Vol. 14. NO. 3
E LE CTROPHYSIOLOGIC STUDIE S
Derived Epicardial Potentials Differentiate Ischemic ST Depression
From ST Depression Secondary to ST Elevation in Acute Inferior
Myocardial Infarction in Humans
DAVID KILPATRICK. MD, FRACP, ANTHONY J. BELL. MBBS, FRACP,
STEPHEN J. WALKER, PHD
Hobart, Tasmania, Australia
It was hypothesized that in acute inferior wall myocardial
infarction, an additional ischemic area in the subendocar-
dium of the noninfarcting territory would produce a selec-
tive current dipole between the infarct& and ischemic
regions. A resistance network model to calculate epicardial
potentials from body surface electrocardiographic poten-
tials was developed and used to examine the hypothesis in
219 patients with acute inferior myocardial infarction. In
the learning set of 110 patients, two characteristic dipole
patterns were observed, each associated with a high mor-
tality rate in the ensuing 15 months when compared with
that in the remaining patients. In the test set of 109
patients, a double-blind analysis of the patterns showed
that the 34 patients with a dipole pattern had a collective
mortality rate of 35% at I5 months compared with a 15
month rate of 5% in the remaining patients.
In the total group of 219 patients, the magnitude of ST
segment elevation and both the magnitude and integral of
the area voltage of ST depression on the epicardium were
significantly correlated with the mortality rate (p < 0.0002
for all variables against death at 15 months). This study
strongly suggests that ST depression due to ischemia can be
differentiated from ST depression secondary to the ST
elevation in acute inferior infarction by the examination of
epicardial potential distributions.
(_I Am Co11 Cardioll989;14:695-702)
In acute inferior wall myocardial infarction. anterior ST
segment depression either in the I2 lead electrocardiogram
(ECG) or from body surface mapping has been shown to be
associated with increased morbidity and mortality rates
(I-4). even though this association is still controversial
(5,6). It is difficult to separate ST depression arising
from an area of primary subendocardial ischemia from ST
depression secondary to the ST elevation associated with
the infarct region. We hypothesized that, by examining
the epicardial potential distributions,
differentiate an ischemic source of ST depression from ST
it is possible to
From the Department of Medicine, University of Tasmania, Ausrralia and
Intensive Care Unit, Royal Hobart Hospital. Hobart. Australia.
This study was supported in part by the NHMRC
Australian Capital Territory: National Heart Foundation of Australia. Can-
berra, Australian Capital Territory; Ramaciotti
South Wales; Royal Hobart Hospital Research Trust. Hobart. Tasmania and
‘Tasmaman Development Authority Hobart, Tasmama.
Manuscript received January 30, 1989; rewsed manuscript
March 21. 1989. accepted April 24, 1989.
Address for eormts: David Kdpatrick.
University of Taimama. 43 Collins Street, Hobart. Australia 7000.
of Australia. Canberra.
Foundation. Sydney. New
MD. Department of Medicine.
P~l9X9 by the Amerwan College of Cardiology
depression secondary to infarct-related ST elevation. To
validate this hypothesis, we studied the epicardial potential
distributions in 219 patients with no previous myocardial
infarction who presented with an acute inferior myocardial
infarction and correlated these distributions with clinical and
Theoretical considerations. We postulate that if there was
a region of acutely infarcted muscle surrounded by normal
muscle, the electric field set up by this infarcted region
would be symmetric, with approximately equal current flow
surrounding the whole boundary of the region of ST eleva-
tion. If, however. there were a region of ST elevation
associated with an acute infarction and an additional region
of ST depression associated with an adjacent region of
subendocardial ischemia, the current distribution would not
be symmetric but the region of ST elevation and the region of
ST depression would form a powerful current dipole on the
surface of the heart. These current fields are illustrated in
Figure 1. We hypothesized that examination of the epicardial
potential distributions would enable the differentiation of ST
depression secondary to ST elevation in an infarcting region
and ST depression from a primary source such as suben-
KILPATRICK ET AL.
EPICARDIAL MAPS AND PROGNOSIS IN INFERIOR INFARCTION
JACC Vol. 14, No. 3
12. Tikhonov AN, Arsenin VY V. H. Solutions of III-posed problems
Washington D.C.: Winston and Sons, 1977.
13. Barr RC, Spach MS. Inverse calculation of QRS-T epicardial potentials
from body surface potential distributions for normal and ectopic beats in
the intact dog. Circ Res 1978;42:661-75.
14. Moses LE, Emerson ID, Hosseini H. Analyzing data from ordered
categories. N Engl J Med 1984;311:442-8.
15. Barr RC, Spach MS. Human inverse epicardial potentials computed from
body surface potentials in patients with implanted pacemakers (abstr).
Circulation 1980;62(Suppl IIIkIII-343.
16. Tovama S. Suzuki K. Takahashi T. Yamashita Y. Euicardial isowtential
mapping from body surface isopotential mapping in myocardial infarction.
1 Electrocardiol 1985;18:277-85.
17. Toyama S, Suzuki K, Takahashi T, Yamashita Y. MyocardiaI Infarction
size and location: a comparative study of epicardial isopotential mapping.
thahium-201 scintigraphy, electrocardiography and vectorcardiography. J
Electrocardiol 1987;20:203-I I.
18. Fore FN, Smith GT, McNamara JJ. Prediction of infarct size with
baboons: a proposed model for accurately determining the efficacy of
therapeutic interventions. Circ Res 1978;43:455-65.
Holland RP, Brooks H. Precordial and epicardial surface potentials
during myocardial ischemia in the pig: a theoretical and experimental
analysis of the TQ and ST segments. Circ Res 1975;37:471-80.
Frank E. Electric potential produced by two point current sources in a
homogeneous conducting sphere. J Appl Physics 1952;23:1225-8.
Samson WE, Scher AM. Mechanism of S-T segment alteration during
acute myocardial injury. Circ Res l%o,8:780-7-7.
Kleber AG. Janse MJ. Cauelle FJC Van. Durrer D. Mechanism and time
course of S-T and T-Q segment changes during acute regional myacardial
ischemia in the pig heart determined by extracellular and intracellular
recordings. Circ Res 1978;42:6Of13.
Holland RP, Brooks H. Spatial and nonspatial influences on the TQ-ST
segment deflection of ischemia: theoretical and experimental analysis in
the pig. J Clin Invest 1977;60:197-214.