Demonstration of differential ventricular overdrive pacing during long RP' supraventricular tachycardia.

We described the differential ventricular overdrive pacing during long RP' supraventricular tachycardia and discussed about its response leading to the dianosis.

The optimal slow pathway ablation site in atrioventricular nodal reentrant tachycardia cases with an inferiorly located His bundle.

INTRODUCTION: The optimal slow pathway (SP) ablation site in cases with an inferiorly located His bundle (HIS) remains unclear. METHODS AND RESULTS: In 45 patients with atrioventricular nodal reentrant tachycardia, the relationship between the HIS location and successful SP ablation site was assessed in electroanatomical maps. We assessed the location of the SP ablation site relative to the bottom of the coronary sinus ostium in the superior-to-inferior (SPSI), anterior-to-posterior (SPAP), and right-to-left (SPRL) directions. The HIS location was assessed in the same manner. The HIS location in the superior-to-inferior direction (HISSI), SPSI, SPAP, and SPRL were 17.7 ± 6.4, 1.7 ± 6.4, 13.6 ± 12.3, and -1.0 ± 13.0 mm, respectively. The HISSI was positively correlated with SPSI (R2 = 0.62; P < .01) and SPAP (R2 = 0.22; P < .01), whereas it was not correlated with SPRL (R2 = 0.01; P = .65). The distance between the HIS and SP ablation site was 17.7 ± 6.4 mm and was not affected by the location of HIS. The ratio of the amplitudes of atrial and ventricular potential recorded at the SP ablation site did not differ between the high HIS group (HISSI ≥ 13 mm) and low HIS group (HISSI < 13 mm) (0.10 ± 0.06 vs. 0.10 ± 0.06; P = .38). CONCLUSION: In cases with an inferiorly located HIS, SP ablation should be performed at a lower and more posterior site than in typical cases.

Diverse Phenotypic Manifestations in a Family with a Novel RYR2 E4107A Variant.

Cardiac ryanodine receptor (RyR2) gain-of-function mutations cause catecholaminergic polymorphic ventricular tachycardia (CPVT). Conversely, RyR2 loss-of-function mutations cause a new disease entity, termed calcium release deficiency syndrome (CRDS), which may include RYR2-related long QT syndrome (LQTS). Importantly, unlike CPVT, patients with CRDS do not always exhibit exercise- or epinephrine-induced ventricular arrhythmias, which precludes a diagnosis of CRDS. Here we report a boy and his father, who both experienced exercise-induced cardiac events and harbor the same RYR2 E4107A variant. In the boy, an exercise stress test (EST) and epinephrine provocation test (EPT) did not induce any ventricular arrhythmias. QTc was slightly prolonged (QTc: 474 ms), and an EPT induced QTc prolongation (QTc-baseline: 466 ms, peak: 532 ms, steady-state: 527 ms). In contrast, in his father, QTc was not prolonged (QTc: 417 ms), and neither an EST nor EPT induced QTc prolongation. However, an EST induced multifocal premature ventricular contraction (PVC) bigeminy and bidirectional PVC couplets. Thus, they exhibited distinct clinical phenotypes: the boy exhibited LQTS (or CRDS) phenotype, whereas his father exhibited CPVT phenotype. These findings suggest that, in addition to the altered RyR2 function, other unidentified factors, such as other genetic, epigenetic, and environmental factors, and aging, may be involved in the diverse phenotypic manifestations. Considering that a single RYR2 variant can cause both CPVT and LQTS (or CRDS) phenotypes, in cascade screening of patients with CPVT and CRDS, an EST and EPT are not sufficient and genetic analysis is required to identify individuals who are at increased risk for life-threatening arrhythmias.

Catheter ablation of the left-sided variant of right top pulmonary vein in a case with persistent left superior vena cava.

A 50-year-old woman underwent catheter ablation for atrial fibrillation. Preoperative computed tomography revealed a left-sided variant of the right top pulmonary vein (PV) and a persistent left superior vena cava. The right top PV was successfully isolated through a wide antral circumferential ablation line simultaneously with the right PVs.

Demonstration of the discrepancy between AT-wave morphology on 12-lead ECG and AT mechanism in scar-related AT.

