Author + information
- Received May 4, 2018
- Revision received July 19, 2018
- Accepted August 23, 2018
- Published online October 31, 2018.
- Brian J. Hansen, BSca,b,
- Jichao Zhao, PhDc,
- Ning Li, MD, PhDa,b,
- Alexander Zolotarev, BSca,d,
- Stanislav Zakharkin, PhDa,
- Yufeng Wang, BScc,
- Josh Atwalc,
- Anuradha Kalyanasundaram, PhDa,b,
- Suhaib H. Abudulwaheda,
- Katelynn M. Helfrich, BSca,
- Anna Bratasz, PhDb,
- Kimerly A. Powell, PhDb,
- Bryan Whitson, MDb,e,
- Peter J. Mohler, PhDb,f,
- Paul M.L. Janssen, PhDa,b,
- Orlando P. Simonetti, PhDb,g,
- John D. Hummel, MDb,f and
- Vadim V. Fedorov, PhDa,b,∗ ()
- aDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, Columbus, Ohio
- bDavis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, Ohio
- cAuckland Bioengineering Institute, The University of Auckland, Auckland, New Zealand
- dPhystech School of Biological and Medical Physics, Moscow Institute of Physic and Technology, Dolgoprudny, Russian Federation
- eDepartment of Surgery, The Ohio State University Wexner Medical Center, Columbus, Ohio
- fDepartment of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio
- gDepartment of Biomedical Engineering, The Ohio State University Wexner Medical Center, Columbus, Ohio
- ↵∗Address for correspondence:
Dr. Vadim V. Fedorov, Department of Physiology and Cell Biology, The Ohio State University Wexner Medical Center, 5196 Graves Hall, 333 West 10th Avenue, Columbus, Ohio 43210-1218.
Objectives This study sought to improve atrial fibrillation (AF) driver identification by integrating clinical multielectrode mapping with driver fingerprints defined by high-resolution ex vivo 3-dimensional (3D) functional and structural imaging.
Background Clinical multielectrode mapping of AF drivers suffers from variable contact, signal processing, and structural complexity within the 3D human atrial wall, raising questions on the validity of such drivers.
Methods Sustained AF was mapped in coronary-perfused explanted human hearts (n = 11) with transmural near-infrared optical mapping (∼0.3 mm2 resolution). Simultaneously, custom FIRMap catheters (∼9 × 9 mm2 resolution) mapped endocardial and epicardial surfaces, which were analyzed by Focal Impulse and Rotor Mapping activation and Rotational Activity Profile (Abbot Labs, Chicago, Illinois). Functional maps were integrated with contrast-enhanced cardiac magnetic resonance imaging (∼0.1 mm3 resolution) analysis of 3D fibrosis architecture.
Results During sustained AF, near-infrared optical mapping identified 1 to 2 intramural, spatially stable re-entrant AF drivers per heart. Driver targeted ablation affecting 2.2 ± 1.1% of the atrial surface terminated and prevented AF. Driver regions had significantly higher phase singularity density and dominant frequency than neighboring nondriver regions. Focal Impulse and Rotor Mapping had 80% sensitivity to near-infrared optical mapping–defined driver locations (16 of 20), and matched 14 of 20 driver visualizations: 10 of 14 re-entries seen with Rotational Activity Profile; and 4 of 6 breakthrough/focal patterns. Focal Impulse and Rotor Mapping detected 1.1 ± 0.9 false-positive rotational activity profiles per recording, but these regions had lower intramural contrast-enhanced cardiac magnetic resonance imaging fibrosis than did driver regions (14.9 ± 7.9% vs. 23.2 ± 10.5%, p < 0.005).
Conclusions The study revealed that both re-entrant and breakthrough/focal AF driver patterns visualized by surface-only clinical multielectrodes can represent projections of 3D intramural microanatomic re-entries. Integration of multielectrode mapping and 3D fibrosis analysis may enhance AF driver detection, thereby improving the efficacy of driver-targeted ablation.
- atrial fibrillation
- contrast-enhanced cardiac magnetic resonance
- multi-electrode mapping
- optical mapping
This work was supported by National Institutes of Health grants HL115580 and HL135109 (V.V.F) and T32HL134616 (B.J.H.), American Heart Association Grant in Aid 16GRNT31010036 (V.V.F.), and Health Research Council of New Zealand (J.Z.). Dr. Simonetti receives research support from Siemens. Dr. Hummel is a consultant to Abbott Laboratories. Dr. Fedorov has received research support from Abbott Laboratories. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Clinical Electrophysiology author instructions page.
- Received May 4, 2018.
- Revision received July 19, 2018.
- Accepted August 23, 2018.
- 2018 American College of Cardiology Foundation
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