Prompt reperfusion of patients with acute myocardial infarction (MI) and ST-segment and T-wave changes on 12-lead ECG markedly improves outcomes, including reducing mortality.1-3 A patient with acute coronary syndrome (ACS) and concomitant left bundle-branch block (LBBB) presents diagnostic and management challenges, as the classic ECG findings of ST-segment elevation MI (STEMI) are obscured by the repolarization changes of LBBB. In addition to dubious ST-segment changes in ischemia, LBBB places patients at greater risk for acute MI, heart failure, and death.4
For more than 60 years, clinicians have recognized the diagnostic and management challenges of patients with chest pain presenting with concomitant LBBB.5 Altered ventricular depolarization in patients with LBBB masks characteristic ECG changes of MI, and patients with new or persistent LBBB and acute MI have worse prognoses.4,6 Patients with suspected STEMI and LBBB (regardless of chronicity) represent a small but substantial proportion of the ACS cohort, and this patient subset has increased adverse clinical outcomes and higher complications following acute MI.4 These patients are more likely to be older, female, and have a history of preexisting cardiovascular disease, are more likely to suffer acute MI, stroke, heart failure, and death compared with patients who do not have LBBB.4 Determining which patients in this subset should receive emergent reperfusion is challenging.
Uncertainty about the optimal approach to identifying acute MI in patients with LBBB has contributed to delays in diagnosis and prolonged time to revascularization.2 Historically, the American College of Cardiology/American Heart Association (ACC/AHA) guideline was to treat all patients with new (or presumed new) LBBB and symptoms of acute MI as a STEMI equivalent, mandating emergent reperfusion with fibrinolytics or percutaneous coronary intervention (PCI).7,8 This treatment approach resulted in heterogeneous and altered management approaches with diverse outcomes. Newer guidelines eliminate the concept of treating patients with presumed new LBBB and chest pain as a STEMI equivalent based on more recent angiographic data that question the validity of this principle.4,9,10 The 2004 AHA guideline recommended reperfusion therapy for all patients with LBBB and symptoms of acute MI, resulting in overtreatment of many patients with an aggressive and expensive therapy. The 2013 AHA guideline suggested the opposite extreme—not to treat patients with LBBB and symptoms of acute MI as STEMI-equivalent, and thus not to treat with reperfusion therapy. The drastic change from using reperfusion therapy for all patients with LBBB to using it for none significantly reduces false-positive treatments but fails to recognize that some patients with chronic LBBB do have STEMI and could die if treatment is delayed.11 Hence, the need for a reliable diagnostic tool to diagnose STEMI in patients with new or chronic LBBB. Clinicians should become comfortable using the Sgarbossa criteria when faced with a patient with LBBB and chest symptoms. These criteria are particularly helpful in this setting due to their high specificity and positive predictive value. Using this tool will allow an objective triage, recognizing those patients who actually need aggressive therapy.
Despite the repolarization changes from LBBB and distorted ST segments, noninvasive diagnostic ECG criteria have been validated to further triage patients with LBBB and chest pain. The Sgarbossa ECG criteria for diagnosing acute MI in patients with LBBB have been posited to meet this diagnostic challenge.9 The addition of the ST/S ratio (creating the modified Sgarbossa criteria) lends further diagnostic validity.12 These criteria form part of a diagnostic algorithm for rapid diagnosis while minimizing treatment decision extremes.11 However, these criteria are not without controversy. The strength of this tool is on the side of diagnostic specificity with fewer false-positive acute MI diagnoses; however, the low sensitivity of 20% could result in undertreatment. Other studies suggest there may be no improvement over clinical judgment alone. Some have advocated additional criteria to improve sensitivity.4 This article reviews the management dilemma of chest pain and LBBB, the expanded Sgarbossa criteria, and recently proposed treatment algorithms.
PATHOPHYSIOLOGY OF LBBB
Below the level of the atrioventricular (AV) node and bundle of His, the conduction system trifurcates into a single right bundle and a bifascicular left bundle. The main left bundle branch further divides into the anterior and posterior fascicles. Compared with the right bundle branch, the left bundle is larger and anatomically deeper within the myocardium. These structural characteristics provide a degree of protection for the left bundle branches, requiring a significant ischemic injury to result in damage and conduction delay. LBBB can occur in otherwise healthy hearts but far more commonly is a marker of underlying structural or ischemic heart disease. Conditions associated with LBBB formation include aortic stenosis, hypertension, acute MI, chronic ischemic heart disease, heart failure, and cardiomyopathy.
