Anterior ST elevation: Anterior STEMI? A mysterious case.

A male in his 60's was brought in for intoxication and agitation.  15 minutes after arrival he was calm but complaining of chest pain.  He was given aspirin and this ECG was recorded.  It seems that the patient had ongoing chest pain at the time of the ECG:

There is sinus rhythm.  There is a significant Q-wave in III and aVF, with T-wave inversion in lead III, suggestive of inferior MI of unknown age.  There is anterior ST elevation with a prominent T-wave.  It seems as if this was noticed after the troponin I returned at 4.1 ng/ml, at which point the "anterior STEMI/early repol rule" was applied and the result was a value of 24.5 (greater than 23.4, so there was worry for anterior STEMI)

The patient was taken emergently to the cath lab and found to have a 95% RCA in-stent thrombotic lesion that was stented, and 90% right posterolateral branch to the posterior wall, with dissection, that was angioplastied.  The pain was gone after treatment.

After PCI, this ECG was recorded (it is unclear if there was active chest pain or not):

Now it really looks like an anteroseptal MI, but is it?

He was taken back to the catheterization laboratory, and there was no change.  There was a small right ventricular marginal branch with only TIMI-I flow, however, this was unchanged compared with the previous angiogram.  So is this ST elevation with massive T-waves due to right ventricular MI?

The troponin I peaked at 8 ng/ml.  Echo showed a normal RV, no increase in right sided pressures, and no anterior wall motion abnormality, but it did show a posterior wall motion abnormality.

This may be another example of "posterior reperfusion T-waves".  Here is another example of this.  Dr. Brian Driver, Dr. Gautam Shroff, and I have studied this in patients with STEMI of the RCA or circumflex, and found that in patients who have involvement of the posterior wall, the T-wave amplitudes in V2 and V3 increase after reperfusion.

The ST elevation in this case makes it more uncertain and mysterious.

Here is the physiology: When there is reperfusion of a myocardial wall, the overlying leads record T-wave inversion (negative T-waves).  If we record the posterior wall from anterior (V1-V3), and the posterior wall T-wave is negative (posterior vector negative), then its positive vector is anterior and, if recorded from the anterior wall, it will be added to the positive vector of the positive anterior T-wave, resulting in larger T-waves than before.  Simultaneous posterior leads could document this, if recorded.

In this case, there is also anterior ST elevation, and if this truly reflects the posterior wall, then one would expect not just T-wave inversion, but also ST depression on posterior leads, if they had been applied.

The next morning, this was recorded:

There is some resolution of the anterior ST elevation and T-waves.

I do not have a confirmed explanation for this "anterior" ST elevation with large T-waves.

It is probably due to a combination of right ventricular STEMI and posterior reperfusion T-waves.