LBBB in Patients With Suspected MI: An Evolving Paradigm

Patients with a suspected myocardial infarction (MI) in the setting of a left bundle branch block (LBBB) present a unique diagnostic and therapeutic challenge to the clinician. A diagnosis of MI with electrocardiogram (ECG) is especially difficult in the setting of LBBB because of the characteristic ECG changes caused by altered ventricular depolarization. The Sgarbossa criteria1 were first introduced over 20 years ago to improve the diagnostic accuracy for MI in the presence of LBBB; others have subsequently modified the criteria to improve sensitivity.2 Here we review the pathophysiology of LBBB in MI, discuss current guidelines, and highlight evolving paradigms for the diagnosis and treatment of suspected MI in patients with LBBB.

In contrast to the right bundle branch, the left ventricular conduction system is a large, diffuse structure that typically requires a significant insult to result in widespread injury. When a new LBBB is caused by MI, the infarction site is usually anterior or anteroseptal, and the MI usually involves a large territory of myocardium. Most cases of LBBB in suspected MI are therefore not a result of focal infarction. Instead, extensive myocardial damage involving a large portion of the distal conduction system is usually required to cause LBBB. This explains why acute LBBB caused by transmural MI is associated with a poor prognosis. In rare circumstances, acute LBBB may be caused by a more discreet MI just distal to the bundle of His.

Contemporary studies suggest that acute LBBB from transmural infarction is relatively uncommon. LBBB is more often a pre-existing marker of underlying structural heart disease; those with LBBB have increased risk for cardiovascular mortality, coronary artery disease, heart failure, and sudden cardiac death.3,4 The LBBB itself can be the result of an aging or fibrotic conduction system, chronic ischemic heart disease, left ventricular hypertrophy, adverse ventricular remodeling from congestive heart failure, or valvular heart disease.

The diagnosis of MI in the setting of LBBB is especially challenging by ECG. Because left ventricular activation is delayed in LBBB and the initial septal activation is from right to left (opposite of the normal situation), septal Q waves indicative of an MI are absent. Additionally, secondary ST-T wave abnormalities that occur in LBBB obscure the recognition of injury currents in ischemia and infarction. The most widely accepted tools to aid in the diagnosis of MI in the presence of LBBB are the Sgarbossa criteria. Sgarbossa et al.1 identified three ECG criteria that may improve the diagnosis of MI in patients with LBBB:

  1. ST-elevation of ≥1 mm and concordant with the QRS complex (5 points)
  2. ST-segment depression ≥1 mm in lead V1, V2, or V3 (3 points)
  3. ST elevation ≥5 mm and discordant with the QRS complex (2 points)

ST-segment concordance with the QRS complex has a specificity approaching 98% but with limited sensitivity (~20%) (Table 1).5 Thus, the Sgarbossa criteria are informative if present but not reassuring if absent and cannot be used to exclude MI. In order to improve diagnostic accuracy, Smith et al.2 developed the "modified Sgarbossa criteria," in which the original absolute 5 mm criterion is replaced with a proportion: ST elevation/S-wave amplitude of ≤ -0.25). The authors reported improved diagnostic sensitivity from 52 to 91% in identifying angiographically proven MI but with reduced specificity compared with the original Sgarbossa criteria (90 vs. 98%). The modified Sgarbossa criteria have subsequently been validated in a separate cohort.6

Table 1: Sgarbossa Electrocardiogram Criteria for the Diagnosis of MI in the Presence of LBBB5,10

Table 1
Sensitivity, specificity, and positive and negative likelihood ratios are presented as summary statistics (95% confidence intervals) for score of ≥3 and ≥2.
*ST-segment deviation is measures at the J point. Concordance and discordance of ST segments are determined by comparison with the main direction of the QRS complex.

