Introduction: Identifying the origin of nonpulmonary vein atrial fibrillation (AF) triggers (NPVTs) after pulmonary vein isolation (PVI) can be challenging. We aimed to determine if noninvasive electrocardiographic imaging (ECGi) could localize pacing from common NPVT sites. ECGi combines measured body surface potentials with heart-torso geometry acquired from computed tomography (CT) to generate an activation map.
Methods: In 12 patients with AF undergoing first time ablation, the ECGi vest was fitted for preprocedural CT scan and worn during the procedure. After PVI, we performed steady-state pacing from 15 typical anatomic NPVT sites at a cycle length of 700-800 ms. We co-registered the invasive anatomic map with the CT-based ECGi epicardial activation map to compare ECGi predicted to true pacing origin.
Results: In the study cohort (67% male, 58% persistent AF, and 67% with left atrial dilation), 148 (82%) pacing sites had both capture and adequate anatomy acquired from the three-dimensional mapping system to co-register with ECGi activation map. Median distance between true pacing sites and point of earliest epicardial activation derived from the ECGi maps for all sites was 17 mm (interquartile range, 10-22 mm). Assuming paced sites treated as regions with a radius of 2.5 cm, the earliest activation site on ECGi map falls within the region with 94% accuracy.
Conclusion: ECGi can approximate the origin of paced beats from common NPVT sites to within a median distance of 17 mm. A rapidly identified region may then be the focus of more detailed catheter-based mapping techniques to facilitate successful localization and ablation of NPVTs.
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http://dx.doi.org/10.1111/jce.16347 | DOI Listing |
J Cardiovasc Electrophysiol
September 2024
Cardiac Electrophysiology Section, Department of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Introduction: Identifying the origin of nonpulmonary vein atrial fibrillation (AF) triggers (NPVTs) after pulmonary vein isolation (PVI) can be challenging. We aimed to determine if noninvasive electrocardiographic imaging (ECGi) could localize pacing from common NPVT sites. ECGi combines measured body surface potentials with heart-torso geometry acquired from computed tomography (CT) to generate an activation map.
View Article and Find Full Text PDFJACC Clin Electrophysiol
November 2023
Section of Cardiac Electrophysiology, Division of Cardiovascular Medicine, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania, USA. Electronic address:
Background: Targeting nonpulmonary vein triggers (NPVTs) of atrial fibrillation (AF) after pulmonary vein isolation can be challenging. NPVTs are often single ectopic beats with a surface P-wave obscured by a QRS or T-wave.
Objectives: The goal of this study was to construct an algorithm to regionalize the site of origin of NPVTs using only intracardiac bipolar electrograms from 2 linear decapolar catheters positioned in the posterolateral right atrium (along the crista terminalis with the distal bipole pair in the superior vena cava) and in the proximal coronary sinus (CS).
Cell Rep
April 2023
Center for Interdisciplinary Research in Biology (CIRB), Team "Ca(2+) Signaling and Microbial Infections," Collège de France, CNRS UMR7241/INSERM U1050, PSL Research University, 75005 Paris, France; Laboratoire de biologie et Pharmacie Appliquée (LBPA), CNRS UMR8113/INSERM U1282, Team "Ca(2+) Signaling and Microbial Infections," Ecole Normale Supérieure Paris-Saclay, Université Paris Saclay, 91190 Gif-sur-Yvette, France; Institute for Integrative Biology of the Cell (I2BC), CNRS UMR9198/INSERM U1280, Team "Ca(2+) Signaling and Microbial Infections," CEA, Université Paris-Saclay, 91190 Gif-sur-Yvette, France. Electronic address:
Upon activation, vinculin reinforces cytoskeletal anchorage during cell adhesion. Activating ligands classically disrupt intramolecular interactions between the vinculin head and tail domains that bind to actin filaments. Here, we show that Shigella IpaA triggers major allosteric changes in the head domain, leading to vinculin homo-oligomerization.
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