Chest pain with serial ECGs – can you guess the sequence?

 Written by Jesse McLaren

A 45-year-old presented with 24 hours of intermittent chest pain. Below are serial ECGs focusing on the inferior leads and aVL. Can you guess the sequence?

 

First, what’s the interpretation of each ECG on its own?

#1

 

There’s T wave inversion in III/aVF and a taller T wave in aVL and V2. On it’s own this is nonspecific, but in the right context this could be diagonal occlusion (if active chest pain) or infero-posterior reperfusion (if resolved chest pain).

#2

 

Normal ECG

 

 

#3.

There’s discordant T wave inversion in aVL, which is reciprocal to inferior T waves that are tall relative to the QRS but not bulky. On it’s own this is nonspecific, but in the right context this could be inferior OMI (if active chest pain) or reperfused high lateral (if resolved chest pain).

 

 

#4.

Obvious infero-postero-lateral STEMI(+)OMI, regardless of context

 

 

Now let’s put them in order: what was the sequence?

 

The most likely would be #2) initially normal, then #3) subtle OMI, then #4) obvious STEMI, and then #1) reperfusion:

In other words, the patient with an initially normal ECG develops an acute coronary occlusion, with ECGs that progress from subtle to obvious, and then reperfuse after angiography. But that’s not always the case.

 

Now let’s look at the actual sequence, with the addition of clinical context, and see how the patient was managed:

 

The patient received aspirin from EMS and arrived at triage painfree (ECG #1). But 90 minutes later troponin returned at 70ng/L (normal <26 in males and <16 in females), and a repeat ECG was done (ECG#2) for recurring chest pain. The patient received nitro but the pain persisted, and the ECG was repeated 10 minutes later (ECG#3). The patient received more nitro, but the pain continued, and another ECG was done just 6 minutes later (ECG#4).

So the patient arrived with spontaneous reperfusion(ECG#1). When the pain recurred the ECG normalized(ECG#2), but this is pseudonormalization: the coronary artery has spontaneously reoccluded, and the T waves are on their way up. Just 10 minutes later the repeat ECG showed subtle OMI(ECG#3), with rising T waves and reciprocal STD in aVL. Looking at each ECG in isolation and without clinical context, the Queen of Hearts called the first 3 ECGs ‘not OMI’. But in sequence and with the clinical context of resolved and then recurring and refractory chest pain, the ECGs show subtle spontaneous reperfusion progressing to reocclusion. With serial ECGs that are ‘STEMI negative’ the physician could have waited for serial troponin levels or referred the patient as “non-STEMI”. But with ongoing pain despite nitro and dynamic subtle ECG changes, a fourth ECG was repeated just 6 minutes later, showing obvious STEMI(+)OMI (ECG#4), and the cath lab was activated.

 

What was the outcome and final diagnosis?

By the time of angiography 20 minutes later the RCA had spontaneously reperfused again: it was 90% occluded and had normal TIMI 3 flow. The patient had a 5^th ECG after angiography, which was normal (this time truly normalized, not pseudonormalized):

Post-cath trop was 300ng/L but was not repeated after. There were no follow up ECGs, which would have shown infero-posterior reperfusion TWI like the first ECG.

 

The discharge diagnosis was STEMI based on the STEMI positive ECG and code STEMI activation, with culprit lesion on angiography. This is one of the 20% of true positive STEMI that have open artery and normal flow by the time of the angiogram, showing that STEMI paradigm does not require a totally occluded artery at angiography.

And yet more than a quarter of ‘non-STEMI’ have an occluded coronary artery on delayed angiography, and yet are still discharged with a diagnosis of ‘non-STEMI’. So neither STEMI ECG criteria nor angiographic findings on their own sufficiently identify the pathology of acute coronary occlusion. Whereas the OMI paradigm incorporates, ECG, troponin, echo and angiographic findings to capture the dynamic nature of occlusion/reperfusion.

 

If acute MI is a movie, what film are we watching?

 

ECGs are 10 second snapshots in time, and with 4 columns on a page each lead only shows 2.5 seconds – so these are like still shots from a movie. The angiogram is a longer shot but does not represent the entire movie, and is separated in time from when the earlier scenes when the initial ECG was done. But if MI is a movie, what film are we watching?

