Monday, March 3, 2014

Pseudo High Lateral STEMI -- How not to be deceived by ST elevation in aVL

This ECG was shown to me with no other information:

My response was: this is normal variant ST elevation in I and aVL. 

"Why?" I was asked.  First, I will say that many of my interpretations are subjective, based on pattern recognition that is not always translatable into a rule.

But I believe I can at least partly transform my interpretation into a rule here:   Even though there is some minimal reciprocal ST depression in lead III, the ST elevation is in the setting of a well-formed R-wave in aVL.  Moreover, there is a proportionally (proportional to the R-wave) small T-wave.  T-wave size and morphology is at least as important as ST elevation in diagnosing MI.  Also, there are well-formed J-waves in I and aVL.

High lateral MI is the MI location that is most difficult to diagnose largely because the R-wave voltage in Lead aVL is often very small, and thus any ST elevation or T-wave amplitude may also be small, though when scrutinized it is often proportionally excessive.  This does not apply here.  There is plenty of R-wave amplitude with which to judge the ST segment and T-wave.

There are no other findings on the ECG to support MI:

1. Lateral MI is frequently associated with posterior MI, but here there is no precordial ST depression

2. High lateral MI from first diagonal occlusion (D1) is frequently associated with ST elevation in V2.  Well there is indeed ST elevation in V2, but this is normal variant ST elevation:  if you use the Smith formula, STE60 V3 = 1.5, computerized QTc = 392, and R-wave amplitude is 10.5 mm; formula = 21.50 (significantly less than 23.4, so very unlikely to be MI).

3.  There is no ST elevation in V5 and V6.

Pretest Probability

If this were a person at risk for STEMI: risk factors, older age, crushing chest pain, I would highly recommend serial ECGs, immediate formal echo, etc.  But not cath lab activation.

In this case, as it turned out, the patient was less than 40, had no risk factors, and had primarily abdominal pain and vomiting. 

Certainly I would not obect to serial ECGs, but no more aggressive investigation is warranted.

Also, do not hesitate to consult someone with more expertise.  This is usually, but not always, a cardiologist


It turns out that the cath lab was activated, coronaries were normal, and the patient ruled out.

Unfortunately, this happened on a late in the evening, so that the cath team had to be called into the hospital and it was an unfortunate use of resources.

All serial ECGs were identical.  The patient ruled out by serial troponins.


1. Use cath lab resources wisely, especially depending on your institution's own resources
2. Remember the importance of proportionality
3. Remember the importance of the T-wave in STEMI
4. Soft ECG findings should be more deeply scrutinized when the pretest probability is low
5. f you are worried, use other resources, especially immediate high quality echo, to look for wall motion abnormality.


  1. Is there a left lateral accessory pathway ?

    1. I see why you ask that, but no: the PR interval is normal and the QRS duration is normal. Of course, anyone can have a concealed path.

  2. Would you approach the patterns in leads I and aVL as a variant of early repolarization? (E.g. well-developed R and T waves, J-point with a hook, convex-upward ST segment)

    I've seen quite a few ECGs in young African-American males that had this sort of STE, and I've chalked it up to ER. However, the usual definitions I've seen don't describe a high-lateral pattern, just inferior and left-anterior leads.

    Your reasoning here is reassuring to me, but I'm wondering why I haven't seen any explanations in textbooks or the literature prior to your post.

    1. Not everything has a paper written on it. I have seen so many of these I should write one.

  3. Thanks for this Dr Smith. I have seen several ECGs like this recently and I have struggled to explain to others why it is not a STEMI, fortunately they have mostly not had cardiac sounding chest pain and medics have been happy for serial ECGs and TNIs. If the history sounded like MI I would probably go down the echo route. Is this a common normal variant? I find this kind of STE much easier to explain as early repol/high take off if in all/most leads or precordial leads. It's that psuedo reciprocal change pattern in III that is hard to explain.

    However I have had one young patient who presented with cough, SOB and some substernal discomfort in whom this ECG pattern was new (had a normal ECG earlier that week). I new it wasn't an MI but I couldn't explain the changes. I discussed it with the cardiologist who said to rule out conditions that could cause a structural shift in coronary anatomy such as pneumothorax or mediastinitis. the CXR showed a widened mediastinum and subsequent echo and CT showed a severely dilated but non-dissecting aortic root (7cm)! I still can't get my head round how this caused these changes.

    1. Charles, do you know that this caused the ECG changes? Or are they a coincidence?
      Thanks for the great comments!

    2. Don't know for sure and would go for coincidence if I hadn't seen a completely normal ECG from earlier that week. Will try and send you the traces when I can.

  4. Just saw an identical case a few weeks ago. Exact same ST elevation in I, AVL upsloping, with similar morphology in III. Again it was a young man with no risk factors and predominantly GI symptoms of burping, vomiting. Serial troponins and ECG were negative. Thanks for writing this up!

  5. What if the ecg realy flatten st elevation 1 avL& the patien in ventolin spray and terbutalin for chronic Asthma..should isdn 5 mg sl be given?

    1. I'm sorry I don't understand the question


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