Viral symptoms, then acute chest pain and this ECG. What do you do?

A late 30's male presented with fever, sore throat, headache, vomiting, and body aches ("bones hurting") for 2 days.

He presented to the ED because he developed sudden severe, sharp, pleuritic (but not positional), substernal and left mid to lower chest pain.

He had this ECG at time 0

What do you think?

There was an old ECG for comparison:

Very normal

Interpretation:
There is serious widespread ST elevation that could easily by due to a wraparound LAD with anterior and inferior MI.  It could also be due to pericarditis or myocarditis, but I always say that "you diagnose pericarditis at your peril."

If you thought it might just be early repolarization, we could use the formula to assess this:
QTc = 358
RAV4 = 7
QRSV2 = 15
STE60V3 = 4

Formula value = 18.72, consistent with LAD occlusion.

The clinical presentation is very suggestive of myo-pericarditis.  But one should always remember that acute MI is a far more common pathology than myo- or pericarditis.

Other thoughts:
There is no abnormal PR depression.
The T-waves are taller than expected for myo-pericarditis, and more typical of acute MI.
The location in V2-V4 as much as inferior and lateral is unusual for myo-pericarditis.
Exam revealed no friction rub

What do you want to do?

A bedside echo was done immediately.  Here is the parasternal short axis, performed by a real expert in emergency department point of care cardiac ultrasound:

There does not appear to be an anterior wall motion abnormality.

This makes anterior MI less likely, but wall motion abnormalities are very tricky, and POCUS is very poor at identifying them.

They did not see any WMA anywhere.

There is no effusion.

The first troponin returned at 43.2 ng/mL (very high)!

At this point I would seriously consider activating the cath lab, or at least getting a formal contrast echo.

Another ECG was recorded at 1.5 hr:

Increasing ST elevation in II and V4-V6

A 2nd troponin returned at 81.78 ng/mL


Another ECG was recorded at 3.5 hrs:

No great change

A 3rd troponin returned at 100.2 ng/mL:

Another ECG recorded at 8 hr

CRP 204 mg/L (normal is less than 5): this strongly supports an infectious etiology.

Here is the troponin profile:

The providers were convinced that this was myocarditis and did not ever take the patient to the cath lab.

I would have been very nervous about this, especially after finding wall motion abnormalities on the formal echo:

Here was a delayed formal contrast echo:

The estimated left ventricular ejection fraction is 45%.
Decreased left ventricular systolic performance mild .
Regional wall motion abnormality- distal inferior hypokinesis.
Regional wall motion abnormality-inferolateral hypokinetic

This demonstrates that POCUS is NOT sensitive enough for wall motion abnormalities.

I was relieved to see this MRI result:

MRI IMPRESSION
1) Mildly decreased LV function with no focal wall motion abnormalities.
2) Normal dimensions of all cardiac chambers.
3) Extensive myocardial delayed enhancement, sparing the subendocardium,
consistent with myocarditis. There is also subtle pericardial enhancement
concerning for pericarditis, without pericardial effusion.



Learning Points:

1.  Myocarditis can look exactly like acute MI on the ECG, and have identical troponins and wall motion abnormalities.  I think it is risky to assume myocarditis based only on clinical presentation.  Perhaps I'm too conservative.
2. POCUS is insufficient to rule out wall motion abnormalities.

Another similar case:

Teenager with chest pain and slightly elevated troponin. What happens then?

Cases of acute MI that were initially misdiagnosed as myo- or peri-carditis:

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

"Pericarditis" strikes again

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MY Comment by KEN GRAUER, MD (1/10/2020):

===================================

I like this case because it proves what we know = Medicine is not 100%. Try as we may — we never attain “perfection” — but instead we aim to come as close as we can to diagnosing or excluding the most worrisome clinical possibilities in the most time-efficient and least harmful manner possible (ie, while the risk from acute cardiac catheterization is small in experienced hands — adverse effects can occur, so the procedure is not100% benign).

• For clarity — I’ve reproduced in Figure-1 the initial ECG in this case ( = ECG #1) — and the prior (comparison) tracing on this patient (ECG #2).

Figure-1: The initial ECG and the prior (comparison) tracing in this case (See text).

Regarding ECG #1: I agree with the essentials of Dr. Smith’s interpretation of this tracing. I’ll add some additional points:

• There is a regular sinus rhythm at ~80-85/minute.
• There is significant baseline artifact in a number of leads. NOTE: I feel it important to mention this degree of artifact — because it does impact on our interpretation in this case (ie, makes it near impossible to assess whether certain key leads with ST elevation also manifest PR depression ...).
• All intervals (PR/QRS/QTc) are normal. The frontal plane axis is indeterminate (ie, a nearly isoelectric QRS in all 6 limb leads). There is no chamber enlargement.

