53 year old male with a suspicious ECG – Conclusion

This is the conclusion to 53 year old male with a suspicious ECG.

Let's take another look at the 12-lead ECG.

This one was really challenging because we all know that reciprocal changes are strongly supportive of acute STEMI. However, this case is an excellent reminder of something else — the importance of clinical correlation! 

Remember "Step 7" in the Six Step Method for 12-Lead ECG Interpretation? While I acknowlege the possibility of a clinically silent acute myocardial infarction, my department's STEMI Alert protocol requires that the patient be experiencing signs and symptoms consistent with ACS. It need not be chest pain, but it would have to be an anginal equivalent if chest pain were absent.

This ended up being called benign early repolarization at the hospital.

Aside from the lack of clinical correlation, were there any clues that this was not an acute STEMI? 

When I sent this ECG to Stephen Smith, M.D. of Dr. Smith's ECG Blog he pointed out that the QTc was only 360 ms. He gave it a 3% probability of being an acute STEMI (perhaps it would have been less had I told him the patient was completely asymptomatic). That was a very good point! The QTc is almost always prolonged in the setting of ischemia.

I can't give you an exact cut-off but it's something I'll be keeping a close eye on going forward for these tough cases.

Another thing that interests me about this case is that it reminds me of the incredible diversity of ST-changes that fall under the banners of "benign early repolarization", "early repolarization", or "repolarization abnormality".

I think these phrases are often a substitute for "we don't know why ST-elevation is present but we don't think it's a STEMI." However, the phrase "repolarization abnormality" is pretty generic. After all, what is the ST-elevation of acute STEMI if not a repolarization abnormality?

I understand the reluctance of physicians to use the word "benign" especially when some studies suggest that "benign" early repolarization may be a weak marker for sudden cardiac death. But it can all be very confusing for those trying to learn how to differentiate the ST-elevation of acute STEMI from other causes of ST-elevation.

Let's consider some examples.

This is from 23 year old male CC: Chest pain

This one was labeled a "repolarization abnormality". 

Here's another great example from Tweet about ECG leads to mystery – Is this a mimic or the real thing?

This one is similar to our "53 year old male with a suspicious ECG" in that the inverted T-wave in lead aVL looks like a reciprocal change. However, the patient was a 19 year old African American male, ventilator dependent, with an elevated temperature. Not exactly a presentation we associate with acute STEMI.

Here's an ECG that I had forgotten about until I found it on my hard drive last week. I don't remember who sent it to me but I remember being told that the potassium came back in the normal range (and that it was not a STEMI).

This is an impressive looking ECG! I would definitely be worried about acute anterior STEMI. However, two findings point toward benign early repolarization. First, the QTc is only 389 ms! Second, R-wave progression is intact (average R-wave height in leads V2-V4 is greater than 5 mm).

Finally, let's look at a "classic" case of benign early repolarization (BER). This is from the "Early Bird Gets the Worm" case at EMS1.com.

Now we see all of the classical features of benign early repolarization. Notched J-points. Upwardly concave ST-elevation. Short QTc. Absence of reciprocal changes.

Unfortunately, as you can see, it's not always this easy! 

So what should you do?

Remember the 41 year old male CC: Chest pain?

In this case the QTc was relatively short at 394 ms and R-wave progression is intact. However, something about it doesn't look right. The ST-segments in lead aVL are upwardly convex (non-concave) and the ST-segments are flat and almost downsloping in lead III (a possible reciprocal change).

This turned out to be acute STEMI but it was serial ECGs that clinched the diagnosis! That and the fact that the "story was good."

So remember, always correlate the ECG to the history and clinical presentation and perform serial ECGs.

4 Comments

  • Brandon Oto says:

    It seems like there aren’t as many studies that examine the predictive value of clinical findings + ECG findings for MI, versus just the latter. We know that many CP patients with STE are BER; I would be interested how many asymptomatic STE patients are likewise. This is a great reminder about how much the PPV value of even as alarming a finding as STE with reciprocal changes is still heavily dependent on the population you’re looking at (asymptomatic dude off the street, versus patient who brought himself to the ED). Hence the challenges in any screening-type diagnostic situation.

  • 12leadekg says:

    @tom B  I understand the QTC of 360 ms making this likely BER.  However, I thought that with BER there would be no ST depression in the recripical leads

  • There shouldn't be, Jeff! This is a very unusual case.

  • alvin halpern says:

    good point about r wave progression intact… in anteroseptal MIs, there is poor r  wave progression… but, still in the field, this is a r/o STEMI and transported to the appropriate facility..this was a great 12 ekg to discuss.  ..  thank you

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