Is it MI or pericarditis?

This is a 48 y.o. male with a history of Bipolar disorder, polysubstance abuse, spontaneous pneumothorax x2, who presents for chest pain x 4 hours. The patient was in his usual state of health until this afternoon when he noticed the gradual onset of bilateral chest pain. He had a relapse of crack use this AM. He describes the pain as bilateral, radiating to the left arm, worsening over time, and associated with mild SOB and also some pleuritic chest pain. There is no relation of pain to exertion or meals, and no associated diaphoresis, nausea or vomiting. No recent long sedentary periods. No recent trauma, but has been doing more manual labor than usual. Pt has not had chest pain with crack use before.

Here is his initial ECG:

Sinus.  Normal QRS.  ST elevation in all leads that is not inconsistent with early repol or pericarditis, especially since there is J-wave notching (in lead aVL).  However, look closely at aVL: there is actually a bit of ST depression here.  That should not happen with either pericarditis or with early repol, especially when there is J-wave notching.  One should suspect that this is reciprocal ST depression.

Here is his previous ECG for comparison, recorded 7 months prior:

Here there is none of the ST elevation seen in the above ECG.  In fact, the T-waves are normal here, whereas they are large above.  The ones above, then, are not necessarily due to early repol.  There is a change.  The most important change, though, is the ST elevation in inferior leads and the reciprocal depression in aVL.

 Here I place them on the same page for better comparison:

This comparison makes it obvious that the new ST elevation is diffuse: inferior, anterior, lateral. aVL is NOT elevated! .  

Here I have magnified II, III, aVF, and aVL for better comparison:

Now the difference in ST segments, especially aVL, is obvious

Here I have magnified V1-V3 for better comparison: 

Now the new ST elevation in V1-V3 is obvious

The Emergency physician started therapy for NSTEMI.  The first troponin returned at 2.25 ng/mL. The cardiology fellow then opined that this was myopericardititis and instructed to stop the heparin. However, this is not myopericarditis. It cannot be because there is reciprocal ST depression in lead aVL.  Additionally, the T-wave enlargement in V2 and V3 happens only rarely in pericarditis.  Besides MI, the only explanation for that is the occasionally seen month to month variation in early repol.

Follow up:

The troponin peaked at 23.6.  The echo showed an inferior and anterior wall motion abnormality.  Thus, it was not pericarditis.  Angiogram showed a ruptured plaque in the proximal LAD, with distal embolization of thrombus to the apex.  This was a "type III," or "wraparound" LAD which supplies both anterior and inferior walls. 

Even without the angiogram, the rapid rise and fall of troponin establishes the diagnosis as MI, not myopericarditis.

The stenosis was minimal, and the ACS occurred in the setting of cocaine use, so the therapy was eptifibatide and heparin for 72 hours, with no PCI.

Lessons

1) Pericarditis should never be assumed when there is even a hint of reciprocal ST depression.  Only Localized pericarditis (most pericarditis is "diffuse" inflammation of the entire pericardium) ever has reciprocal ST depression, and localized pericarditis is very rare.  I suspect that many cases of "localized pericarditis" are really STEMI that went undiagnosed.

2) Wraparound or Type III LAD ACS mimics pericarditis because it leads to diffuse ST elevation.