Wednesday, October 5, 2011

Inferior ST Elevation: what is the Diagnosis?

You can read this post here, or watch a video presentation of it:

I was handed this ECG, without any clinical information, while on my way to see another patient:
There is sinus rhythm.  There is ST elevation diffusely: 2 mm in V2, 3.5 mm in V3, 2.5 mm in V4, 1.5 mm in V5, and 1 mm in V6, 1.5 mm in lead II, 1 mm in leads III and aVF.  R-waves are well formed, and in fact there is high voltage.  T-wave to ST ratio is greater than 4 in lead V6, making pericarditis unlikely (also there were no symptoms of pericarditis).  The computerized QTc is 386 ms.   There are marked J-waves in II and V4-V6, with slurring of the R downstroke in III and aVF.  There is no reciprocal ST depression anywhere except aVR; in particular, there is none in aVL.  Not only is there no ST depression in aVL, there is actually a bit of STE in lead I.   These are all classic signs of early repolarization.
I immediately recognized this as early repolarization of inferior, lateral, and anterior leads, and went on my way. Some time later, I found out that the residents had initiated an aggressive workup because they were worried about the ECG.

It turns out that this was a 27 yo African American male who presented with pressure-like (non-pleuritic) chest pain and dyspnea.  He appeared very anxious and was hyperventilating and he had just had an episode of what sounds like carpal spasm.  Clinically, he was having a panic attack.  His ECG did not worry me.

Is there LVH on the ECG?  By voltage there does seem to be, but this was a young thin male and high voltage without LVH is common in this situation.

Most early repolarization is in precordial leads, where it is so common that it is considered normal to have baseline ST elevation on the ECG.  I have put up many posts on this topic, and on differentiating ER from LAD occlusion. But there is also early repolarization in inferior or lateral leads, and when present, it is virtually always present in anterior leads as well.

Here is a case of a 45 year old with chest pain:
There is ST elevation in inferior leads only, with no reciprocal ST depression in aVL.  There is a slight T-wave inversion in aVL.
Inferior MI was diagnosed by the emergency physician and the patient needed to be flown by helicopter to the cath lab.  The arteries were clean.  There was no MI.  This was the patient's baseline ECG.   It was a false positive.

How would you be able to know this from the ECG alone?  If there are no changes in aVL, it is highly unlikely to be inferior STEMI.  If there is simultaneous lateral MI, it is possible that aVL may be silent, but in this case V5 and V6 have very minimal ST elevation.  Would you be certain that it is not STEMI?  No, but you should suspect that it is a false positive.  If you have immediate echocardiography available, you could prove that it is early repolarization by showing good contraction of the inferior wall.  Serial ECGs may be useful.  Or perhaps you need to just activate the cath lab and risk a false positive.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.

Is there danger to early repolarization itself?

Ha├»ssaguerre et al. performed a case control study of patients with idiopathic ventricular fibrillation, and found that many more of these patients than of controls had baseline inferior or lateral early repolarization.  Tikkanen et al. performed a longitudinal community study, following people for a mean of 30 years.  They found early repol pattern in inferior and/or lateral leads in 3.5% and 2.5% a , respectively, and in both locations in only 0.1%.  These patients had a small but significant increased long-term risk of death from cardiac causes (Relative Risk = 1.28 for 1mm, 2.98 for 2 mm of inferior STE). 

No one is certain what to do with this information, and it certainly does not impact emergency medicine, in which the problem remains: is it STEMI or not? 

1.  Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med 2008;358(19):2016-23.
2.  Tikkanen JT, Anttonen O, Junttila MJ, et al. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med 2009;361(26):2529-37.
3.  Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61.


  1. I like the video format. Thanks :-)

  2. Thanks. I'm trying to survey the audience about it, but I'm apparently not techno-savvy enough to get the survey monkey to pop up.

  3. How about the T waves in V3-v6 in the above EKG? They are really sharp, either as in the hyperkalemia or as in the De-winter T. Thanks:)

    1. It is appropriate to check the K, but T-waves like this can be normal.

  4. How about the T waves in V3-v6 in the above EKG? They are really sharp, either as in the hyperkalemia or as in the De-winter T. Thanks:)


Recommended Resources