41 year old male CC: Chest pain – Answer

Thank you for all of the excellent comments on this case! I was delighted to see such a high level dialog when I checked my blog this morning.

Normally I would to answer each of you individually, but since there are 22 comments (so far) I thought I would try a different strategy and post the answer, along with tips for the correct interpretation of this ECG (at least in the context of “STEMI / not a STEMI” while you are out in the field).

This was not a STEMI.

It was most likely left ventricular hypertrophy with a strain pattern and mild hyperkalemia.

First, let’s look at the 12-lead ECG and make the case for LVH.

You’ll recall from my previous posts on the topic that I’ve said it’s more important to recognize the so-called “strain pattern” than the voltage criteria.

The reason is simple.

If the “strain pattern” isn’t causing a problem (mimicking an acute anterior STEMI) then you’re waisting your time calculating the QRS voltage.

This ECG has the general appearance of “T-wave discordance”. In other words, the T-waves are deflected opposite the main deflection of the QRS complex, which is highly suggestive of a secondary ST-T wave abnormality.

In this case, the most likey cause is left ventricular hypertrophy.

I say “generally appearance of T-wave discordance” because it’s not true in every lead. That’s why I mentioned in a previous post that there are “some caveats”.

When I’m looking for appropriate T-wave discordance, I mentally remove isoelectric or equiphasic leads, particularly in the transition zone (the point at which a QRS goes from mostly negative to mostly positive in the precordial leads).

Let’s circle the leads I would mentally remove from this 12-lead ECG to decide whether or not “T-wave discordance” is present.


With those leads removed, are the T-wave deflected opposite the QRS complexes?


Could that be a coincidence?

Highly unlikely!

The high lateral leads in particular are showing a very typical looking strain pattern.

This can be a problem because it could easily be mistaken for “lateral ischemia” or reciprocal changes secondary to acute STEMI!

Does this ECG meet the voltage criteria for LVH?

Not exactly, but I believe we can make the case using the Romhilt-Estes point scoring system. This ECG would get at least a 4 (probable LVH), and it’s right on the borderline for left atrial enlargement and delayed intrinsicoid deflection in leads V5 and V6 which would give it a score of 5 or 6.

But I don’t think that’s important.

The next question we want to ask is, is the degree of the secondary ST-T wave abnormality proportional to the amplitude of the QRS complex in the opposite direction?

The answer is yes.

Remember, we’re looking at the ST-segments and the T-waves together.

At first glance it looks like there might be more ST-elevation in lead V1 than lead V2. However, I believe this is an optical illusion created by the biphasic P-waves in lead V1, as well as the more defined (less diffuse) J-points in lead V1.

Let’s blow this up a little bit.


When we use the TP-segments as a baseline, we can see that it’s debatable as to whether or not lead V1 shows more ST-elevation, but it’s obvious that lead V2 shows a more pronounced ST-T wave abnormality.

The T-waves seem a little bit narrower than we might have expected with LVH, perhaps with a slightly later take-off. Also, the QTc is well within “normal” at 419 ms.

I don’t have the exact lab value, but the feedback I received on this case was that the patient had a potassium level that was “on the high end of mild hyperkalemia” (so I’m guessing between a 6 and 7).

Consider the following graphic that compares the T-waves of hyperkalemia to the T-waves of acute anterior STEMI.


There isn’t much documentation out there as to what hyperkalemia is supposed to look like in the presence of a secondary ST-T wave abnormality, but you’ll notice that with hyperkalemia, the T-waves are narrow and have a late take-off, while with acute anterior STEMI, the T-waves are more “broad-based”.

This was a very difficult case. So what can we learn from it?

In my mind, it’s very simple (and it needs to be simple for field use — complicated equations involving calipers are not simple).

T-wave discordance strongly suggests the possibility of a secondary ST-T wave abnormality. That being the case, I would wait for changes on serially obtained ECGs before calling a STEMI Alert.

Remember, in some studies LVH is the most common cause of ST-elevation in chest pain patients, so we need a solid strategy to deal with this STEMI mimic!

I hope we can continue our useful discussion about this ECG! I look forward to reading more of your comments.

See also:

41 year old male: CC: Chest pain


  • Ahh, another good case. I am glad I got it, well except for the hyper K. It did strike some good discussion, which is great. This is another example of why using the TP-segment as a baseline/isoelectric line for comparison is a better habit than using the PR-segment–when possible. Thanks for clearing up the V1 vs. V2 confusion, and the equiphasic lead discordance, I didn't know that.

