ISCHEMIC ST DISPLACEMENT/Vincent, Abildskov, Burgess
R: Computer processing of exercise electrocardiograms. In Trends in
Computer-Processed ECGs, edited by Van Bemmel JH, Willems JC.
Amsterdam, North Holland Publ Cie, 1977, pp 383-406
27. Froelicher Jr VF, Yanowitz FG, Thompson AJ, Lancaster MC: The correlation of coronary angiography and the electrocardiographic response
to maximal treadmill testing in 76 asymptomatic men. Circulation 48:
597, 1973
28. Erikssen J, Enge I, Furfang K, Storstein 0: False positive diagnostic tests
and coronary arteriographic findings in 105 presumably healthy males.
Circulation 54: 371, 1976
29. Cornfield J: Statistical classification methods. In Computer Diagnosis
559
Methods, edited by Jacques J. Springfield, Ill, CC Thomas, 1972
30. Pipberger HV, Schneiderman MA, Klingeman JD: The love-at-first-sight
effect in research. Circulation 38: 822, 1968
31. Redwood DR, Borer JS, Epstein SE: Whither the ST segment during exercise. Circulation 54: 703, 1976
32. Sheffield LT, Reeves TJ, Blackburn H, Ellestad MH, Froelicher VF,
Roitman D, Kansal S: The exercise test in perspective. Circulation 55:
681, 1977
33. McHenry P: The actual prevalence of false positive ST segment
responses to exercise in clinically normal subjects remains undefined. Circulation 55: 683, 1977
Mechanisms of Ischemic ST-Segment Displacement
Evaluation by Direct Current Recordings
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G. MICHAEL VINCENT, M.D., J. A. ABILDSKOV, M.D.,
AND MARY Jo BURGESS, M.D.
SUMMARY The electrophysiologic basis of ischemic ST-segment
displacement was investigated in 40 open chest dogs. Epicardial and
subendocardial electrograms were recorded with direct current
coupled amplifiers during partial and complete coronary artery occlusion. The time course and magnitude of DC potential changes, and
the effects on the DC potentials of heart rate and subendocardial
ischemia were investigated.
TQ segment depression, representing loss of resting membrane
potential, was found to be the consistent and most specific mechanism
of "ST displacement" due to ischemia. True ST-segment displacement, due to alterations of phase 2 of the transmembrane action
potential, occurred less frequently, and was not specific for ischemia.
The DC potential changes were similar in both subendocardial and
epicardial tissue. Increased heart rate by atrial pacing increased the
magnitude of TQ segment depression and produced subendocardial
ischemia during partial coronary flow reduction.
The findings have importance in the clinical interpretation of STsegment displacement. Potential limitations in the use of precordial
ST-segment mapping to estimate infarct size or severity are
described. The results help explain the variable and conflicting findings of previous studies investigating the mechanisms of ST displacement, and may help explain the poor correlation between rapid atrial
pacing-induced ST displacement and coronary artery disease defined
by angiography. Electrocardiographic interpretation based on
physiologic data such as those presented in this study should improve
the usefulness and accuracy of the electrocardiographic examination.
ST-SEGMENT DISPLACEMENT, one of the most useful
signs of acute ischemic heart disease, has at least two major
possible physiologic mechanisms: localized loss of resting
membrane potential and alteration of the transmembrane
action potential waveform or time of onset of the action
potentials.' Action potential waveform changes resulting in
ST displacement include alterations in the duration,
amplitude, and slope of phase 2. The time of onset of the action potential may be altered by conduction abnormalities
which result in delayed activation and therefore delayed
repolarization. Previous studies investigating the relative
frequency anid magnitude of these two mechanisms have
produced conflicting results."'' These variable results, plus
the increased interest in the use of ST-segment displacement
brought about by precordial ST-segment mapping, and body
surface isopotential mapping, indicate that further elucidation of the underlying physiologic mechanisms is needed.
In the standard electrocardiogram, using capacitor
coupled (A-C) amplifiers, both TQ segment and true STsegment displacement appear as "ST-segment displacement," and the two cannot be differentiated. The technique of recording cardiac potentials using direct current
coupled amplifiers does, however, allow the identification of
these two mechanisms individually. Using this technique,
loss of resting membrane potential is manifest by a depression of the TQ segment (baseline), while action potential
waveform or timing changes are manifest by a shift of the
true ST segment.' 6 These two separate mechanisms are illustrated in figure 1. Previous studies using this technique
have reported variable results, some indicating only TQ segment depression,9- " and others reporting both mechanisms
to be present, but with variable relative importance.` This
study describes the time course and magnitude of changes in
direct current recorded epicardial and endocardial electrograms from ischemic cardiac tissue in the experimental
animal. Additional new information is reported on the effect
of heart rate on the DC recorded electrogram. Through the
use of coronary artery flow probes to document the
magnitude of coronary artery flow reduction, the effects of
partial flow reduction and subendocardial ischemia are
described.
Methods
The mechanism of ST displacement produced by com-
From the Cardiovascular Research and Training Institute and Cardiology
Divisions, University of Utah School of Medicine and LDS Hospital, Salt
Lake City, Utah.
Supported in part by Program Project Grant HL 13480 from the National
Institutes of Health, Award 73-710 from the American Heart Association,
and a Research Award from the Utah Heart Association.
Address for reprints: G. Michael Vincent, M.D., Department of Medicine,
LDS Hospital, Salt Lake City, Utah 84143.
Received June 7, 1976; revision accepted May 27, 1977.
CIRCULATION
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90 mV
Baselineos lh
e
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FIGURE 1. Diagrammatic representation initially described by
Samson and Scher' of "ST segment displacement." Panel A shows
shortening of the action potential and phase 2 slope changes. The
surface DC electrocardiogram shows elevation of the true ST segment. Panel B shows loss of resting membrane potential in the intracellular recording and depression of the baseline (TQ segment) in
the surface electrocardiogram. For simplicity, T waveform changes
which would be expected with action potential changes in A are not
sho wn.
plete or partial occlusion of a coronary artery was studied
using myocardial electrograms recorded with direct current
coupled amplifiers. The studies were performed in open
chest mongrel dogs, under pentobarbital or morphine and
chloralose anesthesia, with mechanical ventilation with
room air. Several types of recording electrodes were used.
Most frequently the electrode was an insulated silver wire,
.005 inches in diameter, with the insulation scraped for 1-2
mm, and this area was chloridized. Epicardial recordings
were obtained from wires sutured through the very
superficial epicardial tissue, as well as from saline moistened
cotton wick electrodes, saline-agar filled plastic cups of 0.25
to 1.0 cm diameter, chloridized silver discs of 0.5 to 1.0 cm
diameter, and silver-silver chloride discs of 7 mm diameter.
Subendocardial recordings were obtained from wires
sutured through the ventricular wall and out again, so that
the scraped area was placed in the subendocardium and
anchored there by a previously placed knot adjacent to the
scraped area. A chloridized silver wire inserted subcutaneously in the hind leg served as a reference electrode.
The first occlusion was performed one hour after electrode
placement to allow the injury currents due to electrode
placement to disappear or stabilize. The amount of true STsegment and TQ-segment change during each experiment
was determined by taking the difference between the control
and the intervention states. Thus, while there was some "STsegment" displacement in 20% of control recordings, the
magnitude and relative amount of TQ and ST-segment displacement were not different in this circumstance from
recordings where the control tracings showed no ST displacement. The electrodes were placed in the distribution of
the isolated artery, at sites judged to be ischemic by visual
observation of color and wall motion changes during occlusion. An average of five unipolar electrograms was recorded
in each experiment at a sensitivity of 10 or 20 mV/cm on a
multichannel Grass pen recorder or Dixon light beam oscillograph. The direct current differential preamplifiers used
in this study were specifically designed and fabricated in our
laboratory using techniques to maximize DC recording
characteristics. The input stage employs selected monolithic
VOL 56, No 4, OCTOBER 1977
dual field effect transistors and dual low drift operational
amplifiers physically configured for maximum thermal inertia. All active and passive components used were selected on
the basis of minimum temperature coefficient and noise.
After a 10 minute warm-up period the long term DC voltage
drift was <10 tV/hr. The input impedance was 1011 ohms.
This differential electrometer type input minimized drift due
to the large dynamic range of source impedances encountered in the electrocardiographic recording. The
preamplifiers had a frequency response of DC to 10 KHz
and a voltage gain of 10. Noncardiac potential shifts due to
amplifier drift, electrode polarization or skin potential
changes around the reference electrode were not uncommon.
To prevent this artifact from being mistaken for cardiac
potential changes due to ischemia, data were taken only
from those recordings in which the baseline potential following release of the occlusion returned to the control value.
The polarity of the recording system was such that a positive
wave was inscribed when the exploring electrode became
positive with respect to the reference electrode. The TQsegment level was measured just prior to the QRS complex.
True ST-segment level was measured immediately after the
J point.
Complete coronary occlusion of either the left anterior
descending artery or the circumflex artery was performed in
30 animals by applying traction on a piece of umbilical tape
passed underneath the vessel. Ischemic areas of variable size
were obtained in different animals by varying the location of
the occlusion. Approximately 120 occlusions were performed, and 600 electrograms recorded. Control recordings
of epicardial and subendocardial electrograms, and a Y lead
body surface electrocardiogram were made prior to each
occlusion and continuous recordings were made during coronary occlusion of 5 to 20 minutes duration, and for 4 to 6
minutes following release of the occlusion. In those experiments with 10 to 20 minute occlusions, the pericardium
was loosely closed over the electrodes, warm saline pads
were placed on the heart, and the chest wall was closed prior
to obtaining control and occlusion records.
The effect of partial coronary artery occlusion, producing
variable degrees of coronary flow reduction, was investigated in 10 additional dogs. The animals were prepared
as previously described. A Statham coronary flow probe was
placed on the proximal left anterior descending artery or circumflex artery, and connected to a Statham SP 2202
flowmeter, from which mean coronary flow could be read
directly. Coronary flow reduction of the desired amount was
obtained using an inflatable silastic cuff placed around the
artery distal to the flow probe, making sure no significant
branches exited between the probe and the occlusion cuff.
Several occlusions of variable degree were performed in
each animal, with randomly selected reductions in mean coronary flow of 10-100%. Control recordings were made prior
to each occlusion, and continuous recordings made during 5
minutes of flow reduction, and for 5 minutes following
release.
Results
TQ and ST-Segment Changes
In all experiments, depression of the TQ segment occurred and was the major cause of "ST-segment dis-
ISCHEMIC ST DISPLACEMENT/Vincent, Abildskov, Burgess
CONTROL
I MEN
OCCLUSI
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2I
MAFTER
2 MU MIN 1AFTE
RELEASE
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RELEASE
20mvI
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FIGURE 2. Simultaneous epicardial electrograms recorded from four electrodes. The electrodes were distributed randomly in the ischemic area, with some more toward the center of the ischemic area than others. A t one minute of occlusion TQ depression is apparent in all recordings. After two minutes of occlusion the TQ depression has increased. The STsegment take-off is slightly elevated or isoelectric in all recordings. The marked change in T waveform is apparent, and
this figure emphasizes that major changes in action potential downstroke shape and timing can occur without significant
alteration of phase 2 and the true ST segment.
placement." True ST-segment shifts were of less magnitude
and variable, with both ST depression and elevation occurring. Four representative epicardial recordings are shown
in figure 2. The mean TQ and ST-segment changes occurring with 15 minute occlusions are shown in figure 3. The
TQ depression began within 30 seconds, and increased in
magnitude during occlusions up to 20 minutes, but usually
reached a near maximum degree by about 5 minutes. There
were only small changes in the true ST-segment level. The
results of shorter occlusions, 3 to 5 minutes in duration, involving 12 experiments and 53 electrograms showed a
similar time course and magnitude of TQ and true STsegment change, with the TQ segment usually returning to
the control level within 60-90 seconds. The occlusions maintained for 20 minutes or longer frequently led to changes
which persisted following release of the occlusion. In these
circumstances it was impossible to determine if the persistent changes were due to early infarction, or to artifact due
to electrode polarization or amplifier drift, and for this
reason occlusions longer than 15 minutes in duration were
not included in the analysis. The peak magnitude of TQ
depression was as much as 12-14 mV and occurred in the
center of the ischemic area. The amount of depression
decreased toward the periphery of the lesion. TQ depression
occasionally began several seconds earlier in subendocardial leads than in epicardial leads, but the peak
magnitude of depression was similar in both.
T waveform was markedly altered with occlusion. The T
wave was usually inverted in both subendocardial and epicardial recordings in the control state, and became positive
in both during ischemia.
Variable Coronary Flow Reduction and Subendocardial Ischemia
In the studies with variable coronary flow reduction, myocardial ischemia as evidenced by post release reactive
hyperemia measured by flowmeter occurred with reductions
of flow of 5-10%. Usually no electrocardiographic changes
were present at that time. T wave changes occurred at
3
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7 16
9
10 11 12 13 14 15
i
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FIGURE 3. The time course and magnitude of potential changes
occurring during 15 minute coronary artery occlusion. In these
animals the pericardial sac and chest wall were closed after electrode application. The data are from four experiments in which 14
electrograms were recorded. Mean values and standard error for
TQ and STchange are shown. Comparing TQ and ST, P < 0.001 at
each point in time of occlusion. The mean ST segment remains essentially at the control level. Significant TQ depression develops,
with rapid decrease in TQ level for the first five minutes, and a
slower rate of change through 15 minutes.
VOL 56, No 4, OCTOBER 1977
CIRCULATION
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CONTROL
3 MN
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FIGURE
4.
Heart rate is
effect of partial coronary flow reduction. Coronary flow has been reduced to 25% of the control flow.
100/mmn A and C are recordings from epicardial wire electrodes. B is a recording from a subendocardial
The
electrode. The subendocardial
recording shows TQ depression with partial flow reduction, with little change
in the
epicar-
recordings. During complete occlusion, there is prominent TQ depression in all electrograms, and slight ST elevation
the subendocardial recording, with no change from control values of the ST segments in the epicardial recordings.
dial
in
30-50% flow reduction. TQ-segment depression, at control
heart rates of 100-140/min occurred when the flow was
reduced by 50-70%. True ST displacement, when it
developed, occurred at approximately the same level of flow
reduction as TQ depression. As with complete occlusion, the
magnitude of TQ depression exceeded that of true ST displacement. Figure 4 shows the changes in epicardial and
subendocardial leads with 75% coronary flow reduction at a
heart rate of 100/min. TQ-segment depression is present in
the subendocardial lead, but there are no TQ-segment or
true ST-segment changes in the epicardial leads. The electrogram changes during complete occlusion demonstrate
that all electrodes were well within the distribution of the
occluded vessel.
Effect of Heart Rate
Subendocardial ischemia could also be produced by
alterations in heart rate during partial occlusion. Figure 5
shows recordings from a subendocardial lead and an overCONITOL
120/MIN
EPI
10
_
1
MIN AT
160/MAN
lying epicardial lead. Progressive increase in paced heart
rate in the presence of 60% reduction in coronary flow
produced prominent TQ and true ST changes in the subendocardial recording, with only minimal changes in the epicardial recording. Figure 6 shows the effect of increased
heart rate in the presence of normal coronary flow, and
demonstrates no change in TQ segment in the subendocardial recording, indicating that increased heart rate of this
degree produced no ischemia. There is decreased T wave
amplitude and slight true ST elevation consistent with the
well known alterations of action potential waveform due to
heart rate.
The heart rate also had a major effect on the magnitude of
DC displacement due to complete coronary occlusion.
Figure 7 shows the mean TQ and true ST-segment displacement occurring in a series of dogs in which occlusion at heart
rates of 120/min and 180/min were compared. True STsegment displacement is similar at both rates; however, TQsegment depression occurs earlier and to a greater degree at
I MIN AT
135/MIN
IMIN AT
220/MIN
IMIN AFTER
RETURN. TO I2DAN
______
u'!
