Monday, December 5, 2016

Right Precordial T-wave Inversion

This was posted on Facebook EKG club by Massimo Bolognesi, from Italy.  He is a highly respected Sports Medicine Cardiologist.

He graciously allowed me to re-post it here.

"This ECG was recorded on an asymptomatic 50 year old marathon runner who presented for pre-participation screening."

(This ECG could easily be seen in an ED chest pain patient, and I have seen many)

What do you think?

Sinus bradycardia.
There is high voltage.
There is ST elevation in V2 and V3
There are inverted T-waves in V2 and V3
There are prominent U-waves in V2 and V3

Many responders were worried about ischemia or hypertrophic cardiomyopathy.

Here was Massimo's response:

"I'm very sure of Early Repolarization (ERP) diagnosis in this case. 
First because I have a good eye on ECGs of endurance athletes
Second because I see a lot of these tracings
Third because the stress test determines the disappearance of ECG abnormalities found at rest
Fourth because the echocardiogram is normal
Fifth and last, the clinical presentation speaks clearly."  


I (Smith) have seen many similar ECGs in ED chest pain patients.  I have always believed them to be benign for the reasons described below.  But I have never had any data to support my beliefs, so I've never posted them.

Notice also that the QTc is very short. First, one must realize that the last wave is a U-wave, which is common in ERP.  So the QT must not be measured in V2 or V3.  The QT as measured in other leads is about 420 ms, with a preceding RR of 1500ms, resulting in a Bazett corrected QT interval of 345 ms. This short QT at least makes ischemia all but impossible.  ERP is, of course, associated with an increased long term risk of sudden death, but only marginally and only if in inferior or lateral locations

In addition, many readers of this Facebook post were worried about ischemia, including Wellen's syndrome ("What if this patient had presented with chest pain?"): 

Even in the setting of ischemia, the ischemia would not be represented by this ECG. This is a classic pattern and the QT is so short as to make ischemia very unlikely.  This is a normal variant.  I have seen this innumerable times in chest pain patients in the Emergency Department. At first glance, it may appear to be similar to ischemic T-waves, but it is not. The large upright U-wave, this high voltage, and the short QT interval differentiate it from ischemia.  

It is important to remember that even a patient with a normal variant could have a myocardial infarction, just as patients with completely normal ECGs may have MI.  

It is only to say that the ischemia is not represented on this ECG.

See this post on Benign T-wave Inversion.

Here is a relevant post on the inverted T-waves of Persistent Juvenile T-wave Pattern with many other the normal variants of T-wave inversion.


  1. Hi, first thank you for your blog, i followed it for many years with great interest.

    I would like to discuss the ERP with the light of this 2015 consensus paper

    For the ERP diagnosis you now need
    1-a end QRS slur/notch

    It didn't appear clear to me that this patient present QRS notch/slur.



    1. Sam, for the purposes of differentiating MI from non-MI, I use the term "early repol" interchangably with "normal variant ST elevation." These definitions are for research purposes to classify and risk stratify patients' risk of long term sudden death (v fib). By the strict definition, they have a higher risk.

    2. Thank you for your response !

  2. Steve:

    I recently saw a similar patient who was an ultramarathoner with a similar EKG pattern.

    T wave inversion in leads V2-V3 has been reported to be 3x more likely in endurance athletes; see

    And this paper describes a displacement of the RV toward the left axilla measured by cardiac MRI as likely explanation:

    Brosnan MJ, Claessen G, Heidbuchel H, Prior DL, La Gerche A. Right Precordial T-Wave Inversion in Healthy Endurance Athletes Can Be Explained by Lateral Displacement of the Cardiac Apex. JACCCEP. 2015;1(1):84-91. doi:10.1016/j.jacep.2015.03.007.

  3. (trying to repost my comment, I think I lost connection before posting last time)

    Great post! I agree fully with your interpretation that it is not ischemia and perhaps some useful notes can be added. The T-wave inversions are asymmetric here (in ischemia, they are typically symmetric) and the T-wave inversions are actually concordant with the QRS direction. Taken together, ischemia becomes even less likely (on top of your comments).

