Management of Patients With LBB and Suspected MI
The initial rationale for using ST-segment elevation on ECG as a decision point for early reperfusion therapy in patients with suspected ACS was the high specificity for identifying patients who had complete occlusion of a coronary artery and who were most likely to benefit from treatment with a fibrinolytic agent. In this regard, a new (or presumably new) LBBB was thought to be equivalent to ST-segment elevation. However, recent data have called into question the principle that suspected ACS with a new or presumed new LBBB should be treated as a STEMI equivalent. In the fibrinolytic era, a diagnosis of AMI typically was not confirmed angiographically, but rather biochemically with creatine kinase, creatine kinase-myocardial band, or both. As primary PCI became more feasible, a larger number of studies were able to confirm AMI angiographically. Overall, these studies have demonstrated that less than half of all patients with suspected ACS and LBBB ultimately will be diagnosed with an AMI (Table 1). Moreover, a significant proportion of those patients with AMI will not have an occluded culprit artery at catheterization, and thus are classified more appropriately as having a non–ST-segment elevation myocardial infarction (NSTEMI), unstable angina, or non-ACS presentation (Table 3). 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 AMI, they are unlikely to benefit from early reperfusion therapy. In addition, fibrinolytics have been shown to offer no benefit, and in fact may be harmful, to patients with NSTEMI.
The significant variability in the prevalence of AMI complicated by LBBB reported in prior studies may be partially explained by diagnostic criteria with poor specificity for AMI. Because circulating biochemical markers of myocardial necrosis can be associated with structural heart disease, heart failure, kidney disease, and other comorbid conditions, patients with LBBB may have been misclassified previously as having AMI based solely on biochemical testing. Moreover, because elevated cardiac biomarkers are associated with greater risk in many non-ACS conditions compared with ACS, it is likely that some of the excess risk associated with LBBB reflects comorbid conditions not related to incident LBBB.
In addition to the more accurate classification of AMI in the primary PCI era, it is also possible that the distribution of new versus old LBBB has changed. For example, in 2 reports from the 1970s, the proportion of AMI patients with new (compared with old) LBBB ranged from 53% to 61%. In contrast, a recent study by Chang et al. reported that new LBBB was observed in only 29% of LBBB patients. Because patients hospitalized with myocardial infarction increasingly are older; are more likely to be female; are more likely to have coexisting conditions such as hypertension, dyslipidemia, and diabetes mellitus; and are more likely to have undergone previous coronary revascularization, the prevalence of chronic LBBB likely is increasing, despite a general decline in overall incident STEMI. This phenomenon suggests that chronic LBBB may have become more common, whereas incident LBBB in AMI has decreased, because of longer life expectancy and better survival for patients with heart failure and other coexisting conditions. Furthermore, other studies have demonstrated no difference in the prevalence of AMI between patients with chronic LBBB and new or presumed new LBBB, suggesting that true myocardial infarction-associated LBBB is indeed rare.
As pressures to reduce reperfusion times have increased, and acute cardiac care—both in the emergency department and in the ambulance—is increasingly driven by protocol, LBBB of unknown duration has emerged as a frequent reason for false activation of the cardiac catheterization laboratory for primary PCI. In this setting, a false activation is defined as an activation in which the coronary angiogram does not identify a culprit artery consistent with STEMI. Because only a minority of patients with LBBB ultimately are diagnosed with AMI, false-positive cardiac catheterization laboratory activation is frequent. In a single-center study of 1,335 patients, Larson et al. reported that the prevalence, of false-positive catheterization laboratory activation was 14% overall, but among patients with LBBB at presentation, the rate of false activation was 44%. These findings have been confirmed in a recent PCI study demonstrating that 39% of the 98 patients with new LBBB, most of whom even had concordant ST-segment changes on ECG, did not have an occluded culprit coronary artery on angiography. In our experience, it is not uncommon for catheterization laboratory activation to occur in patients with atypical chest pain or evidence of new onset heart failure in whom LBBB is present but cannot be confirmed to be old.
Urgent catheterization for all-comers can lead to an increased risk of complications related to the invasive procedure, resulting in prolonged hospital length of stay and higher costs and decreased quality of life for providers. In centers where primary PCI is not readily available, these issues obviously are more concerning given the risks of bleeding, particularly intracranial hemorrhage, with fibrinolytic therapy; the risks of fibrinolytic therapy may be magnified in patients with LBBB who generally are older and have higher rates of hypertension. Alternatively, given that patients with LBBB are less likely to receive reperfusion therapy (because of comorbid conditions or lack of diagnostic accuracy of the ECG procedure), there is appropriate concern that delays in diagnosis and therapy may lead to missed opportunities to reduce morbidity and mortality in patients with LBBB and true AMI. For example, a decision analysis found that routine administration of fibrinolytic therapy to all patients with LBBB and possible AMI would result in a small but significant mortality reduction; however, this approach may lead to unnecessary administration of fibrinolytic therapy to most patients who do not have AMI. It should be noted that this analysis was performed more than 10 years ago, based on epidemiological data suggesting a higher proportion of STEMI-equivalent AMI in patients with LBBB than seems to be the case today. In the modern era, the risk-to-benefit ratio may be even less favorable. Therefore, as systems of care improve and delays in transfer for primary PCI decrease, applying a routine transfer strategy for patients with suspected AMI and LBBB may preserve the benefit of reperfusion therapy for the highest-risk patients while minimizing potential harm associated with administering fibrinolytic therapy to patients without occluded arteries.
