Sometimes even ST Elevation meeting criteria is not enough to be convincing

Written by Emre Aslanger.  Emre is a new Editor of the Blog.  He is an interventionalist in Turkey.

A 50 something-year-old man with a history of newly diagnosed hypertension and diabetes, for which he did not take any medication, presented a non-PCI-capable center with a vague, but central chest pain. His vitals were normal and his first ECG was as shown below:

There is obvious ST segment elevation (STE) in anterior leads. STE in lead I and II are more subtle. The presence of J notch in V6 might have deceived the physician into thinking of early repolarization, but this can also be seen in anterior OMI. Note that QRS amplitudes are somewhat lower than expected and there is poor R wave progression. Add to these the slight reciprocal ST depression in lead III and aVF. 

   

There are tall and peaked T waves in anterior leads. Hyperacute T waves are generally described as such in many textbooks, but actually the majority of hyperacute T waves are “bulky” rather than being “peaked”, this is an example just happens to be both. Also not only the bulk of the T wave does matter, but also its proportion to the corresponding QRS complex is important. You can find many examples on this blog attesting that. Here, for example, T waves in lead II and aVF looks out of proportion to their respective QRS complexes in isolation.

 

Is this a subtle ECG ? I am sure that it is not for the readers of this blog. But I frequently witness that the diagnosis of OMI, especially anterior OMI, becomes much harder when there is no clear (although we have subtle ones here) reciprocal changes. This was a clearly diagnostic ECG that makes me think of a proximal left anterior descending artery (LAD) occlusion. 

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Smith: 

--Lead III is another giveaway.  You would not see this ST depression with a down-up T-wave in normal variant ST Elevation.

--How about the Formula for differentiating normal STE from Anterior OMI?

We do not see the computerized QTcB, but I measure it at 426 ms

RAV4 = 5.5 mm, QRSV2 = 12.5; STE60V3 = 3.5 mm

Formula = 22.51, all but diagnostic of LAD occlusion 

Dr. Aslanger performed the external validation of the formula. Full text here:

A tale of two formulas: Differentiation of subtle anterior MI from benign ST segment elevation

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This ECG was at 14:52. 

It is understood that the attending physician thought this ECG might have been more likely to be compatible with ‘early repolarization’ in the context of atypical chest pain and he ordered a hsTnT test, which turned out to be negative (11 ng/L, normal <14 ng/L). A second ECG was taken at 15:16.

If the first ECG was not diagnostic, the change between these two should have been. This is also a clear ECG for the readers of this blog, but may be hard for someone who is not used to seeing non-mainstream ECGs. There is STE in inferior leads now (The unfortunate thing about these leads is the conventional naming that labels them as inferior, which could not be more misleading in electrophysiological terms. See bibliography). STE in inferior leads is a frequent finding in distal LAD occlusions (not necessarily in “wraparound” LADs, which is already more or less a finding for many LADs that you will find if you look for), because apically directed ST segment vector is not pulled upwards by more dominant basal anterior segments. This is a bad ST vector orientation, because it causes widespread STE and one of the most important mistakes that needs to be avoided here is thinking of the diagnosis of pericarditis. 

Look at the STE in lead II, aVF. They are so out of proportion to their respective QRS complexes so that they are diagnostic even by themselves. Such an out-of-proportion STE is virtually never seen in pericarditis. Also note poor anterior R wave progression, again this is not a feature of pericarditis. I don’t even mention about the dynamic change between two ECGs. Also note how hyperacute T waves of proximal occlusion pattern changed into an apicolateral one. This ECG series shows many different examples of the findings bearing the same title. 

But why did the proximal LAD OMI pattern change into a distal LAD OMI pattern here ? Wait for the angiogram.  

With the false reassurance of negative troponin, confusing changes on ECG and atypical chest pain, a third ECG was taken much later (which was similar to the fourth taken at our institution, see below), at 17:40. I don’t know the reason why it took so long, but a second troponin turned out to be positive by then and the patient was referred to our hospital for “emergency PCI”. 

He arrived to our hospital one hour later. The ECG in ER is shown below:

ECG is still diagnostic but we are watching the natural course of myocardial infarction here. I have trouble understanding the chain of events that resulted in the unacceptable delay and cost the patient’s anterior wall.

Here is the angiogram: 

There is a thrombotic ostial LAD lesion in addition to widespread atherosclerotic involvement, fortunately reperfused by itself. You may see a filling defect in distal LAD, most probably due to an embolization from proximal lesion. Also note that LAD does not extensively wrap-around apex and supply inferior wall. The lesion was successfully stented, but it was unfortunately done after a significant myocardial loss. 

Fortunately, peak troponin was only 1090 ng/L and next day EF was 45-50% with apical and mid anterior hypokinesia. The patient was (and we, his caregivers were)  really lucky to get away with such a limited damage.        

