Tuesday, February 18, 2020

32 yo with right sided chest pain. Zero ST Elevation, but that does not matter.

This was sent by a reader.  He does a nice job of examining the whole case, so I leave it (mostly) in his words.

32 yo M Sudden onset localized, ‘sharp’ right sided chest pain for 1 hr. 7/10 at worst, now 4/10 with some radiation to both arms. no associated symptoms.
PMH - MS, Cholesterol, Smoker.
FH - Father MI 45
Obs - BP 133/83, RR 20, Sats 95%, examination unremarkable. Bloods pending.

Reader's interpretation:
Sinus rhythm approx 65bpm
normal axis
non-specific inter-ventricular conduction delay (IVCD) versus incomplete RBBB. QRS 100ms
Subtle 'sagging' ST depression I, aVL, V6. no ST elevation
Very tall anterior T waves V1-5 that are symmetrical and disproportionately large (particularly in V4) but neither very peaked or blunted.
The QTc is normal to short, around 400ms
The R wave progression is slow with potential pathological Q waves V3, I, aVL

Reader's comment:
Although I felt the anterior T waves may be hyperacute suggesting a STEMI equivalent (OMI) I did not feel this was diagnostic at the time. Given the atypical pain and well looking patient the initial plan was serial ECGs, CXR, morphine and review with initial bloods in an hour. Not for lab unless evolving ST elevation. This plan was agreed with the on call cardiology registrar.

This was recorded shortly later, (The reader does not give the exact timing):

Reader's interpretation
Overall very similar to the first trace.
There is a reduction in the T wave amplitude and T wave in version in aVL.
There is reduced R wave amplitude in V3 and a new narrow Q wave in V4.
There is perhaps 0.5-1mm ST elevation in V1 only.
I felt these changes were due to chest lead positioning, V1-2 were placed too high for the initial ECG.

Clinical course
Subsequent ECGs over the next 2 hours were similar. The patient looked well and the pain was now a mild ache 1/10 (Smith comment: because of the morphine?).  The CXR was unremarkable as were bloods except high sensitivity Troponin I at 110 ng/L (99th percentile 34 ng/L).  (Smith comment: this is diagnostic of acute MI, and even with a negative ECG, is reason to activate the cath lab if there is ongoing pain, which of course morphine might eliminate)

I treated him as an NSTEMI with Clopidogrel (already loaded with aspirin), Fondaparinux and commenced atorvastatin and bisoprolol. He was admitted directly to the cardiac ward and placed on telemetry. 

When I returned to check on him later in the night shift the patient was sleeping and there were no further ECGs to review.

The following morning the ECG below was recorded. This shows QS complexes throughout the anterolateral leads that suggests a completed extensive anterior STEMI. Repeat Troponin was greater than 10,000 ng/L (large MI, we do not have the peak)


The patient was taken to the lab and a total occlusion of the mid LAD (after a large diagonal) was treated successfully with PCI and stenting. There was also bystander disease and a staged PCI to the proximal RCA was planned. The patient did well and was discharged without significant LV dysfunction or other complications.


In hindsight I feel there are very few alternative causes for an ECG like this other than an acute LAD occlusion. I believe this is one of those 'subtle STEMI' cases where neither the ECG nor the symptoms are very obvious or severe and the usual evolution is not seen.

I think of these cases as 'insidious infarcts' and I have seen this in all infarct territories and I do not think they are particularly rare. Essentially the patient is fairly comfortable and the ECG is not obvious but the patient ended up with Q waves, huge troponins and we missed the opportunity to reperfuse the artery when it counts. These patients tend to be younger and do well but I have no doubt that their future risk of heart failure, arrhythmias and premature death is greatly increased compared to if they had PPCI and standard STEMI treatment. Needless to say cases like this have had a significant impact on me and make me strive to be better at spotting subtle ECG patterns and advocating for patients like this having emergent angios.

What could have been done differently.
Applying Smith's subtle anterior STEMI v early repolarisation (4 variable) equation to the first ECG gives a score of 20.6 suggesting STEMI (> 18.2). Although this is arguably outside it's indications as there is a fairly clear Q wave in V3 (note there are lots of exclusions for using this equation). (Smith comment: if exclusions are there because they are indicative of acute LAD occlusion.  If any one of the 8 are present, it is LAD occlusion until proven otherwise.  Here is a link to use of the formula).

A bedside echo (especially with speckle tracking if available) may have helped if there were regional wall motion abnormalities. 

FOAM resources that promote recognition and early treatment of 'STEMI equivalent' patterns are promoted by Stephen Smith and Pendell Meyers. This is summed up in their proposed OMI/NOMI terminology to replace STEMI/NSTEMI.

Links for the anterior STEMI v early repolarisation equation below.

Smith comment:

1. Morphine should never be given until you are committed to the cath lab.  Pain was 1/10 probably due to morphine.
2. One must learn how to recognize hyperacute T-waves.  These ones are the real thing and cannot be anything else.  The first ECG is absolutely diagnostic of acute LAD occlusion and the cath lab should be activated immediately.
3. Young people do have MI!!

Here are 2 recent cases that are similar:

Case 2. This patient was brought by EMS.  The hyperacute T-waves were immediately recognized by the medics and the patient went expeditiously to the cath lab.   1972765.
Diagnostic hyperacute T-waves in V2-V5Even the small ones are hyperacute, as they are huge in proportion to the QRS and they are "Fat" and symmetric.

This was the patients ED ECG:
Again, diagnostic hyperacute T-waves in V1-V5.

Case 3. Here is a case that was diagnosed and treated immediately, but the myocardium was completely infarcted anyway, without ever developing any ST elevation.

Prehospital ECG:
de Winter's T-waves in V2
Hyperacute in V1-V6, II and aVF
They are symmetric and fat, and also tall.  They tower over the QRS.  The T-wave in V6 is not at all large in any absolute sense, but it is huge in proportion to the QRS.

Here is the ED EDG:
de Winter's T-waves in V3, hyperacute from V1-V6.

And the post-reperfusion ECG:

Even though there was never ST Elevation, and the patient underwent rapid reperfusion, there are fully developed QS-waves, indicative of profound anterior wall infarction.

Furthermore, a hyperacute T-wave need not be large, or even proportionally large:  Sometimes a hyperacute T-wave is only symmetric, but not large, as Case 3 below:

Case 3.

Small T-waves that are hyperacute just because they are symmetric.  
The T-waves in II, III, and aVF are hyperacute only because of their symmetry.
I recognized these hyperacute T-waves immediately as part of a study we are doing.  No one else saw them at all.  Another clue is of course the slight STD with T-wave inversion in aVL. 
The next day angiogram, and their disappearance after reperfusion, proved that they were indeed hyperacute Ts due to RCA OMI.

Here is the post reperfusion ECG:

Here is how normal assymetric inferior T-waves look:

Hyperacute T-waves:

Ten (10) Examples of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD occlusion

MY Comment by KEN GRAUER, MD (2/18/2020):
Our most sincere THANKS to the reader who submitted this case. CREDIT to him/her — for his/her soul-searching account! Hindsight is always much easier in the “retrospectoscope”. I’ll focus my comments on a few additional thoughts to those made by Dr. Smith.
  • For clarity — I’ve reproduced and labeled the first 2 ECGs in this case in Figure-1.

Figure-1: The first 2 ECGs that were shown above in this case (See text).

MTHOUGHTS on this Case  Although the patient in this case is young (32yo) — he is a smoker — his family history is worrisome (father with MI at age 45) — and, his symptoms are new, and these new symptoms led to presentation in the ED.
  • Especially when there are concerning features in the history — The onus has to be on us to rule out (rather than to rule in) the possibility of an acute cardiac event. As a result — IF the initial ECG is not normal, we need to prove that the ECG abnormalities are not acute (rather than the other way around).
  • IF in doubt after evaluating the patient the best you can — Err on the side of caution. Better to cath a patient who doesn’t need it — than not to cath someone who does.

Regarding ECG #1  The reader was systematic in their interpretation, and he/she identified the main abnormal findings. LOOKING CLOSER at ECG #1:
  • In the limb leads — larger and wider-than-expected Q waves are present in leads I and aVL. That said, I wasn’t convinced these limb lead Q waves were significant to the case at hand — and I thought overall ST-T wave changes in the limb leads of ECG #1 were nonspecific.
  • NOT SO in the chest leads. Starting from a definite R wave in lead V1 (3 mm in amplitude) — there is Loss oR wave from V1-to-V2. That this is real-until-proven-otherwise, is supported by the very wide and deep Q wave in lead V3 (BLUE arrow) This suggests anterior MI has occurred at some point in time.
  • The reader correctly identified, “very tall anterior T waves in V1-thru-V5 that are symmetrical and disproportionately large (particularly in lead V4)”. In a patient with new symptoms — especially in association with loss of R wave + the very-large-and-wide Q wave in lead V3 — this description by the reader is how I would define hyperacute anterior T waves.
  • I would add that T waves are fatter-than-they-should-be at their peak (at least in leads V1, V4 and V5) — and, that these T waves are wider-than-they-should-be at their base (at least in leads V1, V3, V4 and V5) — therefore, clearly to be assumed hyperacute in a patient with new symptoms until proven otherwise.

