1081
Importance of the Great Vessels in the
Genesis of the Electrocardiogram
D. Kilpatrick, S.J. Walker, and A.J. Bell
The electrocardiogram is the graphic representation against time of the difference in potential
between points of the body caused by the current field of the heart. To examine the origin of this
current field, a method of transforming body surface electrocardiographic data to the
epicardial surface has been developed. The computed epicardial current density distributions
in 219 patients with acute inferior myocardial infarction showed that, in 89% of patients, the
current flow out of the heart during the ST segment came from two regions, not only from the
infarction region but also from a region over the great vessels. This finding suggests that
current flows from the ischemic region, through the low-resistance pathway provided by the
intracavity blood, out the great vessels, and back to the epicardium. A similar pathway has been
hypothesized when ischemia causes endocardial ST elevation, such as during a stress test or
with unstable angina. To test this hypothesis, a group of patients with ST depression on the
12-lead electrocardiogram, not associated with ST elevation, was examined with body surface
mapping. Ninety-four percent of patients had epicardial current density distributions that
showed a region of current flow out of the heart and over the great vessels that was consistent
with this hypothesis. This could explain the poor localization of coronary artery disease by
electrocardiographic techniques when there is ST depression on the body surface. (Circulation
Research 1990;66:1081-1087)
he electrocardiogram (ECG) is the temporal
record of the potential difference between
two points on the body surface recorded with
time. The potential difference is set up by the current
field generated by the heart.' The regional information from the body surface ECG in general bears a
relation to the source; however, ST segment depression has been found to be a poor localizing sign in
coronary artery disease, especially with exercise.2-6
We have studied patients with acute inferior
infarction by use of body surface mapping and an
inverse transformation7'8 to produce epicardial surface potential distributions. The epicardial maps
during the ST segment showed a positive region over
the superior aspect of the heart in addition to the
expected inferior ST elevation. This suggested a
selective current path from the infarcting endocardium that traveled out of the heart through the great
vessels. We hypothesized that this current path might
T
From the Department of Medicine, University of Tasmania,
Hobart, Australia.
Supported by grants from the National Health and Medical
Research Council of Australia, the National Heart Foundation of
Australia, the Royal Hobart Hospital Research Trust, and the
Tasmanian Development Authority, Hobart, Australia.
Address for correspondence: D. Kilpatrick, Department of
Medicine, University of Tasmania, 43 Collins St., Hobart, Australia
7000.
Received May 11, 1989; accepted November 15, 1989.
also be active in conditions such as ischemia, in which
there was ST depression on the body surface 12-lead
ECG. To test this hypothesis in patients with ST
depression, we examined the epicardial ST maps of
patients with ST depression but who showed no
evidence of ST elevation on the 12-lead ECG.
Materials and Methods
Collection of Body-Surface
Electrocardiographic Potentials
The system for acquisition, display, and recording
of the body surface electrocardiographic data has
been described previously.9'10
In brief, a jacket with a fixed array of 50 electrodes
is wrapped around the patient starting from a position 7.5 cm to the right of the sternum, so that the
second column of electrodes is on the midsternal
line. A bedside display of the sampled electrocardiographic signals enables bad leads to be selected and
replaced by an interpolation from the surrounding
leads. Linear baseline drift is corrected by interpolation between baseline points picked manually in
successive TP segments.
The number of electrodes in contact with the
patient varies with the size of the patient, which
enables virtually all patients to be studied. Electrode
positions are calculated from the degree of overlap of
the jacket, which is recorded at the time of mapping.
1082
Circulation Research Vol 66, No 4, April 1990
Although electrode positioning varies between patients, body surface maps comparable among patients
are produced by using an interpolation scheme that
takes into account the size of each patient. A spline
interpolation method is used. This method produces
32 columns each of 12 rows that are evenly distributed around the thoracic surface. This format is
comparable with that used by other groups. A complete recording can be made within 5 minutes of
approaching the patient.
The Inverse Transformation
The epicardial potentials are calculated from the
body-surface data by multiplying that data by a
matrix derived from a numerical model of the electrical properties of the human torso. The technique
used to model the torso has been described previously.7'8 Briefly, the model simulates, on a nonuniform
rectangular grid, a three-dimensional resistor network that resembles the human torso both geometrically and electrically. The lungs, spine, sternum,
and heart were included in the model. The values
used for tissue resistivity in the model are those
published by Rush et al.11 The torso geometry has
been digitized from computed tomographic scan data
obtained from a 40-year-old male subject in whom 22
computed tomographic scan slices were available,
spaced at 1 cm. In the region of the heart, the slices
were spaced 1 cm apart; elsewhere, slices were
spaced 2 cm apart. No interpolation between slices
was performed. To produce torso models of realistic
size, the last (lowest) slice was repeated several times
at a spacing of 2 cm to give an overall torso height of
45 cm. The extended region started just below the
lungs and was homogeneous except for the inclusion
of the spine.
