Is this Myo-pericarditis? Or OMI with subsequent pericarditis? Does the angiogram always explain the ECG findings?

A 57 y.o. male with a history of diabetes presented with sharp, substernal chest pain with radiation to the bilateral shoulders that started approximately 40 hours prior to presentation.  Patient reports that this pain came on suddenly, is worse when he lays down and better when he sits up.  It is non-exertional but is worsened when he takes a deep breath.  

He denies any preceding illnesses, fevers, chills, cough, runny nose.  Patient states that he has never had a history of heart problems.  He reports that he is not taking any medications for his diabetes at this time.  He has never had a blood clot before.  He has not noticed any swelling in his legs.

An ED ECG was recorded:

What do you think?

There is sinus tachycardia, which should make you pause when you are considering ACS, as most ACS has a normal heart rate unless it is causing decreased stroke volume.  

There is ST Elevation in inferior and lateral leads, and ST depression in V1 and V2.  There is perhaps excessive PR depression in lead II.  There is no Spodick's sign (downsloping TP segment), which was recently reported to be found in about 30% of pericarditis and 5% of OMI.  But Spodick's sign is particularly unreliable in tachycardia since the TP segment is too short to demonstrate much downsloping.

Because there is a flat T-wave, this has the appearance of pericarditis, but with one important exception: there is ST depression V1 and V2.  Pericarditis does NOT have any ST depression EXCEPT in aVR and possibly V1.   Myocarditis, which may be localized (in this case, to inferior, posterior, and lateral walls) may indeed have ST depression.

In addition, the flat T-wave may simply be the beginnings of T-wave inversion in leads manifesting OMI.

Remember: you diagnose pericarditis at your peril.

A 2nd ECG was recorded 30 minutes later:

No significant change

The first troponin I (4th generation) returned at 23.1 ng/mL (very high, consistent with myocarditis or subacute OMI).

How about myo-pericarditis?  The symptoms of myocarditis are very similar to pericarditis, the ECG of myocarditis looks just like this one, and there may be a very elevated troponin, and also a wall motion abnormality.  Unlike pericarditis, there can be ST depression in myocarditis, as it is often localized to one myocardial territory, whereas pericarditis is diffuse (diffuse STE).   

Myo-pericarditis is quite likely here.  The only way you can avoid an angiogram is to have an echocardiogram that does NOT have a wall motion abnormality, but that would be unlikely even in myo-pericarditis.

So the cath lab was activated:

Angiogram:

Interventionalist note: "50-something male with 2 days of chest pain worse with rest and on taking a deep breath. Pain is better with movement. In the ER he was noticed to have marked ST elevation in inferolateral leads with PR depression and PR elevation in aVR. Bedside echo by ER physician showed wall motion abnormality in anterolateral and septal wall.  The (contemporary, not hs) troponin I was 23.1 ng/mL.  He was emergently taken to the cath lab."

Coronary angiogram:

Left main: large caliber and normal.

LAD: Large caliber vessel that wraps around the apex. It has mild diffuse disease throughout. There are small caliber diagonal branches without any significant stenosis.

LCX: large caliber vessel. OM1 and OM2 are small to moderate caliber vessels without any stenosis. OM3 (3rd Obtuse Marginal branch of the circumflex) is a large caliber vessel and has a 70% focal stenosis at the proximal segment. It bifurcates into a large superior branch and a small inferior branch. There is TIMI3 flow in the vessel.

RCA: moderate caliber dominant vessel without significant stenosis. It gives a small PDA and PL branch both of which has non obstructive disease.

Assessment:

"Based on patient history of 2 days of chest pain (worse with respiration and lying down, improved with exertion), and EKG his presentation is most likely consistent with myo-pericarditis. He does have stenosis of OM3 which is a large caliber vessel but has TIMI-3 flow and no clear evidence of plaque rupture. It was therefore decided not to intervene on the lesion."

This ECG was recorded after first angiogram:

Now there are much larger T-waves in V2 and V3.  The ST Depression is gone.  

These look like posterior reperfusion T-waves.

Was that lesion in OM3 perhaps an OMI lesion?  Did it spontaneously open up, resulting in the resolution of STD in V2, V3 and development of posterior reperfusion T-waves?

The troponin peaked at 26.6 ng/mL

A Twist

Later, the interventional team looked at the angiogram again and realized that the lesion in OM3 was indeed ruptured plaque, that it was "hazy" (which implies thrombus) and that the flow was less than TIMI-3.  So this was indeed an OMI of a large 3rd Obtuse Marginal off the circumflex.  

The patient went back for a second angiogram and stent.

Another ECG was recorded after the 2nd angiogram:

Not much different.

An echocardiogram was done:

No effusion

EF = 47%

Regional wall motion abnormality-lateral .

Regional wall motion abnormality-inferolateral (e.g., posterior by the new nomenclature)

This ECG was recorded 2 days later:

This still looks like pericarditis.

Discussion:

What happened?  The patient had an acute OMI of the 3rd Obtuse Marginal branch of the circumflex.  He did not present until 40 hours after onset (hence, first trop very elevated).  He had enough transmural infarction to develop post-infarction pericarditis, which resulted in positional and pleuritic pain, and persistent ST Elevation without large T-waves.   

In this case, the ECG findings and troponin and echo were not distinguishable from an initial insult of myo-pericarditis (which is often localized, and thus mimics OMI) 

So he had OMI followed by postinfarction pericarditis, mimicking myo-pericarditis.