Regarding Q-R-S-T Changes — There are no Q waves — R wave progression may be slightly delayed (ie, the R wave becoming taller than the S is deep between V4-to-V5 — with persistence of S waves through to lead V6). The most remarkable finding is the marked, diffuse ST elevation without any reciprocal ST depression (other than in leads aVR and V1 — both of which commonly show ST-T wave depression with pericarditis).

• ECG Findings in ECG #1 that are consistent with acute pericarditis (or acute myo-pericarditis) include: i) Upward-sloping ST elevation in most leads (in 9/12 leads in ECG #1 = all leads except leads III, aVR and V1); ii) The appearance of the ST-T wave in lead II resembles that in lead I (whereas with acute MI, ST-T wave appearance in lead II resembles lead III — and not lead I ); iii) There are no Q waves, and none of the reciprocal ST depression that is typically seen with proximal LAD occlusion (although inferior reciprocal ST depression may be absent with more distal LAD occlusion!); iv) There is an increased (>0.25) ST/T wave ratio is seen in lead V6; and, v) I think ( = my opinion) there is some (slight-but-real) PR depression (in leads II, V2-thru-V5) + PR elevation in aVR in ECG #1 (supported by the absence of these PR segment changes in ECG #2, which is the prior tracing).
• Finally — the Clinical History in this case ( = a relatively younger adult male with a 2-day history of fever + viral symptoms + pleuritic chest pain) — is clearly consistent with acute pericarditis. The markedly elevated troponin makes this case consistent with acute myopericarditis.
• NOTE — Virtually all of the above points (plus an overview of the ECG stages of acute pericarditis) are made in similar fashion in My Comment at the bottom of the Dec. 13, 2019 Dr. Smith post.

KEY POINT — There is much wisdom in Dr. Smith’s saying, “You diagnose pericarditis (or myopericarditis) at your peril” — and, I have learned from Dr. Smith to repeat this phrase each time I’m confronted with a case like this one!

• That said — I definitely do understand the conviction of the providers at the bedside, that this patient had acute myocarditis and not acute OMI (though I would really have liked to have heard a confirmatory pericardial friction rub on auscultation). No rub was heard.
• I believe comparison of the prior tracing ( = ECG #2) with the initial ED tracing ( = ECG #1) further supports acute myocarditis as the likely diagnosis (although this comparison does not rule out the possibility of acute OMI).
• BUT — “Ya gotta be there”. I may well have also been convinced this patient had acute myocarditis given the findings we have been told. That said, Dr. Smith’s point is excellent — namely, that ECG findings of acute OMI and acute myocarditis may be identical — and, clinical findings may also be similar — such that the only way to sometimes be distinguish with certainty between these 2 conditions in the acute situation may be by acute cath. This can be challenging! — and sometimes you need more certainty with your presumed diagnosis ...

Extra Credit QUESTION: So — WHICH extremity is responsible for the artifact in ECG #1?

ANSWER: Given that artifactual baseline undulations are largest in standard leads I and III (and absent in lead II) — and, artifact is greatest in augmented lead aVL (and present but reduced in leads aVR and aVF) — the left arm is the source of the artifact.

• NOTE: It is clinically relevant to learn how to quickly identify WHICH extremity is the cause of artifact — because the sooner you do, the quicker you may be able to correct the problem (ie, faulty lead connection/inadequate skin contact — or perhaps a tremor in that extremity).
• For my approach on how to quickly identify the extremity causing artifact — Please SEE My Comment at the bottom of the Sept. 27, 2019 Dr. Smith post.

P.S. (My Confession): I was not going to mention Spodick's Sign as an ECG finding in acute pericarditis — but given Matt C's question below, I now feel the need to do so.

• I illustrate and explain Spodick's Sign in Figure-2. As I explain in the legend to this Figure — while I fully acknowledge the world renown of Dr. David Spodick in this field — in my experience ( = my opinion) — this sign has not been helpful to me.
• That said — I do agree with Matt that Spodick's Sign clearly does appear to be present in the above tracings. (This is just not the reason I thought ECG #1 showed acute myopericarditis).
• I excerpted Figure-2 from Section 12 on Pericarditis, from my ECG-2014-ePub. For those who want to read more on "My Take" regarding the ECG Diagnosis of Acute Pericarditis — CLICK HERE for a download of this Section.

Figure-2: Spodick's Sign — excerpted from Grauer K, ECG-2014-ePub (See Text).