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J Am Coll Cardiol, 2005; 46:39-41, doi:10.1016/j.jacc.2005.04.002
© 2005 by the American College of Cardiology Foundation
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EDITORIAL COMMENT

Left Bundle Branch Block in Acute Myocardial Infarction

Benign or Malignant?*

L. Julian Haywood, MD, FACC{dagger},*

{dagger} Keck School of Medicine, University of Southern California, and the Electrocardiography Department, Los Angeles County + USC Medical Center, Los Angeles, California.

* Reprint requests and correspondence: Dr. L. Julian Haywood, LAC + USC Medical Center, 1200 North State Street, Box 305, Los Angeles, California 90033. (Email: jHaywood{at}hsc.usc.edu).


Right bundle branch block (RBBB) and left bundle branch block (LBBB) occur commonly in routine electrocardiographic testing, with RBBB often occurring in young patients without apparent organic heart disease, and LBBB more often encountered in older patients with co-existing evidence of organic heart disease and systemic hypertension (1–3). The classic dissections of Lev (4) lent credence to speculation regarding the anatomic pathways associated with the conduction system and their vulnerability to specific anatomical lesions (5,6).

As attention has become focused on the management of individuals with suspected acute coronary insufficiency or infarction, the utility of the electrocardiogram (ECG) as an adjunct to the diagnosis of acute myocardial infarction (AMI) or injury in patients with LBBB has received renewed attention (7–11). Three specific patient settings might be encountered:

1 When the patient has LBBB on admission and recent previous ECGs do not show LBBB, the patient is presumed to have new-onset LBBB, which many investigators and current guidelines accept as the equivalent of electrocardiographic findings supportive of AMI (12,13). The question is raised as to whether it is reasonable to expect that new-onset LBBB in the setting of AMI would have characteristics different from new-onset LBBB in the absence of AMI.
2 When the patient has LBBB on arrival and is known to have LBBB on previous ECGs, the question is raised as to whether the presence or absence of specific characteristics of the LBBB pattern can reliably differentiate between the presence or absence of new injury or infarction.
3 When the patient has LBBB on arrival and no pre-existing ECG is available for comparison, the question arises as to whether there are electrocardiographic characteristics that, if present or absent, could reliably distinguish between patients with new injury or infarction and those without.
Multiple investigators have dealt with aspects of this problem. In a substudy of 681 patients from the Global Utilization of Streptokinase and TPA for Occluded Arteries (GUSTO)-1 and Thrombolysis and Angioplasty in Myocardial Infarction (TAMI)-9 trials, LBBB was encountered in 8% of the patients and thrombolytic therapy was credited with reducing the mortality associated with persistent bundle branch block (both RBBB and LBBB), but persistent block still conferred a higher mortality. Transient block was more common in this study than persistent block, at least in part because of the use of continuous monitoring to detect the presence of bundle branch block (14).

In a much larger review of data from the National Registry of Myocardial Infarction, 6.7% of 297,832 patients had LBBB (n = 19,467), whereas RBBB was almost as common and both were associated with higher rates of co-morbidity and had a worse prognosis in comparison to those without conduction delay. In comparison to patients with ST-segment elevation without bundle branch block, RBBB was a stronger predictor of in-hospital mortality and LBBB was less predictive (15).

Sgarbossa et al. (16) proposed specific electrocardiographic criteria for the diagnosis of AMI in the presence of LBBB based on the criteria performance as applied to 131 patients in the GUSTO-1 trial who had AMI and LBBB in comparison to patients from the Duke database who had LBBB and were clinically stable. The application of the most efficient of the criteria was associated with a high specificity and low sensitivity.

In an evaluation of the previously mentioned criteria in a community-based cohort of 83 patients with 103 presentations of suspected AMI, the criteria proposed by Sgarbossa et al. (16) performed poorly because of a low sensitivity of 10%, although the specificity was high at 82%. The investigators concluded that a sensitivity of 80% and a specificity of 90% would be required for electrocardiographic criteria in the presence of LBBB to be useful in the selection of patients to receive thrombolytic therapy (17).

