Munrogottlieb0441

The objective of this study was to present a new system, the Automatic Arrhythmia Origin Localization (AAOL) system, which used incomplete electroanatomic mapping (EAM) for localization of idiopathic ventricular arrhythmia (IVA) origin on the patient-specific geometry of left ventricular, right ventricular, and neighboring vessels. The study assessed the accuracy of the system in localizing IVA source sites on cardiac structures where pace mapping is challenging.

An intraprocedural automated site of origin localization system was previously developed to identify the origin of early left ventricular activation by using 12-lead electrocardiograms (ECGs). However, it has limitations, as it could not identify the site of origin in the right ventricle and relied on acquiring a complete EAM.

Twenty patients undergoing IVA catheter ablation had a 12-lead ECG recorded during clinical arrhythmia and during pacing at various locations identified on EAM geometries. The new system combined 3-lead (III, V

, and V

) 120-ms QRS integrals and patient-specific EAM geometry with pace mapping to predict the site of earliest ventricular activation. The predicted site was projected onto EAM geometry.

Twenty-three IVA origin sites were clinically identified by activation mapping and/or pace mapping (8, right ventricle; 15, left ventricle, including 8 from the posteromedial papillary muscle, 2 from the aortic root, and 1 from the distal coronary sinus). The new system achieved a mean localization accuracy of 3.6mm for the 23 mapped IVAs.

The new intraprocedural AAOL system achieved accurate localization of IVA origin in ventricles and neighboring vessels, which could facilitate ablation procedures for patients with IVAs.

The new intraprocedural AAOL system achieved accurate localization of IVA origin in ventricles and neighboring vessels, which could facilitate ablation procedures for patients with IVAs.

This study sought to assess the rate and outcomes of premature ventricular contractions (PVC)-cardiomyopathy from the CHF-STAT (Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure) trial, a population with cardiomyopathy (left ventricular [LV] ejection fraction of<40%) and frequent PVCs (>10 PVCs per hour).

PVCs are associated with heart failure and PVC-cardiomyopathy. The prevalence of PVC-cardiomyopathy and outcome benefits of PVC suppression are not clear.

A secondary analysis of the CHF-STAT study was performed to compare the rate of successful PVC suppression (≥80% PVC reduction), LV recovery (defined as improvement in LV ejection fraction of≥10% points), and PVC-cardiomyopathy between amiodarone and placebo groups at 6months. PVC-cardiomyopathy was defined if both PVC reduction of≥80% and LV ejection fraction improvement of≥10% were present at 6months. Cardiac events (death or resuscitated cardiac arrest) were compared between PVC-cardiomyopathy versus non-PVC-cardiomyopathyrdiomyopathy in the CHF-STAT study was significant regardless of ischemic substrate (29%, overall population; 41%, nonischemic cardiomyopathy). Treatment of PVC-cardiomyopathy with amiodarone is likely to improve survival in this high-risk population.

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.

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.

This study evaluated the association of the post-ablation scar with stroke risk in patients undergoing atrial fibrillation (AF) ablation.

Late gadolinium enhancement-cardiac magnetic resonance studies have reported a direct association between pre-ablation left atrial scar and thromboembolic events in patients with AF.

Consecutive patients with AF were classified into 2 groups based on the type of ablation performed at the first procedure. Group 1 involved limited ablation (isolation of pulmonary veins, left atrial posterior wall, and superior vena cava); and group 2 involved extensive ablation (limited ablation+ ablation of nonpulmonary vein triggers from all sites except left atrial appendage). During the repeat procedure, post-ablation scar (region with bipolar voltage amplitude<0.5mV) was identified by using 3-dimensional voltage mapping.

A total of 6,297 patients were included group 1, n=1,713; group 2, n=4,584. Group 2 patients were significantly older and had more nonparoxysmal AF. selleck compound Nineteen (0.3%) thromboembolic events were reported after the first ablation procedure 9 (1.02%) in group 1 and 10 (0.61%) in group 2 (p=0.26). At the time of the event, all 19 patients were experiencing arrhythmia. Median time to stroke was 14 (interquartile range 9 to 20) months in group 1 and 14.5 (interquartile range 8 to 18) months in group 2. Post-ablation scar data were derived from 2,414 patients undergoing repeat ablation. Mean scar area was detected as 67.1 ± 4.6% in group 2 and 34.9 ± 8.8% in group 1 at the redo procedure (p<0.001).

Differently from the cardiac magnetic resonance-detected pre-ablation scar, scar resulting from extensive ablation was not associated with increased risk of stroke compared with that from the limited ablation.

Differently from the cardiac magnetic resonance-detected pre-ablation scar, scar resulting from extensive ablation was not associated with increased risk of stroke compared with that from the limited ablation.