Clinical Controversies
The initial rationale for using ST-segment elevation on ECG as a decision point for early reperfusion therapy in patients with suspected ACS was the high specificity for identifying patients who had complete occlusion of a coronary artery and who were most likely to benefit from treatment with a fibrinolytic agent. In this regard, a new (or presumably new) LBBB was thought to be equivalent to ST-segment elevation. However, recent data have called into question the principle that suspected ACS with a new or presumed new LBBB should be treated as a STEMI equivalent. In the fibrinolytic era, a diagnosis of AMI typically was not confirmed angiographically, but rather biochemically with creatine kinase, creatine kinase-myocardial band, or both. As primary PCI became more feasible, a larger number of studies were able to confirm AMI angiographically. Overall, these studies have demonstrated that less than half of all patients with suspected ACS and LBBB ultimately will be diagnosed with an AMI (Table 1). Moreover, a significant proportion of those patients with AMI will not have an occluded culprit artery at catheterization, and thus are classified more appropriately as having a non–ST-segment elevation myocardial infarction (NSTEMI), unstable angina, or non-ACS presentation (Table 3). 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 AMI, they are unlikely to benefit from early reperfusion therapy. In addition, fibrinolytics have been shown to offer no benefit, and in fact may be harmful, to patients with NSTEMI.
The significant variability in the prevalence of AMI complicated by LBBB reported in prior studies may be partially explained by diagnostic criteria with poor specificity for AMI. Because circulating biochemical markers of myocardial necrosis can be associated with structural heart disease, heart failure, kidney disease, and other comorbid conditions, patients with LBBB may have been misclassified previously as having AMI based solely on biochemical testing. Moreover, because elevated cardiac biomarkers are associated with greater risk in many non-ACS conditions compared with ACS, it is likely that some of the excess risk associated with LBBB reflects comorbid conditions not related to incident LBBB.
In addition to the more accurate classification of AMI in the primary PCI era, it is also possible that the distribution of new versus old LBBB has changed. For example, in 2 reports from the 1970s, the proportion of AMI patients with new (compared with old) LBBB ranged from 53% to 61%. In contrast, a recent study by Chang et al. reported that new LBBB was observed in only 29% of LBBB patients. Because patients hospitalized with myocardial infarction increasingly are older; are more likely to be female; are more likely to have coexisting conditions such as hypertension, dyslipidemia, and diabetes mellitus; and are more likely to have undergone previous coronary revascularization, the prevalence of chronic LBBB likely is increasing, despite a general decline in overall incident STEMI. This phenomenon suggests that chronic LBBB may have become more common, whereas incident LBBB in AMI has decreased, because of longer life expectancy and better survival for patients with heart failure and other coexisting conditions. Furthermore, other studies have demonstrated no difference in the prevalence of AMI between patients with chronic LBBB and new or presumed new LBBB, suggesting that true myocardial infarction-associated LBBB is indeed rare.
As pressures to reduce reperfusion times have increased, and acute cardiac care—both in the emergency department and in the ambulance—is increasingly driven by protocol, LBBB of unknown duration has emerged as a frequent reason for false activation of the cardiac catheterization laboratory for primary PCI. In this setting, a false activation is defined as an activation in which the coronary angiogram does not identify a culprit artery consistent with STEMI. Because only a minority of patients with LBBB ultimately are diagnosed with AMI, false-positive cardiac catheterization laboratory activation is frequent. In a single-center study of 1,335 patients, Larson et al. reported that the prevalence, of false-positive catheterization laboratory activation was 14% overall, but among patients with LBBB at presentation, the rate of false activation was 44%. These findings have been confirmed in a recent PCI study demonstrating that 39% of the 98 patients with new LBBB, most of whom even had concordant ST-segment changes on ECG, did not have an occluded culprit coronary artery on angiography. In our experience, it is not uncommon for catheterization laboratory activation to occur in patients with atypical chest pain or evidence of new onset heart failure in whom LBBB is present but cannot be confirmed to be old.
Urgent catheterization for all-comers can lead to an increased risk of complications related to the invasive procedure, resulting in prolonged hospital length of stay and higher costs and decreased quality of life for providers. In centers where primary PCI is not readily available, these issues obviously are more concerning given the risks of bleeding, particularly intracranial hemorrhage, with fibrinolytic therapy; the risks of fibrinolytic therapy may be magnified in patients with LBBB who generally are older and have higher rates of hypertension. Alternatively, given that patients with LBBB are less likely to receive reperfusion therapy (because of comorbid conditions or lack of diagnostic accuracy of the ECG procedure), there is appropriate concern that delays in diagnosis and therapy may lead to missed opportunities to reduce morbidity and mortality in patients with LBBB and true AMI. For example, a decision analysis found that routine administration of fibrinolytic therapy to all patients with LBBB and possible AMI would result in a small but significant mortality reduction; however, this approach may lead to unnecessary administration of fibrinolytic therapy to most patients who do not have AMI. It should be noted that this analysis was performed more than 10 years ago, based on epidemiological data suggesting a higher proportion of STEMI-equivalent AMI in patients with LBBB than seems to be the case today. In the modern era, the risk-to-benefit ratio may be even less favorable. Therefore, as systems of care improve and delays in transfer for primary PCI decrease, applying a routine transfer strategy for patients with suspected AMI and LBBB may preserve the benefit of reperfusion therapy for the highest-risk patients while minimizing potential harm associated with administering fibrinolytic therapy to patients without occluded arteries.