Tuesday, January 14, 2020

A 40-something with sharp chest pain, worse with lying down, better leaning forward

A 40-something y.o. male with only PMH of DM and tobacco use presented with chest pain.  

Patient complained of 2 days of sharp, constant, sternal chest pain, 10/10, waxing and waning, worse with laying down and improved with leaning forward or walking.  

He has not had pain like this before.

Here is his ED ECG:
Diffuse ST Elevation.
The only reciprocal depression is in aVR
There is a lot of PR depression.
The inferolateral T/ST ratio is low (i.e., T-waves are not large in spite of STE)

What do you think?

This was texted to me and my answer was this:

"This looks like myo- or pericarditis, but you diagnose myopericarditis at your peril."

Since pain has been present so long, then troponin should be elevated in either MI or myocarditis.  If elevated, the patient needs the cath lab to be certain it is not acute coronary occlusion (occlusion myocardial infarction -- OMI).

Initial troponin I was 23.11 ng/mL (see profile below).

Here is the formal echo:

Regional wall motion abnormality-inferolateral.

Since it could not be definitively proven that this was myocarditis and not acute MI, the cath lab was activated.

Culprit Lesion: Hazy, 70% stenosis of the mid-OM3; Successful PCI with excellent angiographic results, with normalization of flow post-PCI

Learning Points

How is this possible???
How can acute MI have positional and pleuritic chest pain??
How can the ECG in acute MI look exactly like myo- or pericarditis??

2 reasons:

1.  The clinical presentation of acute MI can be protean.  (Those who think that it cannot present like myocarditis have not been around long enough.)   It can present with pleuritic chest pain, positional chest pain, NO chest pain, or just about any other symptom!

See this case:

Should Troponin be a Vital Sign? Perhaps, but only if Interpreted Using Pre-test Probability.

2. Acute MI can result in post-MI pericarditis.

Follow up

In this case, the final clinical diagnosis was presumed acute MI with post infarction pericarditis.

How can you make the diagnosis short of an angiogram?

1.  If there is no new wall motion abormality on a high quality contrast echo, then it is not OMI.  If there is, then it may be either OMI or myocarditis.

2.  MRI, but this takes some time.

3.  Clear pericardial friction rub

4.  Pericardial effusion.

5.  Clear viral syndrome, elevated CRP change the probability, but do not rule out OMI.

Finally: Among these options, only MRI and angiogram will rule out post infarction pericarditis.

Myocarditis is not so common that, if you do an angiogram on all cases, that you will be doing hundreds of unnecessary angiograms.  Furthermore, although PCI has a significant complication rate, angiogram has a vanishingly low complication rate, especially in patients who are previously healthy.

So why risk missing an acute MI (an OMI)?

You diagnose pericarditis and myocarditis at your peril (actually, at your patient's peril).

MY Comment by KEN GRAUER, MD (1/14/2020):
If I ever decided to write another ECG textbook — I would want to use the ECG in this case for illustrative purposes because: i) It shows a number of ECG findings that are highly typical for Acute PericarditisandiiIt also shows features that are not typical for simple acute pericarditis.
  • For clarity — I have reproduced and labeled the ECG in this case in Figure-1.

NOTE: Although we have frequently discussed distinction between acute pericarditis — acute myopericarditis — repolarization variants — and acute MI — differentiation between these entities remains problematic in practice. Hopefully the points emphasized in this case will assist simplifying the task of the emergency care provider.
  • By way of reference — I reviewed the ECG Stages of Acute Pericarditis (including assessment of the ST Segment/T Wave Ratio) in My Comment, at the bottom of the 12/13/2019 SSmith ECG Blog post.
  • I further reviewed ECG findings of Acute MyoPericarditis (including recognition of Spodick’s Sign) in My Comment, at the bottom of the 1/10/2020 SSmith ECG Blog post.

Figure-1: The ECG shown in this case (See text).

QUESTION #1: Which ECG findings in Figure-1 are typical for simple Acute Pericarditis?

