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ECG Discrimination Between Right and Left

Circumflex Coronary Arterial Occlusion in


Patients With Acute Inferior Myocardial
Infarction *
Radhakrishnan Nair and D. Luke Glancy
Chest 2002;122;134-139
DOI 10.1378/chest.122.1.134

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ECG Discrimination Between Right and


Left Circumflex Coronary Arterial
Occlusion in Patients With Acute
Inferior Myocardial Infarction*
Value of Old Criteria and Use of Lead aVR
Radhakrishnan Nair, MD; and D. Luke Glancy, MD

Study objectives: Prior studies have proposed several ECG criteria for identifying the culprit
artery in patients with acute inferior myocardial infarction (MI). We applied each criterion to our
patients to assess its utility. In doing so, we discovered a previously unreported, but highly useful,
criterion utilizing lead aVR.
Study design: Retrospective review.
Patients: Thirty consecutive patients with symptoms of acute MI, ST-segment elevation in the
inferior ECG leads, an appropriate rise and fall of creatine kinase and troponin I levels, and
coronary arteriography within 7 days of the onset of symptoms.
Measurements: The ECG recorded within 24 h of the onset of symptoms that had the most
prominent ST-segment changes was analyzed. In the 12 standard leads and in lead V4R,
ST-segment elevation or depression was measured 0.06 s after the J point.
Results: Four previously described criteria were useful in identifying the right coronary artery
(RCA) or the left circumflex coronary artery (LCX) as the culprit: ST-segment elevation in lead I,
ST-segment more or less elevated in lead II than in lead III, ST-segment elevation > 0.5 mm in
lead V4R, and various combinations of ST-segment elevation or depression in leads V1 and V2. A
new criterion was found to be at least as useful as any previously described: the presence and
amount of ST-segment depression in lead aVR.
Conclusions: At least five different ST-segment criteria help to identify the RCA or the LCX as the
culprit artery in patients with acute inferior MI. One of these, the amount of ST-segment
depression in lead aVR, has not been reported previously and needs validation in a larger study.
(CHEST 2002; 122:134 139)
Key words: coronary angiography; coronary occlusion; coronary thrombosis; ECG; myocardial infarction, acute, inferior
Abbreviations: LAD left anterior descending coronary artery; LCX left circumflex coronary artery;
MI myocardial infarction; RCA right coronary artery

anterior myocardial infarction (MI), the


W ithocclusion
is nearly always in the left anterior
descending coronary artery (LAD). With inferior
MI, however, either the right coronary artery (RCA)
or the left circumflex coronary artery (LCX) may
contain the culprit lesion, and mortality and morbidity in part are determined by the location of the
occlusion.1,2 For example, in patients with inferior
*From the Section of Cardiology, Department of Medicine,
Louisiana State University Health Sciences Center and the
Medical Center of Louisiana, New Orleans, LA.
Manuscript received July 24, 2001; revision accepted December
13, 2001.
Correspondence to: D. Luke Glancy, MD, Louisiana State University Health Sciences Center, 1542 Tulane Ave, Room 441, New
Orleans, LA 70112; e-mail: bkuss@lsuhsc.edu

MI who have right ventricular infarction, the culprit


artery virtually always is the RCA.3 Such patients,
including those in whom ECG evidence of right
ventricular MI is masked,4 are at increased risk for
death,5,6 shock,4 6 and arrhythmias,57 including
atrioventricular block. Thus, identifying the culprit
artery in acute inferior MI helps define those in
whom aggressive reperfusion strategies are likely to
yield the most benefit.
Coronary arteriography is the best means of determining the culprit artery in acute inferior MI.
When both the RCA and LCX are severely diseased,
however, deciding which is the culprit can be difficult, and we have seen several examples of angioplasty being performed on a chronic lesion while the
acute occlusion was ignored. In such circumstances,

134

Clinical Investigations

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having an independent predictor of the culprit artery, such as the ECG, can be very helpful.
Several studies2,3,8 15 have proposed ECG criteria
to aid in identifying the culprit artery in acute
inferior MI. The purpose of this study has been to
apply these various criteria to the ECGs of our
patients with acute inferior MI to determine which
of them have utility. In addition, we describe a
previously unreported ECG criterion that we have
found useful in identifying the artery containing the
culprit lesion.
Materials and Methods
Thirty consecutive patients at the Medical Center of Louisiana
who had symptoms compatible with acute MI, ST-segment
elevation in the inferior ECG leads, an appropriate rise and fall
of creatine kinase and troponin I levels, and coronary arteriography within 7 days of the onset of symptoms were included in
the study. Exclusion criteria were bundle-branch block, prior
Q-wave MI, prior coronary artery bypass graft operation, and
inability to identify the culprit lesion (in two patients, one of
whom had normal coronary arteriographic findings). A lesion was
considered to be the culprit when it occluded or severely
narrowed the artery and was ulcerated and/or contained thrombus. In each of the 30 patients included in the study, the authors
and the arteriographers who performed the study agreed independently on the culprit artery and lesion within that artery.
For each of the 30 patients, the ECG that was recorded within
24 h of the onset of symptoms and had the most prominent
ST-segment changes was chosen for analysis. In each of the 12
standard leads, and in V4R when it was recorded, ST-segment
elevation or depression was measured 0.06 s after the J point with
the aid of a handheld magnifying lens. Measurements were made
to the nearest 0.25 mm (0.025 millivolts). The TP segment of the
ECG was used as the isoelectric line unless tachycardia caused
fusion of the T and P waves, in which case the PR segment was
used. Previously proposed criteria for identifying the culprit were
then evaluated using our patients data, and a new criterion, the
amount of ST-segment depression in lead aVR, was tested.

Results
In 25 of 30 patients, the culprit lesion was in the
RCA while in 5 patients it was the LCX (Table 1). In
four of five patients with ST-segment depression
1.0 mm in lead aVR, the culprit lesion was in the
LCX. Conversely, the culprit lesion was in the RCA
in 24 of the 25 patients with ST-segment elevation
(2 RCA), an isoelectric ST segment (18 RCA), or
ST-segment depression 1.0 mm (4 RCA, 1 LCX)
in lead aVR.
ST-segment elevation in lead III exceeded that in
lead II in 26 patients, and 23 of them had an RCA
culprit lesion. In three patients, the LCX contained
the culprit. Of the three patients in whom STsegment elevation in lead II exceeded that in lead
III, the culprit lesion was in the LCX in two patients
and in the RCA in one patient. The RCA contained

Table 1ECG Correlation With Culprit Artery


ST-Segment Finding and
Lead
Elevated, isoelectric, or
depressed 1 mm aVR
Depression 1 mm aVR
Isoelectric or depressed I
Elevation I
Elevation III II
Elevation III II
Elevation II III
Elevation 0.5 mm V4R
Isoelectric or
elevated 0.5 mm V4R
Depression V4R
Elevation V1, depression V2
Elevation V1 V2
Isoelectric V1, depressed V2
Depression V1, V2
Other pattern V1, V2

Culprit Artery
RCA (n 25)

LCX (n 5)

24

1
25
0
23
1
1
12
2

4
2
3
3
0
2
0
2

0
3
8
6
3
5

2
0
0
0
5
0

the culprit lesion in the one patient in whom STsegment elevation in lead II equaled that in lead III.
Right-sided precordial leads were obtained in 18
patients. In each of the 12 with 0.5 mm STsegment elevation in V4R, the RCA contained the
culprit lesion. In two of the four patients with
0.5 mm ST-segment elevation or an isoelectric
ST-segment in V4R, the culprit lesion was in the
RCA, and in two patients it was in the LCX. Each of
the two patients with ST-segment depression in V4R
had the culprit lesion in the LCX.
When the ST-segment was depressed both in lead
V1 and V2, the culprit lesion was in the LCX in five
patients and in the RCA in three patients. With any
other pattern in leads V1 and V2, the culprit was in
the RCA (Table 1). ST-segment elevation in lead I
was found in only three patients, each of whom had
the culprit lesion in the LCX. Conversely, of 27
patients with an isoelectric (3 RCA) or depressed (22
RCA, 2 LCX) ST-segment in lead I, 25 patients had
the culprit lesion in the RCA.
ECG findings with features typical of RCA and
LCX occlusions are illustrated in Figures 1, 2, respectively. The sensitivities, specificities, and predictive values of the various ST-segment changes for
culprit lesions in the RCA and LCX are shown in
Table 2.
Discussion
Among our 30 patients with acute inferior MI, the
culprit lesion was in the RCA in 25 patients and in
the LCX in 5 patients, a ratio of 5:1. Ten other
studies of patients with acute inferior MI have found

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135

Figure 1. ECG showing changes of acute inferior MI due to proximal occlusion of the RCA:
ST-segment elevation lead III II; ST-segment elevation lead V1 with depression V2, strongly
suggesting both acute right ventricular and acute posterior injury; ST-segment elevation 0.5 mm in
lead V4R; ST-segment depression lead I; and ST-segment depression of 1.0 mm in lead aVR.

RCA to LCX ratios ranging from 2.2:1 to 7.0:1, and


averaging 3.9:1.2,3,8 15 Thus, the RCA is much more
likely than the LCX to contain the culprit lesion in
patients with acute inferior MI. Rarely, acute inferior
MI may result from occlusion of the recurrent LAD
branch,2,3 which is the terminal portion of a wraparound LAD, but this was not the case in any of our
patients. Occasional studies also have included a few
patients with normal coronary arteriographic findings2 and others in whom the culprit lesion could not
be identified.3 We excluded two such patients from
our study.
In addition to statistical probability, several ECG
criteria help identify the RCA or the LCX as the
artery containing the culprit lesion (Tables 1, 2).
Each of these criteria is based on one of two
anatomic facts. First, the myocardial distribution of
the RCA is slightly rightward in the frontal plane,
and consequently the current of injury resulting from
its occlusion will be reflected more in lead III than
lead II. Conversely the distribution of the LCX is
slightly leftward in the frontal plane, and the current
of injury from its closure will be seen more in lead II
than lead III. Similarly the current of injury with
RCA occlusion is more or less perpendicular to the
axis of lead aVR, whereas the current of injury
resulting from occlusion of the LCX has a mean

vector that forms an obtuse angle with the axis of


aVR. Therefore, significant ST-segment depression
in aVR is more likely to occur with LCX occlusion.
An injury vector leftward enough to cause STsegment elevation in lead I is common with LCX
occlusion, but rare with RCA occlusion.9
Second, the RCA provides almost all of the blood
supply to the right ventricle, which is anterior as well
as rightward. When the RCA is occluded proximal to
one or more of its major right ventricular branches,
ST-segment elevation is likely to be seen in lead
V4R.16 Similarly the ST segment in lead V1 (V2R)
may be elevated even when the more leftward
precordial leads show ST-segment depression due to
the posterior injury that so frequently accompanies
acute inferior MI, and Mak and colleagues17 have
drawn attention to this infrequent but highly specific
finding for right ventricular infarction due to RCA
occlusion. Evidence of acute right ventricular infarction is important, not only because it identifies the
RCA as harboring the culprit lesion, but especially
because it predicts a greatly increased morbidity and
mortality.4 7 Consequently, right precordial leads, or
at least a V4R lead, should be recorded in all patients
with acute inferior MI. ST-segment depression in V1
and V2 indicates posterior injury and is typical of
LCX occlusion. All 5 of our patients with LCX

136

Clinical Investigations

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Figure 2. ECG showing changes of acute inferior MI due to occlusion of the LCX distal to its first
obtuse marginal branch: ST-segment elevation in lead II III; ST-segment depression leads V1, V2
suggesting acute posterior injury; ST-segment depression lead V4R; ST-segment elevation in lead I; and
ST-segment depression 1.0 mm in lead aVR. This ECG shows features that also may be seen in
acute, diffuse pericarditis: ST-segment elevation in leads I, II, III, aVF, V4 through V6, and ST-segment
depression in leads aVR and V1. ST-segment depression in leads aVL through V2, and V3, however, is
not a feature of acute, diffuse pericarditis, but is typical of acute inferior MI due to occlusion of the
LCX distal to its first obtuse marginal branch.

occlusion had ST-segment depression in both V1 and


V2, but only 3 of our 25 patients with RCA occlusion
had this pattern. Any other ST-segment pattern in
leads V1,V2 identified the RCA as containing the
culprit lesion in each of 22 patients.
Unlike earlier studies,12,15 we did not find the ratio
of ST-segment depression in lead V2 or V3 to
ST-segment elevation in lead aVF or III to be helpful
in identifying the artery with the culprit lesion. We
did find, however, that quantifying ST-segment depression in lead aVR in our 30 patients distinguished

a culprit LCX ( 1 mm) from a culprit RCA


( 1 mm or no depression) as well or better than
other criteria. Because our study is small and because the amount of ST-segment depression in aVR
has not previously been used to identify the culprit
artery in patients with acute inferior MI, the true
usefulness of these new criteria need to be evaluated
in a larger study. One disadvantage of the aVR
criteria is that ST-segment changes in that lead are
rarely large, and distinguishing 1-mm depression
from lesser amounts may be difficult.

Table 2Utility of ECG Signs in Identifying the Culprit Artery*

ST-Segment Finding

Sensitivity, %

Specificity, %

Positive
Predictive
Value, %

96
100
96
86
88

80
60
40
100
100

96
93
89
100
100

80
100
67
67
63

80
60
40
100
100

96
100
96
86
88

80
100
67
67
63

96
93
89
100
100

RCA
aVR 1, 7, 2 1 mm
I 7, 2
1 III 1 II
1 V4R 0.5 mm
Not 2 V1, not 2 V2
LCX
2aVR 1 mm
1I
1II 1III
V4R 2, 7, 1 0.5 mm
2 V1, 2 V2

Negative
Predictive
Value, %

*1 elevated; 2 depressed; 7 isoelectric.


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137

Lead aVR usually has been ignored in ECG


diagnosis, but the Duke group and other eminent
electrocardiographers have made a rational case for
the increased use of the reciprocal of lead aVR
( aVR) in diagnosis.18 Goldberger19 long ago
pointed out the utility of an initial r or R wave in lead
aVR in distinguishing infarct-related from positional
Q waves in the inferior leads, and Menown and
Adgey20 found ST elevation in lead aVR predictive
of higher creatine kinase levels both in patients with
inferior and in those with lateral acute MI. Wellens
and Conover21 and Viik et al22 have found that ST
elevation in lead aVR or depression in aVR when
combined with ST-segment depression in other
leads indicates more severe subendocardial ischemia. Engelen et al23 reported ST-segment elevation
in lead aVR to be one of the predictors of LAD
occlusion proximal to the first septal perforator in
patients with acute anterior MI. Yamaji and associates24 found ST-segment elevation to occur more
frequently in lead aVR than any in other lead in
patients with acute left main coronary arterial obstruction, and they have been able to distinguish left
main from proximal LAD obstruction using the ratio
of ST elevation in aVR to that in lead V1. Lead aVR
also has been found useful in diagnosing acute
pulmonary embolism, and various ventricular and
supraventricular arrhythmias.25 From our current
findings, it appears that ST-segment change in aVR
also may have a role in distinguishing RCA from
LCX occlusion in patients with acute inferior MI.
Because the right arm is opposite the vector of the
subepicardial ventricular current of injury in acute,
diffuse pericarditis, ST-segment depression in lead
aVR not only is the rule, but is one of the ECG
criteria of acute, diffuse pericarditis. All of the ECGs
used in this study were recorded within 24 h of the
onset of symptoms, a time too early for the changes
of infarct-related regional pericarditis.26 Because the
ST-T changes in this entity usually mimic the ST-T
changes seen with the acute infarct several days
earlier, it is possible that such changes would be
different in RCA and LCX occlusions, but we have
no data to support or deny that hypothesis.
In conclusion, our study confirmed the utility of
four previously described parameters for identifying
the RCA or the LCX as containing the culprit lesion
in patients with acute inferior MI. The calculated
sensitivities, specificities, and predictive values were
similar to those previously reported.8,9,11,13,14 In addition, we found a previously unreported parameter,
the amount of ST-segment depression in lead aVR,
also to be an accurate predictor, an observation that
needs validation in a larger group of patients.

ACKNOWLEDGMENT: We thank Mrs. Brenda Kuss for her


assistance with this article.

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139

ECG Discrimination Between Right and Left Circumflex Coronary


Arterial Occlusion in Patients With Acute Inferior Myocardial Infarction
*
Radhakrishnan Nair and D. Luke Glancy
Chest 2002;122; 134-139
DOI 10.1378/chest.122.1.134
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