Author + information
- Received March 21, 2017
- Revision received May 17, 2017
- Accepted May 17, 2017
- Published online June 19, 2017.
- aPhysiology and Cell Biology Department, Ohio State University Wexner Medical Center, Columbus, Ohio
- bAuckland Bioengineering Institute, University of Auckland, Auckland, New Zealand
- ↵∗Address for correspondence:
Dr. Vadim V. Fedorov, The Ohio State University Wexner Medical Center, 300 Hamilton Hall, 1645 Neil Avenue, Columbus, Ohio 43210-1218.
Recent studies strongly suggest that the majority of atrial fibrillation (AF) patients with diagnosed or subclinical cardiac diseases have established or even pre-existing fibrotic structural remodeling, which may lead to conduction abnormalities and re-entrant activity that sustain AF. As conventional treatments fail to treat AF in far too many cases, an urgent need exists to identify specific structural arrhythmogenic fibrosis patterns, which may maintain AF, to identify effective ablation targets for AF treatment. However, the existing challenge is to define what exact structural remodeling within the complex 3-dimensional (3D) human atrial wall is arrhythmogenic, as well as linking arrhythmogenic fibrosis to an underlying mechanism of AF maintenance in the clinical setting. This review is focused on the role of 3D fibrosis architecture in the mechanisms of AF maintenance revealed by submillimeter, high-resolution ex vivo imaging modalities directly of human atria, as well as from in silico 3D computational techniques that can be able to overcome in vivo clinical limitations. The systematic integration of functional and structural imaging ex vivo may inform the necessary integration of electrode and structural mapping in vivo. A holistic view of AF driver mechanisms may begin to identify the defining characteristics or “fingerprints” of re-entrant AF drivers, such as 3D fibrotic architecture, to design optimal patient-specific ablation strategies.
This work was supported by National Institutes of Health Grant HL115580 and American Heart Association Grant in Aid #16GRNT31010036 (to Dr. Fedorov), and Health Research Council of New Zealand (to Dr. Zhao). The 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 March 21, 2017.
- Revision received May 17, 2017.
- Accepted May 17, 2017.
- 2017 American College of Cardiology Foundation
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