A validation study of the accuracy of the atrial pace map assessed with intracardiac pattern matching: Potential utility of non-pulmonary vein mapping.

BACKGROUND: Identification of infrequent nonpulmonary vein trigger premature atrial contractions (PACs) is challenging. We hypothesized that pace mapping (PM) assessed by correlation scores calculated by an intracardiac pattern matching (ICPM) module was useful for locating PAC origins, and conducted a validation study to assess the accuracy of ICPM-guided PM. METHODS: Analyzed were 30 patients with atrial fibrillation. After pulmonary vein isolation, atrial pacing was performed at one or two of four sites on the anterior and posterior aspects of the left atrium (LA, n = 10/10), LA septum (n = 10), and lateral RA (n = 10), which was arbitrarily determined as PAC. The intracardiac activation obtained from each pacing was set as an ICPM reference consisting of six CS unipolar electrograms (CS group) or six CS unipolar electrograms and four RA electrograms (CS-RA group). RESULTS: The PM was performed at 193 ± 107 sites for each reference pacing site. All reference pacing sites corresponded to sites where the maximal ICPM correlation score was obtained. Sites with a correlation score ≥98% were rarely obtained in the CS-RA than CS group (33% vs. 55%, P = .04), but those ≥95% were similarly obtained between the two groups (93% vs. 88%, P = .71), and those ≥90% were obtained in all. The surface areas with correlation scores ≥98% (0[0,10] vs. 10[0,35] mm2, P = .02), ≥95% (10[10,30] vs. 50[10,180] mm2, P = .002) and ≥90% (60[30,100] vs. 170[100,560] mm2, P = .0002) were smaller in the CS-RA than CS group. CONCLUSIONS: ICPM-guided PM was useful for identifying the reference pacing sites. Combined use of RA and CS electrograms may improve the mapping quality.

Optimal timing of electrical cardioversion for acute decompensated heart failure caused by atrial arrhythmias: The earlier, the better?

The optimal timing for electrical cardioversion (ECV) in acute decompensated heart failure (ADHF) with atrial arrhythmias (AAs) is unknown. Here, we retrospectively evaluated the impact of ECV timing on SR maintenance, hospitalization duration, and cardiac function in patients with ADHF and AAs. Between October 2017 and December 2022, ECV was attempted in 73 patients (62 with atrial fibrillation and 11 with atrial flutter). Patients were classified into two groups based on the median number of days from hospitalization to ECV, as follows: early ECV (within 8 days, n = 38) and delayed ECV (9 days or more, n = 35). The primary endpoint was very short-term and short-term ECV failure (unsuccessful cardioversion and AA recurrence during hospitalization and within one month after ECV). Secondary endpoints included (1) acute ECV success, (2) ECVs attempted, (3) periprocedural complications, (4) transthoracic echocardiographic parameter changes within two months following successful ECV, and (5) hospitalization duration. ECV successfully restored SR in 62 of 73 patients (85%), with 10 (14%) requiring multiple ECV attempts (≥ 3), and periprocedural complications occurring in six (8%). Very short-term and short-term ECV failure occurred without between-group differences (51% vs. 63%, P = 0.87 and 61% vs. 72%, P = 0.43, respectively). Among 37 patients who underwent echocardiography before and after ECV success, the left ventricular ejection fraction (LVEF) significantly increased (38% [31-52] to 51% [39-63], P = 0.008) between admission and follow-up. Additionally, hospital stay length was shorter in the early ECV group than in the delayed ECV group (14 days [12-21] vs. 17 days [15-26], P < 0.001). Hospital stay duration was also correlated with days from admission to ECV (Spearman's ρ = 0.47, P < 0.001). In clinical practice, early ECV was associated with a shortened hospitalization duration and significantly increased LVEF in patients with ADHF and AAs.

Beyond the lens: Unveiling the invisible atrioventricular node in the era of high-density mapping.

