Abstract
The least understood aspect of re-entrant cardiac arrhythmias is how they start spontaneously. The known mechanisms for re-entry induction involve the application of premature electrical stimuli or rapid pacing, whereas in a clinical setting, re-entry often occurs at normal heart rates. Here, we propose a physiological mechanism of re-entry onset at normal and slow heart rates, which is based on structurally determined heterogeneities. Using a two-dimensional tissue model with Luo-Rudy II kinetics, we study electrical propagation in the presence of macroscopic coupling heterogeneities. We find that spiral wave re-entry occurs if steep and smooth coupling gradients are situated side by side, with the critical steepness depending on the frequency of stimulation. We demonstrate how bradycardia can unmask a slow endogenous pacemaker in a poorly coupled region, subsequently leading to spiral wave re-entry. In the presence of coupling heterogeneities, a single excitation coming from the less coupled region may induce spiral wave re-entry.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