Each computed tomographic slice was divided into
a grid with a resolution of 7.5 mm when in the vicinity
of the heart; as the distance from the heart increased,
the resolution increased to 1 cm and then to 1.5 cm.
The model contained 34,914 nodes (points at which
potential calculations are performed). There were
7,237 nodes on the body surface and 807 on the
epicardial surface. Intracardiac blood masses were
not modeled; the inverse calculations are not affected
by the internal structure of the heart because the
epicardial surface nodes at which the potentials are
calculated form a closed surface surrounding the
heart. This surface envelops all cardiac chambers and
transects the great vessels at the point at which they
leave the heart. No attempt was made to model the
anisotropic skeletal muscle layer. Although this is
possible when using a resistor-network model, the
data on muscle fiber distribution and orientation are
not easily available and are not easily incorporated
into the model.
By use of the model, the epicardial potential
distribution (h) and the torso surface potential distribution (b) were related by the following matrix
equation:
Th=b
(1)
where T is a matrix that reflects the geometry of the
torso. To construct the matrix T, the epicardial nodes
were first grouped to form 50 source regions of
approximately equal size, which covered the epicardium, and the potential was assumed to be equal at
all of the nodes within any one source region. Thus,
the vector h has 50 components: the potentials at the
50 epicardial source regions. The number of epicardial source regions chosen affects the inverse calculation, and some preliminary results of calculations
with 26, 50, 74, and 98 regions have been published.12
The vector b has 160 components, corresponding to
160 potentials at body surface sites where (interpolated) body surface map data were measured.
A regularization method13 was used to solve Equation 1 for h in terms of T and b. The solution
obtained is given by the equation:
h= (TtT+ aI)- 'Ttb
(2)
where I is the appropriately sized identity matrix, Tt
is the transpose of matrix T, and a is a parameter that
determines the amount of "smoothing" present in
the solution. The choice of a was made so that the
calculated epicardial potentials were at physiologically reasonable levels while maintaining good correspondence between the measured body surface data
and the body surface distribution that would be
generated by the calculated epicardial potentials.
There are also statistical methods for determining
the optimum value of a14 that require assumptions to
be made about the nature of the body surface noise
and the epicardial potentials.
Calculation of Epicardial Current Densities
Once epicardial potential distributions have been
calculated, it is simple to relate body surface potential
to the current density flowing out of an epicardial
region. This computation essentially considers the
potential at each epicardial node and adjacent nonheart nodes; Ohm's law is used to calculate currents
flowing between the nodes. The resolution for these
current maps is the same as the resolution of the
isopotential maps: 50 equal-sized regions around the
heart, each with an approximate surface area of 5 cm2.
Data Display
The epicardial potentials are plotted as isopotential contour maps on the surface of the heart. These
are displayed on six perspective views generated as
though one were looking at the heart in situ from
viewing positions that were anterior, left lateral,
posterior, right lateral, inferior, and superior to the
heart. The solid lines are positive isopotential contours, the heavy solid line is the zero contour, and the
dashed lines are negative isopotential contours (see
Figures 1-5). The boundary of the heart visible in
each view is shown by the finely spaced dotted line.
Kilpatrck et al Great Vessels and the ECG
Patient Selection
Inferior Infarction. All patients who were entered
into a study of the prognosis of inferior infarction were
entered into this study. 10"5 All patients presented with
no previous history of infarction and with QRS duration 0.1 second or less, 12-lead electrocardiographic
evidence of at least 1 mm of ST elevation in at least
two of leads II, III, and aVF, an enzyme rise, and a
history typical of acute myocardial infarction.
ST Depression. Patients who were routinely
mapped in coronary care and who showed ST depression of at least 0.1 mV in at least two of the 12
standard leads and who had no detectable ST elevation were chosen for this group.
Grouping System
To group similar ST potential distributions, a hierarchical clustering technique was used.16 The measure
of similarity between two distributions was taken to be
their correlation coefficient, which is calculated as
follows: Given two potential distributions A and B,
considered as vectors (ai) and (bi), correlation
coefficient=A.B/IAIIBI, where A.B=laibi and
=v%,ibi. The correlation coefficient is
JAl
independent of the magnitudes of the two vectors and
gives an indication of the similarities in both pattern
and position of maxima and minima. Similar maps
have a correlation coefficient near 1.0. Dissimilar
maps have a correlation coefficient near 0.00, and
maps similar in pattern but with positive and negative
values exchanged have a correlation near -1.0. Correlation coefficients have been applied to body
surface maps previously in an attempt 1) to distinguish normal body surface maps from those taken
from patients with myocardial infarction,'7 2) to
assess the similarity between modeled and measured body surface maps in theoretical studies,'8
and 3) by ourselves, to group patients with inferior
infarction in a clinical correlation.'0
=VIa`,lBl
Statistical Analysis
Epicardial maps were analyzed on a regional basis,
with regions over the great vessels selected for examination. Maps of both potential distribution and
current density were examined. An area of positive
potential over the great vessels was diagnosed when
there was a confluent area of at least three of the
nine superior epicardial regions positive with respect
to the Wilson central terminal. With the current
density maps, the current coming out of the heart is
equal to that flowing into the heart so that a positive
region represents current out of the heart. A positive
area was defined as a confluent area with at least
three of nine superior regions being positive.
