(Circulation. 1996;94:2424-2428.)
© 1996 American Heart Association, Inc.
Articles |
Incidence and Clinical Relevance of the Occurrence of Bundle-Branch Block in Patients Treated With Thrombolytic Therapy
Duke University/VA Medical Center, Durham, NC.
Correspondence to Andrea Natale, MD, VA Medical Center, 508 Fulton St, Box 111A, Durham, NC 27705.
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Abstract |
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Background Whether thrombolytic therapy alters the incidence and clinical outcome of bundle-branch block is unclear.
Methods and Results We examined the occurrence of new-onset bundle-branch block, both transient and persistent, in 681 patients with acute myocardial infarction enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction 9 and Global Utilization of Streptokinase and t-PA for Occluded Arteries 1 protocols. Each patient underwent continuous 12-lead ECG monitoring for 36 to 72 hours with the Mortara ST monitoring system. Bundle-branch block was characterized as right, left, alternating, transient, or persistent. The overall incidence of bundle-branch block was 23.6% (n=161), with transient block in 18.4% (n=125) and persistent block in 5.3% (n=36). Right bundle-branch block was found in 13% (n=89) of the population; left bundle-branch block was found in 7% (n=48). Alternating bundle-branch block was seen in 3.5% (n=24) of patients. Left anterior descending artery infarcts accounted for most bundles (54%, n=79). Patients with bundle-branch block had lower ejection fractions, higher peak creatine phosphokinase levels (P<.0001), and more diseased vessels (P<.019). Mortality rates in patients with and without bundle-branch block were 8.7% and 3.5%, respectively (P<.007). A higher mortality rate was observed in the presence of persistent (19.4%) versus transient (5.6%) or no (3.5%) bundle-branch block (P<.001).
Conclusions Thrombolytic therapy reduces the overall mortality rate associated with persistent bundle-branch block. However, persistent bundle-branch block remains predictive of a higher mortality rate than either transient or no bundle-branch block. Continuous 12-lead ECG monitoring provides an accurate characterization of the incidence and type of conduction disturbances after acute myocardial infarction.
Key Words: bundle-branch block • myocardial infarction • conduction • mortality • thrombolysis
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Introduction |
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Bundle-branch block has been reported in 8% to 18% of patients with acute myocardial infarction and has been associated with an increased risk of complete heart block and sudden death.1 2 3 4 5 6 7 8 9 10 11 12 13 A significant amount of these clinical data, however, is based on the presence of persistent as opposed to transient bundle-branch block, the prognostic implications of which have yet to be fully defined.
The introduction of thrombolytic agents such as tissue plasminogen activator and streptokinase has decreased 30-day mortality in patients with acute myocardial infarction by 
25%,14 15 the proposed mechanisms being early reperfusion of the occluded artery and limitation of the myocardial damage. It has been postulated that the occurrence of bundle-branch block is intimately related to the amount of myocardium (including the septum) jeopardized by the decrease in blood flow from arterial thrombosis.1 13 16 If the occurrence of bundle-branch block is in fact related to the degree of myocardial damage sustained during an infarct, one could speculate that the earlier the infarct-related artery is reperfused, the more myocardium will be salvaged, with less likelihood of persistent insult to the conduction tissue. Whether the use of thrombolysis has indeed affected the development and clinical outcome of bundle-branch block is at present unknown. To assess this issue, we analyzed the incidence and clinical relevance of transient and persistent bundle-branch block in a series of consecutive patients with acute myocardial infarction treated with thrombolytic therapy who also underwent continuous 12-lead ECG monitoring for 36 to 72 hours.
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Methods |
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Study Population
The study population included 721 consecutive patients with acute myocardial infarction enrolled in both the Global Utilization of Streptokinase and t-PA for Occluded Arteries (GUSTO) 1 and Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) 9 trials who were also part of substudies examining ST-segment recovery and reperfusion. Exclusion criteria included patients who were monitored for a period of <36 hours and those with preexisting bundle-branch block. Subjects and methodology for the two trials and their respective substudies were described previously in detail.17 18 Briefly, the GUSTO 1 study randomized patients admitted within 6 hours of myocardial infarct onset to receive, in addition to intravenous heparin, one of four therapeutic regimens: tissue plasminogen activator alone, streptokinase alone, a combination of the two agents, or streptokinase with heparin. Major end points were in-hospital and 30-day mortality. In the TAMI 9 protocol, in addition to the use of standard tissue plasminogen activator, patients admitted within 6 hours of infarct onset were randomized to receive either an intravenous perfluorochemical emulsion (Fluosol) or placebo. Clinical outcome was then assessed both in hospital and at 30 days.
