpacing 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 colocalized 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 < .001]. 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.

Right ventricular outflow tract electroanatomical abnormalities in asymptomatic and high-risk symptomatic patients with Brugada syndrome: Evidence for a new risk stratification tool?

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 < .01) and bipolar LVAs (p < .01) compared with asymptomatic individuals. A substrate size of unipolar LVAs more than 14.5 cm2 (area under the curve [AUC]: 0.92, p < .001] and bipolar LVAs more than 3.68 cm2 (AUC: 0.82, p = .001) distinguished symptomatic from asymptomatic patients. Patients with ventricular fibrillation inducibility (23/54) demonstrated broader endocardial unipolar (p < .001) and bipolar LVAs (p < .001) than noninducible patients. The presence of unipolar LVAs more than 13.5 cm2 (AUC: 0.95, p < .001) and bipolar LVAs more than 2.97 cm2 (AUC: 0.78, p < .001) predicted a positive PVS. CONCLUSION: Extensive endocardial electroanatomical abnormalities identify high-risk patients with BrS. Endocardial HDEAM may allow risk stratification of asymptomatic patients referred for PVS.

High-risk atrioventricular block in Brugada syndrome patients with a history of syncope.

BACKGROUND: Determining the etiology of syncope is challenging in Brugada syndrome (BrS) patients. Implantable cardioverter defibrillator placement is recommended in BrS patients who are presumed to have arrhythmic syncope. However, arrhythmic syncope in BrS patients can occur in the setting of atrioventricular block (AVB), which should be managed by cardiac pacing. The clinical characteristics of BrS patients with high-risk AVB remain unknown. METHODS: This study included 223 BrS patients with a history of syncope from two centers. The clinical characteristics of patients with high-risk AVB (Mobitz type II second-degree AVB, high-degree AVB, or third-degree AVB) were investigated. RESULTS: During the 99 ± 78 months of follow-up, we identified six BrS patients (2.7%) with high-risk AVB. Three of the six patients (50%) with AVB presented with syncope associated with prodromes or specific triggers. Four patients (67%) were found to have paroxysmal third-degree AVB during the initial evaluation for BrS and syncope, while two patients developed third-degree AVB during the follow-up period. The incidence of first-degree AVB was significantly higher in AVB patients than in non-AVB patients (83% vs. 15%; p = .0005). There was no significant difference in the incidence of ventricular fibrillation between AVB and non-AVB patients (AVB [17%], non-AVB [12%]; p = .56). CONCLUSION: High-risk AVB can occur in BrS patients with various clinical presentations. Although rare, the incidence is worth considering, especially in BrS patients with first-degree AVB.

Pulsed field ablation selectively spares the oesophagus during pulmonary vein isolation for atrial fibrillation.

AIMS: Extra-atrial injury can cause complications after catheter ablation for atrial fibrillation (AF). Pulsed field ablation (PFA) has generated preclinical data suggesting that it selectively targets the myocardium. We sought to characterize extra-atrial injuries after pulmonary vein isolation (PVI) between PFA and thermal ablation methods. METHODS AND RESULTS: Cardiac magnetic resonance (CMR) imaging was performed before, acutely (<3 h) and 3 months post-ablation in 41 paroxysmal AF patients undergoing PVI with PFA (N = 18, Farapulse) or thermal methods (N = 23, 16 radiofrequency, 7 cryoballoon). Oesophageal and aortic injuries were assessed by using late gadolinium-enhanced (LGE) imaging. Phrenic nerve injuries were assessed from diaphragmatic motion on intra-procedural fluoroscopy. Baseline CMR showed no abnormality on the oesophagus or aorta. During ablation procedures, no patient showed phrenic palsy. Acutely, thermal methods induced high rates of oesophageal lesions (43%), all observed in patients showing direct contact between the oesophagus and the ablation sites. In contrast, oesophageal lesions were observed in no patient ablated with PFA (0%, P < 0.001 vs. thermal methods), despite similar rates of direct contact between the oesophagus and the ablation sites (P = 0.41). Acute lesions were detected on CMR on the descending aorta in 10/23 (43%) after thermal ablation, and in 6/18 (33%) after PFA (P = 0.52). CMR at 3 months showed a complete resolution of oesophageal and aortic LGE in all patients. No patient showed clinical complications. CONCLUSION: PFA does not induce any signs of oesophageal injury on CMR after PVI. Due to its tissue selectivity, PFA may improve safety for catheter ablation of AF.

Pulsed field ablation prevents chronic atrial fibrotic changes and restrictive mechanics after catheter ablation for atrial fibrillation.

