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