Tuesday, December 10, 2019

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

This is a previously healthy male teenager who was awoken by chest pain.   He was seen at another hospital and found to have a slightly elevated troponin, then underwent a CT pulmonary angiogram (PE) protocol which revealed a right sided pneumonia.  He was treated with Ceftriaxone and azithromycin.

The pain is described as located in the midsternal area, radiating to the right arm, described as 8-9/10 and worse with deep inspirations.  He endorsed cough, fever, and body aches in the previous days.

Here is the initial ECG:

Time zero:
Sinus rhythm. 
There is PR depression: see especially leads II and V5.
The ST segment is not elevated relative to the TP segment, but it is elevated relative to the QRS onset.
QRS onset is the best location for ST segment comparison, and is the location recommended by Universal Definition of MI. Why?
PR depression is due to the negative atrial repolarization wave.  That wave is still resulting in J-point depression, so there should be J-point depression relative to the TP segment.
But here the J-point is NOT depressed, so there is actually ST elevation.
There is no reciprocal ST depression in aVL.
See here for explanation of the atrial repolarization wave.

This ECG is pretty typical of myopericarditis, and fits the clinical syndrome.
This ECG was read initially as normal, and cardiology was not concerned.

The first troponin I returned at 0.081 ng/mL (0.030 is URL).

He was admitted.

A second troponin I returned at 0.122 ng/mL.

Another ECG was recorded at 4 hours and was essentially the same.

In the evening, he became diaphoretic and complained of 9/10 continuous chest pain.  This ECG was recorded at 16 hours:
Computer reads ***Acute MI***
It's not clear to me why the computer read this as such.
What I find interesting here is the new Q-wave in lead III.

This interpretation triggered a rapid response. The pediatric team felt it might be ACS, but on review of his prior ECGs, it was thought to be really unchanged from the 2 prior and more consistent with myocarditis.

The troponin I returned at 9.3 ng/mL, then at 13.65 ng/mL.

The next AM, the patient had still more chest pain, and had this ECG recorded:

25 hours
Marked PR depression.
Inferior Q-waves remain.
Now there is marked ST Elevation in inferolateral leads.
T-waves are not much higher than STE, typical of myopericarditis.
The only STD is in aVR, also typical of myopericarditis.

The troponin returned at 9.45 ng/mL.

An emergent echo was done and showed a wall motion abnormality of the distal septum and anterior wall.

Echo does not necessarily differentiate acute MI from pericarditis: both may have wall motion abnormalities.

There was a CT chest image from the previous day.
This is not easy to read.  
The septum appears a bit darker than the rest, and you might be fooled into thinking there is ongoing ischemia here.  
But I showed it to our expert and chief of radiology, Gopal Punjabi, and he read it as normal. 

Dr. Punjabi has a fantastic radiology blog on Spectral CT: https://www.ctspectral.com/

A negative CT should not be relied upon to rule out ischemia.
However, had there been an area of decreased perfusion, the positive predictive value would be good.
See an examples of CT ischemia here.

Another troponin returned at 23.89 ng/mL.

Here is the troponin profile:

An MRI was done.  Thanks again to Dr. Punjabi for these images and explanations:

Since the is subendocardial sparing, this cannot be infarction, as the subendocardium is the most susceptible region in infarction.

Overall MRI impression:

This showed moderately depressed left ventricular systolic function with ejection fraction of 36-40% with regional wall motion abnormality involving the distal septum and part of the apex.  There was a small pericardial effusion.  On delayed enhancement imaging, there was evidence for patchy areas of delayed enhancement most marked in the distal anteroseptal and apical myocardium as well as the basal and mid segment of the anterolateral walls. The T2-weighted fat-suppressed images showed evidence of edema and areas of delayed enhancement.  There is also mild and diffuse pericardial enhancement all consistent with patchy myopericarditis.

30 hours
Near normalization of ST segments.
Q-waves in III remain.

CRP returned at 43.8 mg/L.
He tested positive for enterovirus.


Many EKGs in acute MI are highly suggestive of myo- and peri-carditis and are misdiagnosed as Myo- or Peri-carditis.

This is why I frequently write: "You diagnose pericarditis at your peril."

In someone over age 30, MI is far more likely.
Under 20, myocarditis is far more likely.

But young people do have MI, due to anomalous coronary arteries, coronary artery dissection, Kawasaki dz, even atherosclerotic plaque rupture, and other etiologies.

