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Epicardial and endocardial ST potential mapping in ischaemia

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Li, Danshi (1997) Epicardial and endocardial ST potential mapping in ischaemia. PhD thesis, University of Tasmania.

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Abstract

The electrocardiographic change associated with ischaemia is typically ST segment
depression which is usually most prominent over the left chest wall. The position of
the ST depression does not predict the ischaemic territories in the myocardium or the
involved coronary arteries.
To evaluate the source of ST depression, a sheep model of subendocardial ischaemia
using partial coronary artery ligation coupled with atrial pacing was developed.
Ischaemia was induced initially in either the left anterior descending coronary artery
or the left circumflex coronary artery territory and subsequently in the territory of the
other vessel. The ischaemic regions were documented by a fluorescent microsphere
technique. During ischaemia potentials were mapped simultaneously from the
endocardium and the epicardium. The distributions of epicardial potentials from
either ischaemic source were very similar (0.77±0.14, P<0.0001), both showing ST
depression on the free wall of the left ventricle, and no association between the ST
depression and the ischaemic region. At the same time, the endocardial ST elevation
was directly associated with the region of reduced blood flow. Insulating the heart
from the surrounding tissue with plastic increased the magnitude of epicardial and
endocardial ST and QRS potentials and decreased the potentials from limb leads,
implying that the ST depression arises from current paths within the myocardium
rather than external. Increasing the percent stenosis of a coronary artery increased
epicardial ST depression at the lateral boundary and resulted in ST elevation starting
from the ischaemic centre as ischaemia became transmural. These results suggest
that the major source of ECG changes is the lateral boundary between ischaemic and
normal territories. This postulate was supported by the spatial flow distributions
which showed a sharp lateral flow change but a gradual transmural flow transition.
In conclusion, ST segment depression can not distinguish an ischaemic region even
from the epicardium. The ischaemic source does relate spatially to the endocardial
ST change but not to the epicardial ST change. The current paths during
subendocardial ischaemia must be in the myocardium and probably originate from
the injury current which flows at the lateral boundary. These effects are not
explained by conventional ECG theory but they do explain why body surface ST
depression does not localise cardiac ischaemia in humans.
The electric and pathophysiologic basis of remote ST depression occurring with ST
elevation during acute myocardial infarction remains controversial. To explore the
possible mechanism of such ST depression, different sizes of myocardial infarction
were produced. The epicardial and endocardial ST potentials were measured and
correlated with regional myocardial blood flow measured by fluorescent
microspheres. Epicardial ST distributions showed that occluding a small vessel
produced the expected ST elevation over the infarcting region with little ST
depression over the noninfarcting region, whereas either the occlusion of the left
anterior descending coronary artery or the left circumflex coronary artery resulted in
a powerful electrical dipole with ST elevation over the infarcted region and ST
depression over the noninfarcted region. Examination of fluorescent microsphere
delivery into the tissues showed that with smaller infarcts the flow remained
unchanged in the noninfarcted region (1.09±0.19 to 1.12±0.15, P>0.05). With large
infarcts there was approximately a 30% flow reduction in the noninfarcted region
which directly correlated to the perfusion pressure drop (r=0.82, P<0.001). These
findings suggest that ST depression reflects extensive infarction and is associated
with reduced perfusion of the noninfarcted myocardium. The reduced perfusion may
have a significant reversible role in the poor prognosis of these patients.

Item Type: Thesis (PhD)
Copyright Holders: The Author
Copyright Information:

Copyright 1997 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:

Thesis (Ph.D.)--University of Tasmania, 1998. Includes bibliographical references. Contents: Pathophysiology of myocardial ischaemia and infarction - ST segment shifts in experimental studies and clinical practice - Measurement of regional myocardial blood flow by fluorescent microspheres - Subendocardial ischaemic model and its validation - Epicardial and endocardial ST potential mapping of the subendocardial ischaemia - Epicardial and endocardial ST potential mapping of the transmural ischaemia

Date Deposited: 19 Dec 2014 02:36
Last Modified: 14 Jul 2017 02:28
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