DIAGNOSIS OF MI IN
BUNDLE BRANCH BLOCKS
MI IN BUNDLE BRANCH
• The ECG diagnosis of MI is more difficult when the baseline
ECG shows a bundle branch block pattern that may precede or
be a complication of the infarct or the patient has a paced
• The frequency of bundle branch block was best assessed in a
review of almost 300,000 infarctions from the National
Registry of Myocardial Infarction investigators.
• Right bundle branch block was present in approximately 6
percent and left bundle branch block in 7 percent of
• RIGHT BUNDLE BRANCH BLOCK WITH MI —
• The effect of right bundle branch block (RBBB) must be
considered in both Q wave (ST elevation) and non-Q wave
(non-ST elevation) infarctions.
• Q wave MI —
• Does not usually interfere with the diagnosis of a Q wave MI.
• Myocardial infarction most often involves the left ventricle
and therefore affects the initial phase of ventricular
depolarization, sometimes producing abnormal Q waves.
• In contrast, RBBB primarily affects 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.
• These changes are due to delayed depolarization of the right
ventricle, while depolarization of the left ventricle is not
• The net effect is that the ECG
patterns are combined when
complete RBBB and a Q wave
infarct occur together, and the
criteria for the diagnosis of a Q
wave MI are the same as in patients
with normal conduction:
– Due to the bundle branch block,
the QRS complex will be
abnormally wide (0.12 sec or
more), lead V1 will show a
terminal positive deflection,
and 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;
• There are, however, problems that can occur with
interpretation of the ECG in patients with RBBB and acute
• Large clinical trials in which serial ECGs are performed have
shown both false-positive and false-negative diagnoses of MI in
the presence of RBBB
• After revascularization, for example, Q wave durations in
patients who develop RBBB can shorten significantly, primarily
in the inferior leads, suggesting that the initial orientation of
wavefronts can change and that false-negative results may be
obtained in patients with inferior infarction
• There has been a case report of a woman with an acute anterior
MI in whom the initial ECG revealed a small R wave in leads
V1 and V4.
• These R waves were replaced by Q waves after the
development of RBBB associated with PR-interval
• The coexistence of left anterior fascicular block with or
without RBBB can be associated with Q waves suggestive of
an anterior MI; in this setting, the altered initial vector is
attributed to the left anterior fascicular block .
– These Q waves can often be distinguished from pathologic Q waves in
an acute MI by their short duration (0.02 sec versus 0.04 to 0.05 sec
with an infarction) and their presence in only leads V2 and/or V3.
• A new posterior wall infarct in the presence of RBBB might
be expected to increase the anterior forces in the right
precordial leads but this has not been systematically studied.
• RBBB-Non-Q wave MI —
• There may be some diagnostic difficulties in interpreting the
ECG in patients with RBBB who have a non-Q wave MI.
– RBBB is typically associated with secondary ST-T changes
due to abnormal right ventricular repolarization.
– Thus, leads with an R' wave (leads V1, V2, and sometimes
V3) will show T wave inversions.
– In contrast, 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 ST-T changes may be due to ischemia, or to other
factors such as drug effects or electrolyte abnormalities
• The proportion of patients with LBBB and acute chest pain
having an acute MI in different studies has been between 13 to
• As a result, inaccurate diagnosis can lead to both
undertreatment and unnecessary overtreatment of patients.
• In one report, for example, thrombolysis was given to only 73
percent with LBBB and an acute MI and to 48 percent of
patients with LBBB and chest pain but no biochemical
evidence of infarction.
• In addition to difficulties in ECG interpretation, approximately
one-half of patients with LBBB and an acute MI do not have
chest pain .
• These patients are much less likely to receive appropriate
medical therapy (eg, aspirin, beta blockers) or reperfusion
• LEFT BUNDLE BRANCH BLOCK WITH MI —
• Left bundle branch block (LBBB) is present in approximately
7 percent of acute infarctions .
• The diagnosis of MI in the presence of 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
• Two issues need to be addressed:
• The impact of LBBB on the diagnosis of acute MI; and
• The effect on diagnosis of a prior MI.
• 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 can occur.
• Because of these difficulties, careful attention to the strength
of the clinical history and confirmation of the diagnosis of an
acute MI by cardiac enzyme elevations is essential.
• Acute MI —
• The sequence of repolarization is altered in LBBB, with the ST
segment and T wave vectors being directed opposite to the
• 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 as in the
Sgarbossa criteria .
• 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.
• Sgarbossa criteria —
• 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 .
• Among 26,003 North American patients who had a
myocardial infarction confirmed by enzyme studies, 131 (0.5
percent) had LBBB. A scoring system, often called the
Sgarbossa criteria, was developed from the coefficients
assigned by a logistic model for each independent criterion, on
a scale of 0 to 5.