AIMS: 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. METHODS AND RESULTS: Cardiac magnetic resonance was performed pre-ablation, acutely (<3 h), and 3 months post-ablation in 41 patients with paroxysmal atrial fibrillation (AF) undergoing pulmonary vein (PV) isolation with PFA (n = 18) or thermal ablation (n = 23, 16 radiofrequency ablations, 7 cryoablations). Late gadolinium enhancement (LGE), T2-weighted, and cine images were analysed. In the acute stage, LGE volume was 60% larger after PFA vs. thermal ablation (P < 0.001), and oedema on T2 imaging was 20% smaller (P = 0.002). Tissue changes were more homogeneous after PFA than after thermal ablation, with no sign of microvascular damage or intramural haemorrhage. In the chronic stage, the majority of acute LGE had disappeared after PFA, whereas most LGE persisted after thermal ablation. The maximum strain on PV antra, the LA expansion index, and LA active emptying fraction declined acutely after both PFA and thermal ablation but recovered at the chronic stage only with PFA. CONCLUSION: Pulsed field ablation induces large acute LGE without microvascular damage or intramural haemorrhage. Most LGE lesions disappear in the chronic stage, suggesting a specific reparative process involving less chronic fibrosis. This process may contribute to a preserved tissue compliance and LA reservoir and booster pump functions.

Use of high-density activation and voltage mapping in combination with entrainment to delineate gap-related atrial tachycardias post atrial fibrillation ablation.

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 <0.1 mV (0.14 ± 0.095 mV, 51 of 134 AT, 41%), and almost always <0.5 mV (0.03-0.5 mV, 133 of 134 AT, 99.3%). The use of multipolar Orion, HDGrid, and Pentaray catheters improved our accuracy in delineating ultra-low-voltage areas critical for maintenance of the circuit of endocardial gap-related AT. Conventional ablation catheters often do not detect any signal (noise level) even using adequate contact force, and only multipolar catheters of small electrodes and shorter interelectrode space can detect clear fractionated low-amplitude and high frequency signals, critical for re-entry maintenance. We performed a diagnosis in 112 out of 134 AT (83.6%) using only activation mapping and in 134 out of 134 AT (100%) using the combination of activation and entrainment mapping. 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.

Local abnormal ventricular activity detection in scar-related VT: Microelectrode versus conventional bipolar electrode.

BACKGROUND: Conventional bipolar electrodes (CBE) may be suboptimal to detect local abnormal ventricular activities (LAVAs). Microelectrodes (ME) may improve the detection of LAVAs. This study sought to elucidate the detectability of LAVAs using ME compared with CBE in patients with scar-related ventricular tachycardia (VT). METHODS: We included consecutive patients with structural heart disease who underwent radiofrequency catheter ablation for scar-related VT using either of the following catheters equipped with ME: QDOTTM or IntellaTip MIFITM. Detection field of LAVA potentials were classified as three types: Type 1 (both CBE and ME detected LAVA), Type 2 (CBE did not detect LAVA while ME did), and Type 3 (CBE detected LAVA while ME did not). RESULTS: In 16 patients (68 ± 16 years; 14 males), 260 LAVAs electrograms (QDOT = 72; MIFI = 188) were analyzed. Type 1, type 2, and type 3 detections were 70.8% (QDOT, 69.4%; MIFI, 71.3%), 20.0% (QDOT, 23.6%; MIFI, 18.6%) and 9.2% (QDOT, 6.9%; MIFI, 10.1%), respectively. The LAVAs amplitudes detected by ME were higher than those detected by CBE in both catheters (QDOT: ME 0.79 ± 0.50 mV vs. CBE 0.41 ± 0.42 mV, p = .001; MIFI: ME 0.73 ± 0.64 mV vs. CBE 0.38 ± 0.36 mV, p < .001). CONCLUSIONS: ME allow to identify 20% of LAVAs missed by CBE. ME showed higher amplitude LAVAs than CBE. However, 9.2% of LAVAs can still be missed by ME.

Ligament of Marshall ablation for persistent atrial fibrillation.

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.

Ventriculoatrial interval variation following atrio-His block during wide-QRS-complex tachycardia with 1:1 ventriculoatrial relationship: What is the diagnosis?

A wide QRS-complex tachycardia with 1:1 ventriculoatrial conduction may present diagnostic difficulties, and multiple pacing maneuvers are often required for an accurate diagnosis. We report a case, in which observation of transient ventriculoatrial interval variation following atrio-His block quickly led to the diagnosis.