暂无摘要。

Atrial fibrosis in the right atrium (RA) presenting as a low-voltage zone might be the mechanism of atrial fibrillation (AF) and intra-atrial conduction delay. The impact of scar homogenization in RA on intra-atrial conduction delay is unknown. We describe a patient with paroxysmal AF and significant intra-atrial conduction delay with repetitive atrial flutter, triggered from the lateral free wall in the RA between the significant low-voltage zone and slow conduction area after pulmonary vein isolation. Linear ablation along the trabeculated lateral free wall in the RA to homogenize the scar was successfully performed, and the intra-atrial conduction delay improved ultimately.

暂无摘要。

Prior studies have described a variety of mechanisms for atrial fibrillation (AF) originating in the right atrium (RA). In this study, we report a series of patients in whom an extensive right atrial free wall low-voltage zone (LVZ) served as the AF substrate.
Five patients with a clinical syndrome of paroxysmal AF and atrial tachycardia (AT) underwent electrophysiologic evaluation. Five patients (3 M; age 52 ± 7 years) had symptomatic paroxysmal AF for (28 ± 17 months) not responsive to medical therapy. At the initial EP study, AT was inducible in four patients and was spontaneous in one patient. In all patients, tachycardia instability precluded detailed AT mapping. Sinus or pace maps indicated an extensive LVZ in the lateral RA trabeculated free wall which consisted of regions of low amplitude complex signals interspersed between electrically silent areas. Radiofrequency ablation aimed at rendering the LVZ electrical inert was successful in eliminating AF in four of five patients. At a follow-up of 28 ± 15 months, one patient had an isolated recurrence of AF. However, two patients required repeat ablation for recurrent AT.
An extensive LVZ in the trabeculated RA free wall constitutes an unusual substrate for AF. These patients also demonstrate unstable ATs originating from the same zone. Radiofrequency ablation to render the low-voltage zone electrically inert is an effective strategy to manage AF and AT.

Atypical atrial flutter (AFL) is common in patients with postsurgical atrial scar, with macro- or microscopic channels in the scar acting as substrate for reentry. Heterogeneous atrial scarring can cause varying flutter circuits, which makes mapping and ablation challenging, and recurrences common.
We hypothesize that dynamically adjusting voltage thresholds can identify heterogeneous atrial scarring, which can then be effectively homogenized to eliminate atypical AFLs.
We studied consecutive patients who presented to Electrophysiology laboratory for atypical AFL ablation with history of atriotomy and included the patients with multiple, varying flutter circuits during mapping in our study. We excluded patients with stable flutter circuit that was sustained and could be localized using traditional entrainment and activation mapping strategy. In the included patients, we performed detailed high-density voltage map of the atrium of interest. We adjusted voltage thresholds as needed to identify heterogeneity and channels in the scarred regions. A thorough scar homogenization was performed with irrigated smart-touch ablation catheter. Re-inducibility of tachycardia, and immediate and long-term outcomes were studied.
Of five studied cases, one was female; age 66 ± 10 years. All five had prior surgical substrate. All the patients had multiple flutter morphologies, which varied as we mapped the AFL. After scar homogenization, tachycardia was not inducible in any patient. No recurrence of flutter was noted during a mean follow-up duration of 450 ± 27 days.
High-density voltage mapping and homogenization of the scar can be an effective strategy in eliminating complex scar-mediated atypical AFL with multiple circuits.

暂无摘要。

Atrial fibrillation (AF) ablation has emerged as the preferred rhythm control strategy for symptomatic paroxysmal AF refractory or intolerant to at least one class I or III antiarrhythmic medication. Since the initial observation by Haissaguerre and colleagues, of pulmonary vein triggers initiating atrial fibrillation (AF), pulmonary vein isolation (PVI) has become the cornerstone for paroxysmal AF ablation therapy.

UNASSIGNED: Left atrial (LA) scarring, a consequence of cardiac fibrosis is a powerful predictor of procedure-outcome in atrial fibrillation (AF) patients undergoing catheter ablation. We sought to compare the long-term outcome in patients with paroxysmal AF (PAF) and severe LA scarring identified by 3D mapping, undergoing pulmonary vein isolation (PVAI) only or PVAI and the entire scar areas (scar homogenization) or PVAI+ ablation of the non-PV triggers.
UNASSIGNED: Totally, 177 consecutive patients with PAF and severe LA scarring were included. Patients underwent PVAI only (n = 45, Group 1), PVAI+ scar homogenization (n = 66, Group 2) or PVAI+ ablation of non-PV triggers (n = 66, Group 3) based on operator\'s choice. Baseline characteristics were similar across the groups. After first procedure, all patients were followed-up for a minimum of 2 years. The success rate at the end of the follow-up was 18% (8 pts), 21% (14 pts), and 61% (40 pts) in Groups 1, 2, and 3, respectively. Cumulative probability of AF-free survival was significantly higher in Group 3 (overall log-rank P <0.01, pairwise comparison 1 vs. 3 and 2 vs. 3 P < 0.01). During repeat procedures, non-PV triggers were ablated in all. After average 1.5 procedures, the success rates were 28 (62%), 41 (62%), and 56 (85%) in Groups 1, 2, and 3, respectively (log-rank P< 0.001).
UNASSIGNED: In patients with PAF and severe LA scarring, PVAI+ ablation of non-PV triggers is associated with significantly better long-term outcome than PVAI alone or PVAI+ scar homogenization.

暂无摘要。

BACKGROUND: Radiofrequency ablation for ventricular tachycardia is an established therapy. Use of chemical agents for scar homogenization represents an alternative approach. The purpose of this study was to characterize the efficacy of collagenase (CLG) application on epicardial ventricular scar homogenization.
RESULTS: Myocardial infarcts were created in Yorkshire pigs (n=6) by intracoronary microsphere injection. After 46.6±4.3 days, CLG type 2, type 4, and purified CLG were applied in vitro (n=1) to myocardial tissue blocks containing normal myocardium, border zone, and dense scar. Histopathologic studies were performed to identify the optimal CLG subtype. In vivo high-density electroanatomic mapping of the epicardium was also performed, and border zone and dense scar surface area and late potentials were quantified before and after CLG-4 application (n=5). Of the CLG subtypes tested in vitro, CLG-4 provided the best scar modification and least damage to normal myocardium. During in vivo testing, CLG-4 application decreased border zone area (21.3±14.3 to 17.1±11.1 mm(2), P=0.043) and increased dense scar area (9.1±10.3 to 22.0±20.6 mm(2), P=0.043). The total scar area before and after CLG application was 30.4±23.4 and 39.2±29.5 mm(2), respectively (P=0.08). Late potentials were reduced by CLG-4 application (28.8±21.8 to 13.8±13.1, P=0.043). During CLG-4 application (50.0±15.5 minutes), systolic blood pressure and heart rate were not significantly changed (68.0±7.7 versus 61.8±5.3 mmHg, P=0.08; 77.4±7.3 versus 78.8±6.0 beats per minute, P=0.50, respectively).
CONCLUSIONS: Ventricular epicardial scar homogenization by CLG-4 application is feasible and effective. This represents the first report on bioenzymatic ablation of arrhythmogenic tissue as an alternative strategy for lesion formation.