ABSTRACT
Atrioventricular nodal reentrant tachycardia (AVNRT) is one of the most common types of paroxysmal supraventricular tachycardia. The autonomic nervous system (ANS) activity is known to affect sudden episodes of AVNRT, but the detailed underlying mechanism is not fully understood. In this work, we update our recent compact multifunctional model of the rabbit atrioventricular node (AV) with ANS control to simulate AVNRT. The refractoriness of model cells is modulated by one ANS coefficient, causing a change in the effective refractory periods, conduction delays, and intrinsic frequency of pacemaker cells. Using the model, we examine the onset, sustainability, and spontaneous termination of typical slow-fast and atypical fast-slow forms of AVNRT under ANS modulation. The conditions for the onset and sustainability of AVNRT can occur independently of each other in various combinations. Differences in the effective refractory periods of the slow and fast pathways of the AV node during anterograde and retrograde conduction determine the form of AVNRT. For the first time, the possibility of identifying hidden processes occurring inside the AV node using a computer model is shown, allowing us to come closer to understanding the role of ANS control during AVNRT. The results obtained are consistent with clinical and experimental data and represent a new tool for studying the electrophysiological mechanisms of this type of arrhythmia.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
New figures have been added, existing figures have been rearranged, and text has been updated to clarify the findings of the paper.
