Friday, February 5, 2016

Apparent Pseudo-STEMI patterns are not necessarily Pseudo. Beware.

This was contributed by an ECG enthusiast who wishes to remain anonymous.

LVH is a well-described “mimic” of STEMI. However, a diagnosis of LVH does not exclude an acute coronary occlusion, and the clinical context, including symptoms and old ECGs, must be taken into account.

A 50 year-old woman came to the ED with recent-onset chest pain.:
She had a history of hypertension, as well as concentric LVH on a very recent echo. Furthermore, she had markedly elevated systolic BP > 200 mm Hg.

Her initial ECG:
There is STE in lead III, < 1 mm, as well as STD with inverted T waves in leads I and aVL. This pattern of STE and STD could represent an early or subtle inferior coronary occlusion. However, the R wave in aVL is ≥ 11 mm, basically diagnostic for LVH.  

Smith comment: the voltage only barely meets LVH criteria, but the morphology of the T-wave inversion in aVL has the "hockey stick" shape often seen in LVH.  Furthermore, the inferior T-waves are not as large as one would suspect with a coronary occlusion (see example at bottom).  I would agree with the contributor that it does not look like the typical ST-T of subtle inferior MI.  But, remember, coronary occlusion can show almost nothing on the ECG.  If it can show nothing, then very subtle abnormalities could be something.

The ECG raised concerns for inferior MI, but it was decided that the STE and STD were due to repolarization changes of LVH. Nonetheless, a repeat ECG was obtained 1 hour later:
Not significantly evolved from the prior ECG.

These ECGs were compared with an ECG from 1 week prior:
Although there is T wave flattening in leads I and aVL, there is no suggestion of LVH on this ECG. In fact, the ST segments in I and aVL are slightly elevated, and those in the inferior leads II and aVF subtly depressed.

Smith comment: The change from one month ago is diagnostic of ischemia.  

I very much doubt that LVH on the ECG, with ST-T repolarization abnormalities, can develop over one month.  Serial ECGs are very helpful, but frequently show no or minimal evolution over one hour.  One need only see this recent case I posted for another example of absence of evolution.

Contributor continued:
Given the previously documented LVH on echo, as well as the lack of evolution over 1 hour, the new ECG changes were attributed to a combination of acute hypertension, LVH, and different patient and limb-lead positioning. The patient received aspirin, morphine, and nitroglycerin. The first troponin was below the 99% cut off, and she was admitted to telemetry for serial troponins.

Smith comment: I think it would have been appropriate to dial up the Nitro until the BP is normal, then repeat the ECG.  If the ST segment abnormalities remain, then either angiography or emergency formal echo is indicated.  If they resolve, then perhaps the findings are due to the severe hypertension.  That is exactly what happened in this really interesting case.

Contributer continued
Wait, why did she have an ECG from a week ago?
She had been admitted earlier in the month for an NSTEMI without ECG changes. On angiography, a drug-eluting stent was used to open a total RCA occlusion. (The ECG above was post-PCI.)

With this knowledge that she had received PCI to the coronary region of concern on the ECG (the RCA typically supplies the inferior wall) only weeks ago, the plan was made to manage her ongoing pain medically, and she was admitted to a telemetry bed.

ECGs were repeated at 5 hours post-arrival: 
Although the R wave in aVL is still diagnostic for LVH, the STD/TWI in leads I and aVL have resolved, as has the STE in III and aVF. This proves that they were due to ACS, not LVH.

And 6 hours post-arrival:
The R wave in aVL has regressed to her baseline height, while T wave inversions in III and aVF suggest spontaneous reperfusion of the inferior wall. 

The 8-hour troponin returned at 6.7 ng/mL. (Smith comment: we don't know the peak, and it is not a reliable indicator of infarct size as it depends on reperfusion, which makes it rise high and quickly, infarct size, collateral circulation, and assay.  However, this certainly is consistent with an acute coronary occlusion, although her ECGs did not meet criteria for STEMI).  She went to angiogram the next day and the RCA was indeed (persistently) occluded.  The RCA territory, however, was now well supplied by left to right collaterals, so that the damage was not extensive.  No PCI was done except for on two unrelated diagonals (off the LAD).

Why did she have an acute occlusion after getting stented?
Unfortunately, after her PCI earlier in the month, she had been discharged home without a Plavix prescription. In combination with aspirin, this medication is essential for preventing in-stent thrombosis. Her echo, which during her earlier admission had shown only concentric LVH, now had an akinetic basal inferior segment. She was presumed to have had an early in-stent thrombosis of the RCA DES due to insufficient platelet inhibition.

Brief review: LVH and inferior STEMI
LVH is well appreciated as producing STE in leads V1-V3, mimicking anterior STEMI. However, no proven criteria permit a clear distinction between acute anterior ischemia and LVH.

This situation is even less clear for inferior STE when LVH criteria are met. A recent review of LVH and STEMI highlights that “there is confusion whether the exclusion of STE thresholds in patients with LVH is limited to leads V2-V3 or applies to all leads.”

On the one hand...

On the one hand, LVH frequently manifests ST changes that mimic inferior STEMI. 
For example:
Example 2 from Life in the Fast Lane:

Case 4 from this post on Dr. Smith's ECG blog:

Case 6 from this post on Dr. Smith's ECG Blog:

On the other hand...
On the other hand, these clear examples of LVH easily met precordial-lead criteria for LVH, as well as limb-lead criteria. Our patient, however, only met limb-lead criteria, and just barely.

Furthermore, it is plausible that the change in axis was because the limb-lead electrodes had been placed differently (e.g. on chest instead of arms) than the prior ECG, or the patient positioned differently (e.g. seated versus supine). However, such changes would not produce the ST changes we see, especially over so short a period of time.

Dr Smith has a great case that also demonstrates the peril of attributing new inferior ST changes to LVH. A patient with chest pain had this ECG:
It meets criteria for LVH based on aVL, but the ST-T are far out of proportion to the QRS amplitude.  This was diagnosed as MI by the emergency physician, but the interventionalist would not take the patient to the cath lab because he was convinced it was due to LVH.
Furthermore, there was a previous ECG for comparison:
Again, the previous ECG makes the diagnosis definite


  1. Overall GREAT post. In the interest of academic discussion — I will present another perspective on how I would interpret the first 5 ECGs that you show.

    The problem with ECG #3 that is shown here ( = the ECG from 1 week prior) — is that the frontal plane axis is different (ie, lead III is predominantly upright — vs lead III in ECGs #1,2 in which the QRS was predominantly negative in lead III). THIS may account for the lack of LVH voltage seen previously in lead aVL — and in my opinion, makes it very difficult to say whether the change between ECG #3 and ECG #2 is indicative of ischemia (it might be due to the axis shift … which in my experience may account for subtle ST-T wave differences).

    That said — in a patient with NEW chest pain — there IS (in my opinion) a difference between ECGs #1 and 2 — in that there is subtle-but-real increase in T wave amplitude in leads II and aVF on ECG #2. While true that heart rate in ECG #2 is a bit faster than it was in ECG #1 — the frontal plane axis IS the same — so although subtle and in no way definitive, I would be suspicious of something that may be acute simply based on this subtle difference between ECGs #1 and 2 …

    ECG #4 (ie, repeated @ 5 hours post-arrival) is of course diagnostic as you emphasize — as frontal plane axis is the same as in ECGs #1,2 and there is now obvious change in ST-T wave morphology in each of the limb leads.

    Note in ECG #5 (@ 6 hours post-arrival) — that frontal plane axis has again shifted (lead III is predominantly positive again) — and once again, I think it may be this frontal plane axis shift that contributes to the change in QRS amplitude in lead aVL … (It would be so NICE if we could just see baseline tracings in sinus rhythm for these 2 different frontal plane axes … — so that we can say with certainty what the baseline R wave amplitude in lead aVL should look like with each axis …).

    I like the 3 examples you then give re potential for confusion between LVH and inferior STEMI — although in EACH case, while I couldn’t be certain — I would have suspected the changes seen were from LVH (and/or ischemia) and not from acute STEMI (simply based on morphologic appearance). In contrast — the final 2 ECGs (taken from your excellent June 1, 2012 post) are a WONDERFUL example (as per my comment on that post) of how despite obvious LVH, the ST-T wave appearance clearly indicates acute ongoing STEMI (which of course is confirmed by finding the previous tracing).

    BOTTOM LINE: You make wonderful points about potential confusion that may arise when assessing for ACS/acute STEMI in the setting of underlying LVH. I just wanted add the importance of integrating frontal plane axis into ECG assessment when comparing serial tracings. I base my comments on many years of religious serial observations within a large family medicine population of patients that this potential effect from shift in frontal plane axis may have on QRST limb lead appearance. THANKS (as always) for your great presentation!

    P.S. Steve — It would be great if you could NUMBER your figures (would really make it much easier to clarify which ECG is being referred to when comments are made). THANK YOU for considering!

    1. Thanks, Ken. Yes, I will remember to number the figures

  2. Another very intersting and very instructive case; thanks a lot.
    Only just a question on your statement 'if the ST segment abnormalities remain, then either angiography or emergency formal echo is indicated. If they resolve, then perhaps the findings are due to LVH'. According to your experience do the repolarization changes due to LVH resolve completely?.
    Let me make also a general comment.
    In comparison with other difficult ECGs where there are validated helps (for example LBBB->modified Sgarbossa or differentiation between early repol and MI->formula), 'paradoxically' in very frequent clinical situation such as LVH and chest pain, which all we face every day, there are too many uncertanties in order to proper evalutate these difficult ECGs.
    I hoped that the Armstrong R/S ratio could be of help until I've read your articles and this blog…
    Therefore, Dr. Smith, I will very highly appreciate your opinion on that; more precisely I would like to know what is your approach to these cases. In other word, and for the sake of clarity, what do you consider first, besides the clinical context, prior available ECGs (which all we know are the exception than the rule), serial ECGs, echocardiogram: Armstrong's ratio, Tampl/QRSampl ratio (not necessarily in that order) etc.?

    Mario Parrinello

    1. Mario,
      You pointed out a typo in my case. I did not mean to say that about LVH. I have changed it to the following, which is what I meant to say:
      If the ST segment abnormalities remain, then either angiography or emergency formal echo is indicated. If they resolve, then perhaps the findings are due to the severe hypertension.
      As for the last question, that is very difficult and very case specific. For this, case, the change is diagnostic. If one did not have that previous ECG, then one would first treat the hypertension and see if that resolves the pain and ECG findings. If not, perhaps activate, or get an emergent formal echo. If there is a WMA, then activate. If there is no wall motion abnormality on a contrast echo read by an expert, then there is not significant ongoing epicardial ischemia.
      Steve Smith

  3. Dr. Smith, thank you for your reply

  4. Clopidogrel treatment failure is surprisingly common. No evidence for changing to an alternative P2Y12, though.

  5. Explain about pseudo STEMI please..

    1. Kaviraj,
      PseudoSTEMI means ST elevation that is not due to MI (not due to coronary occlusion), but may appear at first glance or to the non-expert to be an MI.


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