Blocks in the interventricular conduction system involving both fascicles of the left bundle result in characteristic and diagnostic ECG changes (Table 1). Understanding ST-segment concordance is a critical aspect in recognizing LBBB on a patient's ECG and in using the diagnostic criteria in patients with acute MI. Concordance refers to the relationship between the major QRS (or RS) waveform and the vector of the ST segment. A concordant ST segment is oriented in the same direction as the terminal QRS waveform. In patients with LBBB, the ST segment is discordant with the QRS. This ST-segment discordance interferes with clinical interpretation of acute ischemic changes. In the baseline LBBB pattern, the characteristic notched R (an abnormal widening of QRS complex with a notched, rabbit-ears appearance, Figure 1) is followed by repolarization, yielding marked ST-segment depression in leads V5 and V6. Also in the baseline LBBB pattern, in leads V1 and V2, the rS complex normally is negative with repolarization, resulting in ST-segment elevation (Figure 1). These findings have traditionally made it difficult to interpret acute ischemia in a patient with a STEMI. Thus, in a patient with underlying, asymptomatic LBBB, an ECG will show ST-segment depression in leads V5 and V6, and ST-segment elevation in leads V1 and V2. Additional leads may also reveal distorted ST segments.
Interpreting ST-segment and T-wave inversions is key to chest pain evaluation, especially in the acute setting. In fact, the initial ST-segment sum is the main variable influencing “door to fibrinolytics” time; the largest ST deviations result in the shortest times to treatment.13 Patients with chest symptoms and either a presumed new LBBB or a chronic LBBB present the clinician with a diagnostic dilemma because the most powerful diagnostic tool (ST-segment change on ECG) has historically been presumed unreadable in these patients. Uncertainty about the age or time of onset of the LBBB further complicates clinical decision making.
LBBB chronicity is difficult to determine without reviewing the patient's previous ECGs—a notable contributing factor is that the onset of LBBB often is asymptomatic.4 Patients with acute MI who present with LBBB have greater in-hospital mortality (22.6%) than patients without LBBB (13.1%) yet are less likely to receive interventions known to improve survival.14 Research shows that much of the time these interventricular conduction delays are transient in nature, a myocardial reaction to an ischemic insult. Diagnostically, in a patient with new LBBB and clinical findings that suggest ACS, the transient LBBB pattern may infer myocardial ischemia, but this is not always the case.
The prevalence of LBBB has been estimated at 0.1% to 0.4% in middle-aged men in unselected populations.15 The prevalence increases with age with a reported prevalence of less than 1% at age 50 years, rising to more than 17% among octogenarians.15 Studies demonstrate an increase in mortality, sudden death, ischemic heart disease, and heart failure in patients with LBBB compared with those without LBBB.15 Between 1% and 9% of patients seeking evaluation for suspected acute MI have LBBB (chronicity uncertain).11,16
EVOLUTION AND HISTORY OF MANAGEMENT
Optimal management of patients with acute MI and evolving myocardial ischemia depends on rapidly identifying coronary occlusion and promptly providing reperfusion therapy.11,17 Triaging patients with chest pain relies heavily on identifying ST-segment elevation on a standard 12-lead ECG.13 Controlled studies have analyzed the diagnostic power of the initial ECG in patients presenting with and without chest pain. Optimum ECG variables for detection of acute MI included new ST-segment elevation at the J point in at least two contiguous leads (Figure 2); specifically, elevation of 2 mm or more in men, or 1.5 mm or more in women in leads V2 and V3 and/or elevation of 1 mm or more in one other contiguous chest or limb lead.18 With this model, 83% of patients were correctly classified with 56% sensitivity and 94% specificity.13
ECG manifestations of STEMI in patients with LBBB may be obscured or mimicked, causing treatment problems on both sides of the spectrum.11 This has resulted in undertreatment and overtreatment of ischemia and AMI in patients with chest pain and LBBB. The potential for overtreatment based on older (2004) AHA guidelines, or under treatment based on newer (2013) AHA guidelines explains the pressing need for noninvasive diagnostic tools for this patient group.11
In 1996 and 2004, the American College of Cardiology and American Heart Association (ACC/AHA) published guidelines for managing patients with concomitant STEMI and LBBB, and recommended emergent reperfusion therapy with fibrinolytics or PCI if the patient presented for treatment within 12 hours of symptom onset.7,8 These guidelines were based on older data from fibrinolytic trials in which the diagnosis of acute MI was confirmed biochemically rather than angiographically.11 Relying on biomarkers in patients with LBBB may overestimate the prevalence of acute MI. More recent studies have evaluated the actual incidence of acute MI in patients with LBBB based on angiographic evidence.9,11 Studies indicate that 6% to 51% of all patients with suspected ACS and LBBB will ultimately be diagnosed with acute MI.4 Even in patients with known new LBBB and chest pain, MI is actually diagnosed in a minority.19 The 1996 and 2004 guidelines likely resulted in unnecessary reperfusion therapy for many patients.
