Five Compelling Reasons Why New or Presumed New LBBB (without any other qualification such as Sgarbossa’s or Smith’s criteria) Should NOT be treated as STEMI

My presentation (contra-argument) during the "debate" with Prof Dr. Rashidi Ahmad from UMMC during the 2nd National Emergency and Critical Care Symposium 2015 in Ipoh (08 August 2015)

 

New or Presumed New LBBB To Be Treated As a STEMI Equivalent? A Debate from Chew Keng Sheng

The 6-page companion notes below can also be downloaded at: http://tinyurl.com/pern38t OR at the following URL in slideshare.net:
http://www.slideshare.net/cksheng74/new-or-presumed-new-lbbb-to-be-treated-as-a-stemi-equivalent-a-contra-argument-companion-notes-51407783

1. Recent evidences suggest that new or presumed LBBB does not predict STEMI any more than old LBBB or no LBBB

a.  Chang et al (2009): observational, 7937 patients with CP admitted to ED; 55 with new or presumed new LBBB, 136 had old LBBB, and 7746 had no LBBB. The rate of AMI was not significantly different between the 3 groups (7.3% vs 5.2% vs 6.1%; P = 0.75). Authors conclude, “ED patients with a new or presumed new LBBB are not at increased risk of AMI. The presence of LBBB, whether new or old, did not predict AMI.”

b.  Jain et al (2011): Retrospective, n = 892, only 36 (4%) of whom had new LBBB. Out of these 36, only 14 patients (39%) had final diagnoses of acute coronary syndromes (12 – AMI, 2 UA), 13 (36%) had cardiac diagnoses other than acute coronary syndrome (e.g. acute heart failure, complete heart block, AF, aortic stenosis, hypertensive emergency) and 9 (25%) had noncardiac diagnoses. Which means, only approx 1/3 of new or presumed new LBBB ultimately has AMI. Out of these 36 patients, almost all patients - 32 underwent PCI (3 in the non-ACS cardiac diagnoses and 1 non-cardiac group did not). Which means, new or presumed LBBB results in up to 2/3 of unnecessary PCIs.

c.   Kontos et al (2011): observational, n= 401 LBBB undergoing their institutional MI rule-out protocol, including serial cardiac biomarkers and PCI. LBBB were classified as chronic, new, or if no ECG was available, as presumably new. 37% new LBBB, 27% presumed new LBBB. A total of 116 patients (29%) had MI, with no significant difference in terms of frequency as well as the infarct size of MI was similar among patients with chronic LBBB, new LBBB, or LBBB of unknown duration. Concordant ST changes were the most important predictor of MI (odds ratio 17, 95% CI 3.4-81, P < .001) and an independent predictor of mortality (odds ratio 4.3, 95% CI 1.3-15, P < .001); “new” or “presumably new” (a.k.a. chronicity) was neither predictive.

d.   Wong et al (2005) in the HERO-2 (Hirulog and Early Reperfusion or Occlusion) trial; n= 300 with LBBB (92 with and 208 without ST-segment changes) and 15,340 no LBBB. AMI occurred in 80.7% of LBBB patients and 88.7% of controls (p = 0.006). What’s more interesting is when they analyzed LBBB with or without concordant ST changes: LBBB with ST-segment changes similar risk of 30-day mortality (even slightly higher) compared to STEMI patients without LBBB (odds ratio [OR] 1.37, 95% confidence interval [CI] 0.78 to 2.47). It is those STEMI patients with LBBB that has NO concordant ST-segment changes that has demonstrated lower mortality than STEMI patients without any LBBB (OR 0.52, 95% CI 0.33 to 0.80).  LBBB with concordant ST-segment elevation or lead V1 to V3 ST-segment depression independently predicted higher 30-day mortality but the absence of concordant ST-segment elevation or lead V1 to V3 ST-segment depression during LBBB independently predicted a lower 30-day mortality rate than that of patients with no LBBB.