    The notion that this ECG shows early repolarization, however, does not fit with recent guidelines (MacFarlane et al, JACC 2016), nor does it fit with the decade old description by Haissaguerre et al (NEJM, 2008). The end-QRS J-peak is 1 mm only in lead V5, which excludes early repolarization. I agree completely that this is just normal variant ST elevation, augmented by the athlete's heart. I would like to stress the issues with the widespread misunderstanding regarding early repolarization; even recent guidelines got it all wrong (we wrote about this on our blog: It's like early repolarization became a household name for every elevated J point?

    I would also like to add that the corrected QT interval may be somewhat misleading in this scenario, beacuse there is bradycardia, which makes Bazettes formula very shaky (which is why most companies producing ECG machines threw out Bazette's formula).

    It is my personal opinion that QT intervals should not be assessed to judge ischemia (MacFarlane et al, Comperhensive Electrocardiology, Springer 2010, and Y Birnbaum et al 1996, Cor Art Dis).


    1. Dr. Rawshani,
      Thanks for the comments.
      "Early Repolarization" is a term that has been used interchangably with "normal variant ST elevation" in the literature for decades.
      It is only recently that some have tried to restrict its use to the syndrome of J-waves and QRS slurring/notching which predicts a higher long term risk of sudden death.
      For the purposes of STEMI mimics, which is an entirly different context "early repolarization" remains in widespread usage. And indeed, patients with normal variant ST elevation in leads V2-V4 do have short QT intervals due to rapid repolarization!
      As for the QT interval, there are many correction formulas, none work very good, and the only way to actually correct accurately for any patient is to measure the QT interval at a heart rate of around 60 and then measure it for that same person at many other heart rates. There is substantial literature on this and I will have an article (or post) on this soon which I am working on.
      But this technique is of course no use when trying to decide the diagnosis of a patient in front of you: acute ischemia or not?

      As for its presence in ischemia, there is literature showing the the very first ECG change during angioplasty balloon occusion is a lengthening QT interval. My study on early repol (normal variant STE) showed that QT interval was very important in differentiating it from subtle LAD occlusion: The reference are inadequate. Please give title and volume/issue/page number.
      Steve Smith

    2. J point at V3 seems equal to 1mm?
      A nice study on T wave inversion in the athlete:

  4. Nice clinical example of a repolarization variant as discussed by Drs. Bolognesi and Smith. The clinical setting is key. As emphasized in the discussion — the ST-T wave appearance in all 12 leads “looks like” a repolarization variant given: i) the clinical setting; ii) the relatively short QT; and iii) excellent R wave progression. Lead V1 looks peculiar in that T wave inversion is uncharacteristically deep in this lead (especially in view of much less T inversion in subsequent leads). Given this, the prominent negative component to the P wave in V1 makes one wonder if lead placement might be a bit too high. That said, none of this changes the overall impression that this ECG shows a repolarization variant.

    Of interest, Dr. Bolognesi indicates that the Echo was normal, and that ST-T wave findings normalized on performance of an exercise test. Typically, benign repolarization abnormalities normalize on ETT within no more than a few minutes of exercise.

    As a P.S. — even though clinical setting + the overall ECG pattern seen here suggest this is a benign repolarization variant — when doubt exists, prudence sometimes dictates additional testing. In the setting of an asymptomatic athletic individual — a negative family history, no personal history of syncope/presyncope during exercise + normalization of repolarization changes early during ETT + a normal Echo — combine to confirm beyond doubt the benign nature of these ECG findings. In the setting of an ED — serial tracings and obtaining an Echo at the time of chest discomfort symptoms that shows no wall motion abnormality substantially increase clinical suspicion that this ECG is benign.

    GREAT case! Thanks to Drs. Bolognesi and Smith for their discussion!


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