To activate or not to activate?

Written by Pendell Meyers, with edits by Steve Smith

I was texted this ECG with no clinical information:
(This will be called ECG-2)

What do you think?

I replied “Actually I think this might be a false positive.”

The ECG shows sinus rhythm with relatively normal QRS complex followed by large STE in V1-V3, with ~4mm STE in V2. There are no pathologic Q-waves, no terminal QRS distortion. I do not think there is any STD in the inferior leads; there is a tiny amount of PR depression (normal) and the J-point is exactly on line with the PR interval. In lead III the T-wave does slope downward at first, but I just didn’t think this was convincing morphology to be called reciprocal STD.

I was left with concerning anterior STE which may be a normal variant or may be LAD occlusion, so I used the SubtleSTEMI app on my phone:

3 variable


I sent it immediately to Dr. Smith with no clinical information. He saw it on his phone without the QT (so could not use the formulas), and responded: “That is a really tough one. But I think it is actually a normal variant. My best guess, but I am not sure. Did you use the formulas?”

It turns out this was from a male in his 50s with history of smoking and HTN but no known CAD who presented due to chest pain radiating to the right cheek and right arm, which had awoken him from sleep early in the morning. By the time he arrived in the ED, his pain had apparently spontaneously resolved.

Here was his initial ED ECG earlier that morning (ECG-1):

There is a small amount of STE in V1 and V2, but much less than the ECG above. This ECG is easily within normal limits.

The patient had an initial undetectable troponin and was placed in the observation unit for serial troponins and CTCA vs. stress test.

While waiting in the observation unit, the patient suddenly complained of returning chest pain.  This is when ECG-2 was recorded; here it is again:

The following ECG (ECG-3) was recorded 10 minutes later:

Similar findings with dramatic STE in V2. There is no reciprocal STD.

The treating clinicians interpreted his return of pain with dynamic ECG changes and dramatic STE in the anterior leads as a “STEMI,” and activated the cath lab (appropriately).

Here is the result:

Normal left circulation (except for a 40% D1 nonculprit stenosis according to the report).
Normal right circulation.

Non-obstructive CAD, no coronary occlusion. Repeat ECG after cath was unchanged. Serial troponins were all undetectable. Echo was done and was unremarkable.

What do you think the final diagnosis was in the chart?

“Pericarditis,” of course. He was treated with colchicine and discharged. This patient likely did not have pericarditis. It is much more likely that this ECG is simply a normal variant. Normal variants can change dramatically and dynamically as above. It is an unfortunate truth that we have shown on this blog many times.

Let me be clear: we are not advocating that this patient should not have been cathed emergently. Any patient with a concerning clinical picture or ECG may deserve emergent cath. Dynamic and dramatic STE in general does in fact have a significant rate of true positive acute coronary occlusion. Additionally, diagnostic cath (without any coronary intervention) is a very low risk procedure. But expert ECG interpretation can often predict the false positives in the group of dramatic ECG findings.

Would I have activated the cath lab? Assuming his clinical appearance was as concerning as it sounds on paper, I still think it would have been perfectly reasonable to do so, although in the back of my mind I would suspect a false positive. And that is completely acceptable and likely good care, because the ECG cannot identify all acute coronary occlusion. I would make sure that I am not overlooking the possibility of other dangerous etiologies of chest pain including dissection and PE before letting the patient roll away to the cath lab.

When this specific population (benign early repolarization vs. subtle LAD occlusion) was studied, R-wave amplitude in V4 was the most important predictor variable, more important than STE. QRS amplitude in V2 and QTc were also as important as STE. This is because acute coronary occlusion does not follow the rules of the “STEMI criteria.” Instead, you must become expert in ECG interpretation by learning from cases such as these.

Smith comment: 

1. Is there an alternative to activating the cath lab if you suspect normal variant?  Yes. If you can get a rapid high quality, bubble contrast enhanced echocardiogram, read by an expert, and, while the patient has symptoms and ECG findings, it shows no wall motion abnormality (WMA), then you can be certain that it is normal variant.

2.  Caveat: However, frequently clinicians do such an echocardiogram after symptoms and ECG findings have resolved. This is hazardous! Although there is usually some residual stunning (WMA),  sometimes the ischemia was so brief that the wall motion completely recovers.  This would be a false negative echo and leave the patient with an unstable plaque and thrombus in the coronary artery that would then not be intervened upon.

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