Overall, studies have demonstrated that less than half of all patients with suspected MI and LBBB ultimately will be diagnosed with an MI. Moreover, a significant proportion of those patients with MI will not have an occluded culprit artery at catheterization and thus are classified more appropriately as having a non-ST-segment elevation MI (NSTEMI), unstable angina (UA), or non-acute coronary syndrome (ACS) presentation (Table 2). This has important implications for the treatment of patients with presumed new LBBB who do not have immediate access to coronary angiography. If many of the patients with LBBB do not have MI, they are unlikely to benefit from early reperfusion therapy. In addition, fibrinolytic therapy has been shown to harm patients with NSTEMI.7

Table 2: Prevalence of STEMI-Equivalent MI in Angiographic Studies of Patients With Suspected MI and LBBB10

Table 2

Because of these considerations, there has been a shift in guideline recommendations for management strategies of MI in the presence of a new or presumably new LBBB. The 2004 guidelines from the American College of Cardiology and American Heart Association recommended that patients with a new or presumed new LBBB undergo early reperfusion therapy with fibrinolysis or percutaneous coronary intervention (PCI) (class I indication).8 However, this strategy can lead to frequent catheterization in a significant proportion of patients who do not have an occluded culprit artery and expose patients to unnecessary risks of fibrinolytic therapy and cardiac catheterization.9 We have previously proposed a more judicious diagnostic approach in stable patients with LBBB who do not have ECG findings highly specific for ST-elevation MI (STEMI) (Figure 1). Clinically or hemodynamically unstable patients with suspected MI and new LBBB should be considered for immediate reperfusion therapy per guidelines. Among stable patients, ECG analysis to assess for ST-segment concordance criteria, along with serial cardiac biomarker testing and bedside echocardiography for wall motion abnormalities should be considered in the evaluation of new LBBB presentation to determine whether emergent reperfusion is necessary.10 The most recent 2013 STEMI guidelines are more consistent with our recommendations and recognize the challenge and uncertainty of diagnosing an MI in the presence of LBBB.11 In the recent version of the guidelines, LBBB is no longer an automatic STEMI equivalent. Rather, the guidelines acknowledge that most cases of LBBB are "not known to be old" when no prior ECG is available for comparison and that "new or presumably new LBBB at presentation occurs infrequently, may interfere with ST-elevation analysis, and should not be considered diagnostic of acute MI in isolation." These new guidelines no longer recommend treating new or presumably new LBBB as a STEMI equivalent with planned emergent reperfusion therapy. They recognize the criteria for ECG diagnosis of acute MI in the setting of LBBB that have been proposed and recommend evaluation using transthoracic echocardiography, cardiac troponin levels, and the clinical status of the patient to aide diagnosis. If the clinical suspicion for acute MI is still unclear, referral for invasive angiography may be necessary to guide therapy.

Figure 1: Proposed Diagnostic Algorithm for Suspected MI and LBBB10

Figure 1


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Clinical Topics: Acute Coronary Syndromes, Arrhythmias and Clinical EP, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Valvular Heart Disease, Atherosclerotic Disease (CAD/PAD), ACS and Cardiac Biomarkers, Implantable Devices, EP Basic Science, Acute Heart Failure, Heart Failure and Cardiac Biomarkers, Interventions and ACS, Interventions and Coronary Artery Disease, Interventions and Imaging, Interventions and Structural Heart Disease, Angiography, Echocardiography/Ultrasound, Nuclear Imaging

Keywords: Angina, Unstable, Biomarkers, Bundle of His, Bundle-Branch Block, Cardiac Catheterization, Coronary Angiography, Coronary Artery Disease, Echocardiography, Electrocardiography, Fibrinolysis, Heart Conduction System, Heart Failure, Heart Valve Diseases, Hypertrophy, Left Ventricular, Myocardial Infarction, Infarction, Myocardium, Percutaneous Coronary Intervention, Thrombolytic Therapy, Troponin, Ventricular Remodeling, Acute Coronary Syndrome

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