  • Hillis says:

    OMG !! Still can't believe t's not STEMI !!! .Very excellent and informative case.. But am still curious does the diagnosis was made according to ECG alone or lab cath. was activated when the patient presented in the ER.

  • VinceD says:

    Very interesting case, thanks for sharing/teaching. I most certainly would have been going with hyperacute T's early in an MI without taking the time to mentally run through my list of STEMI mimics.

  • Tom B says:

    Adam -It's just a personal observation. Whenever I see a concordant T-wave, I take notice. After a while I figured out that it can be a normal finding in isoelectric (very small), equiphasic, or transitional leads.For bifascicular blocks, I noticed that when the terminal deflection transitions from positive to negative in the precordial leads, the lead "above" the transition shows a concordant T-wave almost always.Next time you see a bifascicular block (RBBB/LAFB) look for this finding! Tom

  • Tom B says:

    Dr. Hillis -I agree, this a very interesting STEMI mimic! I can't tell you what the actual diagnosis was (other than mild hyperkalemia). I just know that serial cardiac biomarkers were negative and AMI was "ruled out". No cardiac cath was performed.Tom

  • Tom B says:

    VinceD -This is one of the cases that convinced me that looking for T-wave discordance (a "strain pattern" with narrow QRS complexes) is just as important, and probably more important, than looking for the voltage criteria of LVH.I especially look critically at the high lateral leads for the tell-tale downwardly concave "pouty-lipped" flipped T-waves of LVH with strain.Tom

  • Christopher says:

    I know I got tripped up by not seeing "enough" of the strain pattern and the aVR STE. I think I had myself convinced I would need more of the "strain". I tunnel visioned on the T waves as "hyperacute" rather than hyper-K. But they fit the bill of sharp and pointy!Another good 12L added to ye olde mental algorithm :)

  • Max says:

    Thank you so much for taking the time to post out the answer. I'm sure I'm not alone in the demographic of people who learn better after getting something wrong.Apart from the excellent instruction, and dissection, I wonder if you have any advice on how to present this patient to the ED staff? What I mean is, this patient (from the accounting) has the "look" – and as has been demonstrated here, certainly a cursory/non-expert examination of the 12-lead has enough similarities to a STEMI to warrant increased levels of caution and alarm. Presuming I had enough confidence in my analysis to not activate a STEMI, and tried to explain what my findings were, I would be concerned about the reaction of the receiving ED staff.

  • Brown Frown says:

    Something I've never thought about before this case: the potential for ST depression in leads with positively deflected QRS's. It seems to reason if STE can occur with negatively deflected QRS's why cant the opposite be true which seems to be the case here in I, aVL and V6 …

  • Tom B says:

    Christopher – Sometimes it's hard when different ECG findings "don't match" (like the STE in lead aVR). I find myself asking, "What is the most likely scenario?" or taking the constellation of ECG signs that "go together" (Tom G.'s admonition to "consider the company" any ECG abnormality keeps).I think putting this in the mental algorithm is exactly the right answer! Looking for T-wave discordance should be part of the rule-out process for STE-mimics.Tom

  • Tom B says:

    Max -I agree with you! Failure is the best teacher. As Thomas Edison said, "Every wrong attempt discarded is another step forward." I assume from your question that you do not do ECG transmission?I would simply tell the ED physician that you have an acutely ill chest pain patient with a concerning but inconclusive ECG.If you were pressed, I would say that in your opinion, the "T-wave discordance" suggests a secondary ST-T wave abnormality and there there are no changes on serially obtained ECGs.If it turns out to be a STEMI, then it's a learning opportunity for you.If it turns out to be an STE-mimic (like you thought) then it's a learning opportunity for the ED staff, should they choose to accept it.Tom

  • Tom B says:

    scott -Absolutely! I bring this up when we start talking about calculating TIMI Risk Scores for chest pain patients (for the purposes of identifying higher-risk NSTEMI patients who may benefit from being transported to a PCI center).The same conditions that mimic STE (LVH with strain, LBBB, paced rhythm) also mimic STD! Tom

  • Lead answer says:

    This man has really suffer a lot with this pain . you know when any kind of pain comes he only lead to like just finish me.But this man has some courage to live with it.

  • I can say that he has to suffer from sever pain to reach at this lead level. I would not be consider myself in there cause leading in the hurted battle is just not my game.

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