Results
Inferior Infarction
A typical body surface distribution of potential of a
patient with an inferior infarction is shown in Figure
1. The epicardial potentials and the epicardial cur-
Front
1083
Back
Contour interval 50 ±V
FIGURE 1. Body surface map of a patient with an inferior
infarction. The format is of an unwrapped torso with the right
axilla on the left and right boundares and with the left axilla
in the center. The potentials are referred to a simulated Wilson
central terminal. The heavy line represents a zero potential
line; continuous lines, positive contours; and dashed lines,
negative contours. The contour interval is given for each set of
data.
rent density distribution of the same patient are
shown in Figure 2. The region of ST elevation on the
superior aspect of the heart can be clearly seen in
addition to the inferior ST elevation. This is also seen
as a region of current source centered over the great
vessels. The clinical and body surface electrocardiographic data from this group of inferior infarction
patients are fully described in previous papers.'0,'5
The mean time from the onset of chest pain to
mapping was 7.0 hours. Epicardial maps of both
potential and current density of the 219 patients in
these studies showed that 210 (96%) had a region of
superior ST elevation of potential and 194 (88.6%)
had a region of current flow out of the heart over the
region of the great vessels.
ST Depression
There were 93 patients with ST depression on the
12-lead ECG. Of these, 53 patients had non-Q wave
infarction, and 40 had no evidence of infarction. The
body surface map patterns of these patients were
grouped into seven categories; the mean maps are
shown in Figure 3. In 88 (93.7%) of the epicardial
maps of these patients, a region of current flow out of
the great vessels was seen. The 12-lead ECG and
body surface map of a typical patient are illustrated
in Figure 4. In Figure 5, the epicardial maps of the
patient illustrated in Figure 4 show a similar pattern
superiorly to that seen in inferior infarcts (Figure 2).
Discussion
The Origin of ST Potentials
During the ST segment in patients with infarction,
current flows from the region of ischemia or infarction to the normal muscle and effectively causes the
potential of the infarcting region to be elevated
compared with the normal region.'9'20 In our patients
1084
Circulation Research Vol 66, No 4, April 1990
Anterior
Left lateral
Anterior
Left lateral
Posterior
Right lateral
Posterior
Right lateral
Inferior
Superior
Inferior
-'d-
-
,
Suero~~%
1%%
Superior
Epicardial potential contour 0.5mV
Epicardial current contour 10 pA
FIGURE 2. Epicardial maps of a patient with an acute inferior infarction. Left panel: Isopotential maps. Right panel: Current density
maps. In the two sets of data, the format is identical. The six projections for each epicardium are orthogonal and drawn in perspective.
As a consequence, the contour spacing is nonlinear especially at the edges of each projection. To help orient the plots, a set of coronary
arteries has been superimposed on each epicardium. The left anterior descending coronary artery is seen on the right of the anterior
projection and on the left of the lateralprojection. The circumflex corona?y artery and its branches run down the right border of the lateral
projection and in the center right of the posteriorprojection. The superior plane is oriented with anterior toward the top of the page, as
though one were looking down at the heart from above. The inferior surface is viewed from below the heart looking up; the posterior
portion is uppermost, and the left sidepoints to the left. Thepositions of the coronary arteries in the inferior view are arbitrary and represent
a balanced coronary distribution. P represents the pulmonary artery and A the aorta. The heavy line represents a zero potential line;
continuous lines, positive contours; and dashed lines, negative contours. The contour interval is given for each set of data.
with inferior infarction, the presence of a region of
ST elevation over the great vessels was unexpected.
A possible explanation in these patients is that the
low resistance pathway of the blood appears to form
a selective conduction path from the abnormal region
of endocardium, to both the normal endocardium
and the epicardium, by a circuit including the great
vessels. According to this hypothesis, all patients who
have endocardial ST elevation should show a similar
current path and have superior ST elevation.
The genesis of ST depression on the epicardium
was studied by Holland and Brooks,21,22 who concluded that the presence of endocardial ST elevation, when observed from the epicardium, appeared
as epicardial ST depression. This was explained by
using the solid-angle theory but without consideration of the current flow through the great vessels.
