This case was sent by Lou B, a paramedic and RN.
Since there is less than 1 mm of summed inferior ST depression, this ECG meets these criteria, so it could be early repol.
Comment: I hesitate to use this formula to deny cath lab activation to those whom you think have a STEMI. I advocate it mostly to make you reconsider a diagnosis of benign ST elevation when the value is high. If this patient had chest pain and the value suggested early repol, I would be very hesitant to act on it.
Validation of 4-variable formula (it is now established as superior to the 3-variable formula): https://onlinelibrary.wiley.com/doi/abs/10.1111/anec.12568
Explanation of 4-variable formula:
Computerized QTc was 375 ms
STE60V3 = 6.5 (!)
QRSV2 = 16
RAV4 = 14
Value = 20.24
(The cutoff of 18.2 is best, and this is far above that cutoff, supporting acute LAD occlusion)
The cath lab was activated.
–The coronaries were clean (this is not the gold standard, however, as some patients with ischemic ST elevation may have clean coronaries).
–Troponins were negative (this is very strong evidence against ischemic ST elevation, but not the best)
–All subsequent ECGs before the angiogram were identical
–Unfortunately, we do not have the ECGs from after the angiogram [this is the gold standard — if there is no evolution of the ECG, then the ST elevation is baseline. Ischemic ST elevation will always evolve (resolution of STE +/- development of T-wave inversion, +/- development of Q-waves)].
ACTUAL CORONARY ANATOMY:
LM: A 5 mm vessel which bifurcates into the LAD and LCx coronary artery. The LM coronary artery is free of disease
LAD: A type 3 LAD, which gives rise to usual septal perforators and diagonal branches. The LAD and its major branches are free of disease
LCX: A non-dominant vessel that is moderate caliber in size, which gives rise to several OM branches and continues to complete its course in the AV grove as a small vessel. The LCx and its major branches are free of disease
RCA: A dominant vessel witch gives rise to the PDA and PLA. The RCA and its major branches are free of disease
Note that the angiographer does not just say that there is no obstructive coronary disease. He/she says that the vessels are free of disease. This makes the possibility of acute MI even more remote.
There was no post cath ECG, which if unchanged would absolutely confirm that this is his baseline ECG. However, given that all vessels are “free of disease,” it is almost certain that this is the patient’s baseline ECG, and it is a scary one.
Some patients have scary baseline ECGs. Thus, the 4-variable formula does have false positives. Even if you suspect early repol, you may need to activate the cath lab, or at least do an emergent formal bubble contrast echo. You might find a previous identical ECG, and that is also helpful.
Here is another similar case of scary early repol for whom I did not activate the cath lab.
How did I avoid it?
K. Wang’s comments:
A good case.
It’s important and useful to note that
1) Over 90% of healthy young men have up to 3mm ST elevation in one or more precordial leads normally (Atlas of Electrocardiography by K. Wang,
2) There are three causes of tall T waves; hyperkalemia, hyperacute ischemia and normal variant (Atlas of Electrocardiography by K. Wang, page 171).
The first two are symmetric, the last one, the normal variant, is asymmetric in that the upstroke takes more time than the downstroke.
This case turned out to have both.
Comment by KEN GRAUER, MD (8/9/2018):
Our thanks to Lou B for this insightful case. The “MORAL” of this story reminds me of the valuable lesson I was long ago taught regarding the diagnosis of acute RLQ pain: If acute appendicitis is found 90-95% of the time that you call for surgical consultation — then you are not calling the surgeon often enough (ie, you are missing too many cases of acute appendicitis). The same is true regarding the ECG in Figure-1 — the correct answer (as emphasized by Dr. Smith) — is that in view of the worrisome findings on this tracing, you have to rule out acute STEMI until you prove otherwise.
- I don’t feel bad at all that the cath turned out to be totally normal (ie, free of disease!). Instead, I find it both humbling and highly informative to know that despite the worrisome appearance of this 12-lead tracing — it is all the result of a repolarization variant.
Dr. Smith has expertly detailed the abnormal findings in this case, including a 4-variable formula value = 20.24 (above the 18.2 cutoff). I’ll add the following points from a qualitative perspective regarding my interpretation.
- Leads V2 and V3 are the first findings that “caught my eye”. Both leads show more-than-the-usual amount of J-point ST elevation — and — T waves that look to be disproportionately tall compared to respective QRS complexes in these 2 leads. Repolarization variants canclearly produce the same picture — but the onus is on us to prove that this appearance is the result of a repolarization variant, rather than the other way around.
- My “Go-To” Lead whenever I contemplate acute LAD occlusion is lead aVL. Lack of ST elevation in aVL makes me question the diagnosis of acute LAD occlusion. But there is clear ST elevation in lead aVL in Figure-1.
- Mid- or more distal LAD occlusions do not always produce reciprocal ST-T wave depression in the inferior leads. But proximal LAD occlusions almost always do! So once I’ve detected some ST elevation in lead aVL — I simultaneously look next at all 3 inferior leads (II,III,aVF), to see if there are reciprocal ST-T wave changes. Reciprocal changes are not uniformly seen in lead II — and even when seen, they tend to be more modest than in leads III and aVF. But I especially look for that magic “mirror-image” picture of reciprocal change between leads III and aVL — which IF present, to me means acute STEMI until proven otherwise.
- To clarify what I mean by “mirror-image” reciprocal change — I’ve outlined in BLUE in the Bottom of Figure-1 the mirror-image picture of leads III and aVL. Note that the mirror-image of the ST-T wave in lead III looks virtually identical to the upright image of the ST-T wave in lead aVL — and vice versa.
- NOTE: The T waves in lead III and/or lead aVF may sometimes normally be inverted — especially when the axis is leftward, and the QRS complex in these leads is predominantly negative. But it is rare in my experience to normally see the mirror-image reciprocal picture (with some ST depression) that we see here in lead III of Figure-1. The shape of the ST-T wave in lead aVF also looks atypical for a normal variant.
What Else Can We Learn from this Case? Knowing that the cath in this case was entirely normal — it is worthwhile going back to the initial ECG in Figure-1. Factors against acute STEMI include: i) the fact that there is at least some ST elevation in so many leads on this tracing! (ie, leads I, II, aVL, and V1-thru-V6). Acute STEMI is more likely to localize; ii) there is healthy R wave progression and the QTc looks relatively short (these are 2 qualitative features that are incorporated into Dr. Smiths 3- and 4-variable formulas, which I find to be helpful in reducing the likelihood of acute STEMI); and iii) this 58yo man was not having chest pain. That said, the ECG abnormalities that we do see on this tracing clearly justify ruling out acute occlusion.
- SUGGESTION: Given that we now know the ECG in Figure-1 is the “normal” ECG pattern for this patient — it may be helpful to give him a miniature photocopy of his ECG to carry on his person in the event he ever again presents to an ED because of acute symptoms. Ready availability of his “baseline tracing” may avoid another future cath …
|Figure-1: Initial ECG on the 58yo man in this case at the time EMS arrived (TOP tracing). Bottom — For illustrative purposes, I have inserted the “mirror image” of leads III and aVL outlined in BLUE (See text).