When it comes to coronary occlusion, you can't just say: "Well, myocarditis is more likely, therefore I will not investigate further.  You have to be CERTAIN.   Problem is, it is difficult to be certain wihtout an angiogram and/or MRI.  Echo can have WMA in both.  If there is NO WMA, then it is not coronary occlusion, but if there IS one, then you still don't have a diagnosis.

MRI takes too much time.

Angiogram is quick for diagnosis.

CT angiogram is rapid relative to MRI, and could make the diagnosis.

As above, regular contrast spectral CT, if positive, is fairly accurate for ischemia.  But it is not sensitive.

Here are some more ECG cases of myocarditis in young people:


8 yo with myocarditis:

16 yo with acute MI:

MY Comment by KEN GRAUER, MD (12/10/2019):
This have been a number of posts on Dr. Smith’s Blog, regarding the ECG diagnosis of what Acute Myocarditis is and is not (For example — My Comment on the 7/21/2019 post). Today’s case provides perhaps the best example of serial ECG evolution of this elusive entity. As a bonus — Dr. Smith adds labeled MRI images detailing the finding of “subendocardial sparing” that facilitates distinction between acute MI vs Myocarditis.

For clarity — I focus my attention on the serial ECGs shown in this case, which I put together in Figure-1.
  • For interest — I offer another perspective based on mslightly different interpretation of these serial tracings.
Figure-1: The 4 serial ECGs shown in this case (See text).

I begin with my Systematic Approach to interpretation of ECG #1:

Descriptive Analysis of ECG #1: There is a regular sinus rhythm at ~95/minute. All intervals (PR/QRS/QTc) are normal — and the frontal plane axis is normal at +65 degrees. There is no chamber enlargement.
  • Regarding Q-R-S-T Changes  Small and narrow Q waves are present in multiple leads (ie, leads I, II, III, aVF — and V5, V6). R wave progression is normal — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4.
  • The most remarkable finding on this tracing is that there is slight-to-modest ST elevation in each of the inferior leads (II, III, aVF) — and in lateral chest leads V5 and V6. The shape of this ST elevation is concave up ( = smiley-configuration)  and, there is J-point notching in lead V5, as well as the suggestion of slurring of the terminal part of the QRS complex in lead II.
  • NOTE: The finding of Psegment depression in at least several leads, with PR elevation in lead aVR is among the ECG findings listed as consistent with acute pericarditis/myocarditis. The problem I’ve experienced with this criterion (and I’ve looked for PR depression in virtually every tracing I’ve considered acute pericarditis in, for over the last 30+ years) — is that overall sensitivity and specificity of this finding (in my experience) is lacking. I’ve seen PR depression in both normal variants, and in patients with acute MI. I have therefore found this sign of limited usefulness in most instances when contemplating a diagnosis of acute pericarditis or myocarditis. I did not feel that the slight PR depression in leads II and V5 + PR elevation in lead aVR of ECG #1 contributed to the diagnosis ( = my opinion).
My Clinical Impression of ECG #1: I did not think ECG #1 taken by itself was especially typical of acute pericarditis or acute myocarditis.
  • PEARL #1: The KEY to clinical interpretation of this tracing in my opinion depends on the HISTORY. Our Descriptive Analysis remains the same = Sinus rhythm at ~95/minute + slight-to-modest ST elevation with an upward concavity in the infero-lateral chest leads, with some J-point notching/slurring.

Consider the following Clinical Scenarios:
  • Scenario #1  IF told that ECG #1 was obtained from an asymptomatic young adult being screened (ie, in a pre-sports-participation physical exam — or perhaps as part of the person’s job screening) — I would have interpreted ECG #1 as a normal repolarization variant. As the clinician tasked with reading all ambulatory ECGs for 35 medical providers over my 30-year career as family medicine Attending — I encountered numerous similar tracings in this clinical situation.
  • Scenario #2  IF told instead, that ECG #1 was obtained from an older adult with new-onset chest pain that sounded cardiac — I still would have thought this tracing unlikely to represent an acute cardiac event because: i) The Q waves are all small and narrow, and unlikely to represent infarction; ii) The ST elevation is in several anatomic areas — and the shape of these ST segments (upward concavity = “smiley” configuration), together with some J-point notching/slurring is much more suggestive of a repolarization variant; andiiiThere is no reciprocal ST depression. That said, IF this history of new chest pain was indeed worrisome — the fact that there is some ST elevation would be enough to merit additional evaluation (ie, repeat ECG; serial troponins; Echo during symptoms) until more certainty of the diagnosis could be obtained.
  • Scenario #3  IF told instead that ECG #1 was obtained from a previously healthy male teenager who was awoken by severe, pleuritic chest pain — that occurred in association with recent cough, fever, myalgias, and a CT scan diagnosis of pneumonia ( = which is the clinical history in THIS case) — then Acute Myocarditis needs primary consideration in your differential diagnosis even BEFORE you look at the ECG! In this case — even though I still do not think ( = my opinion) that ECG #1 is diagnostic of acute myocarditis — this tracing certainly could represent an early stage of acute myocarditis (or peri-myocarditis).

