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

References

  1. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med 1996;334:481-7.
  2. Smith SW, Dodd KW, Henry TD, Dvorak DM, Pearce LA. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med 2012;60:766-76.
  3. Schneider JF, Thomas HE, Kreger BE, McNamara PM, Sorlie P, Kannel WB. Newly acquired right bundle-branch block: The Framingham Study. Ann Int Med 1980;92:37-44.
  4. Fahy GJ, Pinski SL, Miller DP, et al. Natural history of isolated bundle branch block. Am J Cardiol 1996;77:1185-90.
  5. Tabas JA, Rodriguez RM, Seligman HK, Goldschlager NF. Electrocardiographic criteria for detecting acute myocardial infarction in patients with left bundle branch block: a meta-analysis. Ann Emerg Med 2008;52:329-336.e1.
  6. Meyers HP, Limkakeng AT Jr, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J 2015;170:1255-64.
  7. Effects of tissue plasminogen activator and a comparison of early invasive and conservative strategies in unstable angina and non-Q-wave myocardial infarction. Results of the TIMI IIIB Trial. Thrombolysis in Myocardial Ischemia. Circulation 1994;89:1545-56.
  8. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction). Circulation 2004;110:e82-292.
  9. Barbagelata A, Ware DL. Denying reperfusion or falsely declaring emergency: the dilemma posed by ST-segment elevation. J Electrocardiol 2006;39:S73-4.
  10. Neeland IJ, Kontos MC, de Lemos JA. Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol 2012;60:96-105.
  11. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013;61:e78-140.
  12. Larson DM, Menssen KM, Sharkey SW, et al. "False-positive" cardiac catheterization laboratory activation among patients with suspected ST-segment elevation myocardial infarction. JAMA 2007;298:2754-60.
  13. Chang AM, Shofer FS, Tabas JA, Magid DJ, McCusker CM, Hollander JE. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. Am J Emerg Med 2009;27:916-21.
  14. Lopes RD, Siha H, Fu Y, et al. Diagnosing acute myocardial infarction in patients with left bundle branch block. Am J Cardiol 2011;108:782-8.
  15. Jain S, Ting HT, Bell M, et al. Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction. Am J Cardiol 2011;107:1111-6.

Clinical Topics: Acute Coronary Syndromes, Arrhythmias and Clinical EP, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Valvular Heart Disease, 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, Biological Markers, 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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