– Sgarbossa EB, Pinski SL, Gates KB, Wagner GS. Early
electrocardiographic diagnosis of acute myocardial infarction in the
presence of ventricular paced rhythm. GUSTO-I investigators. Am J
• ST segment elevation of 1 mm
or more that was in the same
direction (concordant) as the
QRS complex in any lead —
• ST segment depression of 1
mm or more in any lead from
V1 to 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) — score 2
A minimal score of 3 was
required for a specificity of 90
MI IN BUNDLE BRANCH
• The first two criteria are similar to those described above since
the ST segment is concordant rather than discordant with the
• 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.
• In a substudy from the ASSENT 2 and 3 trials, the third
criteria added little diagnostic or prognostic value .
• A Sgarbossa score of ≥3 was highly specific (ie, few false
positives) but much less sensitive (36 percent) in the validation
sample in the original report .
• Similar findings were noted in a subsequent meta-analysis of
10 studies of 1614 patients in which a Sgarbossa score of ≥3
had a sensitivity of 20 percent and a specificity of 98 percent .
• The sensitivity may increase if serial or previous ECGs are
• In addition to their utility in diagnosis, the Sgarbossa criteria
may also predict prognosis in patients with acute MI.
• Attempts to improve ECG diagnosis —
• Several studies have systematically evaluated the value of different
ECG findings of acute MI in LBBB.
• An analysis by Wackers correlated ECG changes in LBBB with
localization of the infarct by thallium scintigraphy .
• The most useful ECG criteria were:
– Serial ECG changes — 67 percent sensitivity
– ST segment elevation — 54 percent sensitivity
– Abnormal Q waves — 31 percent sensitivity
– Initial positivity in V1 with a Q wave in V6 — 20 percent sensitivity
but 100 percent specificity for anteroseptal MI
– Cabrera's sign — 27 percent sensitivity overall, 47 percent for
• Cabrera's sign refers to
prominent (0.05 sec)
notching in the ascending
limb of the S wave in leads
V3 and V4;
Chapman's sign- prominent
notching of the ascending limb of
the R wave in lead V5 or V6
• 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
• Ventricular pacing —
• A similar problem is the diagnosis of an acute MI 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 ≥5 mm in leads with a negative QRS complex .
• Two other criteria with acceptable specificity were:
– ST elevation ≥1 mm in leads with concordant QRS polarity
– ST depression ≥1 mm in leads V1, V2, or, V3
• Prior infarction —
• Changes in the sequence of depolarization in LBBB can also
mask typical findings associated with prior transmural (Q
wave) infarctions. Certain ECG patterns, however may suggest
prior infarction despite LBBB
• Left ventricular free wall —
• 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
• As a result, 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 LBBB.
• Anteroseptal —
• 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 I, aVL,
• 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 LBBB pattern
• Free wall and septal —
• Acute or chronic infarction involving both the free wall and the septum
may produce abnormal Q waves (usually as part of 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
• 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, although
relatively insensitive, marker of anterior infarction .
• Inferior wall —
• 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 .
• 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 inferior MI
– Diagnostic T wave inversion (compete or biphasic with an initial
negative deflection), present in 66 percent with and 6 percent without a
• The presence of either finding was 86 percent sensitive and 91
percent specific for the diagnosis of an inferior wall MI
• Summary — The following points summarize the
electrocardiographic signs of myocardial infarction in LBBB.
• The Sgarbossa criteria have high specificity but low sensitivity
; thus, their presence is highly suggestive of acute infarction
but their absence has little value.
• 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
concordant ST elevations in the lateral leads or ST depression
or deep T wave inversions in leads V1-V3 suggests underlying
ischemia . Thus, close attention should be paid to serial ST-T
• The presence of QR complexes in leads I, V5, or V6, or in II,
III, and aVF with LBBB strongly suggests underlying
• 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
TMT in RBBB
• The resting ECG in patients with right bundle branch block
(RBBB) is frequently associated with T wave and ST-segment
changes in the early anterior precordial leads (V1 to V3).
• Exercise-induced ST-segment depression in leads V1 to V4 is a
common finding in patients with RBBB and is nondiagnostic
• The new development of exercise-induced ST-segment
depression in leads V5 and V6 or leads 2 and aVF, reduced
exercise capacity, and inability to increase systolic blood
pressure adequately are useful for detecting patients who have
CAD and a high clinical pretest risk of disease
• The presence of RBBB decreases the sensitivity of
• The presence of this finding in leads V1 through V4 is
not diagnostic of obstructive coronary disease;
however, if ischemic changes are seen in lead II or
aVF, or in leads V5 or V6, the specificity for coronary
disease is improved.
TMT in LBBB
• Exercise-induced ST segment depression is found in most
patients with LBBB and cannot be used as a diagnostic or
prognostic indicator, regardless of the degree of ST-segment
• The relative risk of death or other major cardiac events in
patients with exercise-induced LBBB is increased
approximately threefold over the risk in patients without this
• The development of ischemic ST-segment depression before
the LBBB pattern appears or in the recovery phase after the
LBBB has resolved does not attenuate the diagnostic yield of
the ST segment shift.