A woman in her 70s with diabetes, hypertension, and hyperlipidemia suddenly developed nausea, diaphoresis, and brief syncope while eating at a restaurant. She did not report any chest pain or pressure.
She was brought to the Emergency Department and this ECG was recorded while she was still feeling nauseous but denied chest pain, shortness of breath, or other symptoms:
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| What do you think? No baseline was available for comparison. |
Sinus rhythm
Grossly normal QRS complex
Less than 1mm STE in II, III, and aVF, as well as V4-6, all with extremely upward concavity
aVL has the smallest possible amount of STD in aVL with a shallow negative T-wave
The T-waves in the inferior leads seem to have potentially large amplitude compared to their QRS complexes
STEMI criteria are not met
Although inferior OMI commonly presents with submillimeter STE in the inferior leads with very subtle reciprocal STD and/or T-wave inversion, the morphology of this ECG is not convincing to me. The T-waves have significant amplitude but they are not "fat" enough to be hyperacute. The morphology of STE is not diagnostic of being due to acute transmural ischemia. It is difficult to describe exactly why, but is something that simply comes with time, after following up hundreds of cases to see the ECG progression and patient/angiographic outcomes.
This ECG was texted to me with no clinical information, with the sender being concerned for possible hyperacute T-waves and STE in the inferior leads.
I replied: "I see why you would be worried about hyperacute T-waves, but they just don't look fat enough to be hyperacute. There is definite STE inferior and lateral but it just doesn't look like true positive STE to me. I wouldn't activate the lab for this EKG alone, but if the patient is clinically compatible with ACS you could call a heart alert. I would do echo for WMA, q15 min EKGs - if it's real it will be dynamic and become clear soon. Let me know what happens." If I had known there was no definite chest pain or pressure this would have been slightly more confident.
I later found out that the cath lab was activated soon after arrival.
The patient went emergently to the cath lab, where all coronary arteries were found to be normal.
Note: Normal coronary arteries at the time of cath of course does not rule out the possibility of OMI. There can be OMI at the time of the ECG followed by spontaneous (or medication induced) lysis, such that the artery is open at the time of cath. This can be so brief that even troponins do not significantly rise. Of course that is very rare. But it demonstrates the point that the angiogram alone cannot be used to adjudicate the presence or absence of OMI. The ECG progression, clinical picture, and biomarkers are also involved in the full diagnosis of OMI. The ECG progression in particular is important: True positive OMI findings on ECG must always resolve or evolve. Conversely, an ECG that remains static throughout the entire clinical course means that the ECG findings were not due to OMI (even if OMI was truly present!).
Serial troponins were negative.
Echo showed no wall motion abnormality.
Most importantly, several repeat ECGs were basically unchanged:
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| This is the ECG the next day. This one likely does meet STEMI criteria in II, III, and aVF. But it is the same morphology as the first ECG. Absolute STE is irrelevant - the fact that the prior ECG did not meet criteria and this one does, is meaningless in my opinion. |
Learning Points:
This was an example of a false positive cath lab activation due to ECG findings that were thought to represent OMI.
Learning how to differentiate hyperacute T-waves from normal variants like this is difficult and requires comparing cases like this with our database of true positive hyperacute T-waves. True hyperacute T-waves are tall, fat, wide, symmetric, and by these properties have large area under the curve compared to the size and morphology of the QRS complex.
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These are fat, symmetric, true positive hyperacute T-waves in III and aVF, with their reciprocal counterpart in aVL. This patient had RCA OMI. From: A female in her 60s who was lucky to get expert ECG interpretation |
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| This case. False positive, proven by no evolution and no evidence of OMI, negative trops, and normal angiogram. |
Use these cases to see more true positive inferior hyperacute T-waves:
You have two hours to save this patient's life
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MY Comment by KEN GRAUER, MD (8/26/2019):
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I find this an important case for helping to clarify the semantics surrounding use of the term “hyperacute” when referring to T wave appearance. I fully AGREE with Dr. Meyers astute ECG assessment and management plan for the initial ECG in this case ( = ECG #1 in Figure-1).
- That said — I offer a different perspective on the semantics that I favor to describe the ECG findings in this case.
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| Figure-1: The 2 ECGs shown in this case (See text). |
MY THOUGHTS on ECG #1: The most remarkable findings in ECG #1 are seen in the inferior leads. That said, systematic assessment of this tracing reveals a number of additional findings of interest:
I AGREE completely with Dr. Meyers that:
Where My Perspective Differs: While the history for this patient is not at all convincing for acute OMI — and, reciprocal changes are lacking — and, chest leads fail to show acute changes — we still have the unescapable finding of T waves that are taller-than-they-should-be in each of the 3 inferior leads. That said:
Why this is all Symantics: Regardless of how one classifies the T waves in the 3 inferior leads of ECG #1 — optimal management will be similar:
MY THOUGHTS on ECG #2: There is essentially NO change in the appearance of ECG #2 compared to ECG #1. We are told that several other ECGs done after the initial tracing all looked the same.