The 12-lead electrocardiogram (ECG) is a fundamental modality to help determine the mechanism and the localization of atrial tachycardias (ATs). Although macroreentrant ATs and focal ATs typically show F-waves and discrete P-waves respectively on the 12-lead ECG, this is not universally the case in scar-related ATs.1, We present three cases clearly showing the discrepancy between the AT morphology on the 12-lead ECG and the AT-mechanism.

Transient left phrenic nerve paralysis after ethanol infusion into the vein of Marshall.

An 80-year-old man underwent catheter ablation for atrial tachycardia (AT), which developed after catheter ablation for atrial fibrillation. The AT was diagnosed as dual-loop tachycardia, which included peri-mitral and roof-dependent ATs. An ethanol infusion into the vein of Marshall resulted in left phrenic nerve paralysis. During the procedure, the phrenic nerve paralysis was completely relieved.

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.

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.

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.

Cardiac vagus nerve denervation by pulmonary vein isolation was effective for swallowing-induced atrial tachycardia.

Swallowing-induced atrial tachycardia (SIAT) is a relatively rare arrhythmia. A 56-year-old woman was admitted to treat atrial tachycardia that occurs by not only eating and drinking but also yawning. Both the right and left upper pulmonary veins were suspected as the earliest activation site of the tachycardia and the abnormal activation of ectopies themselves were suppressed after pulmonary vein isolation (PVI). In a 24-hour Holter electrocardiogram, the HF component of the analysis of heart rate variability was suppressed both at 1 day and at 2 years after ablation. In this case, cardiac vagal nerve denervation by PVI was effective for SIAT.

Paradoxical delayed capture proved the dual-loop tachycardia mechanism of a cavotricuspid isthmus-dependent atrial flutter.

A 37-year-old man underwent catheter ablation for a cavotricuspid isthmus-dependent atrial flutter. Two 20-pole deflectable electrode catheters were placed in a parallel position on the tricuspid annulus and right atrial lateral wall. The dual-loop tachycardia mechanism of the atrial flutter was suggested by paradoxical delayed capture of the lateral wall of the right atrium during entrainment pacing from the lateral tricuspid annulus.

Bilateral Cardiac Sympathetic Denervation for Treatment-Resistant Ventricular Arrhythmias in Heart Failure Patients with a Reduced Ejection Fraction.

The sympathetic nervous system plays an important role in life-threatening ventricular arrhythmias (VAs). Bilateral cardiac sympathetic denervation (BCSD) is performed for refractory VAs. We sought to assess our institutional experience with BCSD in managing treatment-resistant monomorphic ventricular tachycardia (MMVT) in heart failure patients with a reduced ejection fraction (HFrEF).Four patients with HFrEF (EF 30.0 ± 8.2%, New York Heart Association [NYHA] class IV 1) underwent BCSD for MMVT (VT storm 3, repetitive VT requiring implantable cardioverter defibrillator [ICD] therapy 1) refractory to antiarrhythmic drugs, catheter ablation and ICD therapy. BCSD was effective for suppressing VT in 3 patients for whom deep sedation was effective for suppressing VT. One patient remained alive after 14 months of follow-up without episodes of VT. One patient died of acute myocardial infarction before discharge and 1 patient died from unknown cause at 3 days post-discharge. In contrast, BCSD was completely ineffective for suppressing VT in a patient with NYHA class IV for whom deep sedation and stellate ganglion block were ineffective. This patient died on the 10th post-CSD day, despite left ventricular assist device implantation. In all cases, BCSD was successfully performed without procedure-related complications.Despite the limited number of cases, our results showed that BCSD in patients with HFrEF suppressed refractory MMVT in acute-phase except for a patient with NYHA class IV; however, the prognoses were not good. BCSD may be a treatment option at an earlier stage of NYHA and a bridge to orthotopic heart transplantation, even if BCSD is effective for suppressing VAs.

Acute coronary artery occlusion and ischemia-related ventricular tachycardia during catheter ablation in the right ventricular outflow tract.

Coronary artery injury is a rare complication of catheter ablation in the right ventricular outflow tract (RVOT). Furthermore, acute myocardial ischemia usually causes polymorphic ventricular tachycardia (VT) or ventricular fibrillation. We herein describe a case in which catheter ablation for VT originating from the RVOT provoked ischemia-related VTs due to acute occlusion of the left anterior descending artery.

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.

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.

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.

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.