First-in-Man Analysis of the Relationship Between Electrical Rotors From Noninvasive Panoramic Mapping and Atrial Fibrosis From Magnetic Resonance Imaging in Patients With Persistent Atrial Fibrillation
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Background—Late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) imaging can be used to evaluate characteristics of atrial fibrosis. The novel noninvasive epicardial and endocardial electrophysiology system (NEEES) allows for the identification of sources with rotor activity. This study describes a new technique to examine the relationship between rotors and LGE signal intensity in patients with persistent atrial fibrillation (PERS) scheduled for ablation.
Methods and Results—Ten consecutive patients underwent pulmonary vein isolation for persistent atrial fibrillation. LGE CMR of both atria was performed, and NEEES-based analysis was conducted to identify rotors. For each mapping point, the intracardiac locations were transferred onto an individual CMR-derived 3-dimensional shell. This allowed the LGE signal intensity to be projected onto the anatomy from the NEEES analysis. NEEES analysis identified a total number of 410 electric rotors, 47.8% were located in the left atrium and 52.2% in the right atrium. Magnetic resonance imaging analysis was performed from 10 right atria and 10 left atria data sets, including 86 axial LGE CMR planes per atrium. The mean LGE burden for left atrium and right atrium was 23.9±1.6% and 15.9±1.8%, respectively. Statistical analysis demonstrated a lack of regional association between the extent of LGE signal intensity and the presence of rotors.
Conclusions—This is the first study demonstrating that the presence of rotors based on NEEES analysis is not directly associated with the extent and anatomic location of LGE signal intensity from CMR. Further studies evaluating the relationship between rotors and fibrosis in patients with persistent atrial fibrillation are mandatory and may inform strategies to improve ablation outcome.
- Received June 12, 2016.
- Accepted June 29, 2017.
- © 2017 American Heart Association, Inc.