title: Investigating the role of the coronary vasculature in the mechanisms of defibrillation.
abstract: BACKGROUND
  The direct role of coronary vessels in defibrillation, although hypothesized to be important, remains to be elucidated. We investigated how vessel-induced virtual electrode polarizations assist reentry termination.
  
  
  RESULTS
  A highly anatomically detailed rabbit ventricular slice bidomain computer model was constructed from 25-μm magnetic resonance data, faithfully representing both structural and electric properties of blood vessels. For comparison, an equivalent simplified model with intramural cavities filled in was also built. Following fibrillation induction, 6 initial states were selected, and biphasic shocks (5-70 V) were applied using a realistic implanted cardioverter-defibrillator electrode configuration. A fundamental mechanism of biphasic defibrillation was uncovered in both models, involving successive break excitations (after each shock phase) emanating from opposing myocardial surfaces (in septum and left ventricle), which rapidly closed down excitable gaps. The presence of vessels accelerated this process, achieving more-rapid and successful defibrillation. Defibrillation failed in 5 cases (all because of initiation of new activity) compared with 8 with the simplified model (5/8 failures because of surviving activity). At stronger shocks, virtual electrodes formed around vessels, rapidly activating intramural tissue because of break excitations, assisting the main defibrillation mechanism, and eliminating all activity <15 ms of shock end in 60% of successful shocks (36% in simplified model). Subsequent analysis identified that only vessels >200 μm in diameter participated through this mechanism. Consequently, wavefronts could survive intramurally in the simplified model, leading to reentry and shock failure.
  
  
  CONCLUSIONS
  We provide new insight into defibrillation mechanisms by showing how intramural blood vessels facilitate more-effective elimination of existing wavefronts, rapid closing down of excitable gaps, and successful defibrillation and give guidance toward the required resolution of cardiac imaging and model generation endeavors for mechanistic defibrillation analysis.
authors.affiliation: Computing Laboratory, University of Oxford, Oxford, UK. martin.bishop@comlab.ox.ac.uk
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Bishop
authors.forename: Gernot
authors.initials: G
authors.lastname: Plank
authors.forename: Edward
authors.initials: E
authors.lastname: Vigmond
mesh_terms: D000818:Animals; D003198:Computer Simulation; D003331:Coronary Vessels / Q000503:physiopathology*; D004554:Electric Countershock / Q000379:methods*; D006801:Humans; D019028:Magnetic Resonance Imaging, Cine; D011817:Rabbits; D014693:Ventricular Fibrillation / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy*