We just published this online in the American Journal of Emergency Medicine:

ST depression in lead aVL differentiates inferior ST-elevation myocardial infarction from pericarditis

I've written about this topic many times, but this is the first formal study we have done on the topic.

A few highlights:

1. Any ST depression (it might be as little as 0.25 mm, so be careful!) in aVL was extremely sensitive for any coronary occlusion that resulted in inferior infarction. Of 426 inferior MI due to complete coronary occlusion, 418 (98%) had an obvious inferior MI and/or had some ST depression in lead aVL.

2. Even when there was ST elevation in V5 and V6 (35 cases), there was some ST depression in lead aVL in all 35 cases!

3. No pericarditis case had any ST depression in lead aVL (100% specificity, CI 91-100%) .

4. We did not compare inferior early repolarization (as defined as benign inferior ST elevation). Some inferior early repol may have some ST depression in lead aVL, but I believe that this is very uncommon. I have been unable to find a consecutive cohort of proven benign inferior ST elevation to formally study.

5. ST depression in aVL was more accurate than STE in lead III greater than STE in lead II. 88% of inferior STEMI had STE in III greater than II, but 12% did not.

A couple ECGs: These do not come from the study:

This was a middle-aged man with chest pain (Figure A):

There is diffuse ST elevation, but there is no ST depression in lead aVL
Diagnosis?

The above is a case of a patient with chest pain who did not have MI. This was early repolarization.

Figure B. Here is a 40-something with chest pain

What is it?

The above (figure B) was a proven occlusion of an artery supplying the inferior wall (in this case, it was a distal occlusion of an LAD that wrapped around the apex and supplied the inferior wall.
Notice the minimal (less than 1 mm) ST elevation in III. But there is clearly some ST depression in aVL. This makes it all but diagnostic of inferior MI.

Figure C: