Tuesday, October 6, 2015

Best Explanation of Terminal QRS Distortion in Diagnosis of Electrocardiographically Subtle LAD Occlusion

This piece was written by Brooks Walsh, who has some great contributions to this blog.  There are, of course, some additions and edits by Steve Smith.


Two young adult males presented to the ED with chest pain. An ECG was immediately performed in both cases. However, while one patient received emergent PCI for an acute coronary occlusion (ACO), the other only got a sandwich and ibuprofen.

Patient #1
There is ST segment elevation in multiple leads, most of which have an associated J-wave (slurring of the J-point); e.g. in V4-V6, I, II, and aVF. There is no reciprocal depression, the QTc is not significantly lengthened, and the ST segments in V2 – V4, although elevated, are concave upwards. All of these elements point to benign early repolarization.

If you used the LAD occlusion vs. Early Repol formula, using:
1) 3.0 mm for ST elevation, relative to PQ jct., at 60 ms after the J-point in lead V3
2) QTc = 405 ms
3) R-wave amplitude in V4 = 17 mm
You get: 21.9, which effectively excludes LAD occlusion
But you should not have used the formula for this case.  Why not? (the answer is below)

There is now a still more accurate 4-variable formula.
See this post:

12 Example Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

It has also been externally validated:

Patient #2
There is ST segment elevation in multiple leads, most of which have an associated J-wave (slurring of the J-point); e.g. in V4-V6, I, II, and aVF. There is no reciprocal depression, the QTc is not significantly lengthened, and the ST segments in V2 – V4, although elevated, are concave upwards. All of these elements point to benign early repolarization.
Incidentally, the formula value here, using 4.0, 360 ms, and 30 mm R-wave, also excludes LAD occlusion.  It equals 16.2

This is the same interpretation as patient #1. What is the difference? 

Take a closer look at V3 in patient #2.
There is an S-wave which descends below the isoelectric line. This is a normal and expected finding.

Even with dramatic repolarization, lead V3 should manifest an S-wave. There are cases of early repolarization where the S wave is absent in V3, but a J-wave is usually seen in those cases.

For example, patient #2 had a second ECG recorded 10 hours after the initial tracing:
Here, we don’t see an S in V3, but there is a clear “fish-hook” pattern to the J-point, consistent with BER.  Serial troponins, were negative, and echo was normal, and serial ECGs (as shown above) did not evolve significantly. The diagnosis was pericarditis versus early repolarization.

By contrast, reexamine lead V3 in patient #1:
There is no S-wave in this lead, and neither is there a J-wave. This loss of the S-wave is called terminal QRS distortion, and multiple studies suggest that, with an anterior MI, this predicts a larger infarct, with higher mortality, and even a worse response to fibrinolytics or PCI.

An old ECG was obtained for patient #1:
There is minor STE in V2-V4, and J-waves in leads II, aVF, and V4-V6. There is also an S-wave in V3!
Thus, one should suspect that there is LAD occlusion obliterating the S-wave in V3.

One hour after the first ECG was recorded in patient #1, the troponin came back significantly elevated, around 0.07 ng/ml (0.034 99th URL). A second ECG was obtained:
There is no significant evolution from the first ECG, but cardiology was emergently consulted. Following a brief evaluation, the cath lab was activated. A 100% acute occlusion of the proximal LAD was found, and stented.

Following successful PCI, a third ECG was obtained. Note the re-appearance of the S-waves in V3.
This immediate resolution of terminal QRS distortion bodes well for his clinical course, and indeed his follow-up echo was basically normal.


Dan Lee and I studied terminal QRS distortion and found that it was never present in any of 170 proven cases of normal variant ST Elevation (STE in Leads V2-V4).

Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization. 

The study from which the formula was derived only looked at ECG with "subtle" findings of LAD occlusion (as opposed to "obvious").  Of 355 LAD occlusions in both derivation and validation groups, 143 were "subtle" and were studied for the formula.  

In the derivation group, the primary reason for excluding the ECG as "obvious" was terminal QRS distortion in 12 of 121 in the derivation group, and 28 of 234 cases in the validation group.  Thus, in the first case, the formula should not be used because such cases with terminal QRS distortion were excluded.    

The iPhone app for the formula asks you for exclusions.   The sidebar LAD occlusion-BER calculator has red text above it outlining the exclusions.


  1. Superb post for illustrating subtleties in distinction between ERP (early repolarization pattern) vs Anterior STEMI. I wonder if Patient 2 had acute pericarditis (perhaps superimposed on baseline ERP) — as the amount of ST elevation in lead I looks disproportionately great, especially given the modest R wave amplitude in this lead … But the point is well made that Patient #2 is not having a STEMI, whereas Patient #1 is. THANKS for posting!

    1. Ken,
      Possible, but I would not say it looks much like pericarditis either. In any case, not MI!

    2. I think we basically agree. #1 — this isn't a STEMI. #2 — There is a lot of ST elevation in a number of leads. Would be interesting if we had more history on this patient (and especially if a baseline ECG could be found). I completely agree that this 1st tracing in Patient #2 doesn't look like typical pericarditis — but I was at a loss to explain that much ST elevation in lead I ... That said — perhaps it is all a repolarization variant ... THANKS again for this SUPERB Blog post!

  2. As an additional comment for other readers (I know Brooks and Steve know this), I would suggest that if you are reading these ECG's in an acute care setting with ready access to the patient and there is any question at all about the presence or absence of terminal QRS, it would be helpful to actually go look at where the precordial leads were placed on the chest. I've seen plenty of instances where V3 has been placed too far lateral and then risks giving a false-positive impression of S-wave obliteration in that lead.

    Great case!

  3. Steve...

    Regarding the "old ECG" for Patient 1: try as I might, I do not see any J waves in Leads II, aVF or V6 (as it states in the caption). I do see notching at the J point in V4 and V5. What am I missing?

    Jerry Jones MD FACEP FAAEM

    1. Jerry,
      It is only leads V2 and V3 that must have either a J-wave or an S-wave for it to be early repol. This is something I have found in every case of early repol.

  4. Great case and explanation! question: in patients with baseline early repol who presents with STEMI (with or without terminal qrs distorsion). Is it possible to have a preserved j-wave in affected leads? Or is the j-wave always "deleted" when there is a STEMI?

    1. In my experience, it is almost always obliterated. But in my study, there were plenty of LAD occlusions that has some J-waves. See the paper.
      Thanks and great question.

  5. hi,
    nice and difficult case.

    In patient 2, even if the precordial leads looks like BER, fragmented qrs in DI-AVL wit ST elevation and ST depression in DIII-AVF with some down-up aspect would have frighten me.

    1. Olivier,
      Yes, however a QTc of 360 ms is almost impossible in STEMI!! A little known fact.

    2. @ Olivier — Isolated ST-T inversion in lead III (and also in aVF) as was seen in the initial tracing for Patient #2 is not necessarily abnormal. Lead II doesn’t have any ST-T depression (and that’s the lead that counts most!). I agree that the ST elevation (especially in lead I) in Patient #2’s initial tracing is marked and of concern. Dr. Smith indicates that “the differential for Patient #2 was between pericarditis versus early repolarization”. My bet is on acute pericarditis (perhaps upon a baseline of early repolarization) — but I believe the key point Dr. Smith is making is that this initial ECG for Patient #2 is highly unlikely to represent anterior STEMI.

  6. Great case Dr Smith--
    I also find it interesting that the initial algorithm interpretation for patient #1 was "early repol", while the initial machine interpretation for patient #2 was "***ACUTE MI*** !


  7. Does this mean that ANY STE in V2-V3 with absence of J wave and S wave = confirmed STEMI? What if you see terminal distortion without STE? What about the 50% of the R wave STE criteria?

    1. The 50% criteria was used as a prognostic tool in patients with definite STEMI.
      In my modification of the rule, I found that it is never seen in early repol. In other words, if you think an ECG represents early repol, there MUST be either a J-wave or an S-wave in BOTH V2 and V3

  8. Very nice case and such a useful discussion. I could not understand the concept of " STE at 60 ms", how is it actually calculated? I will be grateful if somebody explains that for me please. Thanks

    1. go to minute 23:00 of this lecture. You really should watch the whole lecture:

  9. Thanks a lot Dr Smith for this great case!


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