Citing the overall poor performance of all QRS-based and ST-T-wave based criteria for AMI in the diagnosis of AMI, Maynard et al. (18) propose that body surface mapping be used to improve diagnosis in patients with LBBB; however, both the number of studies and the number of patients involved are very limited.

The report by Wong et al. (19) in the current issue of the Journal presents data to evaluate the Sgarbossa et al. (16) criteria to distinguish between ECGs with LBBB that are indicative of new injury or ischemia and those that are not supportive. The specific measurement criteria are the same as those tested in the previous GUSTO-1 study and are refined and evaluated here in a retrospective analysis of ECGs collected at randomization and 60 min after initiation of thrombolytic therapy in the Hirulog Early Reperfusion/Occlusion (HERO) trial. The criteria tested include:

1 ST-segment elevation measuring ≥1 mm concordant with the QRS in any lead.
2 ST-segment depression measuring ≥1 mm in any of the V1 through V3 leads.
3 Discordant ST-segment elevation measuring ≥5 mm.
Using a criterion of twice the upper limit of normal value for serum troponin as the ‘gold standard’ for confirmation of myocardial injury, the investigators in the Wong et al. (19) study demonstrate a high specificity for the criteria of >l mm elevation in any lead or ST-segment depression in V1 through V3, but low sensitivity and low specificity and sensitivity for ≥5 mm discordant ST-segment elevation in any lead. Because 80% of the 300 patients with LBBB randomized into the HERO trial had enzymatic confirmation of AMI (1.76% of 17,013 total patients enrolled in the HERO trial, all of whom received one of two comparison regimens of thrombolysis), there will be some debate as to whether the listed ECG criteria received an adequate appraisal despite the careful statistical comparisons.

Although the ST-segment elevation criteria identified patients among those with enzymatically confirmed AMI who had higher enzymatic levels and worse 30-day mortality, the low sensitivity indicates that the absence of the criteria was not useful to exclude enzymatically confirmed AMI, albeit LBBB patients without ST-segment elevation had a better 30-day outcome.

A major contribution of this trial—apart from whether or not the electrocardiographic diagnostic criteria results will prove to be convincing in other hands and everyday practice—is the outcome comparisons between patients with and without LBBB. The overall mortality rates of patients with LBBB were significantly higher at 30 days compared to those with normal conduction (16% vs 9.1%, p < 0.0001), confirming the known higher risk attendant to the presence of LBBB. However, when patients with LBBB were compared to an age-matched and geographical origin-matched internal sample of comparable size with normal conduction, the 30-day mortality was lower in LBBB patients (16% vs 22.1%) and the incidence of confirmed AMI was lower in LBBB patients (80.7% vs 88.7%). Although the presence of ST-segment changes during LBBB (versus those with LBBB without ST-segment changes) was associated with higher mortality (21.7% vs 13.5%, p = 0.067), the higher mortality rate was not different from matched controls (21.1% vs 25%, p = 0.563), whereas the mortality was significantly lower in those with LBBB without ST-segment changes compared with matched controls, respectively (13.5% vs 21.6%, p = 0.022).

Thus, this important trial presents three important findings with major clinical implications:

1 Reliable ECG criteria for acute myocardial injury can identify patients with LBBB who are at higher risk for increased mortality despite the use of thrombolytic therapy.
2 The LBBB confers increased risk for mortality in the setting of suspected AMI; however, the increased risk is significantly associated with older age and co-morbidity risk factors.
3 In the absence of electrocardiographic criteria for myocardial injury or infarction, AMI patients with LBBB may be at lower risk for mortality in comparison to age-matched controls, in part possibly due to the "protective" effect of pre-existing angina.
The findings of the study by Wong et al. (19) warrant appropriately sized prospective studies to determine the practicality of the electrocardiographic criteria proposed and the implications of the matched control findings.


    Footnotes
 
* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. Back


    References
 Top
 References
 
1. Hiss RB, Lamb LE. Electrocardiographic findings in 122,043 individuals Circulation 1962;25:947-961.[Abstract/Free Full Text]

2. Shaffer AB, Reiser L. Right bundle branch block system in healthy young people Am Heart J 1961;62:487-493.[CrossRef][Web of Science][Medline]

3. Friedberg CK. Disturbances in conductionheart block and bundle branch block. In: Friedberg CK, editor. Diseases of the Heart. Philadelphia, PA: W. B. Saunders Company; 1966. pp. 583-639.

4. Lev M. Anatomic basis for atrioventricular block Am J Med 1964;37:742-748.[CrossRef][Web of Science][Medline]

5. Racker DK. Atrioventricular mode and input pathwaysa correlated gross anatomical and histological study of the canine atrioventricular region. Anat Rec 1989;224:336-354.[CrossRef][Medline]

6. Flowers N. Left bundle branch blockcontinuously evolving concept. J Am Coll Cardiol 1987;6:684-697.

7. Shupak MG, Lyons WL, Go AS, et al. Should the electrocardiogram be used to guide therapy for patients with left bundle branch block and suspected myocardial infarction? JAMA 1999;28:714-719.

8. Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute myocardial infarction N Engl J Med 2003;348:933-940.[Free Full Text]

9. Wacker FJ. The diagnosis of myocardial infarction in the presence of left bundle branch block Cardiol Clin 1987;5:393-401.[Medline]

10. Canon A, Freedman SB, Bailey BP, Bernstein L. ST-segment changes during transmural ischemia in chronic left bundle branch block Am J Cardiol 1989;64:1216-1217.[CrossRef][Web of Science][Medline]

11. Stark KS, Krucoff MW, Schryver B, Kent KM. Quantification of ST-segment changes during coronary angioplasty in patients with left bundle branch block Am J Cardiol 1991;67:1219-1222.[CrossRef][Web of Science][Medline]

12. Edhouse JA, Sakr M, Angus J, et al. Suspected myocardial infarction and left bundle branch blockelectrocardiographic indication of acute ischemia. J Accid Emerg Med 1999;16:331-335.[Abstract/Free Full Text]

13. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summarya report of the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction). Circulation 2004;110:588-636.[Free Full Text]

14. Newby KH, Pisano E, Krucoff MW, Green C, Natale A. Incidence and clinical relevance of the occurrence of bundle-branch block in patients treated with thrombolytic therapy Circulation 1996;94:2424-2428.[Abstract/Free Full Text]

15. Go AS, Barron HV, Rundle AC, Omato JP, Avins AL. Bundle-branch block and in-hospital mortality in acute myocardial infarction Ann Intern Med 1998;129:690-697.[Abstract/Free Full Text]

16. Sgarbossa EB, Pinski SL, Barbagelata A, et al. GUSTO-1 Investigators Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block N Engl J Med 1996;334:481-487.[Abstract/Free Full Text]

17. Shlipak MG, Lyons WL, Go AS, Chou TM, Evans T, Browner WS. Should the electrocardiogram be used to guide therapy for patients with left bundle-branch block and suspected myocardial infarction? JAMA 1999;281:714-719.[Abstract/Free Full Text]

18. Maynard SJ, Menown IBA, Manoharan G, Allen J, Mc Anderson J, Adgey AAJ. Body surface mapping improves early diagnosis of acute myocardial infarction in patients with chest pain and left bundle branch block Heart 2003;89:998-1002.[Abstract/Free Full Text]

19. Wong C-K, French JK, Aylward PEG, et al. Patients with prolonged ischemic chest pain and presumed-new left bundle branch block have heterogeneous outcomes depending on the presence of ST-segment changes J Am Coll Cardiol 2005;46:29-38.[Abstract/Free Full Text]


Related Article

Patients With Prolonged Ischemic Chest Pain and Presumed-New Left Bundle Branch Block Have Heterogeneous Outcomes Depending on the Presence of ST-Segment Changes
Cheuk-Kit Wong, John K. French, Philip E.G. Aylward, Ralph A.H. Stewart, Wanzhen Gao, Paul W. Armstrong, Frans J.J. Van De Werf, R. John Simes, O. Christopher Raffel, Christopher B. Granger, Robert M. Califf, Harvey D. White for the HERO-2 Trial Investigators
J. Am. Coll. Cardiol. 2005 46: 29-38. [Abstract] [Full Text] [PDF]




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