Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block or a paced rhythm

INTRODUCTION — The diagnosis of acute myocardial infarction (MI) is most typically suspected from the history of chest pain (discomfort) and is confirmed by the presence of abnormal electrocardiograms (ECGs) and elevation of serum troponin. (See "Diagnosis of acute myocardial infarction" and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction".)

The ECG diagnosis of acute and prior MI in patients with right bundle branch block (RBBB), left bundle branch block (LBBB), or a right ventricular (RV) paced rhythm will be reviewed here. The ECG features of RBBB and LBBB are discussed separately. (See "Right bundle branch block" and "Left bundle branch block".)

GENERAL PRINCIPLES — 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 when the patient has an RV paced rhythm [1-6]. The frequency of bundle branch block was assessed in a review of almost 300,000 infarctions from the National Registry of Myocardial Infarction 2 [7]. Right bundle branch block was present in approximately 6 percent and left bundle branch block in 7 percent of infarctions. Patients with bundle branch block were significantly less likely than those without bundle branch block to receive appropriate therapy with aspirin or beta blockers, had more comorbid disease, and had a significant increase in in-hospital mortality.

RIGHT BUNDLE BRANCH BLOCK WITH MI — Clinicians should be familiar with the effects of right bundle branch block (RBBB) in the settings of acute and prior myocardial infarction.

ST elevation — RBBB does not usually interfere with the diagnosis of an acute ST-elevation MI (STEMI). The reason is that MI most often involves the left ventricle (LV) 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 (waveform 1A-B). These changes are due to delayed depolarization of the RV, while depolarization of the LV is not substantially affected. (See "Right bundle branch block".)

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 (duration of 120 ms 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; if the infarction is inferior, Q waves will appear in leads II, III, and aVF.

However, problems can occur with interpretation of the ECG in patients with RBBB and acute MI:

●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 [8]. 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 infarctions [9].

●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 [10]. These R waves were replaced by Q waves after the development of RBBB associated with PR-interval prolongation, suggesting extension of the infarction. However, the Q waves disappeared with resolution of the RBBB.

●The coexistence of left anterior fascicular block with or without RBBB can be associated with Q waves suggestive of an acute anterior MI; in this setting, the altered initial vector is attributed to the left anterior fascicular block [11]. These acute Q waves can often be distinguished from nonacute Q-waves by their short duration (0.02 s versus 0.04 to 0.05 s with a nonacute infarction) and their presence in only leads V2 and/or V3.

●An acute 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.

●Note that the Brugada pattern may simulate RBBB with acute or evolving STEMI.

Non-ST-elevation myocardial infarction — There may be some diagnostic difficulties in interpreting the ECG in patients with RBBB who have a non-ST-elevation MI. RBBB is typically associated with secondary ST-T changes due to abnormal RV 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 non-ST-elevation MI, or to other factors such as drug effects (digoxin) or electrolyte abnormalities, such as hypokalemia.

LEFT BUNDLE BRANCH BLOCK WITH MI — Left bundle branch block (LBBB) is present in approximately 7 percent of acute infarctions [7]. The diagnosis of acute MI in the presence of LBBB is considerably more complicated and confusing than that of right bundle branch block (RBBB). The reason is that LBBB alters both the early and the mid to late phases of ventricular depolarization, and also produces secondary ST-T changes (waveform 2A-B).

Two major issues need to be addressed: the impact of LBBB on the diagnosis of acute MI and the effect on diagnosis of a remote MI [1-3,6]. There are issues that vary with the site of the infarct, and there are changes that are independent of the site of the infarct. 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 biomarker elevations are essential. (See "Diagnosis of acute myocardial infarction".)

Acute myocardial infarction — The sequence of repolarization is altered in LBBB, with the ST segment and T-wave vectors being directed opposite to the main QRS vector. 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 described below.

●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 ischemia [12].

●"Pseudonormalization" of previously inverted T waves is suggestive, however, not diagnostic of ischemia.

