Search

Objective The aim of this study was to assess temporal changes and clinical implications of peridevice leak (PDL) after left atrial appendage closure. Background Endocardial left atrial appendage closure devices are alternatives to long-term oral anticoagulation (OAC) for patients with atrial fibrillation. PDL > 5 mm may prohibit discontinuation of OAC. Methods Patients included in the study had: 1) successful Watchman device implantation without immediate PDL; 2) new PDL identified at 45 to 90 days using transesophageal echocardiography; 3) eligibility for OAC; and 4) 1 follow-up transesophageal echocardiographic study for PDL surveillance. Relevant clinical and imaging data were collected by chart review. The combined primary outcome included failure to stop OAC after 45 to 90 days, transient ischemic attack or stroke, device-related thrombi, and need for PDL closure. Results Relevant data were reviewed for 1,039 successful Watchman device implantations. One hundred eight patients (10.5%) met the inclusion criteria. The average PDL at 45 to 90 days was 3.2 ± 1.6 mm. On the basis of a median PDL of 3 mm, patients were separated into ≤3 mm (n = 73) and >3 mm (n = 35) groups. In the ≤3 mm group, PDL regressed significantly (2.2 ± 0.8 mm vs 1.6 ± 1.4 mm; P = 0.002) after 275 ± 125 days. In the >3 mm group, there was no significant change in PDL (4.9 ± 1.4 mm vs 4.0 ± 3.0 mm; P = 0.12) after 208 ± 137 days. The primary outcome occurred more frequently (69% vs 34%; P = 0.002) in the >3 mm group. The incidence of transient ischemic attack or stroke in patients with PDL was significantly higher compared with patients without PDL, irrespective of PDL size. Conclusions New PDL detected by transesophageal echocardiography at 45 to 90 days occurred in a significant percentage of patients and was associated with worse clinical outcomes. PDL ≤ 3 mm tended to regress over time.

The goal of this study was to characterize the location and electrophysiological properties of left atrial appendage (LAA) atrial tachycardia (AT).The LAA has been reported to be a source of AT and atrial fibrillation (AF) triggers.This study retrospectively reviewed ATs mapped to the LAA. Activation and entrainment mapping were used to determine the mechanism and localize each AT circuit/origin.From 2014 to 2018, a total of 45 patients (mean age 65 ± 10 years; 69% male) had 51 LAA ATs: 43 (84%) after AF ablation and 8 de novo (no prior AF). Overall, 50 (98%) were due to localized re-entry/micro-re-entry, whereas only 1 was a focal triggered AT. All 50 micro-re-entrant LAA ATs were mapped to the anterior base (70%) or LAA ridge (30%), and all were successfully treated with focal ablation; no case required LAA isolation. After successful ablation of the initial AT at the LAA base, 23 (62%) of 37 patients with AF also had inducible macro-re-entrant peri-mitral flutter, but none had AF triggers from inside the LAA.LAA ATs are almost always micro-re-entrant in mechanism and originate from either the anterior base or LAA ridge. AT originating from inside the LAA body is very rare. The anterior and ridge aspects of the LAA-left atrium junction seem to be arrhythmogenic hotspots prone to localized re-entry. These ATs are treatable with focal ablation without LAA isolation but are frequently associated with macro-re-entrant peri-mitral flutter.

The purpose of this study is to determine whether patients on ≥4 weeks of continuous non-vitamin K antagonist oral anticoagulant (NOAC) therapy require transesophageal echocardiography (TEE) before catheter ablation of atrial fibrillation (AF) or atrial flutter and to compare rates of left atrial (LA) thrombus and dense spontaneous echocardiographic contrast (SEC) in patients on NOAC versus warfarin therapy.The impact of NOAC therapy on the rates of LA thrombus detection by TEE in patients undergoing catheter ablation of AF is unknown.Initial TEEs for 388 patients (median age, 65 years; 74% male) on ≥4 weeks of continuous NOAC (n = 183) or warfarin therapy (n = 205) undergoing catheter ablation of AF and flutter were reviewed.After ≥4 weeks of therapy, the prevalence of LA thrombus and LA thrombus/dense SEC among patients on NOACs was 4.4% and 6.0%, respectively, which was comparable with that of patients on warfarin. LA thrombus rates among patients on dabigatran, rivaroxaban, and apixaban were 5.4%, 4.8%, and 0%, respectively (p = 0.46). Predictors of LA thrombus were congestive heart failure (odds ratio [OR]: 5.38; 95% confidence interval [CI]: 1.79 to 16.2; p = 0.003); and persistent AF (OR: 3.27; 95% CI: 1.06 to 10.2; p = 0.040).Despite ≥4 weeks of anticoagulation, the rate of LA thrombus in patients on NOACs before catheter ablation of AF or atrial flutter was 4.4%. This suggests that continuous NOAC therapy does not eliminate the need for TEE before catheter ablation of AF.