Roles of the Purkinje system during electric shocks and arrhythmia.

摘要

The Purkinje system (PS) is a network of fast-conducting fibres that facilitates coordinated ventricular contraction during normal heartbeats. Its roles during abnormal activity are unclear; experimental observations are difficult due to fine fibre geometry. The objective of this thesis was to use computer simulations of bioelectric activity in the heart to better understand roles of the PS during electric shocks and life-threatening episodes of arrhythmia. Several key findings are presented. Firstly, electric fields on the defibrillation scale were applied to the quiescent ventricles with and without the PS model. Due to its unique geometry, the PS is subject to rapid excitation by all fields; depending on how stimulation affects the myocardial volume, this can lead to significant abbreviation of total activation time (tact) compared to cases where the PS is absent, since field-induced PS activations can be passed to coupled ventricular tissue that is excitable post-shock. This effect was most prominent for weaker shocks and for fields oriented along the apico-basal axis, for which the PS shortened tact by more than 30%.;Finally, simulations were performed to explore PS contributions during ventricular fibrillation (VF), which leads to sudden cardiac death. It was determined that breakthroughs from the PS can result in a shift in pathology, from functional reentry driven by multiple rotors to macroscopic anatomical reentry in a circuit including the PS. Furthermore, the model suggested that metabolic factors are the crucial factor in establishing a transmural gradient in activation rate during VF; the PS does not seem to contribute significantly to this phenomenon.;Keywords: Purkinje system, cardiac arrhythmia, defibrillation, atrioventricular reciprocating tachycardia, ventricular fibrillation.;Secondly, a simple model of atrioventricular reciprocating tachycardia (AVRT) was constructed. The PS is a crucial component of the anatomical circuit that sustains this arrhythmia. Clinically, identification of QRS complex fusion during ventricular overdrive pacing (VOP) confirms the presence of AVRT but in approximately 30% of AVRT patients it is never observed. Investigation of VOP in the model revealed that stimulus proximity to the PS obscures fusion; this suggests that non-responders may have more PS endpoints in preferred VOP locations.