‘NSTEMI’ or reperfused OMI? And which lesion is the culprit?

Written by Jesse McLaren

 

An 80 year old with a history of CHF, ESRD on dialysis, and multiple prior cardiac stents presented to the emergency department with 3 days of intermittent chest pain and shortness of breath that resolved after nitro, which felt like prior episodes of angina. The patient was pain free on arrival, and below are the prior and new ECG. What do you think?

Prior on top, New on bottom

 

 

 

There’s normal sinus rhythm, normal conduction, left axis, poor R wave progression and low precordial voltages. Compared with prior there are subtle T wave inversion inferior and lateral. In a patient with resolved ischemic symptoms this suggests infero-lateral reperfusion, usually from the RCA vs left circumflex.

Smith: I looked at the bottom ECG without even looking at the previous, and could see that there is classic morphology of reperfusion, especially in lead III, with recriprocal STD and upright (reciprocal reperfusion) T-wave in aVL.  Then when you compare with the old ECG, the change makes it diagnostic of inferior and lateral reperfusion.

 

 

‘NSTEMI’ or reperfused OMI?

 

The emergency physician ECG interpretation was simply “NSR”. When the hs-troponin I returned at 475 ng/L (compared to baseline of 60), the patient was referred to cardiology as “NSTEMI.” The cardiology interpretation was “left axis, anteroseptal Q, poor R wave progression”, and the patient was admitted as “NSTEMI”. This implies a non-occlusive MI that can safely wait for delayed angiogram.

 

But even without comparison to the prior ECG, the Queen of Hearts identified the ECG as showing reperfused OMI, at risk for reocclusion:

Smith: You can see that the Queen of Hearts sees leads III and aVL just like I did.

What’s the culprit?

 

The next day the patient went to the cath lab, where the interventional cardiologist noted: “ECG did not reveal any acute ischemic changes. There appeared to be Q waves both in the inferior and anterior leads. Reviewing his old ECGs as well there were no significant changes compared to previous.” Angiogram showed a chronic total occlusion of the circumflex, multiple patent stents, and two stenoses: 95% distal RCA and 90% mid LAD.

 

So which was the culprit? As the cath lab report noted, “The culprit vessel unfortunately was not clear due to the fact that he has diffuse coronary artery disease. It is possible either the LAD or RCA is contributing to his presentation. I suspect the RCA lesion is also chronic. His ECG was unfortunately not helpful given it had evidence of Q waves anteriorly as well as Q waves inferiorly on some of the ECGs in the past. We agreed that it was reasonable to revascularize the LAD.”

 

In other words, because the subtle inferior reperfusion was not identified, the culprit RCA was not stented. Over the next couple of days the patient continued to have intermittent chest pain.

 

A few hours after angiogram the patient developed chest pain:

Now the previously inverted infero-posterior T waves are upright (pseudonormalization), and there is reciprocal ST depression in aVL which is highly specific for inferior OMI. The patient has spontaneously re-occluded.

 

Queen of Hearts of Heart identifies this as acute coronary occlusion:

The chest pain resolved after nitro and the ECG was not repeated.

 

The next day the patient had another episode of pain that resolved before assessment:

Reperfused again

The following day the patient had another episode of chest pain:

Spontaneously re-occluded again. This was interpreted as "inferior STEMI" and the cath lab was activated. At the time of the angiogram the RCA was again open at 95%, and stented. Troponin rose from 380 ng/L to 930 ng/L before cath, but was not repeated after. The patient had no further episodes of chest pain.

 

Next day ECG showed reperfusion.

Discharge diagnosis was ‘Non-STEMI’.

 

Here are the ECGs again, focusing on the inferior leads and reciprocal change in aVL:

Take home

1.        The catch-all phrase ‘NSTEMI’ does not differentiate between different pathologies with different management based on the state of the coronary artery: non-occlusive MI (non urgent cath), subtle occlusion MI (emergent cath), and reperfused occlusion at risk of re-occlusion (urgent cath)

2.        The STEMI/NSTEMI dichotomy can make it difficult to identify the culprit lesion, which can be spontaneously reperfused at the time of the angiogram

3.        T waves are very specific markers for the dynamic process of spontaneous reperfusion/re-occlusion

4.        The Queen of Hearts can differentiate subtle reperfused OMI from NOMIs, and help guide cath lab decisions

5.        Further significant myocardial damage could have been avoided by stenting the RCA at the first cath, but this is only possible with accurate ECG interpretation, or with use of the Queen of Hearts.