Definitions
The diagnostic criteria used for the determination of left bundle-branch block included (1) a QRS duration of 
0.12 seconds; (2) the presence of a broad monophasic R wave in leads I, V5, and V6, which is usually notched or slurred; (3) the absence of Q waves in leads I, V5, and V6; (4) delay of onset of intrinsicoid deflection in leads V5 and V6; and (5) repolarization abnormalities (ST and T waves displaced opposite to the major deflection of the QRS complex). Diagnostic criteria for the presence of right bundle-branch block included (1) prolongation of the QRS duration to 0.12 seconds; (2) a secondary R wave (R/) in the right precordial leads, with the R/ greater than the initial R wave; (3) a delay in the intrinsicoid deflection in the right precordial leads >0.05 seconds; and (4) a wide S wave in leads I, V5, and V6.19
ECG Analysis
All patients underwent 36 to 72 hours of continuous 12-lead ECG monitoring with the Mortara ST monitoring system. This system analyzes a 12-lead ECG every 20 seconds and acquires a tracing in the event of any ST-segment change that persists for >60 seconds, including repolarization changes caused by conduction abnormalities. An ECG also is stored at 20-minute intervals. The stored ECGs were downloaded as a digital data stream to 3.5-in diskettes for subsequent analysis.
The ECG data files were reviewed by use of a custom superimposition scoring program for the development of bundle-branch block. If this occurred, the block was characterized as right, left, or alternating, transient, or persistent. Transient bundle-branch block was defined as block that occurred during and was resolved before the end of the monitoring period. The absence of bundle-branch block was confirmed by analysis of the discharge ECG. Persistent bundle-branch block was defined as block that occurred during and persisted throughout the duration of the monitoring period. Persistence of bundle-branch block was also confirmed by analysis of the ECG at discharge. ECG data were interpreted by two experienced reviewers, both of whom were blinded to patient angiographic and clinical outcome. Information acquired regarding the occurrence of bundle-branch block was then correlated to the angiographic and clinical outcome data of each respective trial.
Statistical Analysis
For statistical analysis, the data for baseline and clinical outcome parameters are reported by use of percentages for categorical variables and 50th (25th, 75th) percentiles for continuous variables.
To determine possible univariate correlates of mortality and the occurrence of bundle-branch block, we applied 
2 and Fisher's exact tests for testing proportions and giving odds ratios and 95% CIs.
By using the Breslow day test for the homogeneity of the odds ratio, along with the Cochran-Mantel-Haenszel test, we were able to test the correlation between mortality and bundle-branch block while controlling for the infarct-related artery. A value of P<.05 was considered significant.
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Results |
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Of the 721 patients screened, 681 met the criteria for enrollment into the study. Table 1
gives the baseline clinical and demographic characteristics. A significant proportion of these patients were men with a history of smoking.
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The overall incidence of bundle-branch block was found to be 23.6% (161 patients; 95% CI, 20% to 27%), of which 125 patients (18.4%) had transient and 36 patients (5.3%) had persistent block. Right bundle-branch block was found in only 89 patients (13%); left bundle-branch block was seen in 48 patients (7%); and alternating bundle-branch block was found in 24 patients (3.5%). A strong correlation was found between the infarct-related artery and the presence of bundle-branch block (Table 2). Left anterior descending infarcts accounted for 54% of the bundle-branch blocks, whereas right coronary artery and circumflex artery infarcts were observed in 36% and 6.9% of the bundle-branch blocks, respectively. Table 3 shows the incidence of bundle-branch block subdivided between right, left, and alternating bundle-branch blocks with respect to the infarct-related artery. The incidence of bundle-branch block was found to be higher in those patients with left anterior descending artery infarcts versus other vessel distributions (Fig 1). Factors indicating more myocardial damage by the infarct such as the number of diseased vessels, peak creatine phosphokinase, and ejection fraction were also predictive of the occurrence of bundle-branch block (Table 4). However, the first available Thrombolysis in Myocardial Infarction flow after thrombolytic therapy did not appear predictive for the occurrence of bundle-branch block. A tendency to a higher incidence of bundle-branch block was also seen in older patients and in patients with a history of prior myocardial infarction, diabetes, or hypertension (Table 5).
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With respect to mortality, a strong relationship was found between the presence of bundle-branch block and the occurrence of death. In patients with bundle-branch block, the mortality rate was 8.7% compared with 3.5% in those without bundle-branch block (Fig 2). In addition, when patients were subdivided further into transient (77.6%) and persistent (22.4%) bundle-branch block, a significantly higher mortality was found in the persistent bundle group compared with the transient bundle and no bundle groups (Fig 3). In patients with persistent bundle-branch block, the likelihood of death was six times higher than in those without bundle-branch block (odds ratio, 6.0; 95% CI, 2.6% to 13.5%). In Fig 4, the mortality rates for patients with persistent left and right bundle-branch blocks are compared. Although a difference did exist between these two groups, it did not prove statistically significant. However, the sample size might have been too small to allow definitive conclusions.
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Discussion |
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The major findings of our study are (1) a lower occurrence of persistent bundle-branch block but a higher overall incidence than was reported previously (persistent and transient bundle-branch block), probably because of the use of continuous 12-lead ECG monitoring, and (2) increased mortality with persistent bundle-branch block and a decreased mortality with transient bundle-branch block, suggesting a more "complete" myocardial infarction in the persistent bundle-branch block group and an effective thrombolysis with myocardial salvage in the transient bundle-branch block group.