ANSWER: Typical ECG findings for acute pericarditis that are seen in ECG #1 include the following:
  • There is diffuse ST elevation (ie, in almost all leads — except for right-sided leads III and aVR).
  • There are no more than trivial Q waves (ie, and very narrow septal q waves in several lateral leads).
  • There is no reciprocal ST depression (as is usually seen when there is acute infarction).
  • The ST-T wave appearance in lead II looks similar to what is seen in lead I. In contrast, with acute MI — the ST-T wave appearance in lead II tends to resemble lead III.
  • There is an increased ST/T wave ratio in lead V6 — because T wave amplitude in this lead is modest, and there is a relatively large amount of ST elevation in this lead.
  • There is significant PR depression in multiple leads (GREEN arrows in Figure-1). The amount of PR depression is especially marked in leads V2 and V3. In addition — there is marked PR elevation in lead aVR (PURPLE arrow).
  • Finally — there are aspects of the History that are clearly consistent with a diagnosis of acute pericarditis (ie, chest pain is positional — being exacerbated by lying supine, and relieved by leaning forward).

QUESTION #2: Which ECG findings in Figure-1 are NOT typical for simple Acute Pericarditis?

ANSWER: As typical as the history initially sounded in this case — demographics of this patient do differ from the most common presenting scenario of acute pericarditis.
  • Although there are numerous potential causes of acute pericarditis — an acute viral etiology in a previously healthy younger adult would be the most typical presenting scenario. The patient in this case was somewhat older (ie, in his 40s) — and he had a history of diabetes + longterm smoking. Clearly, he might be predisposed to developing coronary disease.
  • PEARL #1: Despite the above noted ECG findings that are typical of acute pericarditis — the dramatic amount of T wave peaking (especially in lead V3) is much more suggestive of the hyperacute T waves of impending coronary occlusion than of simple acute pericarditis.

PEARL #2: A distinguishing feature between Acute Pericarditis vs Acute MI is that with pericarditis — T waves tend not to invert until after ST elevation has returned to the baseline.
  • In contrast, with acute MI — it is not uncommon to see residual ST elevation while T waves have begun to invert. Therefore, another feature against simple pericarditis in ECG #1 — is the fact that beginning T wave inversion is seen in multiple leads (RED arrows) in which ST segments are still at least slightly elevated.

PEARL #3: When in addition to Pericarditis, there is also Myocarditis (ie, acute MyoPericarditis) — Distinction from Acute MI becomes even more difficult! Troponin elevation by definition implies at least some degree of acute myocarditis.
  • Potential ECG findings of acute Myocarditis (or MyoPericarditis) are many — and they may be identical to the findings of acute MI. Often, there is a combination of ECG findings suggestive on the one hand of acute pericarditis — and, on the other hand, of acute MI (such as we see in Figure-1!).

ISUMMARY  Among KEY POINTs which have been emphasized numerous times by Dr. Smith:
  • You diagnose acute pericarditis (and acute myopericarditis) at your peril (that is, at your patient’s peril)!
  • Neither ECG findings nor clinical history are totally reliable for distinguishing between acute myopericarditis vs acute MI.
  • As was seen in this case — sometimes both conditions may coexist! Thus, the patient in this case had acute MI and then developed post-infarction pericarditis.
  • Sometimes, diagnostic cardiac catheterization may be needed to distinguish between these entities. It is perfectly fine if cardiac cath is sometimes needed to be certain of your diagnosis.


  1. excellent case; so you are saying, steve, that an OMI secondary to the diseased obtuse marginal -3 led to the pericarditis.
    it would interesting to see the ecg's post stent: how much, if any, of the injury pattern improved.
    thank you, steve.
    and i guess, even if there were a pericarditis-related friction rub, or even an effusion, in this case angio was warranted , (no?), because the OMI caused a secondary pericarditis?

    1. THANKS for your comment Tom! I believe you are “right on” — in that thinking in this case postulated a post-infarction pericarditis. Typically, this takes at least “a little” (a day, or two or three) time for such post-infarction pericarditis to develop — but of note, the history in this case DID indicate 2 days of “waxing and waning” positional chest pain — so enough time WAS present for a post-infarction pericarditis to develop. And I believe (in My Comment, written after you submitted your thoughts) that the ECG in Figure-1 DOES show ECG findings typical of BOTH acute coronary disease as well as acute pericarditis. Finally, you are correct that even if a “tell-tale” pericardial friction rub was present — that this would not distinguish between the possibility that BOTH pericarditis + acute coronary disease were present (ie, cath would be warranted regardless!) — and THAT was among the KEY Teaching Points emphasized in this case by Dr. Smith. THANKS again for your input! — :)