Numerous studies have clarified the histological characteristics of the area surrounding the atrioventricular (AV) node, commonly referred to as the triangle of Koch (ToK). Although it is suggested that the conduction of electric impulses from the atria to the ventricles via the AV node involves myocytes possessing distinct conduction properties and gap junction proteins, a comprehensive understanding of this complex conduction has not been fully established. Moreover, although various pathways have been proposed for both anterograde and retrograde conduction during atrioventricular nodal reentrant tachycardia (AVNRT), the reentrant circuits of AVNRT are not fully elucidated. Therefore, the slow pathway ablation for AVNRT has been conventionally performed, targeting both its anatomical location and slow pathway potential obtained during sinus rhythm. Recently, advancements in high-density three-dimensional (3D) mapping systems have facilitated the acquisition of more detailed electrophysiological potentials within the ToK. Several studies have indicated that the activation pattern, the low-voltage area within the ToK obtained during sinus rhythm, and the fractionated potentials acquired during tachycardia may be optimal targets for slow pathway ablation. This review provides an overview of the tissue surrounding the AV node as reported to date and summarizes the current understanding of AV conduction and AVNRT circuits. Furthermore, we discuss recent findings on slow pathway ablation utilizing high-density 3D mapping systems, exploring strategies for optimal slow pathway ablation.

Pseudo-slow-fast atrioventricular nodal reentrant tachycardia: Is the fast pathway a criminal or innocent bystander?

The intracardiac electrograms are shown during scanned single premature ventricular extrastimuli with a decreasing coupling interval in a very short RP tachycardia. What is the diagnosis and is the fast pathway essential for sustaining the tachycardia?

Where is the gap after a 90 W/4 s very-high-power short-duration ablation of atrial fibrillation?: Association with the left atrial-pulmonary vein voltage and wall thickness.

Background: Although pulmonary vein isolation (PVI) for atrial fibrillation (AF) utilizing radiofrequency (RF) applications with a very high-power and short-duration (vHPSD) has shortened the procedure time, the determinants of pulmonary vein (PV) gaps in the first-pass PVI and acute PV reconnections are unclear. Methods: An extensive encircling PVI was performed with the QDOT MICRO catheter with a vHPSD (90 W-4 s) in 30 patients with AF (19 men, 64 ± 10 years). The association of the PV gap sites (first-pass PVI failure, acute PV reconnections [spontaneous reconnections or dormant conduction provoked by adenosine triphosphate] or both) with the left atrial (LA) wall thickness and LA bipolar voltage on the PVI line and ablation-related parameters were assessed. Results: PV gaps were observed in 29 (6%) of 480 segments (16 segments per patient) in 17 patients (56%). The PV gaps were associated with the LA wall thickness, bipolar voltage, and the number of RF points (LA wall thickness, 2.5 ± 0.5 vs. 1.9 ± 0.4 mm, p < .001; bipolar voltage, 2.59 ± 1.62 vs. 1.34 ± 1.14 mV, p < .001; RF points, 6 ± 2 vs. 4 ± 2, p = .008) but were not with the other ablation-related parameters. Receiver operating characteristic curves yielded that an LA wall thickness ≥2.3 mm and bipolar voltage ≥2.40 mV were determinants of PV gaps with an area under the curve of 0.82 and 0.73, respectively. Conclusions: The LA voltage and wall thickness on the PV-encircling ablation line were highly associated with PV gaps using the 90 W/4 s-vHPSD ablation.

Clinical implication of the patient's disease awareness and adherence to medications in patients undergoing atrial fibrillation ablation.

