Acute chest pain with LBBB and obvious OMI, worsening on serial ECGs, but repeatedly missed by physicians and Marquette 12SL

This was written by Hans Helseth. He just graduated from college. He has no medical training, but he has read this blog for years. He is an ECG tech who hopes to go to medical school.

He has never been poisoned by the STEMI/NSTEMI paradigm because he has never been to medical school.  Lucky Hans.

You don't need to have medical training to recognize OMI on the ECG.  You need to be curious, have an open mind, probably have a talent for seeing patterns, and read lots of posts on this blog (where else will you see hundreds of cases of subtle OMI?).

Although the ECGs today are obvious (I hope) to most, it is not realistic for all providers to be good at reading ECGs for OMI.  It takes both too much time and too much ability for pattern recognition.  Which is why it is a perfect use case for AI, and we have produced the PM Cardio Queen of Hearts AI ECG Model to do this for you.  It is awaiting FDA approval (but approved for 1.5 years already in the EU)

Even though these ECGs are obvious, they were missed by both board certified emergency physicians AND by the Marquette 12SL Conventional algorithm!

Case

A 76 year old man with chronic hypertension but no history of coronary disease or myocardial infarction presented to the ED with chest pain at 2343.

His triage EKG is shown below:

There is left bundle branch block, so the EKG must be evaluated for ischemia by Smith-modified Sgarbossa criteria.

There is ST elevation in the inferior leads. There is inappropriately discordant ST elevation in lead III (ST elevation greater than 25% of the height of the QRS complex) and concordant ST elevation in leads II and aVF. These leads all have large hyperacute T waves. There is evidence of transmural ischemia of the posterior wall as well. Leads V1 to V4 have down-up shaped T waves typical of ischemia and atypical of LBBB. There is concordant ST depression in V2 and V4. While the J point in leads V1 and V3 may not show ST depression, with LBBB these leads should have ST elevation. They therefore display “relative ST depression”. There is also evidence of lateral wall involvement in V6, which shows an isoelectric J point rather than the expected discordant ST depression.

Overall, this EKG meets Smith-modified Sgarbossa criteria in multiple leads. For it to be positive for the criteria, it only needs to be positive on one lead!!

In other words, it is overtly and obviously diagnostic of inferior, posterior, and lateral OMI.

Unfortunately, the ED provider did not recognize this pathognomonic ECG. The final interpretation was “Sinus rhythm with left bundle branch block. No priors to compare. No other acute ischemic changes noted.”

The Marquette 12 SL algorithm only flagged the EKG as abnormal for left bundle branch block.

The Queen of Hearts recognizes this as OMI ("STEMI/STEMI Equivalent").

At 0012, the first high sensitivity troponin T (URL 15 ng/L) resulted at 29, slightly elevated. Even in the absence of ECG findings, a patient with persistent chest pain and new elevated troponin should go to the cath lab by current guidelines, but these guidelines are hardly ever followed). Moreover, one should never wait for troponins when the ECG is diagnostic -- myocardium is dying while you wait.

The ED provider repeated the EKG at 0029, nearly 2 hours later:

There are dynamic changes of continued ischemia: The ST elevation and T wave sizes in all inferior leads have increased. The T wave inversion in V2 has become more dramatic. ST elevation has now developed in V6.

None of these changes were appreciated.

The interpretation by the provider read “Repeat EKG showing stable appearing left bundle branch block. No other acute changes”. The Marquette 12 SL algorithm again only noted LBBB.

The Queen of hearts also recognizes this ECG as OMI.

The patient waited in the ED for another hour and fifteen minutes. A third EKG was obtained at 0144 because nursing staff noticed changes in ST elevation on the patient’s monitor:

There is now a tremendous 6-7mm of ST Elevation in lead III!

Amazingly, the Marquette 12 SL algorithm still only recognized LBBB.

The provider interpretation of this EKG read: “Repeat EKG with continued left bundle branch block. Generally has similar appearance but there are some changes noted in inferior leads with rising J-point. Difficult to interpret due to a left bundle branch block.”

It is incredible how findings which appear to those who really know ECGs are obvious, but to most physicians are inscrutable.

At 0208 the ED staff contacted cardiology to discuss the case. Cardiology decided to activate the cath lab emergently for “quite a bit of elevation in II, III, and aVF”.

