Friday, December 2, 2016

ST Elevation in aVL. Reciprocal ST depression in III. Is it MI?

I was reading this ECG in the queue, with no clinical info.

What do you think?

My interpretation was LVH, no evidence of MI.   There was no previous ECG or echo for comparison.

My ECG diagnosis may surprise you, as I have long discussed "ST elevation in aVL with reciprocal ST depression in lead III" as due to high lateral MI.

This is different because:
1) There is saddleback morphology in aVL, and
2) There is also high voltage.

I have previously talked about ST elevation with saddleback morphology in lead V2 as rarely being due to anterior STEMI.  See this post (the only case I've seen in which it was STEMI): 

Anatomy of a Missed LAD Occlusion (classified as a NonSTEMI)

Voltage on this ECG does meet Estes criteria for LVH: 
1) At least one R- or S-wave greater than 20 mm (lead II) = 3 points.
2) ST-T abnormalities in the absence of digoxin = 3 points
Total = 6 points
5 points is definite
4 points is probable
This scoring system comes from this original article.

However, meeting LVH criteria is not critical, as they are not sensitive.  Many cases of LVH show themselves only by the typical repolarization abnormalities.  In this case, we see somewhat typical repolarization abnormalities in leads III and aVF.

Estes criteria are only 34% sensitive for LVH as diagnosed by echo.   

In this paper that used other criteria, the sensitivity for LVH by echo was less than 10%!
At least one of, with or without ST-T abnormalities:
1) R-wave 11 mm in aVL
2) R-wave at least 25 mm in left precordial leads
3) S-wave at least 25 mm in right precordial leads
4) Sum of precordial SV1 or SV2 plus RV5 or RV6 at least 35 mm
5) Sum of lead I plus lead II at least 25 mm.

In both studies, specificity of the criteria was nearly perfect.

Case Continued

This 30-something presented with headache and chest pain.  He had a history of hypertension, apparently completely untreated.  His chest pain had lasted 40 minutes and was now gone.

Blood pressure was 170/105.

Another ECG was recorded several hours later:
No significant change

The history of HTN, the elevated BP, the high voltage, and the saddelback make it very unlikely that this ST elevation is due to STEMI.

The patient ruled out for MI by negative delta troponins.

Here is a post on True Positive ST elevation in aVL vs. False Positive ST elevation in aVL
However, I do not discuss saddleback in aVL in this post.


  1. If I were to see this in the prehospital environmnet, I am still transporting this patient to the hospital, so that the blood tests can be done. I am hoping that the purpose of this was to suggest that a STEMI Alert might not be necessary, but that transport is.

    1. Joe,
      Of course!! One many have a Non ST Elevation MI with a completely normal ECG! In fact, one may have a completely normal ECG when there is 100% acute coronary occlusion. So this is only to say that it is unlikely to be a coronary occlusion. The patient certainly needs further evaluation.
      Steve Smith


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