Take home messages:

• Any coronary occlusion may present with vague symptoms, but when ECG is clear, there should not be any suspicion. ECG hardly ever tells lies! Many times it is more prudent to count on ECG than the patient’s history.
• Troponin can never compensate your limited ECG reading skills or the complete lack thereof.
• Anterior OMI may, and frequently does, present without reciprocal changes.  
• The leads showing STE should not be assumed to be the ones overlying the infarcting segments. It is all about the orientation of ST vector. Because of it the occlusion pattern on ECG may change during the course of OMI.
• Despite a prolonged ECG findings, the damage can rarely be less than expected, due to spontaneous open-and-close cycles, ischemic preconditioning, and the presence of collaterals.

References 

1. Aslanger EK. Considerations on the naming of myocardial infarctions. J Electrocardiol. 2022 Mar-Apr;71:44-46. doi: 10.1016/j.jelectrocard.2022.01.006. Epub 2022 Jan 31. PMID: 35124348.
2. Bozbeyoğlu E, Yıldırımtürk Ö, Aslanger E, Şimşek B, Karabay CY, Özveren O, Değertekin MM. Is the inferior ST-segment elevation in anterior myocardial infarction reliable in prediction of wrap-around left anterior descending artery occlusion? Anatol J Cardiol. 2019 Apr;21(5):253-258. doi: 10.14744/AnatolJCardiol.2019.09465. PMID: 31062754; PMCID: PMC6528511.
3. Aslanger EK, Meyers HP, Smith SW. Recognizing electrocardiographically subtle occlusion myocardial infarction and differentiating it from mimics: Ten steps to or away from cath lab. Turk Kardiyol Dern Ars. 2021 Sep;49(6):488-500. doi: 10.5543/tkda.2021.21026. PMID: 34523597.

 

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MY Comment by KEN GRAUER, MD (11/13/2022):

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Highly interesting case by Emre Aslanger. Among the important points brought out by Dr. Aslanger's discussion are the following: 

• Despite the history of a "vague" type of chest pain and negative initial troponin — extensive infarction nevertheless occurred.
• Anterior OMI is not always accompanied by inferior lead reciprocal changes (Many cases on Dr. Smith's Blog show this same phenomenon).
• ST elevation in both anterior and inferior leads does not necessarily indicate an LAD "wraparound" lesion (Bozbeyoğlu reference documenting this cited by Dr. Aslanger below — with Dr. Aslanger as one of the co-authors).
• The "occlusion pattern" on ECG may change during the course of evolution (in today's case — from a proximal LAD OMI to a more distal LAD OMI pattern, presumably due to embolization from a proximal lesion).
• Extensive atherosclerotic involvement (with multi-vessel disease) — may produce confounding changes on ECG. 
• Spontaneous "open-and-close" cycles of the "culprit" artery may similarly produce confounding ECG changes — with an unpredictable picture of how much myocardial damage is ultimately produced (Many cases of this same phenomenon on Dr. Smith's ECG Blog).

I focus my comment on one additional aspect that led to confounding ECG changes in today's case.

• I initially suspected LA-LL Lead Reversal in the first 2 tracings in today's case. Having been "burned" by this subtle form of lead misplacement on several occasions in the past — my attention was captured by the presence of a P wave in lead I larger than the P wave in lead II. This is virtually never seen with sinus rhythm, given the orientation in the frontal plane of the SA Node with respect to the AV Node.
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• Alas — I was wrong. There is no lead reversal in today's case. The fact that the P wave in lead I remains larger than the P wave in lead II for all 3 tracings confirms that instead of lead reversal — there is an ectopic atrial rhythm!

I'll add a "shifting" frontal plane axis to the confounding ECG changes seen over the course of the 3 ECGs in today's case (ie, lead aVF evolving from a tiny but isoelectric QRS in ECG #1 — to an all positive QRS in ECG #2 — to a predominantly negative QRS in ECG #3). The explanation for this axis shift brings us back to the series of important findings highlighted by Dr. Aslanger:

• Cardiac cath showed widespread coronary disease (and this may produce confounding ECG findings).
• The infarction that ultimately evolved was extensive! (essentially wiping out all positive forces in the chest leads of the last tracing).
• The "occlusion pattern" on ECG changed during the course of OMI evolution (with resultant frontal plane axis shift and dramatic QRST morphology changes over the course of the 3 tracings).

P.S. — Lead reversals do occur! Prior to my "high intensity exposure" on the internet to confounding ECG pictures worldwide — I didn't realize how common lead reversals are in practice. I suspect this is because clinicians aren't as attuned to looking for them.

• It is usually easy to recognize the most common cause of lead reversal — which is mixup of the LA-RA electrodes. But other forms (especially LA-RA lead reversal) — can be far more subtle, and are easily overlooked.
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• There was no lead reversal in today's case.
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• For those interested in examples of Lead Reversal (and HOW to recognize this when it occurs) — Please check out My Comment at the bottom of the page in the August 17, 2022 post in Dr. Smith's ECG Blog. I work through a case of LA-RA lead reversal — and link to 11 other examples of lead reversal that we've published in recent years.