ENDO
A A
FIGURE 5. The effect of heart rate on DC displacement during partial flow reduction. Electrograms from epicardial
(EPI) and endocardial (ENDO) leads are shown. Coronaryflow has been reduced to 40% of the control value. The heart
rate has been sequentially increased by atrialpacing. The control record is afterfive minutes offlow reduction. Progressive
TQ depression occurs in the endocardial lead with increased heart rate. A t 160/min there is some ST elevation; however at
220/min, as ischemia becomes more severe, the ST-segment take-offis slightly depressed. There is only slightflattening of
the T wave in the epicardial lead.
ISCHEMIC ST DISPLACEMENT/Vincent, Abildskov, Burgess
CONTROL
PACING
563
IMMEDIATELY AFTER
RATE 120/MIN
EPI
ENDO |! ,r1||r
MV
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FIGURE 6. The effect of increased heart rate on epicardial and
subendocardial recordings during normal coronary flow. Pacing at
240/min was performed for three minutes prior to recording the
240/min record. The TQ segment remains unchanged in both electrograms, indicating that no ischemia was produced. Increased ST
elevation and flattening of the T wave occurs in the subendocardial
recording during increased heart rate. The post pacing record was
taken immediately upon return to the control rate. The ST and T
waveform returned to the control state within one minute.
the fast rate. An example of this series of experiments is
shown in figure 8.
Discussion
These studies indicate that TQ-segment displacement,
thought to be due to loss of resting membrane potential, is
the major mechanism producing "ST-segment" displacement during cardiac ischemia. Altered action potential
waveform was found to have a less marked role in "STsegment displacement" although it undoubtedly results in
alterations of T waveform. The major current of injury due
to ischemia, therefore, is diastolic. In a recording from a
lead overlying the ischemic segment the loss of resting
potential is manifest as TQ depression. This appears as "St
elevation" on the AC coupled electrocardiogram since the
downward baseline shift is compensated by the capacitor
coupled amplifier returning the baseline to the control level,
producing "elevation of the ST segment." True ST-segment
displacement (systolic injury current), thought to be due to
action potential waveform or timing change, was of less
magnitude, and variable in its expression, since both true ST
elevation and depression were seen. In the series of dogs with
15 minute occlusions in which the chest was closed prior to
occlusion, the ST segment remained essentially isoelectric
(fig. 3). In the dogs with shorter occlusion ST depression was
seen from epicardial recordings, perhaps due to further cooling of the epicardial surface during ischemia. Previous
studies have demonstrated that acute ischemia does produce
shortening of the action potential. However, shortening of
the action potential without significant alteration of phase 2
appears to occur frequently. This was demonstrated by the
frequent finding of an isoelectric true ST segment during
ischemia, indicating that phase 2 relationships were not
altered, even though there had been marked changes in action potential waveform and downstroke timing as shown by
initially negative T waves becoming positive and peaked
during ischemia.
-7
-8
-9
-10
1
2
3
4
TIME(min)
FIGURE 7. The effect ofheart rate on DC potential changes during
complete coronary occlusion. The data arefrom four experiments in
which 16 electrograms were recorded. Sequential occlusions were
performed in each animal at atrial paced rates of 120/min and
180/min. The sequence of rates during occlusion was random.
Mean TQ and ST changes and the standard error are shown. The
TQ depression occurs earlier and to a greater degree during thefast
rate. The difference in TQ level is significant at P < 0.001 at each
time interval during occlusion.
Our results are supported by a study of simultaneous intracellular and epicardial electrograms reported by
Prinzmetal et al.6 The intracellular recordings showed
predominantly loss of resting membrane potential, smaller
changes in phase 3 timing, and even less change in phase 2
duration, amplitude or slope, with the epicardial electrogram showing corresponding amounts of TQ depression, T
wave change and true ST-segment change. In a similar
study, Samson and Scher also observed both loss of resting
potential and action potential waveform changes, but found
more variability in the relative magnitude of TQ and STsegment change, with the magnitude of ST displacement
often exceeding that of TQ depression.' They also found that
true ST displacement usually preceded any change in baseline potential. Our results, in contrast, found baseline potential to change first, or the two to occur simultaneously. Both
of these previous studies, among others,'1 12 showed that
epicardial TQ-segment depression was associated with loss
of resting membrane potential in the intracellular recording,
and that displacement of the true ST segment was associated
with action potential waveform changes, validating the use
of extracellular DC recordings to study these two
mechanisms of "ST displacement."
