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Abstract

This thesis presents a computer simulation of electrocardiographic ST segment shift
in myocardial ischaemia to elucidate the source of ST changes in both subendocardial
and transmural ischaemia.
A realistic torso model was constructed, in which the myocardium was represented
by the bidomain model. In a normal heart, there is no current source during the
ST segment and there is a minimal ST potential field. With myocardial ischaemia,
the transmembrane potential of ischaemic cells changes, allowing current to flow
between the ischaemic and nonischaemic regions, which generates ST segment shift.
The ischaemic regions included in the model were those measured using fluorescent
microspheres in a sheep model, and the transmembrane potentials were generated
from values extracted from the literature.
Subendocardial ischaemia in the territory supplied by either the left anterior descending
coronary artery (LAD) or left circumflex coronary artery (LOX) was simulated,
showing that the current source is produced at the ischaemic boundary, with
the positive source at the ischaemic and the negative source at the normal side of the
boundary. At the intramural boundary, the current flow is highly localised around
the boundary, while at the lateral boundary normal to the endocardium, current
flows both by crossing the boundary and through the intracavity blood. Epicardial
ST depression is seen over the lateral boundary while endocardial ST elevation
appears over the ischaemic region. The source in the septum is not seen on the
epicardium because it is surrounded by highly conductive blood. LAD and LCX
ischaemia share the lateral boundary and produce a similar pattern of epicardial ST
depression on the left free wall.
Transmural ischaemia of varying size was studied. Transmural ischaemia of a small
region produces localised ST elevation over the ischaemic region with little ST depression
elsewhere on the epicardium and a similar pattern on the endocardium with
a much lower amplitude. Ischaemia in either the LAD or LCX territory produces
a strong dipole on the epicardium over the left lateral region, with ST elevation on
the ischaemic region and ST depression on the nonischaemic region. ST depression
in transmural ischaemia is generated with ST elevation and is an integral part of the
source, thus it is inevitable that ST depression on the body surface will be generated
during ischaemia of a large region of myocardium.
The effect of the myocardial anisotropy on ST potentials was also studied. The
inclusion of myocardial anisotropy produces results somewhat closer to measured
results in animal models.
In conclusion, the bidomain model is successful in modelling the ST potential and
the simulation in this study successfully explains the observations of ST segment
shift during myocardial ischaemia. It provides useful guidance for the clinical interpretation
of ST segment shift.

Item Type:	Thesis - PhD
Authors/Creators:	Li, CH
Copyright Holders:	The Author
Copyright Information:	Copyright 1998 the Author - The University is continuing to endeavour to trace the copyright owner(s) and in the meantime this item has been reproduced here in good faith. We would be pleased to hear from the copyright owner(s).
Additional Information:	This thesis presents a computer simulation of electrocardiographic ST segment shift in myocardial ischaemia to elucidate the source of ST changes in both subendocardial and transmural ischaemia. Thesis (Ph.D.)--University of Tasmania, 1998. Includes bibliographical references. This thesis presents a computer simulation of electrocardiographic ST segment shift in myocardial ischaemia to elucidate the source of ST changes in both subendocardial and transmural ischaemia
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