 

In the STEMI paradigm there are only two possible films, which are completely different from each other: ‘STEMI’ depicts on artery that is totally occluded until it is reperfused on emergent angiography, while ‘non-STEMI’ shows a non-occluded artery that can wait to be seen on delayed angiography. But many STEMI spontaneously reperfuse while many ‘non-STEMI’ have totally occluded arteries. Bizarrely, the STEMI/Non-STEMI films are named not after how they end (the patient outcome) but how they begin (whether ECGs meet STEMI criteria, or whether code STEMI is activated), with STEMI(-)OMI still called ‘non-STEMI’ regardless of outcome. This is like categorizing a film that ends in tragedy as a comedy based on an earlier scene.

 

Occlusion MI is a dynamic process that can fluctuate between occlusion, spontaneous reperfusion and spontaneous reocclusion. Each patient with acute MI has their own film (with Non-occlusive MI, or Occlusion MI with or without spontaneous reperfusion or reocclusion), presents at a different time in the show (with acute or subacute presentations), and have corresponding ECGs that show subtle STEMI(-)OMI, obvious STEMI(+)OMI, or no ECG signs of OMI at all (for NOMI or electrocardiographically silent OMI). All these scenes can be missed by STEMI criteria, but looking through the lens of OMI allows us to see much more. By interpreting each still shot, looking at their sequence, and applying them in context, we can piece together the film for each patient.

 

 

Take away

 

1. OMI is a dynamic process that may spontaneously reperfuse or reocclude, and all phases can be missed by STEMI criteria

2. Just as true positive STEMI may have normal flow by the time of the angiogram, OMI is not based exclusively on the angiogram but also incorporates ECG, echo and trop

3. Serial ECGs applied in context can show subtle changes from reperfusion (resolved chest pain with reperfusion T wave inversion) to spontaneous reocclusion (recurring chest pain with pseudonormalization), and reciprocal change is often the more obvious initial change

4. Acute MI is like a film and ECGs are still shots: interpreting each ECG still shot through the lens of OMI, looking at their sequence and applying them in context, can help show each patient’s film and at what stage you are watching

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MY Comment, by KEN GRAUER, MD (6/7/2024):

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Fascinating clinical dissection of today’s case by Dr. McLaren! My thoughts as I read his excellent discussion are simple — namely, that depending on the history (ie, depending on the presence and relative severity of chest pain at the time each of the 4 ECGs shown was done) — a different logical sequence for these 4 tracings could have been proposed!

• For example — the ECG showing inferior lead T wave inversion would logically occur after chest pain resolves (because this ECG is showing reperfusion T waves) — but whether this ECG was the 1st, 2nd, 3rd or 4th tracing in the sequence might depend on when this sequence of recorded ECGs began (ie, Had this patient’s CP already resolved by the time EMS arrived on the scene to record their 1st ECG — or was CP slowly increasing — or maximal – or gradually or rapidly decreasing at the time that EMS arrived?).

The BOTTOM Line in Today’s CASE:

Realistically — Optimal clinical ECG interpretation is not an attainable goal in the absence of correlation to the presence and relative severity of CP at the time each serial ECG is done. Despite this clinical reality — all too many clinicians still fail to document the presence and relative severity of CP at the time each serial ECG is recorded. 

• As is shown in expert fashion by Dr. McLaren throughout his discussion of today’s case — the result is that too many ECGs are erroneously interpreted as “nonspecific”, and too many acute OMI’s are either overlooked or diagnosed only after significant (avoidable) delay.
• Correlating events (symptoms) at each point in the story (ie, at the time each ECG is recorded) — is essential for appreciation of “dynamic” ST-T wave changes that expedite early recognition of an OMI in progress.
• 
  
• SUGGESTION: There is a very simple way to ensure that this critically important correlation between the presence and relative severity of symptoms to each ECG that is done in a patient with chest pain is not lost: Simply write down for every tracing — on the actual ECG recording on a scale from 0-to-10, what the patient's "pain score" is at that time. Then sign this notation, and write down the time. 
• Adherence to this simple suggestion will instantly facilitate review of serial tracings — and make it so much easier to "put together" a cohesive story that will invariably enhance clinical interpretation.