Is there a difference between postinfarction pericarditis and Dressler's syndrome?  Yes.  

Postinfarction pericarditis (sometimes called postinfarction regional pericarditis) occurs very shortly (days) after onset of MI.  See the linked post for details.

Dressler's syndrome (or "post myocardial injury syndrome) has signs and symptoms similar to those seen in patients with acute pericarditis and/or pericardial effusion in other clinical settings, but there is a latency period of weeks to months post-MI, with rare early presentations within one week post-MI. In Dressler's, the initial myocardial injury is thought to release cardiac antigens and stimulate an immune mediated damage response, possibly similar to that in idiopathic pericarditis.

This further illustrates my old saying: "You diagnose pericarditis and your peril."  That is even true when it is clearly pericarditis, because pericarditis may be the result of acute MI!!

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Comment by KEN GRAUER, MD (6/11/2022):

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The topic of acute traumatic pericarditis was just discussed in the June 8, 2022 post by Drs. Nicholson and Meyers. In My Comment on that post (at the bottom of the page) — I contrasted the ECG findings of typical acute pericarditis with those of the patient in that case, who survived among other injuries a penetrating wound to the heart.

Today's case by Dr. Smith illustrates another facet regarding the ECG diagnosis of acute pericarditis. To emphasize — there are multiple potential causes of acute pericarditis. These include:

• Acute viral pericarditis (probably the most common cause in a general population).
• Other infectious conditions (ie, bacterial infections, fungal, TB).
• Inflammatory disorders (ie, RA, SLE, rheumatic fever, other forms of vasculitis).
• Metabolic disorders (ie, uremia from renal failure, hypothyroidism).
• Miscellaneous conditions (ie, cancer, certain drugs, radiation therapy, sarcoidosis, trauma).
• Idiopathic (ie, cause unknown — although many of these are probably undiagnosed viral infections).
• Cardiac causes (ie, post-infarction regional pericarditis, Dressler Syndrome [ie, an autoimmune-mediated response to myocardial antigens, usually seen 2-3 weeks after an MI], post-cardiac surgery).

Also to emphasize is: i) That for all the discussion about pericarditis — this disorder is not a common diagnosis in an emergency setting; ii) When pericarditis occurs — its manifestations may vary depending on which of the above factors are causative; and, iii) The uncommon cardiac causes of Dressler Syndrome and post-infarction regional pericarditis have become even less common in recent years, felt to be a positive result of the increase in reperfusion therapy.

Today's case is interesting in that the patient is felt to have had both an acute OMI and post-infarction regional pericarditis. This 57-year old man presented to the ED with a 2-day history of chest pain, including a pleuritic component (CP worse on taking a deep breath) — and positional change (CP worse on lying supine, and improved on sitting up).

• What pertinent negative was missing from the history provided?
• For clarity — I've reproduced the initial ED from today's case in Figure-1. What ECG findings in today's initial tracing are consistent with acute pericarditis?
• Which ECG findings are against acute pericarditis?

Figure-1: The initial ECG in today's case.

ANSWERS:

• The pertinent negative missing from the history in today's case, is that, "No pericardial friction rub was heard". In my experience of reviewing literally hundreds of internet cases in which the diagnosis of acute pericarditis was suspected — the overwhelming majority of clinicians FAIL to ever mention that they listened for a pericardial friction rub. If Not Mentioned as a positive or negative finding — this usually means that the clinician did not listen for a rub. Failure to listen for a rub is a critical oversight — because IF you hear a pericardial friction rub — then you have made the diagnosis of acute pericarditis! 
• 
  
• ECG findings in Figure-1 consistent with acute pericarditis include: i) Upward sloping ST elevation in multiple leads; ii) The shape of ST-T wave elevation in lead II looks more like lead I than lead III (whereas with acute inferior MI — the ST-T wave shape in lead II looks more like lead III); and, iii) The ST-T wave ratio in lead V6 is >0.25 (whereas it tends to be less than this with repolarization variants) — See My Comment in the June 8, 2022 post for review of these and other ECG findings typical for acute pericarditis.
• 
  
• Of no diagnostic help in Figure-1 are the findings of: i) PR depression — which I found difficult to assess in the inferior leads of this tracing (due to baseline wander). I don't see diffuse PR depression — and even if I did, the specificity of this finding for acute pericarditis is lacking; and, ii) Multiple leads in this tracing show Q waves — however, the q waves in leads I,II,III,aVF and V4-6 are small and narrow (and most likely insignificant).
• 
  
• ECG findings in Figure-1 against the diagnosis of acute pericarditis include: i) There is J-point ST depression in lead V2 (Other than right-sided leads III, aVR and V1 — there should not be ST depression in other leads with acute pericarditis); ii) The T wave in lead V2 is surprisingly tall and peaked (Normally there is a similar shape to the diffusely elevated ST-T waves); and, iii) It looks like there is already a hint of beginning T wave inversion in a number of the leads that show ST elevation (whereas T wave inversion with acute pericarditis typically does not begin until ST elevation has resolved).

Conclusion: Although at 1st glance, it looked like the ECG picture in Figure-1 might be suggestive of acute pericarditis — on further inspection, there are significant ECG features against the diagnosis of acute uncomplicated pericarditis.

• As per the superb discussion above by Dr. Smith — evolution of this case (including the ECG picture on serial tracings) — are consistent with what probably occurred in today's case, namely the combination of acute OMI from LCx occlusion, followed by development of post-infarction regional pericarditis.