title: Arrhythmogenic mechanisms of the Purkinje system during electric shocks: a modeling study.
abstract: BACKGROUND
  The function of the Purkinje system (PS) is to ensure fast and uniform activation of the heart. Although this vital role during sinus rhythm is well understood, this is not the case when shocks are applied to the heart, especially in the case of failed defibrillation. The PS activates differently from the myocardium, has different electrophysiological properties, and provides alternate propagation pathways; thus, there are many ways in which it can contribute to postshock behavior.
  
  
  OBJECTIVE
  The purpose of this study was to elucidate the role of the PS in the initiation and maintenance of postshock arrhythmias.
  
  
  METHODS
  A computer model of the ventricles including the PS was subjected to different reentry induction protocols.
  
  
  RESULTS
  The PS facilitated reentry induction at relatively weaker shocks. Disconnecting the PS from the ventricles during the postshock interval revealed that the PS helps stabilize early-stage reentry by providing focal breakthroughs. During later stages, the PS contributed to reentry by leading to higher frequency rotors. The PS also promoted wave front splitting during reentry due to electrotonic coupling, which prolongs action potential durations at PS-myocyte junctions. The presence of a PS results in the anchoring of reentrant activations that propagate through the pathways provided by the PS.
  
  
  CONCLUSIONS
  The PS is proarrhythmic in that it provides pathways that prolong activity, and it plays a supplementary role in maintaining the later stages of reentry (>800 ms).
authors: Department of Electrical and Computer Engineering, University of Calgary, Calgary, Canada. mdeo@ucalgary.ca
authors: Makarand
authors: M
authors: Deo
authors: Patrick
authors: P
authors: Boyle
authors: Gernot
authors: G
authors: Plank
authors: Edward
authors: E
authors: Vigmond
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000503:physiopathology; D003198:Computer Simulation; D047548:Defibrillators / Q000009:adverse effects*; D004195:Disease Models, Animal; D006352:Heart Ventricles / Q000294:innervation* / Q000473:pathology; D006801:Humans; D011690:Purkinje Fibers / Q000473:pathology / Q000503:physiopathology*; D011817:Rabbits; D012307:Risk Factors; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology