136 SECTION I  Adult Electrocardiography

Figure 7–17 ECG of a 61-year-old woman resuscitated from cardiac arrest but who succumbed to cardiogenic shock on
the same day. Acute injury pattern suggests inferior and right ventricular infarction. The latter was corroborated by the ST
segment elevation in leads to the right of lead V1. In the left precordial leads, ST segment elevation extends to lead V3,
and reciprocal depression is present in leads I, aVL, and V5–V6. There is sinus tachycardia with complete atrioventricular
(AV) dissociation and AV junctional rhythm at a rate of 56 beats/min.

Figure 7–18 ECG of a 65-year-old woman with a posterolateral myocardial infarction attributed to complete occlusion of
the left circumflex coronary artery in its midportion and complete occlusion of the dominant right coronary artery. There was
severe posterolateral hypokinesis with an estimated left ventricular ejection fraction of 10 percent. ST segment elevation is
present in leads I, aVL, and V6 and reciprocal ST segment depression in leads V1 through V3.

whereas in the case of circumflex occlusion, ST
segment in lead I is either elevated or isoelectric.
In the experience of these investigators,23 ST
depression in lead I was predictive of RCA
occlusion in 86 percent of cases and an isoelec-
tric or elevated ST segment in lead I was predic-
tive of circumflex occlusion in 77 percent of
cases.
Numerous earlier studies produced the same
or similar results. Thus Huey et al.41 compared
the ECGs of 40 consecutive patients with acute
MI caused by left circumflex artery occlusion
with those of 107 patients with right coronary
occlusion. In the patients with inferior MI, ST seg-
ment elevation in one or more of leads I, aVL, V5,
and V6 was highly suggestive of occlusion of the left
circumflex artery (see Figure 7–20). Bairey et al.42
also reported that ST segment elevation in the lat-
eral leads identified circumflex artery occlusion
as the cause of inferior MI.
 7  Acute Ischemia: Electrocardiographic Patterns 137

Figure 7–19 ECG of a 48-year-old man with acute occlusion of a large obtuse marginal branch before (A) and 3 hours
after (B) emergency percutaneous coronary angioplasty. Note the ST segment elevation in leads I, aVL, V5, and V6. Recipro-
cal ST segment depression in leads V1–V3 regress after angioplasty.

In patients with inferior MI, ST segment
elevation in lead III exceeding that in lead II,
particularly when combined with ST segment
elevation in lead V1, is a powerful predictor of
occlusion of the right coronary artery proximal
to the acute margin of the heart42 (see Fig-
ure 7–9). Hertz et al.43 reported the same results
with an added finding that reciprocal ST depres-
sion in lead aVL was greater than in lead I.
Leads V5 and V6 are affected by posterolat-
eral ischemia (Figures 7–23 and 7–24). ST seg-
ment elevation >0.2 mV in leads V5 and V6 in
patients with inferior MI correlated with occlu-
sion of an artery (right or circumflex) supplying
a large territory of the myocardium with an
expected high ischemic burden.44 In patients
with an inferior MI with ST segment elevation
in leads II, III, and aVF, the presence of addi-
tional ST segment elevation in leads V5–V6 or
leads I and aVL is a fairly sensitive and specific
marker for left circumflex coronary artery
occlusion.42
Depression of the ST segment in leads V1–V3
tends to indicate a large posterolateral perfusion
defect,32 probably owing to the involvement of
posterior or posterobasal wall, and is more often
associated with occlusion of the circumflex artery
(71 percent) than of the RCA (40 percent).45
LATERAL, INFEROLATERAL, AND
POSTEROLATERAL MI
Lateral wall involvement causes ST segment
elevation in leads V5 and V6. It occurs more fre-
quently in circumflex artery than right coronary
artery occlusion, but independent of the vessel
involved, ST elevation in these leads implies a
larger ischemic area.23
138 SECTION I  Adult Electrocardiography
Figure 7–20 ECG of an 82-year-old man with an acute inferior and posterobasal myocardial infarction, apparently caused
by 95 percent occlusion of the dominant left circumflex artery and 95 percent occlusion of the mid-right coronary artery.
Note the ST segment elevation in leads II, III, aVF, and V2–V6 and the reciprocal ST segment depression in leads aVR and
V1. Left ventricular ejection fraction is 20 percent.
Localizaton of ST segment elevation and reci-
procal ST segment depression varies in patients
with a lateral MI depending on the extent and
location of the MI. Typically, ST segment eleva-
tion in patients with inferolateral MI is present
in leads II, III, aVF, V5, and V6 (see Figure 7–20).
In many cases, however, ST segment elevation
extends to the right of lead V5 (i.e., leads
V2–V4). The lead with maximal ST segment
elevation, however, is usually V6 or V5. Recipro-
cal ST segment depression may be present in
leads I, III, aVL, and V1–V4, but it may also be
absent.
In patients with high lateral MI caused by
occlusion of the left circumflex coronary artery,
the ST segment is usually elevated in leads I,
aVL, V5, and V6; it is depressed in leads III
and aVF and occasionally in lead V1 (see
Figure 7–23).
Posterior wall involvement causes reciprocal
ST depression in right precordial leads. When
present in patients with RCA occlusion, it indi-
cates dominance of this vessel. In case of circum-
flex artery occlusion, the posterior wall is nearly
always involved. Therefore absence of ST seg-
ment depression in the right precordial leads in
inferior MI is strongly suggestive of RCA
involvement.23 In patients with posterolateral
MI, ST segment elevation may be either absent
or present in leads V5 and V6.
In patients with a so-called true posterior MI
(i.e., without ECG evidence of inferior or lateral
MI), ST segment elevation may be present in
leads V7–V9 and reciprocal ST segment depres-
sion in leads V1–V3.46 Routine recording of leads
V7–V9 has been recommended in patients with
suspected MI but with a nondiagnostic 12-lead
ECG.47–49 ST elevation in posterior leads V7–V9
in patients with an inferior MI was associated
with a high incidence of posterolateral wall
motion abnormalities, large infarct, and low
ejection fraction.49 In the study of Wung and
Drew,50 posterior leads V7–V9 contributed signif-
icant additional diagnostic information above
and beyond the standard 12-lead ECG when a
criterion of 0.05 mV instead of 0.1 mV ST eleva-
tion was applied to the posterior leads.
ACUTE INJURY PATTERN IN BOTH
ANTERIOR AND INFERIOR LEADS
In the GUSTO study, a pattern with combined
ST segment elevation in at least two of leads
V1–V4 and more than two leads of leads II, III,
and aVF was present in 179 of 2996 patients with
acute MI. Of these patients, RCA occlusion was
present in 59 percent and distal LAD occlusion
in 36 percent. Patients with combined anterior
and inferior ST segment elevation tended to have
limited MI size and a more preserved LV
function.51
ACUTE INJURY PATTERN IN RIGHT
PRECORDIAL LEADS
Elevation of the ST segment in the right precor-
dial leads V3R and V4R usually signifies the pres-
ence of RV MI.52,53 In patients with RV MI,
ST segment elevation may extend to additional
right precordial leads V5R and V6R52–55 and
 7  Acute Ischemia: Electrocardiographic Patterns 139

Figure 7–21 ECG of a 48-year-old man with an inferoposterior myocardial infarction caused by total occlusion of the
large-caliber circumflex coronary artery. No significant stenoses were present in the left anterior descending and right coro-
nary arteries, but there was a 90 percent stenosis of a small diagonal branch. A, Day of infarction. Note the ST segment ele-
vation in leads II, III, and aVF and reciprocal ST segment depression in leads I, aVL, and V1–V6. B, At 13 hours after
angioplasty of the left circumflex artery. Note the regression of the ST segment deviation and the decrease in QRS duration
from 104 ms to 86 ms.

sometimes to precordial leads V1–V545 (see Fig-
ure 7–24). In the presence of an inferior MI, a
diagnosis of RV MI is supported by a discordant
pattern of ST segment elevation in V1 and ST seg-
ment depression in V2.56 ST segment elevation in
leads V3R and V4R may be present in patients
with acute anterior MI but seldom extends to
lead V5R.57 Moreover, when the ST segment ele-
vation caused by acute anterior MI is present in
leads V3R–V5R, the magnitude of the ST segment
elevation diminishes from V3R to V5R, whereas in
the presence of RV MI, the ST segment elevation
is either the same or increases from V3R to V5R.58
Saw et al.59 found that in patients with inferior
MI, ST elevation in lead III greater than in lead
II was more sensitive than lead V4R in diagnos-
ing RV MI.
Isolated RV infarction is rare, but the diagno-
sis can be verified by echocardiography. In one
reported case, ST segment elevation in the
precordial leads was associated with minimal
ST segment elevation in the inferior leads.60 In
another case, massive ST segment elevation in
the precordial leads was associated with massive
ST segment elevation in inferior leads.44 Such
cases are rare.
TOMBSTONING PATTERN
The term “tombstoning pattern of ST segment in
acute MI” was apparently introduced by Wima-
larathna.61 It is used infrequently to label a
purely monophasic pattern occurring most
often in patients with proximal occlusion of
140 SECTION I  Adult Electrocardiography

RIGHT CORONARY ARTERY MI CIRCUMFLEX CORONARY ARTERY MI

I I

III II III II
Figure 7–22 Schematic presentation of the ST segment vector in inferior wall myocardial infarction showing the differ-
ence between the occlusion of right and left circumflex coronary artery and the corresponding ECG changes in the limb
leads. See text discussion. (From Wellens HJJ, Gorgels APM, Doevedans PA [eds]: The ECG in Acute Myocardial Infarction
and Unstable Angina. Norwell, MA, Kluwer Academic, 2003. With permission of authors and publisher.)

Figure 7–23 ECG of a 63-year-old man with a pattern of high lateral myocardial infarction probably caused by left
circumflex artery disease. Coronary angiography showed 50 percent mid-left circumflex artery stenosis, 75 percent obtuse
marginal artery stenosis, 99 percent proximal left anterior descending artery stenosis, and aneurysmal dilatation of the right
coronary artery. ST segment elevation is present in leads I, aVL, V5, and V6; reciprocal ST segment depression is present in
leads III, aVF, and V1.

LAD coronary artery62 and suggesting a large
infarct and a low LV ejection fraction63 (see
Figures 7–29 and 7–30). It can be seen also in
an agonal ECG (Figure 7–25).
BRUGADA AND OTHER RSR0 PATTERNS
WITH ST ELEVATION IN THE RIGHT
PRECORDIAL LEADS
In patients with an RSR0 pattern in the right precor-
dial leads and absent anterior infarction, ST seg-
ment elevation may be caused by septal ischemia
(Figures 7–26 and 7–27) or by RV MI.53–56,58
Other causes of such a pattern include the syn-
drome associated with sudden cardiac death
described by Brugada and Brugada64 and
arrhythmogenic RV dysplasia (see Chapter 12).
Brugada and Brugada65 described a syndrome
of RBBB, persistent ST segment elevation in leads
V1–V3 (ocasionally in other leads), and sudden
cardiac death that affects predominantly male
patients and is often familial. In some subjects
with this syndrome, the pattern appears inter-
mitently with transient normalization of the
ECG. There are three types of the ECG pattern:
in the most common, type 1, the ST segment is
coved and the elevation is 0.2 mV; in type
2 there is saddleback elevation of 0.1 mV;
and in type 3 the coved or saddleback elevation
is <0.1 mV.66 The ST elevation is augmented by
 7  Acute Ischemia: Electrocardiographic Patterns 141

Figure 7–24 Acute inferoposterior myocardial infarction with right ventricular infarction in a 37-year-old man. ECG was
recorded on the day of the onset of chest pain. A diagnosis of infarction was corroborated by serial cardiac enzyme changes.
Radionuclide angiography revealed an akinetic inferoposterior wall of the left ventricle and severe hypokinesis of the right
ventricle. The left ventricular ejection fraction was 48 percent and the right ventricular ejection fraction 11 percent. Physical
examination revealed marked jugular venous distension. ST segment elevation is present in leads II, III, and aVF and recip-
rocal ST segment depression in leads I and aVL. There is some ST segment elevation in the left precordial leads. Its cause is
uncertain. Marked ST segment elevation in leads V1 and V4R is suggestive of right ventricular infarction. ST segment elevation
in all of the precordial leads subsided the next day.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

VI

Figure 7–25 Monophasic ECG pattern (“tombstone”) of a pulseless unconscious patient recorded shortly before his death.

selective stimulation of a-adrenergic or musca-
rinic receptors and by sodium channel–blocking
antiarrhythmia drugs,67 but reduced by b-adren-
ergic stimulation or a-adrenergic block.68 Many
of these patients have no evidence of structural
heart disease. Mutations of the SCN5A gene,
which encodes the cardiac sodium channel, have
been identified in about 15 percent of patients
with Brugada syndrome who have frequently
bradyarrhythmic complications.69,70 A similar
ECG pattern was present in young male South-
east Asians who died unexpectedly during
sleep71 and in patients with familial cardiomyopa-
thy (arrhythmogenic RV dysplasia) involving the
right ventricle and the conducting system.72–74
Common to these conditions is QRS widening con-
fined to selected leads with ST segment elevation
(usually V1–V3) with normal QRS duration in
remote leads such as I and V6.75 In patients with
RV dysplasia, the shape of the terminal QRS
portion in the right precordial leads has been
likened to the Greek letter epsilon.
The pattern of RBBB with ST segment elevation
in the right precordial leads is not entirely specific
for RV ischemia or Brugada syndrome because it
can occur with other conditions (Figures 7–28
and 7–30). Table 7–1 lists some of the conditions
in which the Brugada type ECG pattern may be
encountered. The largest number is probably in
the unexplained category.76
142 SECTION I  Adult Electrocardiography

V1

V2

V3

V4

V5

V6
A B C D E F

Figure 7–26 Selected electrocardiographic leads before (A), during (B–E), and after (F) balloon occlusion of the proximal
left anterior descending coronary artery in a patient in whom ST segment elevation in leads V1–V3 during occlusion was
associated with a QRS duration increase in these leads. (From Surawicz B, Orr CM, Hermiller JB, et al: QRS changes during
percutaneous transluminal coronary angioplasty and their possible mechanism. J Am Coll Cardiol 30:452, 1997. American
College of Cardiology, by permission.)

CORONARY SPASM, UNSTABLE leads or two or more anatomically contiguous

ANGINA PECTORIS, NON-Q WAVE MI
Acute injury pattern is the diagnostic marker of
coronary spasm, and the lead distribution of ST
segment deviation during coronary spasm is the
same as during myocardial ischemia caused by
other types of coronary occlusion (Figure 7–29).
ST segment elevation has been reported also in
patients with syndrome X, normal coronary
angiograms, and suspected spasm of coronary
arterioles.77 In the presence of unstable angina
pectoris78 and non-Q wave MI,79 an acute injury
pattern is present in a small number of patients.
Other ECG changes accompanying these condi-
tions are discussed in Chapters 8 and 9.
ST SEGMENT CHANGES AS A GUIDE
TO THROMBOLYTIC THERAPY
The ECG plays a crucial role in identifying can-
didates for thrombolytic treatment.80 The indica-
tion for emergent thrombolytic therapy of
suspected acute MI is based on the presence of
ST segment elevation of >0.1 mV in two limb
precordial leads. In the cases of preexisting
ST segment elevation, such as with left bundle
branch block (LBBB), the same rule applies
when the availability of the basic pattern allows
recognition of the ST shift.81 Regression of ST
segment elevation parallels recanalization,82–84
and incomplete resolution of ST segment eleva-
tion is a powerful independent predictor of early
mortality.85–88
Reelevation of the ST segment is a sign of
limited myocardial salvage and suggests ex-
tensive myocardial damage.89–93 In some cases,
in the presence of anterior ischemia, a transient
increase in ST segment elevation (attributed to
adenosine release) preceding and following the
decrease during the first hour has no adverse
consequences.94,95 The magnitude of ST segment
elevation, measured as a sum of the ST shift
voltages, is related to the severity of myocardial
ischemia and not to the size of the area at risk.96
Depression of the ST segment may be recipro-
cal or indicative of additional (presumably sub-
endocardial) ischemia. Shah et al.97 evaluated

Figure 7–27 Superposition of the ECG before and during occlusion of the left anterior descending coronary artery in a
patient whose ECG is shown in Figure 7–20. Note the increased QRS duration during occlusion in leads V1 and V2 but
not in V6. (From Surawicz B, Orr CM, Hermiller JB, et al: QRS changes during percutaneous transluminal coronary
angioplasty and their possible mechanism. J Am Coll Cardiol 30:452, 1997. American College of Cardiology, by permission.)

Figure 7–28 Example of an electrocardiogram (leads
V1–V3) simulating the pattern of Brugada syndrome in a
61-year-old man after surgical replacement of the aortic
valve and a coronary bypass for a 60 percent obstruction
of the left main coronary artery.
the prognostic significance of the resolution of
ST segment depression in patients with acute
MI after thrombolytic treatment. They compared
patients with ST segment depression resol-
ving simultaneously with ST segment elevation
(simultaneous group) and patients with ST seg-
ment depression persisting after ST segment
elevation resolution (independent group). The
in-hospital mortality was significantly higher in
the independent group than in the simultaneous
group or a control group without ST segment
depression.
ST SEGMENT SHIFT DURING
PERCUTANEOUS CORONARY
ANGIOPLASTY
Balloon occlusion of the coronary artery during
angioplasty lasts usually 1.5 to 3.0 minutes. The
behavior of the ST segment during percutaneous
transluminal coronary angioplasty (PTCA) is the
same as during spontaneous myocardial ischemia,
but the magnitude of the ST segment elevation
expressed in percent of QRS amplitude tends to
be smaller. Among patients with acute MI treated
with direct angioplasty, there was a rapid decrease
of ST segment elevation in those with myocardial
reperfusion but not in those with a no-reflow
phenomenon.98
Also, the average number of leads with ST seg-
ment elevation and those with reciprocal
ST segment depression tends to be smaller during
7  Acute Ischemia: Electrocardiographic Patterns 143
PTCA than during acute ischemia. The maximal
ST segment elevation during balloon occlusion
of the LAD coronary artery is located in lead V2,
V3, or V4 (see Figure 7–30) and, during occlusion
of the RCA, in lead III. During occlusion of the
diagonal branch of the LAD coronary artery, max-
imal ST segment elevation may be located in lead
aVL. The results of occlusion of the left circumflex
coronary artery vary. In about one third of cases,
an ST segment shift in the standard 12-lead ECG
is absent; in another third, ST segment elevation
is present in one or more standard leads; and in
the remaining third of cases there is ST segment
depression in leads V2 and V3, which is believed
to represent a reciprocal change of STsegment ele-
vation localized in the back.99 The localization of
the ST segment elevation predicts the site of the
future loss of QRS voltage.100
In theory, an absence of ST segment displace-
ment at the site of presumed acute injury may be
due to cancellation by contralateral ST segment
displacement in an opposite direction; but in
practice such a mechanism is difficult to verify.
The nonhomogeneous intensity of ischemia
detracts from the accuracy of locating the site
of ischemia. Thus it has been shown that balloon
occlusion of the partially stenotic LAD coronary
artery caused reversible ST segment elevation in
the left precordial leads when the collateral cir-
culation was poor or absent. The same proce-
dure in similar patients with good collateral
circulation produced ST segment depression in
the same leads.101,102 Studies during coronary
artery angioplasty showed that the site of
impaired perfusion could be identified with
greater accuracy using a larger array of precor-
dial leads.102 For instance, ST segment elevation
in the left axillary and back leads was specific for
occlusions of the left circumflex and diagonal
branches. ST segment elevation in lead V3R was
present in 82 percent of cases with an occluded
right coronary artery.103
Kornreich et al.102 used 120 leads to con-
struct a body surface potential map in 131
patients with acute MI. They found that the most
abnormal ST segment elevations and depressions
at each MI location were localized in leads out-
side the standard precordial lead positions. This
study supports the prevailing notion that a larger
number of electrodes, such as are employed dur-
ing mapping of the torso, can improve the diag-
nostic accuracy of the ECG.
It has been shown that ST segment behavior has
a predictive value in patients with acute first ante-
rior MIs caused by an LAD coronary artery lesion
treated with rapid reperfusion by angioplasty.
Kobayashi et al.104 found that recovery of LV
144 SECTION I  Adult Electrocardiography

Figure 7–29 Variant angina. Patient had severe coronary artery disease involving all three major vessels, especially the
anterior descending branch, as demonstrated by coronary arteriogram. A, Tracing recorded during angina at rest. B, Tracing
recorded 20 minutes later, after the pain had subsided. The latter tracing is representative of the patient’s baseline ECG. Dur-
ing angina (A), marked ST segment elevation is present in leads II, III, aVL, and V1–V6 with reciprocal ST segment depression
seen in leads aVR and aVL. There is also an increase in the amplitude of the R wave in leads II, III, and aVF, with disappear-
ance of the S waves in leads showing marked ST segment elevation. The resulting complexes resemble the monophasic trans-
membrane potential. Many similar episodes were observed in this patient.

PERSISTENT ST SEGMENT ELEVATION

systolic function was better in patients in whom
ST segment elevation resolved than in those in
whom it did not. Santoro et al.105 found that
reduction in the ST segment elevation after direct
coronary angioplasty was the only independent
predictor of LV function recovery. Microvascular
injury has been suspected to be the cause of persis-
tent ST segment elevation after primary angio-
plasty for acute MI.106,107 (Also see Chapter 8.)
AFTER MI
After healing of the MI, ST segment elevation
persists in about 60 percent of patients with an
anterior infarction (Figure 7–31) and in about
5 percent of patients with an inferior MI.108
Persistent ST segment elevation correlates with
the presence of asynergy.21 It has been shown that
ST segment elevation developed during balloon
 7  Acute Ischemia: Electrocardiographic Patterns 145

Figure 7–30 ECG leads V1–V6 before (left) and during (right) balloon occlusion of the left anterior descending coronary
artery at midlevel. The maximal ST segment shift and maximal S amplitude decrease (percent of baseline value) are in lead
V4. (From Surawicz B, Orr CM, Hermiller JB, et al: QRS changes during percutaneous transluminal coronary angioplasty and
their possible mechanisms. J Am Coll Cardiol 30:452, 1997. American College of Cardiology, by permission.)

with and without persistent ST segment elevation

TABLE 7–1 Conditions Associated with
RSR0 Pattern and ST
Segment Elevation in the
Right Precordial Leads
Brugada syndrome (types 1 to 3)
Arrhythmogenic right ventricular dysplasia
Southeast Asian males at risk of sudden cardiac
death
Ischemia or infarction of the right ventricle
Anteroseptal ischemia or infarction
Pulmonary embolism
Hyperkalemia
Unexplained, not at risk of sudden cardiac death
inflation coincident with the new appearance of
hypocontractility in a region of previously normal
motion109 and that there was a close association
between the magnitude and extent of ST segment
elevation and the extent of asynergy.110 The most
sensitive marker for anterior wall hypocontracti-
lity was ST segment elevation in lead V2; for infe-
rior wall hypocontractility, the most sensitive
marker was ST segment elevation in lead III.
The widely held notion that persistent ST seg-
ment elevation is a marker of a ventricular aneu-
rysm has not been supported by recent studies.
Radionuclide imaging has shown similar global
and regional wall motion abnormalities in patients
after MI.111 If the aneurysm is defined as a “full-
thickness scar that exhibits a localized convex pro-
trusion during both phases of the cardiac cycle,”
two-dimensional echocardiography shows that
the persistent ST segment elevation correlates with
dyskinesia rather than with an aneurysm.112
The well-established relation between persis-
tent ST segment elevation and the paradoxical
motion of LV myocardium112 suggests that stretch
may play a role in the process, but the mechanism
by which stretch might cause ST segment dis-
placement has not been elucidated. The study of
Toyofuku et al.113 supports the hypothesis that
stretch can cause ST segment elevation in the
absence of ischemia. These investigators reported
that in patients with arrhythmogenic right ven-
tricular dysplasia (ARVD) who had no coronary
artery disease, ST segment elevation was induced
by exercise. In their study, significant ST segment
elevation in the right precordial leads developed
in 11 of 17 (65 percent) patients with severe RV
asynergy; the finding proved to be helpful for
diagnosing ARVD noninvasively.
The results of aneurysmectomy have not
helped to locate the site of abnormal potential dif-
ferences. In one study of 74 ECGs with ST seg-
ment elevation before aneurysmectomy, the
pattern remained unchanged in 60.8 percent,
improved in 25.7 percent, and became more
146 SECTION I  Adult Electrocardiography
Figure 7–31 ECG of an 84-year-old woman with a left ventricular aneurysm, a massive anterior myocardial infarction,
5 years after onset. Present are atrial fibrillation, low voltage in the limb leads, intraventricular conduction disturbance sug-
gestive of periinfarction block, and persistent ST segment elevation in leads V2–V6.
pronounced in 13.5 percent of the cases after
aneurysmectomy. The average ST segment ampli-
tude after aneurysmectomy in several studies
was reduced by only one fourth114 (Figure 7–
32). Engel et al.114 found that after an encircling
endocardial ventriculotomy the ST segment eleva-
tion was unchanged, suggesting that the ST seg-
ment elevation did not originate in the injured
tissue adjacent to the aneurysm. The authors
admitted to the possibility, however, that the
encircling procedure could have created new
zones of injury.
RECOGNITION AND SIGNIFICANCE
OF RECIPROCAL ST CHANGES
WITH ACUTE MI
Depression of the ST segment in the presence of
ST segment elevation can be a result of the pro-
cess that caused the injury current responsible
for ST segment elevation. Alternatively, it may
be a marker of an independent additional area
of injury in another location.
It has been shown that a subendocardial
lesion associated with ST segment elevation in
subendocardial electrograms causes a reciprocal
ST segment depression in the epicardial electro-
grams, so long as a layer of nonischemic epicar-
dial muscle is present. However, when ischemia
becomes transmural, ST segment elevation
occurs in the epicardial electrograms. During
acute ischemia, reciprocal ST segment depres-
sion is present in all patients with an inferior
MI (see Figure 7–9) and in 70 percent of patients
with an anterior MI (see Figures 7–7 and 7–10).
When the magnitude of the ST segment elevation
is small because the overall amplitude of the
complex is low, reciprocal ST segment depres-
sion may be more conspicuous than the culprit
ST segment elevation (Figure 7–33).
Echocardiographic studies showed that recip-
rocal ST segment depression did not correlate
with remote wall changes, a finding compatible
with a truly reciprocal change; but this finding
has not been universally confirmed. Thus
nuclear imaging suggests that reciprocal ST seg-
ment change indicates an additional region of
remote ischemia.115 Moreover, angiographic
studies performed within 2 weeks of an acute
MI in 84 patients with inferior MI showed that
patients with anterolateral ST segment depres-
sion had larger infarcts and a higher incidence
of multivessel disease.108 In the same study, the
absence of reciprocal ST segment depression
“virtually precluded multivessel disease.” Also,
among patients with anterior infarction, ST seg-
ment depression in inferior leads occurred in
45 percent and was associated with more exten-
sive infarction, increased morbidity, and a higher
incidence of multivessel coronary disease.116
During the evolution of an inferior wall
infarction associated with ST segment elevation
in lead III, an absent or a disproportionately
small reciprocal ST segment elevation in leads
V1 and V2 was suggestive of an associated infarc-
tion of the right ventricle117 (see Figures 7–9
and 7–16). The same principle was shown to
be applicable when an anterior MI caused by
 7  Acute Ischemia: Electrocardiographic Patterns 147

Figure 7–32 ECG of a 50-year-old man with akinesis of the anterior wall, apex, and inferior wall; hypokinesis of the
lateral wall; and a left ventricular ejection fraction of 20 percent before (A) and after (B) aneurysmectomy. A, Note the absent
r waves and elevated ST segment in leads I, aVL, and V2–V6. B, Note regression of the ST segment elevation and reappear-
ance of r waves in leads V2–V4.

occlusion of the LAD coronary artery was
accompanied by ischemia of the inferior wall.117
The latter was caused by continuation of the
occluded LAD coronary artery beyond the apex
of the heart onto the inferior wall of the left ven-
tricle or by the LAD coronary artery supplying
collaterals to the previously infarcted inferior
wall. Under such circumstances, ST segment ele-
vation in the anterior precordial leads was asso-
ciated with attenuation or reversal of the
reciprocal ST segment depression in the “infe-
rior” leads.118 In patients with acute MI, the sen-
sitivity of MI detection increases significantly by
co-existence of ST-segment elevation and recip-
rocal depression in the 12-lead ECG.118a
ABSENCE OF THE EXPECTED
RECIPROCAL ST SEGMENT DEVIATION
In the presence of the three common types of
Q wave MI (anterior, lateral, inferior), ST seg-
ment elevation is usually associated with recip-
rocal ST depression in one or more of the
standard 12 leads. In the presence of posterior
or anterior subendocardial MI, the acute injury
pattern is manifested by ST segment depression
148 SECTION I  Adult Electrocardiography
Figure 7–33 Low-amplitude ST segment elevation in low-amplitude complexes in leads III and aVF compared with more
conspicuous reciprocal ST segment depression in leads V1–V4. ECG of a 45-year-old man with an inferior myocardial infarc-
tion attributed to occlusion of the proximal left circumflex coronary artery. Left ventricular ejection fraction was 45 percent.
in one or more of the standard leads. The recip-
rocal ST segment elevation may be present only
in the back in the case of subendocardial infarc-
tion and may be difficult to detect in the anterior
leads in the case of posterior infarction because
of the low amplitude of the ST segment deviation
caused by the remote location of the infarction.
The apparent lack of expected reciprocal
ST segment depression in the presence of ST seg-
ment elevation in one or more standard precor-
dial leads may be attributed to one or more of
the following factors:
1. Failure to examine leads aVR and V1, which
are probably relatively close to the postero-
basal part of the left ventricle. These leads
are often less carefully examined than the
other 10 leads, and so the differences
between normal and abnormal patterns in
these leads may be less recognizable.
2. Difficulty of recognizing it owing to the
low amplitude of the ventricular complex
in the leads with expected ST segment
deviation (Figure 7–34).
3. Obfuscation by secondary ST segment
deviations caused by intraventricular con-
duction disturbance or ventricular hyper-
trophy. A common cause is wide terminal
QRS deflection in the presence of incom-
plete or complete RBBB.
4. Coexistence of acute anterior and inferior
injury patterns (Figure 7–35).
5. Diffuse ST segment elevation during the
early stage of anterior infarction with tran-
sient extension of the ST segment elevation
into the territory facing the inferior leads.
6. Associated pericarditis (Figures 7–36 and
7–37). It has been suggested119 that the
disappearance of the reciprocal ST segment
depression or appearance of the ST seg-
ment elevation in the leads with previous
ST segment depression in some cases facil-
itates the diagnosis of infarction-related
pericarditis.
ST SEGMENT ELEVATION: NORMAL
VARIANT AND ACUTE PERICARDITIS
In some young men after onset of puberty an
excessive ST segment elevation occurs as a nor-
mal variant. Mehta et al.120 described this pat-
tern as an elevated concave ST segment, located
commonly in the precordial leads (most conspic-
uously in leads V1–V3) with reciprocal ST seg-
ment depression in lead aVR. The pattern is
often associated with tall peaked T waves, a slur
on the R wave, vertical electrical axis in the fron-
tal plane, and sinus bradycardia.120 The inci-
dence decreases with advancing age. A review
of the literature suggests that, contrary to the
anecdotal reports, the pattern is equally common
in all races.120
The term “early or premature repolarization,”
which is not clearly distinguishable from the
normal male pattern, is frequently applied to
this pattern.121,122 The prematurity implies that
the ST segment shift is attributed to shortening
of ventricular action potentials in some epicar-
dial regions. Rapid early repolarization in these
regions may be expected to produce potential
differences, resulting in a current similar to the
injury current. Consequently, in partial support
of this theory are the observations that exer-
cise123 and isoproterenol abolish the ST segment
elevation, presumably as a result of diminished
 7  Acute Ischemia: Electrocardiographic Patterns 149

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

Figure 7–34 ECG of a 44-year-old woman with acute inferior myocardial infarction and low-voltage ECG. Note that both
the ST segment elevation in leads II, III, and aVF and the reciprocal ST segment depression in leads V1–V4 are approximately
of the same amplitude, in proportion to the QRS amplitude.

Figure 7–35 Absent reciprocal ST depression in the ECG of a 54-year-old man with recent anterior and inferior
myocardial infarction and aneurysmal dilatation of the middle and apical portions of the septum and apical portions of
the inferoanterior and lateral walls of the left ventricle. Estimated left ventricular ejection fraction was 15 percent.

difference between ventricular action poten-
tial durations. However, mapping studies have
not substantiated the rationale for the term
“early repolarization,” because in normal young
volunteers the overlap between the onset of ven-
tricular repolarization and the end of QRS
(which ranged from 4 to 16 ms) did not corre-
late significantly with the ST segment deviation
in the precordial leads.124
The pattern of “early repolarization” (or nor-
mal “male” pattern) may simulate the changes
of acute pericarditis, possibly because they may
be caused by a similar mechanism. In both,
inscription of the ST segment begins before
QRS forces have returned to baseline,122,125 but
the ST segment elevation in pericarditis is
usually present in both limb and precordial
leads. In contrast, ST segment elevation in the
“normal variant” is confined more frequently to
the precordial lead123,126 (see Figure 1–13).
Moreover, the T wave amplitude in the left
precordial leads tends to be greater in persons
with “normal variant” than in those with acute
pericarditis.126 In practice, however, the
distinction between these two patterns may be
difficult.
Persistent multilead ST segment elevation is
present in patients with spinal cord injury at
the C5 to C6 levels (i.e., lesions that completely
disrupt cardiac sympathetic influences).127
These changes were reversed by low doses of
infused isoproterenol. Although the mechanism
150 SECTION I  Adult Electrocardiography

Figure 7–36 ECG of a 72-year-old man 2 days after acute anterior myocardial infarction caused by occlusion of the left
anterior descending (LAD) artery at midlevel with associated pericarditis as evidenced by pericardial friction rub. Both prox-
imal LAD and right coronary arteries were diseased but without critical stenoses. ST segment is elevated in all leads except
V1 and aVR; in the latter the ST segment is depressed.

Figure 7–37 ECG of an 82-year-old woman recorded 2 days after the onset of anterolateral myocardial infarction docu-
mented by echocardiogram, which also showed a ventricular septal defect with a large left-to-right shunt and a small peri-
cardial effusion. Patient died the next day. ST segment is elevated in leads I, II, III, aVL, aVF, and V1–V6; it was depressed in
lead aVR.

of ST segment elevation in these patients has not T WAVE CHANGES (HYPERACUTE

been clarified, the findings demonstrate that nor-
mal sympathetic tone modulates the course or
sequence (or both) of ventricular repolarization.
ST SEGMENT ELEVATION: OTHER
CAUSES
Table 7–2 lists additional causes of ST segment
elevation encountered less frequently than the
conditions discussed previously.
T WAVE PATTERN)
Pointed tall or deeply negative “coronary” Twaves
associated with a prolonged QT interval may
appear either before or after primary ST segment
elevation has begun to subside (Figure 7–39A).
These T wave abnormalities are attributed to pro-
longation of activity in the ischemic regions of the
ventricle.2,141 In some cases the increase in Twave
amplitude may be modest and not easily recog-
nized.142 In the presence of posterior infarction,
 7  Acute Ischemia: Electrocardiographic Patterns 151

TABLE 7–2 Less Common Causes of ST Segment Elevation

Pulmonary embolism and acute cor pulmonale (usually lead III)

Cardiac tumor
Acute aortic dissection128
After mitral valvuloplasty129
Pancreatitis and gallbladder disease130–132 and other catastrophic illnesses133
Myocarditis133,134 (Figure 7–38)
Septic shock
Anaphylactic reaction135
J wave
Hyperkalemia (“dialyzable” current of injury)
With any marked QRS widening (e.g., antidepressant drug overdose136 or class IC antiarrhythmia drugs137,138)
After transthoracic cardioversion139
Following implantable cardioverter defibrillator shocks140

Figure 7–38 Acute injury pattern on the ECG of a 35-year-old man with presumed acute myocarditis presenting as the
first manifestation of previously undetected human immunodeficiency virus (HIV) infection. Elevated levels of cardiac
enzymes on admission suggested the diagnosis of myocardial infarction, but the patient had normal coronary arteries and
no pericardial effusion. The ECG returned to normal within 5 days.

tall upright T waves in the precordial leads are U WAVE

similar to the “hyperacute” T waves seen during
acute anterior ischemia (Figure 7–39B) but usu-
ally are less transient.
QT INTERVAL
During acute myocardial ischemia the QT
interval may shorten, lengthen, or remain
unchanged25 (Figure 7–40). It has been reported
that prolonged QT within the first few hours of
symptoms predicts primary cardiac arrest in
patients with acute MI.143
During acute myocardial ischemia the U wave
may become inverted or increase in amplitude.
The former occurs more often. Transient U
wave inversion, however, may be caused not
only by regional myocardial ischemia but also
by an elevation of blood pressure.144,145 It has
been observed that during acute ischemia the
inverted portion of the U wave appears late;
that is, the U wave is positive-negative, whereas
the U wave related to elevated blood pressure is
negative-positive.146
152 SECTION I  Adult Electrocardiography

Figure 7–39 Two examples of tall T waves exceeding 1 mV in amplitude. A, Hyperacute stage of anterior myocardial
infarction in a 63-year-old man with an occluded left anterior descending (LAD) coronary artery recorded during
the course of thrombolytic therapy. B, Acute inferior and posterolateral myocardial infarction in an 82-year-old man
with an occluded dominant right coronary artery, 90 percent stenosis of the mid-LAD artery, and absent collateral
circulation.

Figure 7–40 Variable QTc values during acute ischemia. A, Normal QT and QTc (344 and 418 ms, respectively) on an
ECG of a 42-year-old man with acute inferior infarction caused by occlusion of the right coronary artery. B, Prolonged
QT and QTc (394 and 451 ms, respectively) in a 49-year-old man with acute inferior infarction caused by occlusion of a
large right posterolateral branch of the right coronary artery.
 7  Acute Ischemia: Electrocardiographic Patterns 153

The reports of U wave inversion during ische-
mia stem mostly from the observations during
exercise or coronary spasm, whereas U wave
inversion is seldom observed during PTCA or
with spontaneous myocardial ischemia. Correla-
tion with myocardial imaging showed that dur-
ing exercise a negative U wave in the anterior
precordial leads was both sensitive and specific
for myocardial ischemia of the anterior wall,
whereas a negative U wave in the inferior leads
was specific but not sensitive for acute ischemia
of the inferior wall.147
Increased U wave amplitude in the precordial
leads is observed occasionally during spontane-
ous myocardial ischemia or during exercise-
induced ischemia (see Chapter 10). It is believed
to be a specific although not a sensitive marker
of significant narrowing of the left circumflex
or right coronary artery.148 It is probably caused
by increased compensatory wall motion of the
nonischemic myocardium and increased sympa-
thetic stimulation.
REVERSIBLE QRS CHANGES
The QRS changes during acute myocardial ische-
mia can be caused by: (1) ischemia of the con-
ducting system; (2) impaired conduction in the
ischemic myocardium; and (3) passive shift of
the QRS deflections resulting from shift of the
ST and TP segments. Bundle branch blocks and
fascicular blocks may follow occlusion of the
LAD coronary artery proximal to the first septal
perforator, or after occlusion of an artery supply-
ing collaterals to the myocardium supplied by
the previously occluded proximal LAD coronary
artery. These conduction disturbances are dis-
cussed in Chapters 4–6.
Elevation of the ST segment and decreased high-
frequency components in the signal-averaged
ECG149 are frequently associated with decreased
amplitude or disappearance of the S wave in the
precordial leads (see Figures 7–8, 7–10, 7–11, and
7–41). Other changes may include the appearance
or disappearance of the Q wave (Figure 7–42)
and an increase in the R wave amplitude150
(see Figure 7–41). In the leads with reciprocal
ST segment depression, the S wave amplitude
may increase and the R wave amplitude may
decrease. These changes take place without
changes in the QRS duration and are assumed
to represent passive shifts of the QRS deflec-
tion. The term “periischemic block” app-
lies to transient QRS changes associated
with increased QRS duration.28,151 Such
changes occur less often than changes in QRS

Figure 7–41 Transient appearance of a Q wave associated with an ST segment shift during acute ischemia. Four precor-
dial ECG leads of an 80-year-old man with obstructive disease of the left anterior descending (LAD) coronary artery. The
patient was admitted on day 1 (A) with a diagnosis of unstable angina pectoris and abnormal T waves. B, ECG recorded
on day 2 after abrupt closure of an intracoronary stent inserted during coronary angioplasty at the midlevel of the LAD artery.
C, ECG recorded on day 3 after an emergent coronary artery bypass graft. Note in B the transient appearance of a Q wave, an
increase in R wave amplitude in lead V2, and disappearance of the S wave in leads V2 and V3. Compared with the ECG in A,
there is a marked decrease of R wave amplitude in all leads in C. (From Surawicz B: Reversible QRS changes during acute
myocardial ischemia. J Electrocardiol 31:209, 1998, by permission.)
154 SECTION I  Adult Electrocardiography

Figure 7–42 Transient disappearance of a QS wave associated with an ST segment shift during acute myocardial
ischemia. Selected ECG leads from a 61-year-old woman with a remote inferior myocardial infarction, obstruction of the
dominant right coronary artery at midlevel, and nonobstructive disease of the left anterior descending and left circumflex
coronary arteries. She was admitted after a new onset of angina pectoris and treated with percutaneous transluminal coro-
nary angioplasty (PTCA) of the right coronary artery. A, Before admission on 8/17/95. B, Before PTCA on 11/3/95 at
10:47 AM. C, After PTCA on 11/4/95 at 5:58 AM. Note the disappearance of the Q wave in lead III associated with the ST seg-
ment shift. The QRS patterns before (A) and after (C) development of an acute injury pattern are similar. (From Surawicz B:
Reversible QRS changes during acute myocardial ischemia. J Electrocardiol 31:209, 1998, by permission.)

configuration caused by a passive ST segment increased R amplitude in 9, decreased R ampli-

shift and sometimes are more pronounced in
selected leads (e.g., V1, V2, III, aVF) than in
the remaining ECG leads (see Figure 7–23).
In a study by Surawicz,150 reversible QRS
changes encountered in 29 patients with acute
MI included new Q waves in 3 cases, decreased
Q wave amplitude in 2 cases, QS change to qRS
or qR in 6, disappearance of QS or Q in 4,
tude in 6, decreased S amplitude by more than
75 percent in 18, and increased QRS duration
in 4. Reversible changes of the initial QRS por-
tion were present in 24 of 29 patients, and those
of the terminal QRS portion occurred in all
patients.
It has been reported that in patients with acute
anterior infarction, distortion of the terminal QRS

Figure 7–43 Portion of the ECG of a 58-year-old man with an acute anterior myocardial infarction attributed to occlusion
of the left anterior descending artery after thrombolytic therapy. Rhythm strip in lead II shows an onset of accelerated ven-
tricular rhythm with retrograde conduction to the atria.
 7  Acute Ischemia: Electrocardiographic Patterns 155

Figure 7–44 Variant angina in a 60-year-old woman with recurrent angina at rest. A, Tracing was recorded during one of
the episodes, revealing ST segment elevation in leads II, III, and aVF, with reciprocal ST segment depression in leads I, aVL,
V2, and V3. B, A few minutes later. Note the appearance of premature ventricular complexes and the development of ven-
tricular tachycardia and fibrillation.

portion on admission predicts a high mortality
rate152 and a greater incidence of reflow impair-
ment after emergency coronary angioplasty.153 In
another study, terminal QRS distortion on admis-
sion was a better predictor of final infarct size
than ST segment measurements.154
VENTRICULAR ARRHYTHMIAS
DURING ACUTE ISCHEMIA
Harris155 showed that one-stage occlusion of the
coronary artery in dogs caused ventricular fibril-
lation in 30 to 50 percent of the animals.
Arrhythmias did not occur, however, when the
occlusion was performed in two stages: first nar-
rowing the vessel, and then closing it after 30
minutes. These observations may be pertinent
to the current concept of ischemic precondition-
ing, which postulates that repetitive attacks of
angina pectoris diminish the severity of myocar-
dial ischemia following coronary occlusion.
Elevation of the ST segment is frequently
associated with the appearance of premature
ventricular contractions (PVCs), which may pre-
cipitate a sudden onset of ventricular fibrillation
(VF) typically displaying the R-on-T phenome-
non. These arrhythmias are sometimes called
“occlusion arrhythmias.” It is of interest that
the “primary VF” during acute ischemia tends
to be a unique, isolated event that rarely recurs
after successful defibrillation and regression of
the acute injury ECG pattern. In a large group
of hospitalized patients with acute MI, the inci-
dence of recurrent VF was 2.4 percent.