VOL 56, No
CIRCULATION
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occwSN
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5 MIN
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1 MAN AFlT
RELEASE
6 MIN
OCCLUSI
1 MIN AT 120
AAAL k u 12 !.WEV~kIAA,<
I MIN AFTER
RELEAS1
;
The effect of heart rate on DC electrograms during complete coronary occlusion. The top and bottom elecepicardial recordings from the center of the ischemic area. The center electrogram is an
epicardial recording from the periphery of the ischemic area. A and B are records of two sequential occlusions in one
animal. Afterfive minutes of occlusion, there is greater TQ depression at the rate of 180/min (B) than at 120/min (A). In
A the rate was increased to 180/min during the sixth minute ofocclusion, with further depression of the TQ segment and
peaking of the T waves, and some ST elevation in the top recording.
FIGURE 8.
trograms in both A and B are
Katcher et al.,5 reporting the effects of ischemia and
levarterenol infusion on the DC recorded electrogram,
described results very similar to ours. They found TQ
depression to be a consistent finding with ischemia, and true
ST displacement less in magnitude, and variable, with both
elevation and depression observed. In our studies, increased
heart rate, even with normal coronary flow, was seen occasionally to produce true ST displacement similar to the
frequent clinical observation of ST-segment displacement on
the electrocardiogram during rapid heart rates. This is consistent with the well known effect of heart rate on phase 2 of
the action potential. The magnitude of phase 2 change due to
increased rate is variable from one region to another. A
potential difference during the plateau phase therefore
develops producing true ST-segment displacement.
Katcher et al. reported ST depression with the intravenous infusion of levarterenol and did not think that
ischemia was present. These combined results suggest that
true ST displacement is not a specific sign of ischemia. TQ
depression, on the other hand, has occurred consistently
with ischemia, and was not seen with either rapid atrial pacing or levarterenol infusion, and would appear to be a more
specific indicator of ischemia. The nonspecificity of true STsegment change is further suggested by the variability of true
ST-segment response during occlusion. While the mean ST
segment remained nearly isoelectric (fig. 3), both ST elevation and ST depression were seen with similar amounts of
TQ depression. This observation may have importance in
the interpretation of ST maps for infarct sizing using standard AC coupled amplifiers. It is possible that an intervention may alter "ST segment" displacement by changing action potential waveform or timing, without actually modifying
the severity or extent of ischemic injury. An example of
this may be present in figure 8B. Following two minutes of
complete coronary occlusion, the heart rate was increased.
TQ depression progressively increased indicating increasing
injury. On the top and bottom recordings after five minutes
of occlusion there is peaking of a positive T wave and slight
true ST elevation. At six minutes of occlusion, after the
heart rate had been returned to 120/min, the magnitude of
ISCHEMIC ST DISPLACEMENT/Vincent, Abildskov, Burgess
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TQ depression remains the same, indicating, as would be expected, that the degree of ischemia remained the same.
However, the true ST segments have returned toward the
baseline, and the T waves are lower in amplitude, suggesting
that the true ST changes and some of the T changes during
the fast rate were not due to increased ischemia but to the
effect of increased heart rate on phase 2 of the action potentials. An estimate of the severity of the ischemia based on
total "ST displacement" (TQ and ST) might therefore give
misleading results. In addition, during ischemia the T waves
become positive and often very peaked with rapid ascent
from the J point into the T wave, giving the appearance of
ST elevation. The ST-segment take-off, however, usually
remains isoelectric and the apparent ST elevation is artificial. This, too, should be considered as a source of error
in ST-segment mapping. Holland and Brooks,'3 from experimental data and theoretical concepts using solid angle
theorem analysis, have emphasized the very complex relationships of TQ and ST-segment displacement, and the
potential difficulty of interpreting changes in TQ-ST displacement secondary to interventions.
