Virtual electrophysiological study of atrial fibrillation in fibrotic remodeling. McDowell, K.; Zahid, S.; Vadakkumpadan, F.; Blauer, J.; MacLeod, R.; and Trayanova, N. PLoS One, 10(2):e0117110, 2015.
bibtex   
@Article{RSM:McD2015,
  author =       "K.S. McDowell and S. Zahid and F. Vadakkumpadan and J.
                 Blauer and R.S. MacLeod and N.A. Trayanova",
  title =        "Virtual electrophysiological study of atrial fibrillation
                 in fibrotic remodeling.",
  journal =      "PLoS One",
  year =         "2015",
  volume =       "10",
  number =       "2",
  pages =        "e0117110",
  robnote =      "We aimed to
                 provide a proof-of-concept that patient-specific virtual
                 electrophysiological study that combines i) atrial
                 structure and fibrosis distribution from clinical MRI and
                 ii) modeling of atrial electrophysiology, could be used to
                 predict: (1) how fibrosis distribution determines the
                 locations from which paced beats degrade into AF; (2) the
                 dynamic behavior of persistent AF rotors; and (3) the
                 optimal ablation targets in each patient. Four MRI-based
                 patient-specific models of fibrotic left atria were
                 generated, ranging in fibrosis amount. Virtual
                 electrophysiological studies were performed in these
                 models, and where AF was inducible, the dynamics of AF
                 were used to determine the ablation locations that render
                 AF non-inducible. In 2 of the 4 models patient-specific
                 models AF was induced; in these models the distance
                 between a given pacing location and the closest fibrotic
                 region determined whether AF was inducible from that
                 particular location, with only the mid-range distances
                 resulting in arrhythmia. Phase singularities of persistent
                 rotors were found to move within restricted regions of
                 tissue, which were independent of the pacing location from
                 which AF was induced. Electrophysiological sensitivity
                 analysis demonstrated that these regions changed little
                 with variations in electrophysiological parameters.
                 Patient-specific distribution of fibrosis was thus found
                 to be a critical component of AF initiation and
                 maintenance. When the restricted regions encompassing the
                 meander of the persistent phase singularities were modeled
                 as ablation lesions, AF could no longer be induced. The
                 study demonstrates that a patient-specific modeling
                 approach to identify non-invasively AF ablation targets
                 prior to the clinical procedure is feasible.",
  bibdate =      "Fri Jun 19 06:43:08 2015",
  pmcid =        "PMC4333565",
}
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