2. Questionable historical origin - Recognition of LBBB in AMI dates back to 1917 in an account by Oppenheimer and Rothschild. As noted by Bauer (1965) many of the patients with BBB had many other confounding risks: they were significantly older, higher frequency of HPT, CHF, previous MI, and cardiogenic shock. Therefore, it is difficult to discern whether increased mortality risk (approximately 2-fold) in BBB were actually due to the BBB it self or it was confounded by age and comorbid conditions. Furthermore, in her article published in the Journal of Electrocardiology Vol. 33 (2000), Sgarbossa questioned whether many of the ECGs recorded in the pre-thrombolytic era were actually recorded in real time when the patients were having acute myocardial infarction or not. In that article the authors say:

“In the prethrombolytic era, however, the management of patients with myocardial infarction (MI) consisted only of pain relief, observation, and treatment of complications. In patients with ECG confounders, such as LBBB, the diagnosis of MI was confirmed through biochemical determinations over several hours or days after admission. Because there was no incentive to collect information on early ECG signs of MI, most studies on the diagnosis of MI in the presence of LBBB included ECGs with old infarctions as well as recordings obtained at widely scattered time-points after acute infarction”

Furthermore, the recommendation by ACC/AHA to use the criteria of new or presumed new LBBB is based on the findings more than 20 years ago. It was based on the pooled data of 9 trials in the FTT group (FTT = Fibrinolytic Therapy Trialists) back in 1991 (more than 20 years ago) showing that STEMI patients with BBB treated with fibrinolysis had lower mortality rate than placebo (18.7% vs 23.6%) but this is at the expense of increased major bleeding risk (1.3% vs 0.3%) and increase in stroke (2.1% vs 1.1%). Furthermore, there are three important caveats in interpreting the FTT group results:

o   these trials did not specify whether the ECG showed RBBB or LBBB

o   whether the conduction abnormalities were new, or whether there were associated ST-segment changes (a.k.a. the chronicity of the BBB unknown)

o   the cohort of STEMI patients with BBB in FTT group was very small, 3.6% of the total cohort

3.   3. Confounding pathogenetic mechanisms:

There are just too many confounders to the pathogenetic mechanism of LBBB in AMI. In a commentary article for example, Neeland et al (2012) say that for an AMI to result in LBBB, it would have required a rather large infarct. This is because, unlike the RBB, which is a discrete bundle that can be injured by a small focal insult, the LBB is a large bundle that is further branched into the anterior superior and posterior inferior fascicles, and therefore, the infarct would have either affected the LBB just distal to the bundle of His or an infarct that affect both anterior and posterior fascicles. As such, although LBBB can occur de novo in AMI, LBBB is more likely a pre-existing marker of underlying structural heart disease such as a fibrotic conduction system – thus, a reflection of the patient’s baseline CVS risks such as long standing HPT causing LVH or left ventricular remodeling resulting from CHF. This is consistent with the observations by Bauer (1964) that show that LBBB in AMI, although can be transient or permanent but most permanent LBBB in AMI are not due to true AMI-related LBBB because these true-AMI related LBBB has very high mortality.

4.   4. Ethical issue of giving fibrinolytics when it is not needed

The bleeding risk: E.g., FTT group data: bleeding risk of fibrinolysis 1.1 – 1.3%. NNT for streptokinase is 25; based on the studies like Chang et al (2009) where the incident of STEMI is the same in the new LBBB vs old LBBB vs no LBBB, and the incident of STEMI is only 1/3^rd of the total cases of new or presumed LBBB, is it ethical to subject the patient to fibrinolytic merely because of new or presumed new LBBB per se? To quote Neeland et al (2012):

“In centers where primary PCI is not readily available, these issues obviously are more concerning given the risks of bleeding, particularly intracranial bleeding, 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.”

5.   5. Unnecessary PCIs. As commented in Neeland et al (2012), presumed LBBB has emerged as a frequent reason for false activation cath lab. In a single study of 1335 patients, Larson et al (2007) – overall false +ve cath lab activation was 14%, but in the LBBB cohort, the rate was 44%! Lopes et al (2011) – 39% out of 98 patients with new LBBB, even including those with concordant ST-changes on ECG did not have positive angio finding. Even worse is in centers that do not have 24/7 PCI service.