Other studies using DC coupling to examine injury potentials have shown variable results. Most have suggested both
mechanisms, but of variable relative magnitude and time
course,'-8 and two studies found only TQ depression.9' In
these two studies body surface leads rather than epicardial
leads were employed, and injury was produced by topical
epicardial application of KCI rather than by ischemia.
Whether these differences in technique account for the
variable results is not known. Alzamora-Castro et al.4 used
both ischemia and topical KCI to produce injury and showed
similar changes with both. Cohen et al.,'4 using magnetocardiography to study the DC shifts with experimental
ischemia, found a steady DC current, comparable to TQ
segment depression and considered to reflect loss of resting
membrane potential, to account for "ST displacement."
There were minor and variable changes in the true ST segment. They also demonstrated that TQ depression occurred
first, or TQ and true ST displacement occurred
simultaneously. These results are essentially identical to
those reported in the present study, and the similar results
obtained using a different technique substantiate the validity
of our findings. Though the variable results of previous
studies are not completely explained, it is clear that all
studies have shown TQ-segment depression. The variability
has been in the amount and type of true ST displacement.
Since action potential waveform can be altered by many factors other than ischemia, it seems likely that differences in
these factors from one study to another account for the
variable results. If this is so, it further indicates the importance of understanding which of the two basic mechanisms
of "ST displacement" is really representative of myocardial
ischemia. As mentioned earlier, we believe the data suggest
TQ depression is the more specific indicator of ischemia.
The electrocardiographic changes during evolution of an
acute infarction would appear to support this suggestion.
Early peaked T waves are seen, similar to these animal
studies, representing shortening of the action potential. "ST
elevation" then occurs. After approximately 24 hours Twave inversion begins as the action potentials from the injured cells lengthen. The "ST segment" elevation, however,
"
565
often persists, even to a prominent degree, during this Twave change. While it is possible that such prominent action
potential shortening and lengthening could occur without
significant concomitant change in an abnormal phase 2, it
seems more likely that phase 2 was not prominently altered
to begin with, and that "ST displacement" is due to baseline
depression as seen in these animal studies.
The studies with partial flow reduction showed subendocardial tissue more vulnerable to develop ischemia in the
presence of coronary flow reduction than epicardial tissue,
as has been frequently stated. There has been considerable
previous debate regarding the mechanism of "ST displacement" with subendocardial injury."5 16 Our results indicate an identical physiologic mechanism to that just
described for the ischemia produced by complete occlusion.
In the case of subendocardial injury the diastolic injury
current would be manifest as TQ depression in a subendocardial lead, as was seen, and this would be represented on
the subendocardial AC electrocardiogram as "ST segment"
elevation. In a surface lead overlying the injured area, TQ
elevation would be expected, and in an AC coupled system
this would appear as "ST depression." The "ST depression"
seen during an exercise test or an anginal episode, for example, would therefore appear to be due to loss of resting membrane potential in the subendocardial tissue. TQ elevation
was not seen in this study, however, and areas of "ST
depression" at the periphery of the ischemic lesion were not
observed, in contrast to some other studies.8' 15, 16 The
magnitude of subendocardial injury currents which could be
obtained in our study was small, and this may account for
the lack of epicardial "reciprocal ST depression." The findings with partial flow reduction and alteration of heart rate
may help explain the poor correlation between atrial pacinginduced ST depression and coronary artery disease as
defined by angiography.'7 Rapid atrial pacing, even with
normal flow and no reactive hyperemia following cessation
of rapid pacing was seen to produce true ST displacement
without TQ change. This would appear to be due to the rate
effect on the action potential waveform rather than
ischemia. However, on the AC electrocardiogram this true
ST change would be indistinguishable from ischemic "ST"
change due to TQ displacement.
