Submitted and written by Parker Hambright MD, peer reviewed by Meyers, McLaren, Grauer, Smith
A man in his late 60s called EMS for acute dizziness, nausea, vomiting, and chest pain shortly after beginning his morning exercise. The symptoms lasted for only about 15 minutes and then resolved spontaneously. He was brought to the ED and evaluated in less than one hour from onset of symptoms. His history included known CAD, HTN, HLD, prior MI with LAD stent, AAA repair, and reported dizziness/vertigo.
Here are his EMS and ED triage ECGs (unclear whether symptoms still present or resolved at time of these ECGs, but it seems that symptoms were likely improved or resolved):
EMS:
ED triage (within 1 hour of onset of symptoms):
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| This baseline ECG shows a normal LBBB. |
Meyers interpretation: The EMS and triage ECGs above have suspicious, but not diagnostic, changes from the baseline ECG. The baseline ECG shows only minimal ST deviations in the limb leads, whereas the triage ECG shows greater ratios of STE in III and aVF and STD in I and aVL, with increased area under the T waves, compared to baseline. But the triage ECG does not have any of the modified Sgarbossa criteria. It is not diagnostic, but potentially suspicious for dynamic changes of the inferior leads signaling inferior OMI. I would not yet be certain from these ECGs alone, but I would certainly get more information including repeat ECGs to see if this concern is playing out.
His initial high sensitivity troponin I (Beckman Coulter Access hsTnI) was less than 6 ng/L (drawn at about 1 hour from onset of symptoms).
The providers seemed to think that his symptoms were more related to his history of vertigo. He was given meclizine and symptoms had improved. He was discharged home.
.............
5 days later he returned complaining of two or three days of intermittent chest pain. He presented when he realized the pain wasn't going away during this most recent episode. He did not have further episodes of dizziness.
Here is his ECG at triage on second presentation:
The ECG above is diagnostic of inferoposterior OMI in LBBB. Findings include concordant STE in II, proportionally excessively discordant STE in III (ST/S ratio = 2/4 = 0.5) and aVF with reciprocal depression in I and aVL, hyperacute T wave morphology in II, III, and aVF, and concordant STD with TWI in V1 and V2. The cath lab was activated and the patient was emergently taken by cardiology to the cath lab.
Angiography demonstrated a 70% stenosis of the proximal RCA and thrombotic (100%) occlusion of the mid RCA. Both lesions were stented and demonstrated TIMI 3 flow after intervention. The prior LAD stent was widely patent, and the LCX had only minor irregularities.
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| Grossly patent left main, LAD, and LCX. |
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| After initial intervention. |
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| Post intervention. |
Troponin I was 3,710 ng/L, then 8,228 ng/L, then no further troponins were measured.
Post cath ECG1:
Less STE and terminal T-wave inversion in inferior leads
("Inferior" Pattern A Wellens' waves in the presence of LBBB)
T-waves have evolved to deeper and more symmetric.
("Inferior" Pattern B Wellens' waves in the presence of LBBB)
The post cath ECGs show inferoposterior reperfusion.
Echocardiogram demonstrated an LVEF of 50% with hypokinesis of the basal inferoseptal segments.
The patient experienced resolution of symptoms, was placed on DAPT, and was discharged on hospital day 2 following an uncomplicated hospital course.
Learning Points:
Use the modified Sgarbossa criteria to help diagnose OMI in the setting of wide QRS complexes such as LBBB and ventricular paced rhythm. But just like all other OMI ECG findings, the ECG starts from normal/baseline and evolves into these diagnostic findings in real time. The first visit ECG in this case is "between" the baseline and the diagnostic inferoposterior OMI ECG; in other words, since we know the pain was resolving, it is likely "on the way down" from more diagnostic OMI findings, on the way back to normal (and then likely reperfusion). Becoming accurate at ECG interpretation for OMI involves learning these progressions. Additionally, we have discussed many times on the blog that the ratio of 25% for excessive discordant STE is more specific but less sensitive than 20%. No criteria are perfect in isolation, and if you understand the OMI progression you will be able to perform better than the modified Sgarbossa criteria alone.
Not even high sensitivity troponins reliably show elevations within the first 1 or possibly even 2 hours since onset of ACS. It is very likely that a second troponin on this patients initial visit would have had a significant "delta" (change, or rise), or even risen above the 99th percentile upper reference limit. In either case, further investigation would have been required.
