title: Terminating ventricular tachyarrhythmias using far-field low-voltage stimuli: mechanisms and delivery protocols.
abstract: BACKGROUND
  Low-voltage termination of ventricular tachycardia (VT) and atrial fibrillation has shown promising results; however, the mechanisms and full range of applications remain unexplored.
  
  
  OBJECTIVE
  To elucidate the mechanisms for low-voltage cardioversion and defibrillation and to develop an optimal low-voltage defibrillation protocol.
  
  
  METHODS
  We developed a detailed magnetic resonance imaging-based computational model of the rabbit right ventricular wall. We applied multiple low-voltage far-field stimuli of various strengths (≤1 V/cm) and stimulation rates in VT and ventricular fibrillation (VF).
  
  
  RESULTS
  Of the 5 stimulation rates tested, stimuli applied at 16% or 88% of the VT cycle length (CL) were most effective in cardioverting VT, the mechanism being consecutive excitable gap decreases. Stimuli given at 88% of the VF CL defibrillated successfully, whereas a faster stimulation rate (16%) often failed because the fast stimuli did not capture enough tissue. In this model, defibrillation threshold energy for multiple low-voltage stimuli at 88% of VF CL was 0.58% of the defibrillation threshold energy for a single strong biphasic shock. Based on the simulation results, a novel 2-stage defibrillation protocol was proposed. The first stage converted VF into VT by applying low-voltage stimuli at times of maximal excitable gap, capturing large tissue volume and synchronizing depolarization; the second stage terminated VT. The energy required for successful defibrillation using this protocol was 57.42% of the energy for low-voltage defibrillation when stimulating at 88% of VF CL.
  
  
  CONCLUSIONS
  A novel 2-stage low-voltage defibrillation protocol using the excitable gap extent to time multiple stimuli defibrillated VF with the least energy by first converting VF into VT and then terminating VT.
authors.affiliation: Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
authors.forename: Lukas J
authors.initials: LJ
authors.lastname: Rantner
authors.forename: Brock M
authors.initials: BM
authors.lastname: Tice
authors.forename: Natalia A
authors.initials: NA
authors.lastname: Trayanova
mesh_terms: D000818:Animals; D003198:Computer Simulation; D047548:Defibrillators; D004554:Electric Countershock / Q000379:methods*; D004599:Electric Stimulation Therapy / Q000379:methods*; D006352:Heart Ventricles / Q000503:physiopathology*; D011817:Rabbits; D017180:Tachycardia, Ventricular / Q000628:therapy*; D014693:Ventricular Fibrillation / Q000628:therapy*
keywords: AF; CL; Computer simulation; DFT; Electric countershock; Electric stimulation; RV; Tachycardia, Ventricular; V(m); VEP; VF; VT; Ventricular fibrillation; atrial fibrillation; cycle length; defibrillation threshold; extracellular potential; right ventricle/ventricular; transmembrane potential; ventricular fibrillation; ventricular tachycardia; virtual electrode polarization; Φ(e)