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MY Comment, by KEN GRAUER, MD (2/8/2025):

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Important case presented today by Dr. McLaren — because it highlights the misinterpretations and misconceptions that continue to be all-too-common in everyday practice.

• To facilitate comparison in Figure-1 — I've reproduced the prior (baseline) ECG on today's patient — together with the initial ECG recorded in the ED.

My Concerns Regarding this CASE:

• The History was Ignored: Today's patient is an 80-year old with known coronary disease — who presents with 3 days of intermittent CP (Chest Pain) — but who was not having any CP on arrival. Embedded in this history are 3 reasons for the ED physician to suspect that any ECG abnormalities that might be seen could be subtle: i) The patient is older with a history of multiple prior stents — therefore highly likely to have significant underlying heart disease (probably multi-vessel) — with potential for significant collateral flow that may attenuate the prominence of new changes; ii) The patient's CP has been intermittent — therefore potential for new ECG changes to be in a state of transition (ie, pseudo-normalization) between the stage of ST elevation and the stage of reperfusion ST depression/T wave inversion; and, iii) The patient's CP has resolved at the time the initial ECG was recorded (which often results in significant reduction, if not elimination of ST-T wave changes).
• Saying the Elevated Troponin was the Result of a NSTEMI: The combination of the history of CP + ST-T wave abnormalities consistent with reperfusion changes (especially in comparison to a prior tracing without such changes) + significant Troponin elevation — is diagnostic of an OMI. As per Dr. McLaren — misdiagnosing today's case as a "NSTEMI" only serves to delay the need for catheterization (at the potential price of losing more myocardium).
• Key ECG Findings in Figure-1 were Missed: — i) Which leads in ECG #1 were misplaced? — and, ii) What important new findings are revealed by lead-to-lead comparison between ECG #1 and ECG #2?

Figure-1: Comparison between the initial ED ECG — with the prior ECG on this patient.

KEY ECG Findings in Figure-1 that were Missed:

It is because the history in today's case so strongly suggests that this 80-year old patient with 3 days of intermittent CP that is no longer present might only manifest subtle ECG abnormalities — that lead-to-lead comparison between ECG #1 and ECG #2 is so important. Without using this simple technique of lead-to-lead comparison — it becomes all-too-easy to miss real but subtle differences between the 2 tracings.

• Comparison between ECG #1 and ECG #2 needs to take into account that the lead V1 and V2 electrodes have been placed too high on the chest in ECG #1. We can instantly recognize this because: i) There is such a deep negative component to the P wave in both of these leads; — ii) There are terminal r' deflections in both V1 and V2; — and, iii) The PQRST complexes in leads V1,V2 look very much like the PQRST complex in lead aVR (See My Comment in the November 4, 2018 post, among many others).
• Turning my attention to ECG #2 — my "eye" was immediately drawn to the 2 leads within the RED rectangles ( = leads III and aVF) — because these leads show: i) Abnormal ST segment coving, with a hint of slight ST elevation; — ii) Terminal T wave inversion, which in association with ST coving that shows no more than minimal ST elevation — is suggestive of some spontaneous reperfusion; — iii) Subtle "scooping" of the ST segment in high-lateral leads I and aVL — which is consistent with subtle reciprocal ST-T wave changes; — and, iv) The absence of these ST-T wave changes in these 4 leads on the prior tracing!
• Looking at the chest leads in ECG #2 — similar subtle-but-real ST segment coving occurs, as was seen in leads III,aVF — here, with a hint of ST elevation in lead V5 — with terminal T wave inversion in leads V5,V6. This suggests recent lateral OMI, now with suggestion of some spontaneous reperfusion.
• Knowing that infero-lateral OMIs are so often accompanied by posterior wall involvement — I interpreted the subtle lack of gently upsloping ST elevation in lead V2 as consistent with the overall picture of recent infero-postero-lateral OMI, most probably with some pseudonormalization and the beginning of reperfusion T waves.

BOTTOM Line: The history in today's case alerts the informed provider to the type of subtle ECG findings that need to be looked for.

• The finding of a significantly elevated initial Troponin ( = 475 ng/L) confirms the diagnosis of recent (and/or ongoing) coronary occlusion ( = an OMI) — until proven otherwise. To call this a "NSTEMI" — is to delay needed catheterization and the chance to salvage viable myocardium.
• ECG findings on the initial ECG are subtle. But IF the informed provider assesses this initial tracing by lead-to-lead comparison with the prior ECG — definite ST-T wave changes will be seen in at least 6/10 leads (with comparison of leads V1,V2 between these 2 tracings invalidated by too-high-placement of these leads in ECG #1).