Inferior MI with positive troponin: Acute STEMI or Old MI with new NonSTEMI?

A 40 year old male without cardiac risk factors and with no h/o CAD presented with a few days of intermittent typical chest pain.  He has a history of "reflux" and asthma.  He seemed to be pain free during this first ED ECG, but he was unclear about it:

Sinus rhythm with a nonspecific intraventricular conduction delay of 138 ms.  There are significant Q-waves in inferior and lateral leads diagnostic of MI, and there is ST elevation in leads III and aVF (less than 1 mm), with T-wave inversion (suggestive of old MI or reperfused MI) with a bit of reciprocal ST depression in aVL.  Prominent R-waves in V1-V3 also suggest posterior extension.

This ECG is typical not of acute inferior STEMI, but of old, or at least subacute STEMI: the T-waves are inverted and there are well-formed Q-waves.  What about reciprocal ST depression in aVL?  This is seen both in acute inferior STEMI and in "old inferior MI with persistent ST elevation," also known as "LV aneurysm morphology."    For this reason, these two entities can be very difficult to differentiate.  We have discussed anterior LV aneurysm frequently in the past.  Though both have ST elevation, Anterior STEMI and anterior aneurysm are much easier to differentiate.

The initial troponin I returned at 0.075 (+), complicating the issue.  Is it a NonSTEMI superimposed on old MI?  If it were subacute STEMI, there would be a much higher troponin.  So a bedside echo was done by the emergency physician.  Here we see the parasternal short axis view, which gives a cross section of the LV, with the anterior wall closest to the transducer and the inferior/posterior wall farthest:

Still picture at end systole: Narrow arrows show thin and akinetic inferior wall, compared to thick arrows which show a normal wall thickness in an area with good myocardial shortening (normal anterior wall motion).

Wall motion abnormalities are seen in both acute and old MI.  However, only old MI has a thin wall (scarred myocardium).  This echo shows a thin and akinetic inferior wall, confirming old inferior MI.  There is very poor LV function.

The patient was treated medically and admitted.   The troponins peaked at a level consistent with NonSTEMI.  Angiogram revealed severe 3 vessel disease with a chronically occluded right coronary artery.  The patient went for bypass surgery.  There was no evolution of ECG changes, nor resolution of ST elevation, confirming these were old findings.