Regarding ECG #2  We are not told how much time passed between the recording of ECGs #1 and #2. The important point, is that although subtle — there has been serial change between these 2 tracings.
  • I thought there was no significant change in the limb leads between ECGs #1 and #2.
  • BUT — there has been further loss of anterior forces — seen as development of a very wide-and-deep Q wave in lead V2 + a Q wave in lead V4 (RED arrows in ECG #2 denoting Q waves).
  • As noted by the reader — T wave amplitude has indeed decreased in multiple leads (ie, the T wave is not as tall in ECG #2 as it was in ECG #1 in leads V1, V2, V3 and V4). Further support that this decrease in T wave amplitude represents a dynamic ST-T wave change — is provided by the unusual short segment of ST straightening that we see in lead V1 (PURPLE arrow) — which replaces the upward-sloping ST segment that we previously saw in lead V1 of ECG #1. This is not artifact. It is real.
  • NOTE: While true that there is now a small negative component to the P wave in leads V1 and V2 of ECG #2 that was not present in ECG #1 — one can not attribute all of the dynamic ST-T changes just described (that occurred in each of the first 4 chest leads) simply to positioning 2 leads (ie, V1,V2) too high on the chest. IF thought that these differences between ECGs #1 and 2 were simply due to lead malposition — then ECG #2 should have been immediately repeated after verifying chest lead placement. This clinical point is important — since IF questions persisted as to whether ECG findings were or were not acutely evolving — demonstration of dynamic ST-T wave change proves that they are.

BOTTOM LINE  Soul-searching cases is TOUGH. But it is an invaluable part of optimizing future treatment. We are indebted to the reader who shared this case with us — so that we can all learn from it.


  1. I would also like to add Tereminal QRS Distortion in V3 on the fisrt ECG, and V2,V3 on the second ECG.

    1. @ Shade — There is "almost" TQRSD — but not quite ... (Please SEE my Answer below to Al, with specifics from Dr. Smith — :)

  2. Terminal QRS distortion in V2-V3 ?


    1. @ Al — I asked Dr. Smith about the same thing. This was his answer: “Technically, by my (Dr. Smith’s) definition in the study, there must be some ST elevation for TQRSD. Also, in ECG #1, there is an S-wave that BARELY goes below the isoelectric line.
      so strictly speaking, it does not have TQRSD. Of course all dichotomous rules in medicine are fallacious. The less S-wave there is, the more likely to be LADO, and the more S-wave, the less likely, overall.” So, there is “almost” TQRSD in ECG #1 — but not quite — but this of course does not matter, because of all of the other signs of definite acute OMI — :)

  3. Ken and Steve...

    A very interesting and sad case. I also have a few points to make.

    1. While this chest pain was atypical because it was sharp and on the right, it was also constant for over an hour and radiated to both arms. Neuromuscular pain that is sharp is usually lancinating with sharp, brief and intermittent episodes that are usually affected by a change in position.

    2. I was immediately struck not only by the very obvious hyperacute T waves but also the flattened and minimally depressed ST segment in aVL. aVL is usually the first lead that I scrutinize closely. This flattening had developed into frank T wave inversion by the second ECG. Enough said.

    3. There was never any impressive STE, but the hyperacute T waves were very impressive - and there was a dynamic nature to them because there was some subtle change in amplitude from tracing to tracing. Hyperacute T waves are actually a subendocardial phenomenon which is why we don't see them as often. Usually by the time the patient arrives in the ER the ischemia has become transmural and the hyperacute T waves are being replaced with the STE of epicardial ischemia. However, some can persist for quite a while. It's also a great time to catch the ischemia because it is usually just beginning and there is a great opportunity to salvage myocardium.

    4. The hyperacute T waves in the precordial leads indicate a very proximal occlusion but the lack of STE in aVL indicates an occlusion distal to D1 (which was confirmed at cath). Because of the hyperacute T's in V1 and V2, I'm wondering if D1 was proximal to S1. This would explain why the prominence of the hyperacute T's fizzles out toward V5 and V6.

    5. The additional disease in the RCA that will require a later stent is very interesting. The ST depression in aVL is reciprocal to something going on in the inferior leads and that could explain it. The bases of the T waves in II, III and aVF are very wide and - though not tall - are likely hyperacute T's as well. The RCA is probably receiving significant collateral circulation from the LAD. When it failed, the myocardium in the RCA distribution became ischemic. When multivessel disease is present and there is collateral circulation being shared, it takes just one vessel to fail and the rest start to fall like dominoes.

    Quite a learning case.

    1. GREAT comments as always Jerry! THANK YOU for your insights on the above subtleties! — :)

  4. Very informative and an absoluetly enjoyable read as always .. highlighting the importance of early detection of coronary occlusions transforming ones practice from damage control to function efficient myocardial resuscitation that undoubtedly will preserve and improve quality of life .. absolutely gold!

    1. @ Dr. Taha — THANK YOU so much for your kind words! Our pleasure — :)

  5. Ken...

    Regarding the questions about terminal QRS distortion, the concept as presented by Birnbaum and Sclarovsky referred to STE > 50% of the R wave height or loss of S wave depth in leads with an rS morphology. I don't see any of that here. This is the original article by Birnbaum et al. if any of the readers are interested: Am J Cardiol 1996;78:396-40

    Also, I don't think one could diagnose terminal QRS distortion when all you have are hyperacute T waves, which are a repolarization abnormality, and not yet affecting depolarization.

    1. Hi Jerry. The concept of TQRSD (Terminal-QRS-Distortion) is one that Steve has studied and written on for a good number of years now (ie, this 2016 post on this blog = http://hqmeded-ecg.blogspot.com/2016/11/paper-published-terminal-qrs-distortion.html ) — but there are MANY more posts on this Blog in which Steve comments and illustrates the criteria he has used. My understanding of the definition he uses differs from what you are citing in the Birnbaum/Sclarovsky article from 1996 — but Steve is the EXPERT — so I’m sending your comment his way for his thoughts. THANKS as always for your active and valuable participation in this ECG Blog! — :)

    2. I use a different definition of terminal QRS distortion, as described in this paper: https://www.ncbi.nlm.nih.gov/pubmed/27658331

      Absence of an S-wave OR a J-wave in EITHER of V2 or V3.

      I do not use if for prognostic purposes, but for differentiating the ST Elevation of LAD occlusion from normal STE. It should only be applied if there is at least 1 mm STE in at least one of V2-V4 AND that is the differential diagnosis.

      In this paper we found that zero of 171 cases of benign ST elevation had TQRSD so defined.

    3. Steve...

      So you are using the TQRSD - as you have defined it - as a diagnostic aid, whereas Birnbaum and Sclarovsky use it primarily for prognostic purposes (they assume the diagnosis of acute ischemia involving the LAD has already been made). For them it represents 3rd degree ischemia, with 1st degree being hyperacute T waves and 2nd degree being STE 50% or less the R wave height.

      Thanks for the reference!

  6. Paramedic here. This is an EKG that I would have transmitted, just looking at the anterior leads my immediate thoughts were (similar to the authors) there aren't many reasons for this morphology and these T waves aside from an MI.

    Reading the cases presented here and reading as many EKGs as possible, makes the abnormalities stand out, (Or like Dr Smith says, makes them stand out like a bad enemy).

    1. THANKS so much for your comments. So glad Dr. Smith's ECG Blog has been helpful! — :)

  7. The submitter writes "their future risk of heart failure, arrhythmias and premature death is greatly increased". I would be concerned about the risk for future HF if there were LV dysfunction, a persistent resting wall motion abnormality on echo, or large infarct size and/or microvascular obstruction on cardiac MRI, not solely on the basis of a high troponin and Q waves on EKG.

    1. @ Michelle — Thanks for your comment. Hard to know about “What IFs?” — but hard for me not to believe that IF this patient with acute mid-LAD occlusion (who consequently developed diffuse chest lead Q waves + troponin > 10,000 ng/L) had been cathed (and reperfused) soon after the initial ECG (instead of the delay until later the next day) — that longterm prognosis would not have been BETTER. Impossible to say “How much better”? — and the only info I see regarding the cath report was that the patient was “without significant LV dysfunction” — which could indicate that there indeed WAS some loss of LV function from before the acute OMI. If it were me — I would like my chances much better being reperfused asap after ECG #1, instead of having to wait until the next day … THANKS again for your comment! — :)


DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

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