Review of LBBB OMI Findings on ECG:
The approach to diagnosing OMI in the presence of LBBB was formerly through the use of the Original Sgarbossa criteria, published in 1996. They consist of the following 3 criteria:
Concordant ST elevation >1mm in at least one lead with positive QRS (5 points)
Concordant ST depression >1mm in at least one of leads V1-V3 (3 points)
Discordant ST elevation >5mm in at least one lead with negative QRS (2 points)
A total of 3+ points was deemed diagnostic of any acute MI (OMI or NOMI)
In 2012, Dr. Smith published a new criterion of “discordant STE >1mm AND >25% S wave amplitude” to substitute the previous criterion of “discordant STE >5mm in leads with negative QRS”. The outcome was "Occlusion," and not just any acute MI. The new modified Sgarbossa criteria consists of the following 3 criteria:
Concordant ST elevation >1mm in at least one lead with positive QRS
Concordant ST depression >1mm in at least one of leads V1-V3
Discordant ST elevation >1mm AND >25% of the preceding S-wave amplitude in at least one lead
This alteration of the criteria removed the arbitrary 5mm STE cutoff and replaced it with a criterion that uses disproportional discordance, rather than a fixed amount of STE. The modified Sgarbossa criteria has been retrospectively validated by Meyers et al. and determined, using the 25% rule, to have a sensitivity of 80% and specificity of 99% for OMI; when the 20% rule is used, sensitivity rises to 84%, with specificity dropping to 94%. This alteration improved sensitivity for OMI in LBBB - particularly in ECGs with low voltage - while not resulting in a statistically significant loss of specificity.
The modified Sgarbossa criteria can be objectively applied to ECGs with LBBB in the setting of ACS symptoms in attempts to identify OMI vs NOMI. A conceptual understanding of the criteria, however, can aid in determining which coronary vascular distribution is most likely to be experiencing an OMI. At the foundation of the OMI progression sequence, some degree ST elevation is expected to occur with an occlusive thrombus involving the anterior, lateral, and inferior walls of the myocardium and ST depression of V1-V4 is expected in posterior wall occlusions. These ischemic changes can also be anticipated in a pre-existing LBBB. The expected ECG changes for OMI in LBBB or ventricular-paced rhythm for the various coronary distributions are listed:
--Anterior (assuming predominantly negative QRS complex): Discordant ST elevation >1mm AND >25% S-wave amplitude in V1-V4
--Lateral (assuming predominantly positive QRS complex): Concordant ST elevation >1mm in leads V5-V6, I, or aVL
--Inferior: Concordant ST elevation >1mm or excessively discordant STE greater or equal to 25% in leads II, III, or aVF, based on QRS
--Posterior (assuming predominantly negative QRS complex in anterior leads): Concordant ST depression >1mm in V1-V3
In an uncomplicated LBBB, abnormal depolarization of the ventricles results in abnormal repolarization and a ST segment discordance of approximately 10% is expected and normal. The recognition of concordant ST segment changes or disproportionally discordant ST segment changes (>25%) as abnormal and concerning for ischemia is paramount to the diagnosis of OMI in LBBB.
In this case, the ECG demonstrated 2 out of 3 of the modified Sgarbossa criteria. The prompt recognition and application of the modified Sgarbossa criteria allowed for timely revascularization and a promising clinical outcome.
See these other LBBB posts:
LBBB: Using the (Smith) Modified Sgarbossa Criteria would have saved this man's life
Acute Chest pain with LBBB. What is going on?
Some Cardiologists still are not familiar with Sgarbossa Criteria.....
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MY Comment, by KEN GRAUER, MD (8/1/2022):
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I am always intrigued by the challenge of interpreting the ECG of a patient with new symptoms and LBBB. Sometimes this assessment is EASY — as was the case for the 4th tracing in today’s case, obtained at the time this patient returned to the ED 5 days later — at which time, the ECG had become clearly diagnostic of acute infero-postero OMI.
- In contrast — ECG findings were far more subtle for the 2nd tracing in today's case (which was the initial ED Triage ECG).
As I have often noted in Dr. Smith’s ECG Blog — I favor a "Qualitative" Approach for assessment of LBBB tracings in patients with new symptoms, especially when modified Smith-Sgarbossa Criteria are not yet satisfied.
- I focus My Comment in today's case on the initial ED Triage tracing — and — on the baseline ECG from 1 year earlier. These are the 2nd and 3rd tracings shown above in the discussion by Drs. Hambright and Meyers — which I've reproduced and put together in Figure-1.
- Because of its suboptimal resolution — it is much more difficult to compare the prehospital EMS tracing with the baseline ECG in today's case. Given that my reading of the prehospital EMS tracing is virtually the same as the initial Triage ECG (with the exception of there being some PVCs on the EMS tracing) — I think for educational purposes, it is reasonable to think of the “presenting ECG” as this initial ED Triage Tracing ( = ECG #2).
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| Figure-1: Comparison of the initial ED Triage Tracing — with this patient’s “baseline” ECG from 1 year earlier (See text). |
What Do I Mean by a "Qualitative" Approach?
While the initial ED Triage Tracing ( = ECG #2) by itself is not diagnostic for acute OMI — "qualitative" assessment of ST-T wave morphology is suspicious for an acute evolving event.
- As helpful as modified-Smith-Sgarbossa Criteria can be — I like to look for ST-T wave changes that I know are not normal in a patient with LBBB. These changes in ECG #2 are subtle — but they are present:
- Since measurements are not used in the qualitative approach — I fully acknowledge that this approach is experiential. That said — this approach has consistently worked well for me over many years.
- Since ST-T wave changes with the qualitative approach may be subtle — the more leads showing abnormal ST-T wave morphology — the greater the likelihood of an acutely ongoing cardiac event.
