Mechanisms of transition from normal to reentrant electrical activity in a model of rabbit atrial tissue: interaction of tissue heterogeneity and anisotropy.
Version 1

Experimental evidence suggests that regional differences in action potential (AP) morphology can provide a substrate for initiation and maintenance of reentrant arrhythmias in the right atrium (RA), but the relationships between the complex electrophysiological and anatomical organization of the RA and the genesis of reentry are unclear. In this study, a biophysically detailed three-dimensional computer model of the right atrial tissue was constructed to study the role of tissue heterogeneity and anisotropy in arrhythmogenesis. The model of Lindblad et al. for a rabbit atrial cell was modified to incorporate experimental data on regional differences in several ionic currents (primarily, I(Na), I(CaL), I(K1), I(to), and I(sus)) between the crista terminalis and pectinate muscle cells. The modified model was validated by its ability to reproduce the AP properties measured experimentally. The anatomical model of the rabbit RA (including tissue geometry and fiber orientation) was based on a recent histological reconstruction. Simulations with the resultant electrophysiologically and anatomically detailed three-dimensional model show that complex organization of the RA tissue causes breakdown of regular AP conduction patterns at high pacing rates (>11.75 Hz): as the AP in the crista terminalis cells is longer, and electrotonic coupling transverse to fibers of the crista terminalis is weak, high-frequency pacing at the border between the crista terminalis and pectinate muscles results in a unidirectional conduction block toward the crista terminalis and generation of reentry. Contributions of the tissue heterogeneity and anisotropy to reentry initiation mechanisms are quantified by measuring action potential duration (APD) gradients at the border between the crista terminalis and pectinate muscles: the APD gradients are high in areas where both heterogeneity and anisotropy are high, such that intrinsic APD differences are not diminished by electrotonic interactions. Thus, our detailed computer model reconstructs complex electrical activity in the RA, and provides new insights into the mechanisms of transition from focal atrial tachycardia into reentry.

Originating from BioModels: http://www.ebi.ac.uk/biomodels-main/MODEL1006230017

SEEK ID: https://testing.sysmo-db.org/models/39?version=1

1 item is associated with this Model:
  • MODEL1006230017.xml (SBML and XML document - 114 KB)

Organism: Not specified

Model type: Not specified

Model format: SBML

Execution or visualisation environment: Not specified

Model image: No image specified

This Model was originally imported from the EBI Biomodels: http://www.ebi.ac.uk/biomodels-main/MODEL1006230017.

help Creators and Submitter
Creator
Submitter
Activity

Views: 771   Downloads: 0

Created: 7th Sep 2012 at 08:59

help Attributions

None

Version History

Version 1 (earliest) Created 7th Sep 2012 at 08:59 by Stuart Owen

No revision comments

Powered by
(v.1.16.0-main)
Copyright © 2008 - 2024 The University of Manchester and HITS gGmbH