Aslanidi2009_RightAtrialTissue_Arrhythmogenesis

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

Aslanidi OV, Boyett MR, Dobrzynski H, Li J, Zhang H. Biophys J
2009 Feb;96(3):798-817 19186122
,
Abstract:

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.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Aslanidi OV, Boyett MR, Dobrzynski H, Li J, Zhang H. (2009) - version=1.0

The original CellML model was created by:
Penny Noble

[e-mail]
The University of Oxford
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