Most experimental situations remove the heart or at
least remove the external conduction pathway by
open-chest procedures. This importance of the lowimpedance great vessels would explain why ST
depression is poorly localized. It would also suggest
that quantitative measures of ischemia should
include leads where ST elevation is seen. On the
body surface, ST depression is shown as a region
whose potential is below that of the reference
terminal, and unless the reference terminal is chosen at an extreme, then there must be regions on
the body surface that are positive compared with
the reference terminal (regions of ST elevation).
Epicardial Potential Calculations
The epicardial potentials are calculated from body
surface map data by using a standard transformation
Kilpatrick et al Great Vessels and the ECG
Fror
Back
..
: -.* |.::
.i::. :::-.. ::i
, ::::--:::E::.
::L -;---;:5---z-
F
::: ::I:-i.:;*:;-: j
~
::-
...: ..:.
......
--:.
:::: _ ...-.
_! -- ::.
_.!.
_,~~~~
:-: :: ::i.:!:.:::i
Mean of 6
...
.::!::
...
~.~.~. ~. .
Interval 20 gV
_:: 1::
..~~~~~~~~~~~~~~~
~
~
: :s:::
Back
.:
.:
~~~~~~~~~~~~~~~~~~~~~~~
....:
-_.
.
.:::': .:
.;-:.-:
.
Froi
1085
aL
av
avL
avF
.......
.-. ...
avR
Intel1
....t
Mean of 27
.....
:: .-.
.--
!..i .'--
Interval 1 0 gV
-
..
vi
,
.......t -..
V2
5...t
:.! ...
Mean of 4
Interva 10 lV
....
....
..
:.
, ,,
Mean of 11
Frort
.,',. ...-,', .-i.
-..
.....,.,.
V4
,.
,..
:
V5
V6
Back
Interval 20 V
FIGURE 3. Average map pattems of the groups of patients
with ST depression on the 12-lead electrocardiogram. Each
map was grouped into one of seven groups by using the
algorithm described in the text, and the average map for each
group was calculated. The format is identical with that in
Figure 1.
derived from a resistive network model of the thorax
of a 40-year-old male. This inverse transformation
requires further validation; however, it produces
sensible results even when used with a single body
model.8 Other workers23,24 also have inverse solutions
that appear stable, but so far none have looked at
acute infarction. The ST elevation seen over the
great vessels was present in most cases and suggests
that future models of current flow in the thorax
should include the great vessels.
In the thorax, the heart is the only current generator. This means that current flowing out of a region
of the heart must also flow back into the heart. As a
consequence, the total current density, over every
heart surface, is zero, and current density distributions on the heart are independent of the reference
terminal. We have used current density transforms in
this paper to overcome any uncertainties in the
relativity of the potentials arising from the use of the
Wilson central terminal.
Clinical Sigificance
The obvious clinical significance of the selective
current path is in the interpretation of ST depression.
Many workers have shown that, although body sur-
FIGURE 4. Top panel: Twelve-lead electrocardiogram of a
patient with ST depression. Bottom panel: Surface map of the
same patient. The map contour is the same as in Figure 1.
face ST elevation was highly related to the region of
ischemia, body surface ST depression was poorly
related if at all.2-6Using precordial body surface map
patterns on exercise, Fox et a125 showed some general
relation of ST change to position especially in singlevessel disease. Montague and colleagues26 were able
to differentiate single-vessel disease through subtle
changes to the map pattern that were statistically but
not positionally related to the ischemic region. If the
current from endocardial ST elevation was flowing
out of the great vessels back to the epicardium, then
most of the epicardium could look negative relative
to the superior aspect of the heart.
We conclude that the great vessels form an important low-resistance current path in the human intact
thorax that must be considered when examining the
genesis of ECGs. This is particularly important with
endocardial events and suggests that ischemia may be
better monitored by sampling from leads representing the great vessels.
Acknowledgments
We wish to thank David Lees for artwork and Peta
Guy for secretarial assistance. We are also grateful to
1086
Circulation Research Vol 66, No 4, April 1990
Anterior
Left lateral
Anterior
Left lateral
Posterior
Right lateral
Posterior
Right lateral
Superior
Inferior
Superior
Epicardial potential contour 0.2 mV
Inferior
Epicardial current contour 1 0 ,uA
FIGURE 5. Epicardial maps of the patient whose electrocardiogram and body surface maps are shown in Figure 4. Left panel:
Isopotential maps. Right panel: Current density maps. The format is identical with that in Figure 2.
Anne Duffield, Wendy Herbert, and Peter Lavercombe and the staff of the ICU, Royal Hobart
Hospital.
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KEY WoRDs epicardial current density * inferior infarction
ST elevation * ischemia * selective current path