What does this ECG with significant ST Elevation represent?

These 2 serial ECGs were texted to me recently.  They were recorded 12 minutes apart:

"Hey Steve, 30-something with one week of chest pain, mostly right-sided, better with sitting up.":

What do you think?

QTc's were 330 ms and 373 ms

This is what I texted back:

These look like they are a very pronounced case of Benign T-wave Inversion.  I do not think this is acute occlusion myocardial infarction (OMI).  Get an emergent contrast echocardiogram.

These are reasons why it does not look like OMI: 

1. flat ST segment in V4

2. huge R-wave in V4

3. very short QT interval

4. J-point notching

5. classic early repol in V3

6. classic features of “Benign T-wave inversion” T-waves in V5, V6.  

I would guess the patient is African American.

Would I blow it off?  No.  I would get an echo.  I am 99% certain that it is not OMI.

An emergent echo was done:

Normal left ventricular size, normal wall thickness and mild to moderate systolic dysfunction.

The estimated left ventricular ejection fraction is 43%.

Global hypokinesis.

The first troponin I then returned quite elevated at 9.8 ng/mL.

In the absence of a wall motion abnormality, especially with global decreased ejection fraction, a troponin that is quite elevated like this strongly suggests global myocarditis.  

When does myocarditis mimic OMI?  Often, myocarditis is more focal, has both focal ST Elevation and focal wall motion abnormalities, as well as elevated troponin, and an emergent angiogram must be done to differentiate the two entities.  Definitive diagnosis is by MRI.

I learned more about the history:

30-something African American with 5-7days of sharp R-sided shoulder/scapula/chest discomfort, presented with sinus tachycardia.  This history of a week of constant chest pain is also much more suggestive of myocarditis.  

OMI is generally of more acute onset, unless there is intermittent angina.  OMI it is very unlikely with a week of constant pain.

2 hours later, this ECG was recorded:

This was interpreted as having Wellens'-like reperfusion T-waves.
I would have said they were also likely due to different lead placement or to common hour-to-hour variation in non-ischemic ST elevation.

However, to be certain, the patient went for an angiogram.

Angiogram was normal

C-reactive protein (CRP) returned at 250 mg/L, consistent with myocarditis.

Serial Troponins remained in the 9-11 range, w/o any large rise and/or fall, also atypical for OMI.

He later underwent an MRI:

1) Mildly decreased LV function with no focal wall motion abnormalities
2) Patchy intramyocardial delayed enhancement compatible with myocarditis.
There is also mild pericardial enhancement consistent with pericarditis.
Overall findings are consistent with myopericarditis.

One month later,  a convalescent ECG was recorded:

The typical benign T-wave inversion is still present.  But the significant ST Elevation is resolved.

Thus, that STE was due to myo-(peri)carditis.

Summary:

It was not benign T-wave inversion, but also not OMI.

When there is worry for OMI, but the ECG and history are just not right, then an emergent contrast echo may be done in lieu of an immediate angiogram.

A wall motion abnormality and elevated troponin may be seen in myocarditis, and then an angiogram must be done to differentiate myocarditis from OMI.

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Comment by KEN GRAUER, MD (7/21/2019):

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This case raises interesting issues relating to HOW to interpret the initial ECG ( = ECG #1 in Figure-1). The patient is a 30-ish year old man, who presented to the ED with a 1-week history of chest pain that was mostly right-sided — and improved with sitting up.

• The ECG was repeated 12 minutes later ( = ECG #2).
• A 3rd ECG was recorded 2 hours later ( = ECG #3).

Additional subtle teaching points arise with close examination of the serial ECGs in this case.

Figure-1: The 3 ECGs that were shown in this case (See text).

THOUGHTS: As I suggested in My Comment to Dr. Smith’s Case from July 19 —  An optimal way to enhance one’s ECG interpretation skills is to always interpret the initial tracing in the context of the brief clinical history given (which in this case, was 1 week of right-sided, positional chest pain in a 30-ish year old man).

• Interpret this initial ECG before you look at additional information (or additional tracings). THEN reconsider your interpretation in the context of whatever additional information you are able to obtain.

Dr. Smith emphasized the KEY point regarding the interpretation of ECG #1 — namely that in view of the history of this patient, these ECG findings are unlikely to reflect acute OMI.

• In addition to the reasons cited above by Dr. Smith against ECG #1 being acute OMI — I would add: i) Upward-sloping ST segments in the leads with the most ST elevation (leads V3, V4); ii) Lack of reciprocal ST depression; iii) Lack of significant Q waves (I believe there is an rSr’ complex in lead aVL); and, iv) The atypical history. Of course, none of these features are definitive — and, as per Dr Smith — emergent Echo + ongoing clinical correlation are essential for attaining maximal certainty that this is not acute OMI.
• A NOTE on the History: When (as occurs in this case) — the patient is a younger adult and, the history is atypical for acute MI (ie, right-sided location; pleuritic and/or positional component to the chest pain) — then the prevalence of acute myocarditis as a diagnostic possibility increases significantly.

So, I did not think that ECG #1 was the result of acute OMI. I also thought this tracing looked unusual for a benign T wave inversion repolarization variant ( = my opinion).

• In my experience — Benign T wave inversion in younger adults is almost always associated with ST segment coving and elevation with T wave inversion that is especially prominent in anterior leads. I’m not used to seeing significant T wave inversion in leads V5 and V6 in benign variants, without seeing any of this in leads V2 and V3. On the other hand — acute myocarditis may present with ECG changes localized to a number of contiguous leads in a pattern less typical for acute OMI or benign repolarization.
• The beauty of troponin and Echo in the ED for cases like this — is that it can rule out benign variant when abnormal results are obtained. As per Dr. Smith — definitive diagnosis was obtained later in this case after cardiac cath and MRI.

Other Interesting ECG Features:

QUESTION: Look at ECG #2 in Figure-1. Does the extra ST elevation we now see in lead V3 reflect progression of acute ischemic changes?

ANSWER: I do not believe there is any significant change between ECG #1 and ECG #2. The limb leads are virtually identical in both tracings. The major difference in the chest leads — is that transition now occurs much sooner in ECG #2 (the R wave is predominant already by lead V3 — whereas transition did not occur in ECG #1 until lead V4). As a result — the shape and relative amount of ST elevation in lead V3 of ECG #2 — is comparable to what we see in lead V4 of ECG #1.

• Instead — I believe lead V2 in ECG #2 is malpositioned because: i) There is actually a terminal r’ in lead V2 that should not be there, especially since there was no terminal positive deflection (no r’) in lead V1; and, ii) It does not make physiologic sense for the T wave in ECG #2 to manifest a 3mm positive deflection in lead V1 — then a barely positive T wave in lead V2 — and, then a markedly positive ST-T wave by lead V3.
• PEARL: When you are depending on being able to pick up fine serial ST-T wave changes between successive ECGs — you may want to consider marking the patient’s chest to ensure similar lead placement for serial tracings. Doing so would have avoided the confusion we are confronted with for assessing chest lead progression in ECG #2.

QUESTION: What about ECG #3 in Figure-1? Was it wrong to consider Wellens’-like reperfusion T waves, given the change in lead V3’s appearance?

ANSWER: Even when the chest is marked to ensure consistent precordial lead placement — there may still be slight tracing-to-tracing variation in QRS morphology and amplitude. Sometimes — this just happens. As a result — judgement is needed when interpreting serial tracings:

• I have no “magic formula” for when to say that the difference between one ECG and the next is due to lead placement variation or axis change — vs — a TRUE significant ST-T wave change due to an acutely evolving infarct. Instead — one develops a “judgment Gestalt” from looking at numerous tracings, and then correlating your impressions by subsequent ECGs and what happened to the patient.
• NOTE: Frontal plane Axis may vary depending on the patient’s position in bed (ie, whether the patient is flat in bed — or to a certain extent inclined due to increased dyspnea when the bed is flat). It is important to appreciate that a change in frontal plane axis may sometimes dramatically alter QRS morphology and resultant ST-T wave appearance. That said — this is not a factor in Figure-1 — since both QRS morphology and frontal plane axis in the limb leads of all 3 ECGs is virtually identical!
• Did YOU notice? — that ECG #3 again shows return to a predominant S wave in lead V3 (whereas the R wave was predominant in lead V3 of ECG #2). This observation suggested to me that for comparison purposes of ST-T wave changes in the chest leads for the 3 ECGs shown in Figure-1 — we should be using ECG #1 and ECG #3 (but not ECG #2).
• Despite the fact that in ECG #3 — lead V3 now shows ST segment coving and fairly deep T wave inversion (that was not seen in ECG #1) — I did not think this was an acute ischemic change because: i) This change is really only seen in a single lead (lead V3); ii) Lead V3 in ECG #3 to me looks like the “natural result” of being a “transition lead” between what we see in leads V2 and V4 of ECG #3; and, iii) I thought the localized ST-T wave findings with little change over 2 hours in this younger adult with symptoms atypical for acute MI was much more consistent with acute myocarditis.

Our THANKS to Dr. Smith for this interesting case!