Dizziness in a 40-something with recent stent for inferior OMI

Dizziness is so unlikely to be OMI without an obvious ECG, that I am going to pretend that this patient presented with chest pain.

The PMCardio Queen of Hearts app asks you, before giving an interpretation of OMI ("STEMI-Equivalent"), whether the patient's clinical presentation is high risk for OMI.  If no, then she will tell you that the case is outside of the intended use group.

So let's pretend this is acute chest pain.  (Anyone can get acid reflux and present with chest pain, no matter the appearance of their ECG, right?)

This was interpreted as hyperacute T-waves in the inferior leads.

What do you think?  

There was a previous ECG for comparison, from an admission for inferior-posterior-lateral OMI (see in particular the pre-discharge ECG, below):

Previous active OMI

Predischarge ECG of previous active OMI

Notice that the T-waves in III and aVF are inverted.  

This further alarmed the providers, and led them to believe that these inferior T-wave are pseudonormalized and hyperacute.

What do you think?  Compare to inferior leads in the presentation ECG:

These T-waves do appear to be large and newly upright.  

However, they are NOT hyperacute

I can see instantly that they are not hyperacute, and so can Pendell.  But I cannot give an objective reason why not.  

Pendell and I have been attempting to numerically define hyperacute T-waves, and although we are making some great progress, our system so far cannot match our subjective accuracy (accuracy determined by angiographic/troponin/echo outcomes).  In fact, our system falsely called many of the T-waves in this ECG as hyperacute.

The Queen of Hearts also knows which large T-waves are hyperacute and which are not:

She knows that it is not OMI

(Unfortunately, most providers no longer have access to the Queen of Hearts because 1) it is not yet FDA approved and 2) thus a provider can only use it in the context of research.)

Why are the inferior T-waves upright when they were inverted on the last ECG?  Why is this not pseudonormalization (which implies re-occlusion)?

The last ECG was 6 months prior.  Over weeks to months, T-waves normalize after acute OMI.   If T-waves become upright in the hours or days after reperfusion (either spontaneous or due to intervention), then that is a sign of re-occlusion!  But you expect normalization if the time period is weeks to months.

Here are 9 cases that involve re-occlusion.

20 cases with pseudonormalization

Case continued

The patient was moved to the critical care area, and cardiology was consulted.  Cardiology correctly interpreted the ECG and did not want to activate the cath lab.  Of course, all other evaluation for possible acute MI is indicated and was undertaken, especially serial troponins.

Further ECGs were recorded:

25 minutes

Are those T-waves slightly smaller?  Maybe, but still the first ECG is NOT hyperacute.

47 minutes

Maybe smaller still?

Next day 

Now they are clearly smaller.

The patient ruled out for MI by serial troponins < 3 ng/L.

Why did they get smaller?  Was it unstable angina?  (Well, really, in this case, there was no angina, only "dizziness")

I don't think so.  I think that T-waves can have some evolution even without infarction.

But beware, because unstable angina does still exist in the era of high sensitivity troponin.

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MY Comment, by KEN GRAUER, MD (12/29/2024):

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I found today's case of interest because it addresses the theme of distinguishing "hyperacute" T waves (ie, indicative of ongoing acute OMI ) — vs T wave evolution not associated with an acute cardiac event.

In  the November 27, 2024 post — Drs. Smith and Meyers describe their ongoing work in association with clinician-researchers at Powerful Medical on developing an objective, mathematically derived and clinically-correlated definition of "hyperacute" T waves. KEY variables being integrated into their logistic regression formula include:

• AUC (Area Under the Curve) of the T waves being looked at.
• Increased Symmetry (as defined by time from T-wave onset-to-peak — compared to time from T-wave peak until T-wave end).
• ST Segment Upward Concavity (objectively measured — with reduced concavity correlating to increased likelihood of hyperacuity).

And so, I found it insightful that both Drs. Smith and Meyers immediately knew that despite the ST-T wave changes seen between today's initial ECG compared to the pre-Discharge ECG of this patient that was recorded following extensive acute infero-postero-lateral STEMI — the T waves in ECG #1 (that I've reproduced in Figure-1) are not hyperacute!

• As shown by Dr. Smith in his above discussion — serial ECGs on today's patient over the course of a day did show changes in ST-T wave appearance. Yet clinical follow-up confirming the absence of acute OMI also confirmed that the T waves in today's initial ECG were not hyperacute.

The above said — I thought it worthwhile to take another LOOK at the 2 key ECGs in today's case.

• When I first saw ECG #1 in today's case, being told to consider a clinical presentation of acute CP — I was clearly concerned.
• The T waves in the inferior leads of today's initial ECG are clearly disproportionately taller-than-expected considering modest amplitude of the QRS in these respective leads (RED arrows in Figure-1). That said — the ST segments in these inferior leads are not elevated, and these inferior lead ST segments manifest a peculiar concave-up slope.
• That said — the tiny, artifact-laden QRS complex in lead aVL manifests a very small amplitude mirror-image opposite picture compared to the ST-T wave picture in the inferior leads.
• Lead V1 in ECG #1 is also abnormal — with a tiny amplitude incomplete RBBB pattern manifesting disproportionately increased ST segment coving and T wave inversion that resolves by lead V2.
• 
  
• IMPRESSION: While I can appreciate how the peculiar inferior lead ST segment upsloping may detract from calling these T waves "hyperacute" — told to consider a history of new CP in association with ECG #1 — serial troponins with repeat ECGs are clearly indicated! (notwithstanding the appropriate decision by cardiology not to activate the cath lab at this time).

Comparison between ECG #1 and ECG #3:

Availability of a previous ECG on today's patient (as seen in Figure-1) — further clarifies that there is a difference in ST-T wave appearance in virtually all 12 leads when one compares ECG #1 with ECG #3.

• I found Dr. Smith's interpretation insightful, that despite the obvious ST-T wave differences between the 2 tracings shown in Figure-1 — the T waves in today's initial ECG are still not "hyperacute" (especially since their appearance is not the result of an ongoing or recent cardiac event).
• It turns out that ECG #3 was recorded ~6 months prior to ECG #1. I wish we could see the evolution of ST-T wave changes in ECG #3 at various points during those interim 6 months.
• Regardless — the serial ECGs shown above by Dr. Smith still show some evolution of ST-T wave appearance over the day that this patient was in the hospital.
• BOTTOM Line: As per Dr. Smith, "T waves can have some evolution even without infarction." That said — prudence dictates that even in those cases in which T waves may not fit the definition of being "hyperacute" — a history of new CP and clear differences in ST-T wave appearance (compared to the last previous ECG on record) — mandates ruling out an acute event (even though this does not necessarily mandate activation of the cath lab).

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