A 20-something male with acute chest pain

I was texted this ECG with the words "sudden onset CP in a 20-something":

What do you think?

This was my response:

"This is abnormal in lateral leads. It probably is a normal variant but I would get a stat echo.

It is out of the bounds of the usual with normal variant because the ST Elevation is so focal to the lateral wall. Most normal variant has as much inferior STE as lateral (and of course without ST depression in aVL).  This is myocarditis versus myocardial infarction. He should get an immediate echo.  Problem is, even myocarditis will have a wall motion abnormality. And then the only way to tell rapidly is with an angiogram.  So if there is a wall motion abnormality, go to the Cath Lab.  Diagnosis will still probably be myocarditis."

I didn't realize it at the time, but this was the 2nd ECG.

Let's go back to time zero:

There was less ST elevation on this one.

Unbeknownst to me, the first troponin I had already returned elevated to 3.0 ng/mL by the time I received the text.


Here is more history:

The patient had an acute onset of epigastric and chest pain this morning. He was in 9/10 pain that last over an hour and did not improve with repositioning.

There was a repeat ECG at 70 minutes (the one texted to me)

There is increased STE in V4-V6.

Here is the echo report:

The estimated left ventricular ejection fraction is 53 %.  Normal left ventricular cavity size.

Regional wall motion abnormality-distal septum anterior and apex, posterior segment, small.

So the patient went for angiogram:

Coronaries were clean.

Here is the ECG recorded after the angiogram:

An MRI was done:

Impression:

1) Decreased LV function with apical wall motion abnormality
2) Normal dimensions of all cardiac chambers
3) Delayed gadolinium enhancement involving the distal inferolateral wall
with subendocardial sparing. Findings are most compatible with
inflammatory etiology such as myocarditis.

Learning points:

Myocarditis can exactly mimic OMI, including having a focal wall motion abnormality.  One usually just needs to take a look with angiogram in these cases.

In case you think that 20-somethings don't get coronary occlusion (OMI), think again:

24 yo woman with chest pain: Is this STEMI? Pericarditis? Beware a negative Bedside ultrasound.

A 16 year old girl has syncope while playing basketball.....

Chest Pain in a Male in his 20's; Inferior ST elevation: Inferior lead "early repol" diagnosed. Is it?

And another interesting case of myocarditis in a 20-something woman:

A Young Woman with Chest Pressure and Subtle, Focal ST Elevation/Depression

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Comment by KEN GRAUER, MD (6/11/2019):

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I LOVE this case — because it is both challenging and demonstrative of many important points.

• As always — I strive to maximize my objectivity as commenter by NOT reading what happened until after I commit to an interpretation of the ECGs in the case.

A total of 3 ECGs were done in this case.

• The 1st ECG shown above — was the ECG that was texted to Dr. Smith with the words, “Sudden onset of chest pain in a 20-something year old male”.
• The 2nd ECG shown above — was the initial ECG that was done in the ED on this patient. This ECG was done 70 minutes earlier.
• The 3rd ECG shown above — is the same as the 1st ECG shown above.
• The 4th ECG shown above — is the ECG that was done after cardiac cath.

For clarity — I have rearranged these 3 ECGs and numbered them ( = ECGs #1, #2, #3) in the sequence that they were done (Figure-1).

Figure-1: The 3 ECGs in this case in the sequence that they were done (See text).

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MY Thoughts on these Tracings: I began by first looking at ECG #2 — which is the ECG that was texted to Dr. Smith. As was the case for Dr. Smith, all I knew at the time — was that ECG #2 was obtained from a 20-something male with sudden onset of chest pain.