The prognosis of patients who develop bundle-branch block depends on the underlying cause. Left and right bundle-branch blocks are usually associated with heart disease but can also develop in normal individuals as well and typically increase with age.20 21 22 In patients with normal hearts, bundle-branch block does not appear to reflect a bad outcome; however, in patients with acute myocardial infarction, the occurrence of new bundle-branch block harbors a poor prognosis, as demonstrated by the higher incidence of congestive heart failure, cardiogenic shock, and ventricular arrhythmias shown in previous studies.3 5 11 22 23 24 25 26 27 In our series, the overall occurrence of bundle-branch block is similar or higher to that reported previously. However, it is evident that most of our patients had transient as opposed to persistent bundle-branch block, which constituted the majority of cases in prior studies.2 3 4 5 6 7 8 9 10 25 It is conceivable that this higher incidence of transient bundle-branch block was due to the administration of thrombolytic therapy, which reduced the amount of myocardial damage and reversed what would have otherwise become a persistent bundle-branch block. On the other hand, a better monitoring technique such as that used in our series might have been responsible for the overall higher incidence of bundle-branch block. In fact, in a retrospective analysis, evidence of transient bundle-branch block was low when standard monitoring techniques were used.28 In this regard, the ST monitor used in our study represents a more effective system because it can furnish continuous 12-lead ECGs, which are stored at least every 20 seconds, thereby maintaining detailed information on the QRS morphology and conduction system disturbances (ie, transient or persistent bundle-branch block, AV block) that otherwise could not be documented. It is clear that in view of the limitation of the monitoring system, previous series did not provide adequate assessments of the actual significance and occurrence of transient bundle-branch block. Conversely, on the basis of our findings, we were able to examine the clinical course, importance, and true incidence of transient bundle-branch block. It was evident that this subset of patients had an outcome similar to that of the group with no bundle-branch block. On the basis of our knowledge of the myocardial architecture, which includes both the conduction system and blood supply, a significant amount of myocardial damage must occur for bundle-branch block to occur.1 13 16 17 29 Therefore, one could speculate that because the use of thrombolytic therapy has been associated with a decreased mortality secondary to early reperfusion and ultimately less myocardial damage, the same relationship must, or at least should, exist between this treatment strategy and the development of transient versus persistent bundle-branch block. In this regard, in a recent small series, complete resolution of right bundle-branch block was reported within 3 hours from administration of thrombolytic agents.30
Before the use of thrombolytic agents, the mortality rate for patients with complete bundle-branch block ranged between 36% and 56%. It is clear from our data that the incidence of death in this patient group was lower than previously reported. However, the mortality rate among those patients with persistent bundle-branch block was still consistently higher, indicating that perhaps thrombolytic agents or other types of therapy (aspirin, ß-blockers) may not have been administered early enough, could not reverse the amount of damage already sustained by the myocardium, or simply did not achieve reperfusion of the infarct-related artery. This is consistent with the open-artery hypothesis and might indicate the need for early and aggressive reperfusion interventions in addition to the other adjuvant therapies previously listed for patients with acute myocardial infarction and bundle-branch block. What we could not ascertain with absolute confidence is whether time to treatment was a determining factor in the development of persistent bundle-branch block and hence patient outcome. Although a 6-hour time to treatment was used, it is understood that some infarcts may begin more silently and later progress to noticeable pain, thereby resulting in an underestimation of the time of infarct onset. In addition, because not all patients received early coronary angiography after institution of thrombolytic therapy, spontaneous late reperfusion cannot be excluded and correlation between transient bundle-branch block and effective reperfusion could not be established.
Regardless of the underlying mechanism, it seems apparent from our study that patients with persistent bundle-branch block still compose a higher-risk group for death and should be treated more aggressively. Whether this should include earlier revascularization, prophylactic pacing, or alternative approaches requires further investigation.
Study Limitations
The major limitation of the present study is the use of historical data to assess the benefit of thrombolytic therapy in our population. However, even though the lack of a matched control population that did not receive thrombolysis may represent a problem, it currently will be considered unethical not to administer thrombolytic agents to patients with acute myocardial infarction.
Conclusions
To the best of our knowledge, this is the first report showing that in patients receiving thrombolytic therapy, the occurrence of persistent bundle-branch block is reduced. Whether this reduction is directly related to the use of thrombolytic agents, coadjuvant therapies, or both cannot be answered by our data. The absolute incidence of death in the bundle-branch block group also appeared lower than that reported before the advent of thrombolytic therapy. However, despite thrombolytic therapy, persistent bundle-branch block still identified a subset of patients with higher mortality rates than those with either transient or no bundle branch.
Received December 20, 1995; revision received May 31, 1996; accepted June 7, 1996.
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