The importance of accurate diagnosis in patients with LBBB is illustrated by the following observations:

●The proportion of patients with LBBB and acute chest pain having an acute MI in different studies has varied considerably (eg, between 13 and 32 percent), with a lower incidence in community-based studies compared with clinical trials [13,14]. As a result, inaccurate diagnosis can lead to both undertreatment of patients with an MI and unnecessary overtreatment of patients without an MI [13,15]. In one early report, for example, thrombolysis was given to only 73 percent of eligible patients with LBBB and an acute MI and to 48 percent of patients with LBBB and chest pain but no biochemical evidence of infarction [15]. None of the latter patients satisfied the Sgarbossa criteria described below for an acute MI.

●In addition to difficulties in ECG interpretation, approximately one-half of patients with LBBB and an acute MI do not have chest pain [16]. These patients are much less likely to receive appropriate medical therapy (eg, aspirin, beta blockers) or reperfusion therapy than LBBB patients with chest pain [16].

Attempts to improve ECG diagnosis — Several studies have systematically evaluated the value of different ECG findings of acute MI in LBBB. A 1987 analysis correlated ECG changes in LBBB with localization of the infarct by thallium scintigraphy [1]. 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 sign – 27 percent sensitivity overall, 47 percent for anteroseptal MI.

Note: Cabrera sign refers to prominent (about 0.05 s in duration) 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 sign) [1]. These eponymous signs have a specificity that approaches 90 percent. However, there may be a high degree of interobserver variability in their accurate identification and their sensitivity is quite low. Likely, the pathophysiology relates to underlying myocardial scarring and fractionation of depolarization electrograms, reflected on the surface leads as QRS notching in conjunction with LBBB.

Sgarbossa criteria — A large trial of thrombolytic therapy for acute MI provided an opportunity to revisit the issue of the electrocardiographic diagnosis of evolving acute MI in the presence of LBBB [2]. 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.

The three original ECG criteria with independent value in the diagnosis of acute infarction and the score for each were:

●ST-segment elevation of ≥1 mm in the same direction as the QRS complex (concordant) in any lead: score 5.

●ST-segment depression of ≥1 mm in any lead from V1 to V3: score 3.

●ST-segment elevation of 5 mm or more that is discordant with the QRS complex (ie, associated with a QS or rS complex): score 2. However, prominent J point elevations may occur in V1 to V2 solely due to LV hypertrophy or in other settings. Therefore, a ratio (expressed in absolute units) in any relevant lead of the amplitude of the ST-elevation lead divided by the S wave amplitude in that lead that equals or exceeds 0.25 has been proposed as having greater accuracy than the original (not normalized) Sgarbossa criterion [17]. A higher ratio indicates relatively greater ST elevation. The diagnostic superiority of this modified (STE/S wave) criterion as compared with the original "Sgarbossa rule #3" was supported by the findings of a retrospective case-control study [18].

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 [2]. 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 [19]. The sensitivity may increase if serial or previous ECGs are available [15] or if the modified criteria (including STE/S wave ratio described above) are used [17,18].

In addition to their utility in diagnosis, the Sgarbossa criteria (and their validated modifications) may also predict prognosis in patients with acute MI (See "Conduction abnormalities after myocardial infarction", section on 'Prognosis'.)

More recent ECG criteria — A 2020 study of new ECG criteria reported enhanced accuracy in diagnosing acute MI in patients with LBBB [20]. The algorithm had sensitivity and specificity for the diagnosis of STEMI similar to that in patients without LBBB. Further validation studies that test their performance compared with older criteria are needed [21].

Ventricular pacing — Similar to preexisting LBBB, RV pacing results in delayed repolarization of the LV that prevents the usual interpretation of ST-segment changes in patients with acute MI. In patients with RV pacing and signs or symptoms of ischemia, modified versions of the original Sgarbossa criteria can be used to identify acute myocardial ischemia with reasonable accuracy [17,22]. The ECG suggests ischemia in the presence of RV pacing if one or more of the following features are present:

●ST-segment elevation of >1 mm in the same direction as the QRS complex (concordant) in any lead.

