Friday, November 6, 2015

New Paper published on Significance of Reciprocal ST depression in lead aVL

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

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:
What is this?

Figure C above is proven pericarditis.

Here is the ECG 2 days later (Figure D):

Pericarditis later still


  1. CONGRATS on publication of your article Steve! NICE to get a “formal study” out there on this important subject! I’d just add 2 points: i) In the ECG shown in Figure A — there IS T wave inversion, but NO ST depression (as you emphasize). It is key to be aware of the difference. Isolated T wave inversion may be normally seen in lead aVL, especially when the QRS is predominantly negative (as it is in Fig. A). So Figure A truly supports your emphasis that this is not a stemi tracing.

    Point ii) — The easiest way I’ve found to explain the concept of reciprocal ST-T depression is to think of a “mirror-image”. Leads III and aVL are almost “magic” in how with acute occlusion, the two leads so often manifest a mirror-image of the other. We see this in Figure B — for which the tiny amplitude complex in aVL manifests an ST-T wave that truly looks (shape-wise) like the mirror-image of the ST-T wave that we see in lead III.

    THANKS again for your work on this subject Steve!

  2. Dear Smith
    dose the V4 in figure C show terminal QRS distortion? Thanks

    1. Terminal QRS distortion is normal in V4. It is only if it is in either V2 or V3 that I get worried

  3. Dear Smith
    Do you mean that there is indeed QRS distortion in V4 in figure C? and If I see V4 QRS distortion in other ECG, it is normal?

    1. Well, it is not really QRS distortion because it is normal to have neither a J-wave nor an S-wave in lead V4. However, even if that were abnormal for V4, this one has a J-wave in V4! So even if V3 looked like V4, it would not be QRS distortion because there is "either a J-wave or an S-wave." in this case there is a J-wave, but no S-wave. So V3 can look like that. Again, V4 can have NEITHER and be normal


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