Electrocardiographic diagnosis of myocardial
infarction in the presence of bundle branch block
The classic electrocardiographic pattern of acute Q wave myocardial infarction
occurs in 50 to 75 percent of patients with the clinical diagnosis of
myocardial infarction (MI). (See
"Electrocardiogram in myocardial ischemia and infarction"
diagnosis of MI is more difficult in some cases because the baseline ECG shows
a bundle branch block pattern or bundle branch block may develop as a
complication of the infarct [1,2
RIGHT BUNDLE BRANCH BLOCK WITH MI
diagnosis of a Q wave MI can be made relatively easily in the presence of
right bundle branch block (RBBB). RBBB affects primarily the terminal phase of
ventricular depolarization, producing a wide R' wave in the right chest leads
and a wide S wave in the left chest leads (show
). These changes are due to delayed depolarization of the right
ventricle, while depolarization of the left ventricle is not affected. (See
"Basic approach to delayed intraventricular conduction"
a more detailed review, see
"Electrocardiographic interpretation of right bundle branch block"
MI usually involves the left ventricle and therefore affects the initial phase
of ventricular depolarization, sometimes producing abnormal Q waves. Thus,
these patterns are combined when complete RBBB and a Q wave infarct occur
• The QRS complex will be abnormally wide (0.12
sec or more) due to the bundle branch block.
• Lead V1 will show a terminal positive
• Lead V6 will show a terminal negative
deflection (wide S wave).
• If the infarction is anterior, there will be a
loss of R wave progression with abnormal Q waves in the anterior leads and
characteristic ST-T changes.
• If the infarction is inferior, Q waves will
appear in leads II, III and aVF.
The net effect is that the criteria for the diagnosis of a Q wave MI in a
patient with RBBB are the same as in patients with normal conduction.
RBBB is typically associated with secondary ST-T changes due to abnormal right
ventricular repolarization. As an example, leads with an R' wave (leads V1,
V2, and sometimes V3) will show T wave inversions. However, ST depressions or
T wave inversions in leads with a terminal S wave (leads V5 and V6) cannot be
attributed to the RBBB alone. Such primary ST-T changes may be due to ischemia,
or other factors such as drug effects or electrolyte abnormalities.
LEFT BUNDLE BRANCH BLOCK WITH MI
diagnosis of MI in the presence of left bundle branch block (LBBB) is
considerably more complicated and confusing than that of RBBB. The reason is
that LBBB alters both the early and the late phases of ventricular
depolarization and produces secondary ST-T changes (show
"Basic approach to delayed intraventricular conduction"
a more detailed review, see
"Electrocardiographic interpretation of left bundle branch block"
As a result, considerable attention has been directed to the problem of
diagnosing acute and chronic MI in patients with LBBB [1,2,3,4
There are issues that vary with the site of the infarct and there are changes
that are independent of the site of the infarct, such as the ST-T changes that
Left ventricular free wall infarction
Infarction of the left ventricular free (or lateral) wall ordinarily results
in abnormal Q waves in the midprecordial to lateral precordial leads (and
selected limb leads). However, the initial septal depolarization forces with
LBBB are directed from right to left. These leftward forces produce an initial
R wave in the mid- to lateral precordial leads, usually masking the loss of
potential (Q waves) caused by the infarction. Therefore, acute or chronic left
ventricular free wall infarction by itself will not usually produce diagnostic
Q waves in the presence of LBBB.
If, however, the loss of lateral force is sufficiently large, late rightward
forces generated by other portions of the left ventricle may predominate,
possibly resulting in S waves in I, aVL and V6. Thus, an anterolateral MI
should be suspected in the appropriate clinical setting if new S waves appear
in leftward leads in a patient with preexisting common LBBB. This is an old
concept that makes electrophysiologic and vectorcardiographic sense; however,
it requires further clinical validation.
！ The presence of
LBBB has a variable effect on the ECG changes that can occur with anteroseptal
MI. Perhaps most important, the leftward shift in the initial vector in LBBB
causes the loss of normal septal q waves in the left-right leads, I, aVL, and
V6. Furthermore, the leftward and posterior orientation of the initial vector
often results in a QS pattern in the anterior leads, V1 and sometimes in V2.
These changes can mask the presence of an anteroseptal MI.
There are, however, other changes that can occur that may suggest the presence
of an anteroseptal or septal MI. The infarct may cause the leftwardly directed
initial vector of LBBB to shift to the right, resulting in "pseudonormalization"
of the initial vector and the reappearance of q waves in I, aVL and V6. If
enough of the septum is infarcted, abnormal QR, QRS, or qrS types of complexes
may appear in the mid- to lateral precordial leads in conjunction with the
Free wall and septal infarction
！ Acute or
chronic infarction involving both the free wall and the septum may produce
abnormal Q waves (usually as part of the QRS, or QrS types of complexes) in
leads V4 to V6. These initial Q waves probably reflect posterior and superior
forces from the spared basal portion of the septum. Small q waves (0.03 sec or
less) may be seen in leads I and V5 to V6 with uncomplicated LBBB. Thus, wide
Q waves (0.04 sec) in one or more of these leads are a more reliable sign of
underlying infarction. As an example, wide Q waves (as part of QR complexes)
in V6, particularly with an R wave in V1, appear to be a specific, though
relatively insensitive, marker of anterior infarction [1
Inferior wall infarction
！ In a
retrospective analysis, 35 patients with LBBB and an unequivocal
inferior MI on thallium imaging were compared to 131 patients with LBBB
without an inferior wall MI [5
Two ECG findings were most useful for the diagnosis of an inferior wall MI:
• Q or QS wave in lead aVF, found in 29 percent
of those with a documented MI versus only 3 percent of those without an
• Diagnostic T wave inversion (compete or
biphasic with an initial negative deflection), present in 66 percent with and
6 percent without a MI.
The presence of either finding was 86 percent sensitive and 91 percent
specific for the diagnosis of an inferior wall MI.
！ The sequence of
repolarization is altered in LBBB, with the ST segment and T wave vectors
being directed opposite to the QRS complex. These changes may mask the ST
segment depression and T wave inversion induced by ischemia. On the other
hand, the diagnosis of an acute MI or ischemia can occasionally be made in a
patient with underlying LBBB if certain ST-T changes are seen, particularly if
the ST-T vectors are in the same direction as the QRS complex:
• The presence of deep T wave inversions in leads
with a predominantly negative QRS complex (eg, V1-V3) is highly suggestive of
evolving ischemia or MI.
• ST elevations in leads with a predominant R
wave (as opposed to QS or rS waves) are also strongly suggestive of acute
• Pseudonormalization of previously inverted T
waves is suggestive but not diagnostic of ischemia.
Studies of acute MI in LBBB
studies have systematically evaluated the value of different ECG findings of
acute MI in LBBB. One study by Wackers, for example, correlated ECG changes in
LBBB with localization of the infarct by thallium scintigraphy [2
The most useful ECG criteria were:
• Serial ECG changes ！ 67 percent sensitivity
• ST segment elevation ！ 54 percent sensitivity
• Abnormal Q waves ！ 31 percent
• Cabrera's sign ！ 27 percent sensitivity, 47
percent for anteroseptal MI
• Initial positivity in V1 with a Q wave in V6
！ 20 percent sensitivity but 100 percent specificity for anteroseptal MI
Cabrera's sign refers to prominent (0.05 sec) notching in the ascending limb
of the S wave in leads V3 and V4; a similar finding is prominent notching of
the ascending limb of the R wave in lead V5 or V6 (Chapman's sign) [2
These signs have a specificity that approaches 90 percent. However, there may
be a high degree of interobserver variability in accurate identification and
their sensitivity is quite low.
A large trial of thrombolytic therapy for acute MI (GUSTO-1) provided an
opportunity to revisit the issue of the electrocardiographic diagnosis of
evolving acute MI in the presence of LBBB [3
Of 26,003 North American patients who had a myocardial infarction confirmed by
enzyme studies, 131 (0.5 percent) had LBBB. A scoring system was developed
from the coefficients assigned by a logistic model for each independent
criterion, on a scale of 0 to 5. The three ECG criteria with an independent
value in the diagnosis of acute infarction and the score for each were:
• ST segment elevation of 1 mm or more that was
in the same direction (concordant) as the QRS complex ！ score 5.
• ST segment depression of 1 mm or more in lead
V1, V2, or V3 ！ score 3.
• ST segment elevation of 5 mm or more that was
discordant with the QRS complex (ie, associated with a QS or rS complex) ！
A minimal score of three was required for a specificity of 90 percent. The
first two criteria are similar to those described above since the ST segment
is concordant rather than discordant with the QRS complex. However, the third
finding requires further validation, since a high take-off of the ST segment
in leads V1 to V3 has been described with uncomplicated LBBB, particularly if
there is underlying left ventricular hypertrophy.
A number of the other criteria, including those of Wackers mentioned above,
were not found to be useful. A difference may be that the GUSTO criteria were
applied within hours of the MI as part of the GUSTO-1 trial, while those of
Wackers were often applied much longer after the acute event. Furthermore,
only the Wackers study attempted to localize the infarct.
Studies of acute MI in ventricular paced rhythm
A similar problem is the diagnosis of an acute myocardial infarction in the
presence of a ventricular paced rhythm which is usually associated with a left
bundle branch block pattern. Thirty-two patients in the GUSTO-1 trial (0.1
percent of enrolled patients) had a ventricular paced rhythm. The only ECG
criterion with a high specificity and statistical significance for the
diagnosis of an acute MI was ST segment elevation
mm in leads with a negative QRS complex [5
other criteria with acceptable specificity were:
• ST elevation
mm in leads with concordant QRS polarity.
• ST depression
mm in leads V1, V2, or, V3.
！ The following points summarize
the electrocardiographic signs of myocardial infarction in LBBB.
• A QS pattern, poor R wave progression, or loss
of R waves in the anterior precordial leads or a QS pattern in II, III, aVF,
or aVL can occur with uncomplicated LBBB.
• LBBB characteristically masks the Q waves of
pure lateral and free wall infarction; it may also mask the Q waves of
inferior or anteroseptal infarction.
• ST segment elevation with tall positive T waves
are frequently seen in the right precordial leads with uncomplicated LBBB.
Secondary T wave inversions are characteristically seen in the lateral
precordial leads. However, the appearance of ST elevations in the lateral
leads or deep T wave inversions in leads V1-V3 suggests underlying ischemia.
Close attention, therefore, should be paid to serial ST-T changes.
• The presence of QR complexes in leads I, V5, or
V6, or in II, III, and aVF with LBBB strongly suggests underlying infarction.
• An anterolateral MI should be suspected if new
S waves appear in leftward leads (I, aVL, and V6) in a patient with
preexisting common LBBB.
• Underlying MI is also suggested by notching of
the ascending part of a wide S waves in the mid-precordial leads (Cabrera's
sign), or of the ascending limb of a wide R wave in V5 or V6 (Chapman's sign).