Early repolarization or LAD occlusion?

41 year old male complaining of chest discomfort.

  • Past medical history: Asthma
  • Medications: Inhaler (unknown type)

EMS finds the patient sitting in a chair.

The patient appears acutely ill. His skin is cool, pale, and diaphoretic. Breath sounds clear bilaterally.

  • Onset: At rest
  • Provoke: Nothing makes the pain better or worse
  • Quality: “Heavy” and “unrelenting”
  • Radiate: The pain does not radiate
  • Severity: 8/10
  • Time: The patient has had similar episodes that cleared up after using his inhaler

Vital signs are assessed.

  • RR: 20
  • HR: 60
  • BP: 112/84
  • SpO2: 91 on RA

The cardiac monitor is attached.


A 12 lead ECG is captured.


What’s going on here?

This following ECG was captured en route to the hospital.


Look very carefully at lead V3!

The S-wave has been lifted up above the isoelectric line!

This is sometimes referred to as “terminal QRS distortion” and it helps differentiate LAD occlusion from early repolarization when it occurs in lead V3.

(See also: Terminal QRS Distortion Due to LAD Occlusion at Dr. Smith’s ECG Blog.)

In this case it’s a change on serially performed ECGs which makes the finding even stronger.

It’s also worth noting that the initial ECG shows upwardly convex ST-segment elevation in lead aVL with terminal T-wave inversion. There is also a subtle reciprocal change in lead III.

This case was difficult because our normal “tricks” to differentiate between acute anterior STEMI and benign early repolarization lead don’t work. R-wave progression is intact and the QTc is not prolonged.

Updated 04/23/2016


  • SoCal Medic says:

    Tom,Let me first start with the axis deveiation since I am still learning that. I am thinking right, because aVL is equal and Lead II is positive. Close? ALso I see the fish-hook appearance at the J Point in V4 and V5, which would be consistant with BER. I dont think it is pericarditis because of the way the patient is presenting with a heavy and unreplenting rather than shapr and pin point. The diffuse elevation does not surprise me with the BER, however I am seeing reciprocal changes in the inferior leads, which I am not sure if it is consistant with a BER presntation and would lean towards the onset of an MI, especially since he has had this before (I would equate it to a stress test, then being scheduled for a PCI, where as this occasion was the culmination of time and mistreatment). Am I close?

  • Tom B says:

    You are close.But let’s start with the frontal plane axis.You are correct that the equiphasic lead in the frontal plane is lead aVL. So the perpendicular lead is lead II. Since lead II is upright, we can estimate the QRS axis in the frontal plane at 60 degrees.If we look at the computer measurement of the QRS axis, it is 56 degrees. So using the hexaxial reference system gets us within 4 degrees, which is very accurate.This is well within the left inferior (normal) quadrant.To use the quadrant method, leads I and aVF are positive. Hence, we know the axis is somewhere in the normal quadrant.To use the speed method using leads I, II, and III; since all three are positive, the axis is normal.Make sense?Tom

  • SoCal Medic says:

    starting too… just repetitive now to build the confidence level

  • Tom B says:

    That’s exactly right! Practice makes perfect.

  • walma says:

    Hey Tom I will take a closer look on lead I (for me there is 1 mm ST elevation), and focus on the “strange” pattern of ST segment in aVL lead, ST segment in this lead probably is going UP. Previous ecg would be helpful (if he got any). I would do serial ecg…I would treat him as AMI patient…Maciek

  • Tom B says:

    Very good observation, Maciek! The upwardly convex (non-concave) ST segment in lead aVL caught my eye, too! Also, excellent suggestion as to performing serial ECGs. I’ve got one more to share for this case.

  • SoCal Medic says:

    Let me make sure I understand this part, Lead I on the reference system is ), and the standard vector travels down to the left, which gives us the 0-90 standard axis. a 0- -30 can be considered phsiological, and anything outside of that pathological. From 90-180, it is Right Inferior saying that the vector is traveling down to the right, rather to the left. Am I close or am I way off?

  • Tom B says:

    That’s exactly right, Christopher!

  • Tom B says:

    Actually, I have 2 more ECGs for this case.

  • SoCal Medic says:

    Well then what are you waiting for? lol. I am curious as to how the rest present. Something that I have gotten into a habit of doing is repeating my 12 Leads with the vitals, regardless of what the intial looks like, just to build the motor memory so it is second nature. What I think as recriprocal changes in this ECG have me curious as to what the serial ones look like.

  • Tom B says:

    I’m glad you scrutinize the ST segments carefully enough to see reciprocal changes in the inferior leads! It’s very subtle. Just a flattening of the ST segment. Good eye!

  • SoCal Medic says:

    That clears up alot there. Thanks for the update but do you have anymore that go with it? What is the general time lapse between ECG’s?

  • Tom B says:

    Rhythm strip at 0955.12 Lead 1 at 1006.12 Lead 3 at 1013.The times are still on the ECGs.

