Simulation of atrial activity by a phase response curve based model of a two-dimensional pacemaker cells array: the transition from a normal activation pattern to atrial fibrillation |
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Authors: | Sarit Abramovich-Sivan Solange Akselrod |
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Institution: | (1) The Abramson Institute of Medical Physics, Sackler Faculty of Exact Sciences, Tel Aviv University, Tel Aviv, Israel, IL |
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Abstract: | In this paper, we present an original model of the atria, based on our hypothesis that atrial cells have features of pacemaker
cells, characterized by their normally longer intrinsic cycle lengths and different type of connection (stronger) than the,
sino-atrial (SA) node pacemaker cells. The atrium is simulated by a two-dimensional array of pacemaker cells (25 × 25), composed
of a region of SA node pacemaker cells (11 × 11) surrounded by atrial pacemaker cells. All pacemakers cells are characterized
by only the most relevant functional properties, those which play the most direct role in the determination of the cardiac
rate and in the mechanism of arrhythmias. These properties are: the intrinsic cycle length, τ, an `internal' feature of each
pacemaker cell, and the phase-response curve (PRC), an `overall collective' function. The PRC embodies the interactions of
each pacemaker cell with its neighboring cells, and thus represents the type of connection (strong, weak, etc.) of the pacemaker
cell with its surroundings. In our model, the SA node region differs from the atrial region by cycle length distribution and
PRCs. We studied the spatial interaction between SA node pacemaker cells and atrial pacemaker cells as a function of the regional
variation of cells properties and as a function of the “electrical” coupling between cells (the PRC), in the SA node region,
in the atrial region, and in a border zone between them. We investigated the influence of those parameters on the activation
pattern, on the conduction time of the array, and on a pseudo-ECG signal. This study demonstrates that by representing the
atrial cells as a population of `pacemaker-like' cells, similar to the SA node pacemaker cells, but differing markedly in
their cycle lengths and cell-to-cell interaction (PRC), we can create a global picture of the atrial system by applying a
simple physical-mathematical model. This approach enables us to explore physiological phenomena related to the genesis and
maintenance of atrial activity. It also reveals the conditions which predispose to atrial arrhythmias and conduction disturbances
(e.g. tachycardia, pacemaker shift, re-entry, fibrillation). In particular, it yields insight into the mechanism of transition
from normal atrial activity to the disordered state of atrial fibrillation. Therefore, this study suggests a new way of looking
at the development of cardiac arrhythmias of atrial origin.
Received: 8 September 1997 / Accepted in revised form: 6 October 1998 |
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