More recent guidelines challenge the practice of treating new LBBB as a STEMI equivalent.9 The 2013 guidelines recognize that new LBBB at presentation actually occurs infrequently, may interfere with ST-elevation analysis, and should not be considered diagnostic of acute MI.9,11 The change in approach from treating all patients with LBBB as if they have STEMI to using the diagnostic tool to target treatment will reduce complications from overuse of PCI and fibrinolytics. The excellent specificity of the original Sgarbossa criteria (Table 2) helps clinicians identify patients who may be truly negative if the score is below 3. These patients do not need to be treated as if they had acute MI. Patients scoring 3 or greater on the original Sgarbossa criteria should be treated. The modified criteria (Table 2) do not use scores but patients who meet even one criterion should receive PCI or fibrinolytics.11
The significant downside of the new guideline is the failure to recognize patients with chronic LBBB who actually do have STEMI. Delaying reperfusion in this population could be fatal or increase morbidity due to undertreatment. Hence, the critical need for a noninvasive diagnostic tool that will accurately determine appropriate interventions for these patients.
The acuity and severity of ACS demands diagnostic tests with sensitivity and specificity. Recent algorithms using the Sgarbossa criteria and the ST/S ratio together add a validated approach.
In 1996, Sgarbossa and colleagues published three independent ECG predictors of acute MI in patients with LBBB.20 These criteria resulted from analysis of more than 26,000 patients in the GUSTO-1 trial. The analysis compared ECGs from two groups: patients with LBBB and confirmed acute MI (the study population) and patients with chronic ischemic heart disease and LBBB (the control group).20 Three independent ECG signs were identified that discriminate for acute ischemia with LBBB. Each ECG predictor was assigned a point value dependent upon its predictive power and validity.13,20
The Sgarbossa criteria are the most validated ECG criteria for diagnosing STEMI in patients with LBBB.20 A score of 2 or less is 95% specific in determining absence of acute MI in patients with LBBB, and a score 3 or greater has a sensitivity ranging from 20% to 79% in determining presence of acute MI in patients with LBBB.17,20 A score of 2 based on fulfillment of only the last criterion is not diagnostic of acute MI and mandates further testing and clinical judgment.17,20
In 2012, Smith and colleagues evaluated a fourth ECG criterion designed to increase the sensitivity of the third Sgarbossa criterion and increase the overall sensitivity of Sgarbossa's diagnostic tool.12 Sgarbossa's rule uses an absolute 5 mm cutoff for discordant ST-segment elevation. Smith and colleagues hypothesized that an ST-segment elevation in leads V1 and V3 proportional to the preceding QRS or S wave may be more useful for diagnosing STEMI in patients with LBBB (Figure 3).12 Their hypothesis was correct, and replacing the third Sgarbossa criteria with the ST/S ratio improved diagnostic sensitivity from 52% to 91%, with specificity remaining near 90%.12
LBBB occurs in 1% of the general population; however, the prevalence of LBBB in patients with acute MI is 6% to 9%.2
LBBB often is a marker of chronic cardiac disease and may define a subset of patients at high risk for morbidity and mortality, especially if they have concomitant acute MI. Patients with LBBB are older, often male, and often have a high burden of comorbidities.15 Although biomarker levels are essential to the diagnosis of acute MI, biomarker elevation does not discriminate between STEMI and non-STEMI (NSTEMI), and ST-segment elevation on ECG is the primary indication for emergency reperfusion therapy.
Identifying STEMI in patients with LBBB is challenging because ST-segment changes may be masked.12,15 Overzealous reperfusion leads to complications from fibrinolysis and unnecessary use of cardiac catheterization. Undertreatment can lead to death or increased morbidity. The modified Sgarbossa criteria is a diagnostic tool designed to increase both sensitivity, specificity, and diagnostic accuracy for STEMI in patients with underlying LBBB, regardless of the age or chronicity of the bundle-branch block. This validated tool has a specificity greater than 90% and a sensitivity of 91% with replacement of the ST/S ratio as the third criterion. The interobserver agreement has been validated as strong in previous studies (k = 0.81).21
Following the 2013 guidelines, a triage algorithm for patients with suspected acute MI and LBBB was developed using Sgarbossa criteria, ST/S ratio, and discerning use of additional diagnostic tools including serial ECGs, serial troponin levels, and bedside echocardiography (Figure 4). Patients with suspected acute MI and LBBB who present with hemodynamic instability or acute heart failure are triaged to PCI or fibrinolytic reperfusion, regardless of ECG criteria. Otherwise, patients with a Sgarbossa score of 3 or greater or an ST/S ratio of -0.25 or less are triaged to reperfusion based on this validated tool. Patients not meeting either of these criteria and who are hemodynamically stable receive further evaluation with bedside echocardiography, serial ECGs, and serial troponin levels to determine whether they should receive angiography or noninvasive cardiac testing.11
Using the modified Sgarbossa criteria for management should facilitate more accurate diagnosis, fewer complications, better resource allocation, and improved risk stratification for patients with chest pain and LBBB.
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