  2. Could that be OMI due to pericarditis? Meaning the other way around...

    1. Sounds like cath showed acute coronary disease — so it doesn’t seem that acute pericarditis was the initial event. Instead, the pericarditis appears to be secondary to the acute MI. P.S. Please note My Comment above (that I believe I added after you had already submitted your question). In my opinion — there ARE several ECG findings in Figure-1 that are NOT typical of simple acute pericarditis — but which rather suggest there was indeed an acute coronary event as the primary problem. THANKS again for your question — :)

  3. Great case.
    In the lead III, there is no reciprocal ST depression?

    1. @ Claudio — THANK YOU for your comment. Reasons I would not consider ST-T wave appearance in lead III as consistent with “reciprocal ST depression” are: i) the J point is not depressed in lead III, so technically there is no ST depression. Instead, it is the T wave that is inverted in lead III; ii) The other inferior leads (ie, leads II and aVF) show ST elevation — so the appearance of lead III is unique among the inferior leads; and iii) Lead III (at +120 degrees) is really a “right-sided” lead — and with acute pericarditis — the principal finding is diffuse ST elevation that tends to be seen in ALL leads EXCEPT for remote, right-sided leads. The 3 leads considered as remote, right-sided leads are leads III, aVR & V1 — and those are the leads that do not uniformly manifest ST elevation with pure acute pericarditis. Therefore — the T wave inversion that we see in this case which is isolated to lead III, is really an EXPECTED findings of acute pericarditis, and not a change of “reciprocal ST depression” — :)

  4. Are we sure that RED arrows correspond to beginning T wave inversion and not to negative U waves ?


    1. In my experience — negative U waves are extremely challenging to identify. It has been rare that I’ve been certain about seeing them. I don’t think I’ve ever seen negative U waves in 7/12 leads … I believe the RED arrows in ECG #1 highlight beginning T wave inversion, and not negative U waves — :)

    2. Ken...

      I totally agree with you. In fact, to say that recognizing inverted U waves is "extremely challenging" may itself be an understatement. The time to locate inverted U waves is BEFORE an OMI and ST deviation occurs. Sometimes the only way to do that is to draw a straight line from the end of the T wave where it rejoins the baseline to the beginning of the P wave. Again, this assumes no ST deviation yet (and no baseline wander). And don't expect a discrete little cup-like inverted wave, either. U waves can be rather wide. Just remember that there is no reason for any negative deflection between the end of the T wave and the beginning of the P wave except for an inverted U wave. Inverted U waves are more indicative of proximal LAD occlusions.

      Also, one other distinction to recall. PIRP begins within just a few days of the coronary event. This is not to be confused with postinfarction pericarditis (Dressler Syndrome) which makes its appearance WEEKS after the OMI.

      Terrific discussion - THANKS!

    3. THANK YOU so much Jerry for your comments! I have been "on the lookout" for negative U waves during the past 3+ decades (ever since Barney Marriott first drew my attention to this finding) — and it remains an elusive finding for me — :)

  5. Amazing case, THANKS!I would like to know if the 4-variable formula can help in this case? When use it your value is 19.976 with STE60JV3 = 2.5 mm, QTc-B = 443 ms, QRSV2 = 13 mm and RAV4 = 14 mm, however it is critical to use it only when the differential is subtle LAD occlusion vs. early repol. In other words, can we use it for distinguishing between acute myopericarditis vs acute MI??

    1. @ Anonymous — I will pass your question on to Dr. Smith, since he is the one who studied and devised the 4-variable Formula. My hunch is that the formula does not apply to this case — because this is not a subtle distinction between repolarization variant vs early anterior OMI — but instead, ST elevation is diffuse, T wave appearance (especially in lead V2) is dramatically peaked (abnormal), and there is terminal T wave inversion in multiple leads. I would think these are qualitative ECG findings that should “catch your eye” regardless of what the formula value happens to be.

  6. Thank you for this excellent case study and your contemporary approach. I am a nurse and your blogspot an excellent addition to my practice. Feel more confident in my ability to interpret ECG and critical approach.

    1. @ Anonymous — THANK YOU for your comment! So glad our ECG Blog has been helpful to you! — :)


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