- KEY Point: The best way to improve on recognition of subtle ST-T wave abnormalities in the setting of LBBB — is to routinely go back and compare the initial ECG of each case you encounter, with follow-up tracings obtained after acute reperfusion.
- For More on the "Qualitative" Approach — Please check out My Comments in the September 17, 2020 post — the April 7, 2019 post — and the May 24, 2019 post in Dr. Smith's ECG Blog.
What Do We See in ECG #2 ( = the initial ED Triage Tracing)?
The rhythm in ECG #2 is sinus at ~60/minute. There is low voltage in the limb leads. The PR interval is prolonged (~0.24 second) — and the QRS complex is wide, consistent with complete LBBB.
- Although difficult to assess because of the low voltage — there is straightening of the ST segment takeoff in each of the inferior leads (slanted BLUE lines in these leads).
- Similar straightening of the ST segment takeoff is noted in lead V5. Note the subtle difference in shape of these "straightened" ST segments — compared to the gentle upsloping (normal) shape of the ST segment in leads V3 and V4 of ECG #2.
- Normally with LBBB — lateral leads (ie, leads I,aVL,V6) manifest a depressed ST-T wave. It is not "usual" to see the amount of terminal T wave positivity highlighted by BLUE arrows in these leads. Again — there is low voltage in these lateral leads, which makes assessment of proportionality especially challenging. But I thought the relative size of the terminally upright T waves in leads I,aVL,V6 of ECG #2 was clearly more than I would normally expect.
To EMPHASIZE:
The above ST-T wave "qualitative" findings are subtle! These changes are not diagnostic of OMI! I was in NO way certain from this single initial ECG that an acute ongoing event was occurring. I would not activate the cath lab for these findings. That said:
- This patient who presented with new chest pain is high-risk for having an acute event given his known history of coronary disease — and — his sudden onset of new symptoms severe enough to prompt EMS delivery to the ED. As a result — we need to lower our "threshold" for identifying ECG findings of concern.
- Although subtle (and not diagnostic) — I thought suspicious ST-T wave findings were present in no less than 7/12 leads in ECG #2 (slanted BLUE lines and BLUE arrows in the Top tracing in Figure-1).
- BOTTOM Line: Errors were made in the management of this case. The patient's chest pain was short-lived — and apparently resolving (if not resolved) by the time ECG #2 was obtained. The best way to tell IF the potentially concerning ST-T wave findings I identify above are real is with follow-up (ie, more than a single ECG in the ED — more than a single troponin in the ED — and being sure to correlate chest pain severity with the timing of serial ECGs and troponins). This was not done.
- NOTE: If today's patient in fact had total coronary occlusion at the time he called EMS — and IF the reason his chest pain resolved (as his history suggests) at the time ECG #2 was recorded, was because there was spontaneous reperfusion of the "culprit" artery — then as per Drs. Hambright and Meyers, the reason frank ST elevation may not have been seen in ECG #2 — may have been because of "pseudonormalization" (ie, ST segments returning to the baseline on their way toward evolving inverted reperfusion T waves).
To Also EMPHASIZE:
My above interpretation was made before I looked at this patient's previous "baseline" ECG from 1 year earlier!
- Seeing this patient's "baseline" tracing ( = ECG #3) — provides confirmation that the ST-T findings that I highlighted in BLUE in ECG #2 were all new compared to this patient's ECG 1 year earlier.
- Terminally positive T waves were present in leads I and aVL of ECG #3. That said — Considering low amplitude of the QRS complex in these leads — Isn't this terminal T wave positivity more marked in leads I and aVL of ECG #2?
- Starting from the flat ST segments in the inferior leads and in lead V4 of ECG #3 — Is there any doubt about the change in ST-T wave appearance, with ST segment straightening in each of these inferior leads in ECG #2? Given the history of new chest pain — I now interpreted these changed ST-T waves as hyperacute until proven otherwise.
In Summary:
As per Drs. Hambright and Meyers — today's patient returned to the ED 5 days later because of recurrent chest pain. To underscore the Learning Points highlighted above:
- Chances are that IF more than a single troponin would have been obtained on the initial ED visit — that a 2nd troponin would probably have been abnormal enough to prompt investigation (instead of sending the patient home).
- I also suspect that IF another ECG would have been done in the ED — that the "pseudonormalization" phase that we are probably seeing in ECG #2 — may have given way to evolution of "tell-tale" reperfusion T waves.
- Additional Learning Point: Qualitative assessment of ST-T wave changes in patients with LBBB and new symptoms can clue you in to an acutely evolving event before frank Smith-Sgarbossa Criteria are satisfied. To "hone" your ability to pick up these subtle findings — Compare the inferior leads in ECG #2 with the inferior leads in the 4th tracing shown above in the presentation by Drs. Hambright and Meyers (ie, the Triage ECG on 2nd presentation). Doing so should illustrate why I immediately suspected that there might be an ongoing acute inferior OMI from the inferior lead ST-T wave straightening in the LBBB tracing shown in ECG #2.
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