Background: The effects of the patient's disease awareness on the management of postablation of atrial fibrillation (AF) are unknown. Methods: One hundred thirty-three AF patients undergoing an initial ablation were given a disease awareness questionnaire with a score of 16 points (8 points about AF in general and 8 points about oral anticoagulants) for the Jessa Atrial Fibrillation Knowledge Questionnaire (JAKQ) before and 1-year-after ablation. We divided them into the poor disease awareness group and good disease awareness group according to the median value (75%) of the total JAKQ score about AF in general, and compared the baseline patient characteristics and the 1-year changes in the JAKQ score, medication adherence, blood pressure, laboratory data, echocardiographic parameters, and AF/atrial tachycardia (AT) recurrence rate between the two groups. Results: Forty-two (31.6%) patients were classified as having poor disease awareness (<75% of the total JAKQ score), which was closely associated with poor medication adherence, hypertension, diabetes, dyslipidemia, and greater left atrial volume (LAV). These trends in the poor disease awareness group remained unchanged 1 year after the ablation. During the 25.3-month follow-up, the AF/AT recurrence rate was significantly higher in the poor disease awareness than the good disease awareness group (23.8% vs. 7.7%; p = .003 by the log-rank test). Conclusions: Poor disease awareness was linked to poor medication adherence, lifestyle-related diseases, and greater LAV before and even 1 year after the ablation, making it a potential surrogate marker for AF/AT recurrence. These findings highlight the clinical significance of disease awareness in AF management.

Recurrent episodes of atrioventricular nodal reentrant tachycardia: Sites of ablation success, ablation endpoint, and primary culprits for recurrence.

Background: Atrioventricular nodal reentrant tachycardia (AVNRT) sometimes recurs even after anatomical slow pathway (SP) ablation targeting the rightward inferior extension (RIE). This multicenter study aimed to determine the reasons for AVNRT recurrence. Methods and Results: Forty-six patients were treated successfully for recurrent AVNRT. Initial treatment was for 38 slow-fast AVNRTs, 3 fast-slow AVNRTs, 2 slow-slow AVNRTs, 2 slow-fast and fast-slow AVNRTs, and 1 noninducible AVNRT. All initial treatments were of RF application to the RIE; SP elimination was achieved in 11, dual AVN physiology was seen in 29, and AVNRT remained inducible in 5. The recurrent AVNRTs included 34 slow-fast AVNRTs, 6 fast-slow AVNRTs, 3 slow-slow AVNRTs, 2 slow-fast and fast-slow AVNRTs, and 1 slow-fast and slow-slow AVNRTs. Successful ablation site was within the RIE in 39 and left inferior extension in 7. In 30 of 39, the successful RIE site was in the same area or higher than that of the initial procedure. Conclusion: For a high majority (around 85%) of patients in whom AVNRT recurs after initial ablation success, the site of a second successful procedure will be within the RIE even though the RIE was originally targeted. Furthermore, a high majority (around 86%) of sites of successful ablation will be higher than those originally targeted.

Systematic observation-based diagnosis of atrioventricular nodal reentrant tachycardia with a bystander concealed nodoventricular pathway.

Background: This study aimed to establish a systematic method for diagnosing atrioventricular nodal reentrant tachycardia (AVNRT) with a bystander concealed nodoventricular pathway (cNVP). Methods: We analyzed 13 cases of AVNRT with a bystander cNVP, 11 connected to the slow pathway (cNVP-SP) and two to the fast pathway (cNVP-FP), along with two cases of cNVP-related orthodromic reciprocating tachycardia (ORT). Results: The diagnostic process was summarized in three steps. Step 1 was identification of the presence of an accessory pathway by resetting the tachycardia with delay (n = 9) and termination without atrial capture (n = 4) immediately after delivery of a His-refractory premature ventricular contraction (PVC). Step 2 was exclusion of ORT by atrio-His block during the tachycardia (n = 4), disappearance of the reset phenomenon after the early PVC (n = 7), or dissociation of His from the tachycardia during ventricular overdrive pacing (n = 1). Moreover, tachycardia reset/termination without the atrial capture (n = 2/2) 1 cycle after the His-refractory PVC was specifically diagnostic. Exceptionally, the disappearance of the reset phenomenon was also observed in the two cNVP-ORTs. Step 3 was verification of the AVN as the cNVP insertion site, evidenced by an atrial reset/block preceding the His reset/block in fast-slow AVNRT with a cNVP-SP and slow-fast AVNRT with a cNVP-FP or His reset preceding the atrial reset in slow-fast AVNRT with a cNVP-SP. Conclusion: AVNRT with a bystander cNVP can be diagnosed in the three steps with few exceptions. Notably, tachycardia reset/termination without atrial capture one cycle after delivery of a His-refractory PVC is specifically diagnostic.