BOTTOM LINE: Dr. Meyers and I are essentially saying the same thing. Considering this patient presented to the ED with new symptoms (including syncope — albeit without chest pain) — ECG #1 is not a normal tracing.
Our THANKS to Dr. Meyers for presenting this case!
- There is baseline artifact in several leads. In ECG #1 — this is most marked in leads II, III and aVF. Since electrical derivation of these 3 leads is shared by involvement of the left leg electrode — this is the probable source of this artifact. I’ll emphasize that despite the artifact — this tracing is clearly interpretable. The reason I note the artifact, is that on occasions when artifact does impair interpretation, it may be helpful to recognize from which extremity the artifact arises (Details on this subject are beautifully described in this article by Rowlands and Moore.)
- Beyond-the-Core: In contrast, the limb lead artifact in ECG #2 is maximal in leads I, II and aVR, with electrical derivation of these 3 leads shared by involvement of the right arm electrode — which is the probable source of artifact in ECG #2.
- There are multiple small and narrow Q waves. These are seen in leads I, II, aVL, aVF; and V3-thru-V6. There appears to be a small-but-present initial r wave in lead III. The clinical significance of these Q waves is uncertain — but their presence should be noted because this finding might be relevant if there was ongoing infarction.
- There is early transition — because the R wave becomes predominant (ie, taller than the S wave is deep) as early as lead V2. This finding could also be relevant — because posterior infarction is among potential causes of early transition.
- Finally — I was struck by how similar the appearance is for QRS complexes and ST-T waves in leads V3-thru-V6 of ECG #1. This made me wonder if there might not be a potential technical mishap in this recording.
I AGREE completely with Dr. Meyers that:
- There is <1 mm ST elevation in the inferior and lateral chest leads.
- There is ST segment flattening with no more than minimal T wave inversion in lead aVL. Lead aVL does not have the appearance of a true “reciprocal change”.
- The T waves in the inferior leads of ECG #1 are each taller-than-expected considering the appearance of the QRS complex in each of these leads.
- Criteria for a STEMI are definitely not met in ECG #1.
- The T waves in each of the inferior leads in ECG #1 are not as “fat” as the T waves in the true positive example of inferior hyperacute T waves that Dr. Meyers shows above.
- Although this 70yo woman with cardiac risk factors did have acute symptoms (ie, nausea, diaphoresis and syncope) — she did not report any chest discomfort! On the whole — her history is not convincing for acute OMI (although we need to remember that not all acute MIs are associated with chest pain).
- I would not activate the cath lab on the basis of ECG #1 alone.
Where My Perspective Differs: While the history for this patient is not at all convincing for acute OMI — and, reciprocal changes are lacking — and, chest leads fail to show acute changes — we still have the unescapable finding of T waves that are taller-than-they-should-be in each of the 3 inferior leads. That said:
- ECG #1 is not diagnostic of acute OMI.
- I would not have activated the cath lab on the basis of ECG #1 alone.
- BUT — this patient did present to the ED with new non-chest pain symptoms (including syncope) that could reflect an acute cardiac event.
- AND — in my opinion, in the absence of a prior ECG for comparison — we can not rule out the possibility that these might be hyperacute T wave changes in the inferior leads of ECG #1.
- A definitive diagnosis can not be made from ECG #1 alone.
- Continued close observation of this patient + frequent serial ECGs + stat Echo in the ED (looking for wall motion abnormality) + serial troponins — will almost certainly yield the correct diagnosis in very short order.
MY THOUGHTS on ECG #2: There is essentially NO change in the appearance of ECG #2 compared to ECG #1. We are told that several other ECGs done after the initial tracing all looked the same.
- I find it of interest that both early transition and a similar appearance of the QRS complex and ST-T waves in lateral chest leads persist in ECG #2 done the next day. This makes a technical mishap much less likely — and makes me wonder if an unusual body habitus might account for these findings ...
BOTTOM LINE: Dr. Meyers and I are essentially saying the same thing. Considering this patient presented to the ED with new symptoms (including syncope — albeit without chest pain) — ECG #1 is not a normal tracing.
- Regardless of whether or not you classify the inferior T waves in ECG #1 as possibly hyperacute or not — additional testing, including repeat serial ECGs, troponin + stat Echo are all needed to arrive at a more certain diagnosis.
- “Ya gotta be there” to make the decision of whether or not to activate the cath lab on the basis of the history and ECG #1. While fully acknowledging that “hindsight is 100% in the retrospectoscope” — for learning purposes, I’ll put forth the thought that repeat ECG, stat Echo and initial troponin could probably have been enough to dissuade the decision to activate the cath lab in this case.
Our THANKS to Dr. Meyers for presenting this case!
