Arrhythmogenesis by single ectopic beats originating in the Purkinje system.
Cells in the Purkinje system (PS) are known to be more vulnerable than ventricular myocytes to secondary excitations during the action potential (AP) plateau or repolarization phases, known as early afterdepolarizations (EADs). Since myocytes have a lower intrinsic AP duration than the PS cells to which they are coupled, EADs occurring in distal branches of the PS are more likely to result in propagating ectopic beats. In this study, we use a computer model of the rabbit ventricles and PS to investigate the consequences of EADs occurring at different times and places in the cardiac conduction system. We quantify the role of tissue conductivity and excitability, as well as interaction with sinus excitation, in determining whether an EAD-induced ectopic beat will establish reentrant activity. We demonstrate how a single ectopic beat arising from an EAD in the distal PS can give rise to reentrant arrhythmia; in contrast, EADs in the proximal PS were unable to initiate reentry. Clinical studies have established the PS as a potential substrate for reentry, but the underlying mechanisms of these types of disorder are not well understood, nor are conditions leading to their development clearly defined; this work provides new insights into the role of the PS in such circumstances. Our findings indicate that simulated EADs in the distal PS can induce premature beats, which can lead to the tachycardias involving the conduction system due to interactions with sinus activity or impaired myocardial conduction velocity.
Deo
Makarand
M
Center for Arrhythmia Research, University of Michigan, Ann Arbor, Michigan, USA.
Boyle
Patrick M
PM
Kim
Albert M
AM
Vigmond
Edward J
EJ
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D003198:Computer Simulation; D006329:Heart Conduction System / Q000502:physiology; D023421:Models, Animal; D011689:Purkinje Cells / Q000502:physiology*; D011817:Rabbits; D016276:Ventricular Function / Q000502:physiology; D018879:Ventricular Premature Complexes / Q000503:physiopathology*