• I interpreted ECG #2 as showing — sinus rhythm — normal intervals (PR/QRS/QT) and normal axis (about +70 degrees) — no chamber enlargement — small lateral (normal septal) q waves — normal R wave progression (with transition between leads V2-to-V3) — and ST elevation in the infero-lateral leads.
• The shape of the elevated ST segments was concave-up (ie, “smiley”-configuration) — with J-point notching in leads V4 and V5. Most of the time — this ST-T wave morphology will be associated with a benign repolarization variant when seen in a 20-something year old male ...
• Looking closer — the amount of ST elevation in leads V5 and V6 seemed a bit more than what is usually seen with benign repolarization variants. That said, in view of normal-appearing ST-T wave morphology (ie, concave-up ST elevation with J-point notching) + normal R wave progression with a relatively short QTc + lack of reciprocal ST depression + the patient’s young adult age — I thought ECG #2 was most likely to reflect a repolarization variant.
• That said — I wanted to know more about this patient before rendering a final interpretation ...

At this point, we learned that ECG #2 was not the initial ECG done on this patient. Instead — the initial ECG was ECG #1, which was done ~70 minutes before ECG #2. I compared these 2 tracings:

• There is artifact in several leads of ECG #1 — but otherwise, ECG #1 and ECG #2 are quite suitable for comparison purposes, because there is no appreciable change in frontal plane axis — and no more than minimal change in chest lead QRS morphology.
• I saw slightly less ST elevation in leads V5 and V6 in the Time = 0 Tracing ( = ECG #1) — BUT — I thought T wave peaking and relative T wave size (compared to the QRS in the same lead) was more in leads I, V3 and V4 in the initial ECG ( = ECG #1) compared to the later ECG ( = ECG #2).
• I definitely wanted to know more about this patient … As per Dr. Smith — the differential diagnosis included: i) A repolarization variant; ii) Acute MI; and, iii) Acute Myocarditis (or Myopericarditis).

At this point — we were told that the 1st troponin had returned elevated to 3.0 ng/mL — and — we were given the additional history that the patient’s chest pain was severe (9/10) lasting over an hour, and not improved by repositioning.

• Echo revealed an EF = 53% + regional wall abnormalities.
• Cardiac cath revealed normal coronaries.

We were then shown ECG #3, done after cardiac cath. Comparing the 3 ECGs in Figure-1 in the sequence the were obtained — it should now be obvious that ECG #3 shows ST-T wave abnormalities clearly consistent with the diagnosis of acute MyoPericarditis:

• There is more ST elevation than-there-should-be in leads V4-thru-V6.
• The T wave in neighboring lead V3 looks disproportionately tall compared to R wave amplitude in this lead.
• There is NO doubt in ECG #3, that the T wave in lead I is hyperacute and associated with more ST elevation than should be seen in this lead with this tiny of a QRS complex. ST-T wave appearance in lead I of ECG #3 clearly looks more worrisome than it did in ECG #2.
• The T wave in lead aVL has become upright in ECG #3 (even though tiny — the T in aVL was flat in both ECGs #1 and #2).
• Putting It All Together — the findings we see in ECG #3 are consistent with acute MyoPericarditis = ST elevation with T wave peaking in multiple leads (Right-sided leads aVR and V1 typically do not manifest ST elevation with pericarditis) + the finding that the abnormal ST-T wave appearance in lead II looks much more like lead I than lead III (with acute inferior MI — it is leads II and III that tend to show similar ST-T wave changes).

My LEARNING Points:

• The usual differential diagnosis for ST elevation in a younger adult includes: i) A repolarization variant; ii) Acute MI; and, iii) Acute Pericarditis (or Myocarditis or Myopericarditis). Sometimes distinction between these 3 entities may be quite difficult when all that one has is a single ECG and a history of “chest pain”. I initially favored a diagnosis of “probable repolarization variant” in this case when all I had to look at was ECG #2.
• History is KEY. Even marked ST elevation is often benign when a young adult is either asymptomatic or presents with atypical symptoms. On the other hand — the severe new-onset chest pain in this case was clear indication of a need for more information + diagnostic testing (ie, stat Echo, troponin, repeat ECGs). Once known that serum troponin was definitely elevated — I knew the ECGs were not simply a repolarization variant ...
• Considering the serial tracings shown in Figure-1 — the ECG findings + the wall motion abnormalities and elevated troponin are all consistent with acute Myopericarditis.