ADDITIONAL NOTES: What’s the alternative?

If new or presumed new LBBB per se should not be treated as STEMI equivalents, what are the alternatives?

1. Add on the Sgarbossa’s 3 criteria

Concordant ST elevation >/= 1 mm, weighted score 5;

Concordant ST depression >/= 1 mm in V1-V3, weighted score 3;

Discordant ST elevation >/= 5 mm, weighted score 2

Tabas et al (2008) in a meta-analysis on the Sgarbossa’s criteria,

N = 2100

11 trials

For a total score of >/= 3 points,

sensitivity is 20% (95% CI 18 – 23%); specificity of 98% (95% CI 97 – 99%)

For a total score of >/= 2 points,

sensitivities ranged from 20% to 79%; specificities ranged from 61% to 100%

Sokolove et al (2000)

Sgarbossa’s criteria has an excellent inter-observer agreement (kappa=0.81, 95% CI  0.80 to 0.83) between cardiologists and emergency physicians for diagnosing AMI.

Concordant STE is the single most specific criteria (Lopes et al, 2011; Jain et al, 2011)

Although Sgarbossa’s criteria is specific, it is not sensitive. But we should remember Sgarbossa’s for LBBB is an add-on criteria for STEMI. Without Sgarbossa’s, the usual definition of STEMI should be applied.

2. Smith’s et al (2011)

Address the weak criteria of discordant ST elevation

Absolute 5 mm was used by Sgarbossa et al

Changed it to ST/S </= -0.25 (meaning magnitude of at least 25% of the R or S whichever greater) increases sensitivity from 52% to 91% at the expense of reducing specificity from 98% to 90%.

3. Neeland et al’s algorithm (2013)

If hemodynamically unstable, e.g. cardiogenic shock, refer for PCI/thrombolytics

If stable, use a more specific criteria (Sgarbossa’s)

If Sgarbossa’s criteria suggestive STEMI – PCI/thrombolytics

If Sgarbossa’s criteria not suggestive – depends on other clinical parameters including echo/serial biomarker

Suggested free web resources:

1.  A MUST READ - 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(2):96-105. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402162/pdf/nihms-388154.pdf

2.  Amal Mattu's ECG Case of the Week: Nov 4, 2013. Available at URL: https://www.youtube.com/watch?v=tf4rjJMSrgQ

3.  Modified Sgarbossa Criteria: Ready for Primetime? In: Academic Life in Emergency Medicine (ALiEM) website Available at URL: http://www.aliem.com/modified-sgarbossa-criteria-ready-primetime/ 

References:

• Chang AM, Shofer FS, Tabas JA, et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. Am J Emerg Med 2009;27(8):916-21. 
• 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(8):1111-6.
• Kontos MC, Aziz HA, Chau VQ, et al. Outcomes in patients with chronicity of left bundle-branch block with possible acute myocardial infarction. Am Heart J 2011;161(4):698-704.
• Wong CK, French JK, Aylward PE, 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(1):29-38.
• Sgarbossa EB. Value of the ECG in suspected acute myocardial infarction with left bundle branch block. J Electrocardiol 2000;33 Suppl:87-92.
• 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(2):96-105.
• Fibrinolytic Therapy Trialists' (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients.  Lancet 1994;343(8893):311-22.
• 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(23):2754-60.
• Lopes RD, Siha H, Fu Y, et al. Diagnosing acute myocardial infarction in patients with left bundle branch block. Am J Cardiol 2011;108(6):782-8.
• Tabas JA, Rodriguez RM, Seligman HK, et al. Electrocardiographic criteria for detecting acute myocardial infarction in patients with left bundle branch block: a meta-analysis. Ann Emerg Med 2008;52(4):329-36
• Smith SW, Dodd KW, Henry TD, et al. 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(6):766-76.
• Sokolove PE, Sgarbossa EB, Amsterdam EA, et al. Interobserver agreement in the electrocardiographic diagnosis of acute myocardial infarction in patients with left bundle branch block. Ann Emerg Med 2000;36(6):566-71.