ECG #2 was obtained that evening ( = 16 hours after ECG #1). At this time — the patient had become diaphoretic, and he was complaining of 9/10 continuous chest pain. Serum troponins were clearly elevated ...

My thoughts on comparing ECG #2 with ECG #1 were the following:
  • Although the Q wave in lead III of ECG #2 is quite deep — a small-but-definitely-present Q wave was seen in lead III of ECG #1. Small and narrow Q waves are seen in virtually the same leads in both tracings. Although definitely deeper — the Q wave in lead III of ECG #2 remains narrow. In addition — there has been slight shift in the frontal plane axis (Note that the QRS in lead aVL of ECG #1 was more negative than positive — and in ECG #2, the QRS in aVL is clearly more positive). As a result — I did not think the deeper Q wave in lead III of ECG #2 was clinically significant.
  • Realizing that there is slight change in frontal lead QRS morphology (because of this axis shift) — I still thought there most probably was an increase in the amount of ST elevation in leads II, aVF, V5 and V6 of ECG #2. Given continuous ongoing symptoms (chest pain) — I interpreted ECG #2 as showing an increase in acute changes.
  • As per Dr. Smith — I felt the overall clinical picture was most consistent with acute myocarditis.

ECG #3 was obtained the next morning ( = 25 hours after ECG #1). Severe chest pain persisted ...
  • As per Dr. Smith — there has been a dramatic increase in the amount of infero-lateral ST elevation. In fact, the ST elevation has become generalized — and, is now present in all leads except leads aVR, aVL and V1 = a pattern typical of acute pericarditis and/or myopericarditis.
  • There is J-point ST depression in lead aVR — which, given the generalized ST elevation in almost all other leads — represents a typical “reciprocal change” for acute myopericarditis.
  • Q waves are unchanged since ECG #2.
  • As per Dr. Smith — Pdepression has become much more definite, and is now present in virtually all leads except leads aVR, aVL and V1. Marked Pelevation persists in aVR. Given this diffuse PR depression, in association with diffuse ST segment elevation — this tracing represents one of the few instances in which I’d agree that PR depression in ECG #3 clearly supports our diagnosis of acute myocarditis.

ECG #4 was obtained later that day ( = 30 hours after ECG #1).
  • Clearly there has been improvement in the ECG appearance of this final tracing. That said — J-point ST elevation remains in multiple leads (ie, leads I, II, aVF; V4, V5, V6). PR depression is clearly less. Q waves remain.

FINAL COMMENT: I thought this case remarkable for the insightful manner in which serial ECG changes unfolded as this case of acute myocarditis evolved.
  • It would have been interesting to see a true baseline ECG on this patient — so that we could know how much of the modest, concave-up ST elevation in ECG #1 represented this patient’s baseline vs an early acute change of his soon-to-evolve acute myocarditis.
  • PEARL #2: One of the BEST ways to HONE your ECG interpretation skills — is to GO BACK after you know the diagnosis — and take another look at serial tracings to see if you can now pick up subtle changes that were overlooked on your initial reading. Doing so — Don’t YOU now agree that ECG #2 shows a subtle but overall increase in the amount of ST elevation compared to ECG #1? (Figure-2).

Figure-2: Comparison of ECG #1 with ECG #2 (See text).

Our THANKS to Dr. Smith for presenting this illustrative case!


  1. some links don't work

    1. @ Anonymous — The links left by Dr. Smith at the end of his discussion were not activated. I have fixed this — and I believe that ALL links are now working. If not — LET ME KNOW! Thank you for letting us know! — :)


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