This study has helped elucidate the mechanisms responsible for "ST displacement" due to early, acute myocardial
ischemia, and described the magnitude and time course of
these changes. It must be remembered that in AC recorded
electrocardiograms "ST displacement" due to TQ-segment
change cannot be differentiated from that due to alterations
of the true ST segment. The results of the present study contribute to understanding the mechanisms of "ST displacement" due to ischemia but do not themselves
demonstrate how this can be directly applied in clinical
medicine. DC recording of the electrocardiogram in patients
presents major technical difficulties and cannot be considered practical at the present time. Further, in the case of
acute myocardial infarction, the baseline potential has
usually been altered prior to initial electrocardiographic examination, and even DC recordings at that time would not
establish whether a baseline or true ST shift had occurred.
Some of the clinical areas in which these data might be
applied, however, include the interpretation of ST-segment
CIRCULATION
566
changes in acute infarction as a measure of extent and
severity of injury, the interpretation of ST changes during
exercise or rapid atrial pacing, and the relationship of heart
rate and partial coronary flow reduction to subendocardial
and epicardial ischemia.
8.
9.
10.
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Sudden Death after Repair of
Tetralogy of Fallot
Electrocardiographic and Electrophysiologic Abnormalities
PAUL C. GILLETTE, M.D., MARK A. YEOMAN, M.D.,
CHARLES E. MULLINS, M.D., AND DAN G. MCNAMARA, M.D.
SUMMARY In order to try to determine the mechanism of sudden death in patients after surgical repair of tetralogy of Fallot, electrocardiographic, intracardiac electrophysiologic, and clinical data
of 51 children who had postoperative intracardiac electrophysiologic
studies were reviewed. Ninety-four percent had developed right bundle branch block (RBBB) and 16 percent had additional left anterior
hemiblock (LAH). Two had had transient complete A-V block
(CAVB) and one had permanent CAVB. Six had a first degree A-V
block and nine had premature ventricular contractions (PVC).
Nine patients were found to have prolonged intra-atrial conduction times, four prolonged A-V nodal conduction, four prolonged HisPurkinje conduction, and five prolonged corrected sinus node
recovery times. Patients with first degree A-V block or LAH did not
have an increased incidence of abnormalities on electrophysiologic
study.
No patient with RBBB and LAH developed complete A-V block or
died. Three of the nine patients with PVCs died, one of intractable
ventricular fibrillation and two suddenly, presumably of dysrhythmia. All three had significant congestive heart failure.
Although late complete A-V block occurs and should be watched
for, ventricular dysrhythmias in patients with PVCs may be the cause
of most sudden deaths after tetralogy repair. We currently are treating all of our postoperative tetralogy patients who have PVCs with
quinidine or propranolol.
ALTHOUGH SURGICAL REPAIR of tetralogy of Fallot
results in an improvement in the duration and quality of life
for most patients, late sudden deaths are known to occur."'
The cause of these deaths has been thought to be dysrhyth-
mias. There is a question as to whether ventricular tachydysrhythmias, complete atrioventricular block, or sick sinus
syndrome is the cause.'-"
Intracardiac repair of tetralogy of Fallot carries the risk
of damage to impulse generating or conducting system as a
result of surgical incision, cannulation or suture. The object
of this investigation was to use surface electrocardiography,
His bundle electrography, atrial pacing, and the atrial extrastimulus technique to study electrophysiological properties
of the sinoatrial node, atria, atrioventricular node, HisPurkinje system and ventricles after intracardiac repair of
From the Section of Cardiology, Department of Pediatrics, Baylor College
of Medicine and Texas Children's Hospital, Houston, Texas.
Supported in part by Grant HL-5756 from the NIH and by USPHS Grant
RR-00188 from the General Clinical Research Branch, NIH.
Address for reprints: Paul C. Gillette, M.D., Section of Pediatric Cardiology, Texas Children's Hospital, 6621 Fannin, Houston, Texas 77030.
Received April 11, 1977; revision accepted May 30, 1977.
Mechanisms of ischemic ST-segment displacement. Evaluation by direct current
recordings.
G M Vincent, J A Abildskov and M J Burgess
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Circulation. 1977;56:559-566
doi: 10.1161/01.CIR.56.4.559
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1977 American Heart Association, Inc. All rights reserved.
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