  • ecgblog says:

    Am I wrong, or could also the anterior high, pointed T waves be hyperacute signs?But about the reciprocal changes you mention, I must admit that I can’t see them. There is maybe a slight 1/2-1 mm ST depression in III. The other reciprocal leads here, II and aVF have elevated ST segments. aVL is also slightly elevated.When I look at this ECG, my first thought is that the ST elevation is global and makes me think of pericarditis.But considering the clinical data here, I’d go for an anterolateral MI here, even with the unsure reciprocal changes.Great strip!PQRST/the ecg blog

  • Tom B says:

    Yes, they are hyperacute looking T waves (and need to be differentiated from the peaked T waves of hyperkalemia).Usually the hyperacute T waves from AMI are broad-based, where the peaked T waves from hyperkalemia are “tighter” with a late take-off, but there’s always that middle-ground where it’s impossible to tell.The “reciprocal” changes I mentioned are very subtle, and present and nothing more than a flattening of the ST segment. In other words, I’m talking more about the contour of the ST segment than ST segment depression, but you’re right, there is about 1 mm of ST segment depression in lead III in the first ECG.Remember that leads III and aVL are the two most “reciprocal” leads in the frontal plane (excluding lead aVR). So look back and forth between leads aVL and lead III when you consider whether or not there are VERY subtle reciprocal changes in the first ECG.You’re also correct that at first glance, this looks like pericarditis or benign early repolarization. You even have “notched” J points in leads V5 and V6. However, the dead giveaway is the difference between the first and second 12 lead ECG.If you compare the two, you have a disappearance of the S wave in leads V3 and V4 with a climbing ST segment and sublte changes in T wave morphology. This suggests dynamic changes in supply v. demand characteristics.Great comments! Tom

  • Hillis says:

    Ok i will start from Z !! activate the cath lab. becouse of the obvious 1mm STE in aVL which is very specific for high lateral MI, interesting here i can see subtle STD in the III only !! not in all the inferior leads .
    The STE in the anterior leads looks like to be more due to BER the R wave in V2-4 is more than 5mm and QTc is more than 0,392s , am i right ?
    I nteresting case , i enjoyed reading the above discussion and curiously waiting the update in this case

  • Jeff B. says:

    At first glance, I say antero-lateral AMI. Cardiac alert and all that good stuff. Unfortunately, my education did not spend a ton of time on the axis deviation curriculum. I know it’s great to know, but, with my short transport times, I have a lot to do in a short amount of time.

    I digress… Was this Pt. beta-blocked? Unless he’s beginning to develop an inferior infarct as well, I’m not used to seeing such a low heart rate with antero-lateral infarct patterns. Then again, I have recently activated a cardiac alert for a gentleman with 7mm elevation in II, III and aVF with a HR of 100 and hypertensive…

    Also, except for in lead III, I am picking up on ST elevation in all leads which might, in the back of my mind, peak my interest as to whether or not he may have pericarditis? That being said, it would not sway my treatment course.

    Great case. Thanks!

  • DR SOHAIL says:

    this is seems to be normal variant ECG

  • Johnny G says:

    Please treat the patient and not the 12 lead.  Remember that a significant portion of acute MIs do not present with any EKG changes at all.  Prime age male with significant chest pain.  If you have a "smoking gun" STEMI thats one thing.  But to not treat a "cardiac event" without an impressive EKG would leave a portion of our patients without proper care.  Just my thoughts, listening for others.

  • Marton Varhegyi says:

    Hi, everybody!

    As far as I can judge this case:

    1. The symptoms and physical signs are consistent with ischaemic origin.

    2. On the (first) ECG there is significant STE in lead I (I would say it concave, but that does not rule out ischaemic origin) and aVL, which we really don't expect for BER (BER affects anterior and/or inferior leads, but not high lateral leads – or it is very unusual). There is also reciprocal STD in III (which is not a miracle…).
    However, I think this patient has BER (look for the J waves in V4-6), but he can also have AMI, as the evolution of the STs shows it.

    3. Many of the males have high take-off in the right praecordial leads. I think this is what some people call BER, but these two things (high-take off and BER) – as far as I know – are different.
    Hight take-off is a normal finding in males, not a variant, and affects usually V1-4, and the height of the take-off [somebody calls it "J point elevation"] is proportional to the depth of the S wave). BER usually affects mid- and/or lateral praecordial and/or inferior leads, with – usually – a J wave.
    So I think this ECG shows high take-off (V2-3 and maybe V4) AND BER (V4-6).
    (Also it's so interesting that in lead II and aVF and maybe III there are no STE, but we might have a feeling that there is a J wave. Maybe there would be the STE of BER, if there were no reciprocal ST deviation which compensates the STE in II and aVF, and overcompensates ST in III – in high lateral AMI the biggest reciprocal STD is expected to be in III.)
    As I wrote in high-take off the STE (or J point elevation) is proportional to the depth of the S wave. If we take this into account we can see there is something not very OK. Look at V2 and V3! The STE is almost the same in these two leads, but the depth of the S save is bigger in V2.

    Nevertheless, it was az interesting case, and the blog is also fantastic! Thanks for it!!!

    Best regards,

    Várhegyi Márton
    medical student, Semmelweis University, Hungary

  • Marton Varhegyi says:

    Hm, as I enlarged the first 12 lead ECG I saw in lead II there is also some (nonsignificant) STE.

    Also interesting that the second 12 lead ECG does not show the reciprocal STD in III, but the STE in lead II is now bigger than in the previous strip, and there is also STE in lead aVF.
    I think this case might not be typical for high lateral injury as we can see STE evolving in lead II and aVF too.

    However, if I had seen the first 12 lead strip (with the symptoms, of course), I would have taken the patient into the catheter lab. (Maybe I would have been wrong.)

  • Chau Son says:


    I think with the first 12 lead EKG I can bring the patient to the cathlab with a lateral STEMI diagnosis, do not need to wait for the next EKG.

  • Tyler says:

    Excellent case, was this confirmed with PCI?

3 Trackbacks

Leave a Reply

Your email address will not be published. Required fields are marked *