At 0210, a repeat troponin resulted at 84.

The patient was finally taken for angiography at 0303, 3 hours and 20 minutes after his first diagnostic EKG:

There is a total thrombotic occlusion of the a large obtuse marginal off the circumflex, which supplies the inferior and posterior walls. (See the Terminology and Semantics section of Willy Frick's cardiac cath guide). It was treated with a drug eluting stent.

This EKG was taken after PCI:

Most of the OMI findings are resolved (though STD in V2 persists), with findings of reperfusion (terminal T-wave inversion in III, with reciprocally terminally upright T-wave in I and aVL and V6).

A post-cath Echo showed a posterior wall motion abnormality, with an ejection fraction of 55%. This patient probably had an ejection fraction of 65-70% prior to the MI.

No troponins were drawn after angiography.

===================================

MY Comment, by KEN GRAUER, MD (1/23/2025):

===================================

The issue of assessing the ECG of a patient with new CP (Chest Pain) and LBBB (Left Bundle Branch Block) periodically resurfaces. Prior dogma used to be that you could not recognize acute coronary occlusion in the presence of LBBB. Despite having long ago exposed this dogma as fallacious — too many providers remain "stuck" with the concept that LBBB masks the ECG signs of acute infarction.

• While true that LBBB may make it more difficult to recognize ECG signs of acute ischemia and infarction — the presence of this conduction defect definitely does not prevent our accurate assessment for acute coronary occlusion in many (most?) cases.
• We've reviewed illustrative cases on this subject often (See My Comment in the September 17, 2020 post and the April 7, 2019 post, among others). Today's case provides yet one more example in which despite oversight by the ED team — the initial ECG in this older man with new CP was absolutely diagnostic of an acute OMI in need of prompt cath.

What are the Findings in the Initial ECG?

As per Hans Helseth — ECG #1 clearly satisfies Modified Smith-Sgarbossa Criteria (See My Comment in the December 16, 2019 post for my approach to incorporating these criteria — and the December 21, 2015 post for illustration by Dr. Smith on how to measure these parameters).

The above said, while fully acknowledging the utility of Modified Smight-Sgarbossa Criteria — there is no need to invoke these criteria in today's case. This is because acute ST Elevation MI as a result of acute coronary occlusion is so obviously present from a qualitative approach based on ST-T wave appearance, rather than measurement.

• I fully acknowledge that my preference for a qualitative approach is experiential. But it has worked well for me over decades. I simply look for ST-T wave changes that I know are not normal in a patient with LBBB.
• My attention in today's initial tracing was immediately drawn to the inferior leads (within the RED rectangles in Figure-1). There simply should not be primary ST elevation, in association with disproportionately "hypervoluminous" ST-T waves in leads II,III,aVF. In this older man with new CP — we can instanly know that this is not normal for LBBB.
• Assessing for reciprocal ST depression is more challenging — because the ST-T wave is normally negative in high-lateral leads I and aVL when there is LBBB. But the BLUE arrows in lead aVL highlight a disproportionate amount of J-point depression. To Emphasize: As an isolated finding — I would not necessarily know that the ST depression in lead aVL is abnormal given the presence of LBBB. But in association with the obviously abnormal inferior lead ST elevation that we see in ECG #1 — I interpret the ST-T wave appearance in lead aVL as a reciprocal change that confirms an acute inferior STEMI.

Further support of acute coronary occlusion is forthcoming from the chest leads in Figure-1:

• As per Hans Helseth — the normal ST-T wave appearance in anterior leads with LBBB is oppositely directed to the deep S waves that are typically seen in leads V1,V2,V3. Qualitatively — this normal appearance is completely lacking in Figure-1. Instead of manifesting upright T waves — the ST-T waves in leads V1 and V2 are negative!
• In lead V3 — the upright T wave is tiny with respect to the 20 mm deep S wave in this lead. And the geometrically straight ST segment in V3 is clearly "out-of-place" for the normally expected upsloping ST segment.

BOTTOM Line: 

In today's patient with new CP and LBBB — qualitative assessment of ST-T wave shape without need for measurement is immediately indicative of acute coronary occlusion in need of prompt cath.

Figure-1: I've labeled the initial ECG in today's case.