●ST-segment depression >1 mm in the same direction as the QRS complex (concordant) in at least one chest lead (ie, V1 to V6).

●ST elevation (mm) / S-wave amplitude (mm) ratio >0.25 (a measure of discordance) from the lead that generates the greatest ST elevation/S wave ratio.

These modified Sgarbossa criteria were validated in a study of patients with RV pacing who presented with signs or symptoms of myocardial ischemia [22]. The diagnosis of acute MI ("occlusion MI") was confirmed by troponin assay values and invasive coronary angiography. The ECG criteria had a sensitivity of 86 percent and a specificity of 83 percent for the diagnosis of acute MI. By comparison, the unweighted "original" Sgarbossa criteria had a lower diagnostic accuracy (sensitivity 56 percent, specificity 90 percent), while the "modified Sgarbossa criteria" had a similar diagnostic accuracy (sensitivity 81 percent, specificity 84 percent). (See 'Sgarbossa criteria' above.)

The use of the ECG to help diagnose ischemia or infarction with other pacing modalities (eg, biventricular pacing, LBB area pacing) is an unresolved issue that is beyond the scope of this topic.

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 LV 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. As a result, acute or prior LV 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 LV 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.

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 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 a prior anteroseptal MI.

There are, however, other changes that can occur that may suggest the presence of a prior anteroseptal or septal MI. The infarct may cause the initial leftward 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 prior 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/lateral and superior forces from the spared basal portion of the septum. Small Q waves (0.03 s or less) may be seen in leads I and V5 to V6 with uncomplicated LBBB. Thus, wide Q waves (0.04 s) 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 prior anterior infarction [6].

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 [23]. Two ECG findings were most useful for the diagnosis of a prior inferior 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 a prior inferior MI.

●Diagnostic T-wave inversion (compete or biphasic with an initial negative deflection), present in 66 percent with and 6 percent without a prior MI.

The presence of either finding was 86 percent sensitive and 91 percent specific for the diagnosis of a prior inferior wall MI.

Finally, intermittent LBBB (or intermittent RV pacing) may induce "memory" T-wave inversions in normally conducted beats that previously showed wide, negative QRS complexes (eg V1 to V3 or V4). These changes may mimic evolving anterior ischemia (Wellens sign) or MI. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Abnormal T waves' and "Electrocardiogram in the diagnosis of myocardial ischemia and infarction", section on 'Left anterior descending coronary T-wave inversion pattern'.)

SUMMARY

●Effect of right bundle branch block in acute ischemia

•STEMI – Right bundle branch block (RBBB) does not usually interfere with the diagnosis of an acute ST-elevation myocardial infarction (STEMI). (See 'ST elevation' above.)

•Non-ST-elevation MI – In patients with a preexisting RBBB and acute ischemia, the ECG findings of T-wave inversions or ST depressions are most reliable to aid in the diagnosis of ischemia in leads not showing a terminal R' wave. (See 'Non-ST-elevation myocardial infarction' above.)

●Effect of left bundle branch block in acute ischemia – In patients with a preexisting left bundle branch block (LBBB) ECG pattern, ischemia or infarction are typically masked.

•Acute infarction – The Sgarbossa criteria can be used to identify acute infarction in the presence of LBBB. (See 'Sgarbossa criteria' above.)

•Prior infarction – Changes in the sequence of depolarization in LBBB can also mask typical findings associated with prior transmural (Q wave) infarction. Certain ECG patterns, however, may suggest prior infarction despite LBBB. (See 'Prior infarction' above.)

•Effect of pacing – Modified Sgarbossa criteria can be used to help diagnose infarction in patients with right ventricular (RV) pacing. (See 'Ventricular pacing' above.)