Tuesday, December 31, 2013

Hyperacute T-waves? Anterior STEMI? No, LVH with PseudoSTEMI pattern!

A woman in her 30's with h/o HTN presented with atypical chest pain after a stressful event.  Here is her ED ECG:
There is sinus tachycardia.  There are very large anterior T-waves, with ST elevation.  However, there is also very high voltage.  Criteria for LVH is clearly reached in aVL, with tyical repolarization ("strain") in aVL.  The ST elevation and tall T-waves are discordant to deep S-waves in V2 and V3.

I took care of this patient and was concerned about the ST-T waves in V2 and V3, but thought that they were almost certainly a result of LVH.  One should not apply the LAD occlusion vs. Benign Early Repol Formula if the patient has LVH.  Had I done so, with a QTc of 375ms, the formula value would have been 26.1, indicating anterior STEMI.  Here is another example of LVH resulting in a falsely positive formula value.

I think that the formula would be more accurate if it took into account the entire QRS, not just the R-wave.  I will be using all the original ECGs to study this hypothesis.

There were no previous ECGs for comparison.

We did a bedside cardiac echo which showed concentric LVH and a well functioning anterior wall.  A repeat ECG 30 minutes later was identical.  We recommended admission for further evaluation but the patient signed out against medical advice.

Her heart rate came down with IV fluids.

I am quite certain that this is the patient's baseline ECG.

Lesson:

1. LVH can result in PseudoSTEMI patterns of various morphologies.  Here are some others.
2. The formula may give false positives in LVH

8 comments:

  1. Steve, I realize that it's difficult to come up.with a formula looking at the ratio of S wave depth:ST elevation for determining LVH versus STEMI, but the ratio here is so notable. Do you feel we're able to feel somewhat reassured by this "proportional" STE?

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    1. Brooks,

      In fact there has been a study published summer of 2012 proposing that an ST/S ratio greater than 0.25 distinguished the STE of STEMI from LVH. It is a difficult stud to do, and though the result was very plausible, I'm not sure the methodology was the best that could be done. I have been meaning to post on that topic for a while. Here is a link to the study: http://www.ajconline.org/article/S0002-9149%2812%2901433-6/abstract. I believe that there will be a good ratio that covers BOTH early repol and LVH: a T/QRS ratio. It may be similar to my LV aneurysm ratio: http://www.ajemjournal.com/article/S0735-6757%2805%2900081-1/abstract

      Thanks,

      Steve

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  2. Can you comment on the PR depression and QRS notching in lead II? Is that of any significance?
    Also, in addition to aVL, does lead V1 show a strain pattern?

    Thanks,
    Jos

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    1. I don't think either are of any clinical significance. Do you?

      Steve Smith

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    2. Jos,

      If this patient does have LAE as Ken suggests below, an increased amount of PR depression due to atrial repolarisation, I believe, may be expected.

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    3. Yes, in leads with all positive P-waves.

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  3. GREAT case Steve! - that clearly supports your important premise that ST-T wave changes of LVH may mimic anterior stemi. That said - I’ll make a few points.

    i) There is voltage - and then there is VOLTAGE. QRS amplitude in this tracing is VERY markedly increased. The R in aVL = 17mm - and S wave depth in lead V2 is over 30mm. Young adults may normally have some increase in QRS amplitude - but rarely to this degree - and definitely NOT with classic LV “strain” changes as are seen in lead aVL. Thus, this patient clearly has marked LVH on her baseline ECG.

    ii) Note also LAA (Left Atrial Abnormality) - with a relatively wide and notched P wave in lead II and a seemingly prominent negative component to the P wave in lead V1. Realizing poor sensitivity and poor specificity of the ECG for assessing atrial chamber size - I’m suspicious of LAE (Left Atrial Enlargement) in view of the Voltage and LV “strain” pattern - which provides further support for the diagnosis of baseline LVH.

    iii) Of note - there is also suggestion of RAA (Right Atrial Abnormality) - in that the P wave in lead I appears pointed - and you have a taller-than-expected and almost pointed P wave in lead V2. Echo would tell if this is real (again, poor specificity of ECG for atrial dimensions) - and it sounds like from your Echo that you saw concentric hypertrophy with a well functioning ventricle - so no “cardiomyopathy” per se.

    iv) Anterior leads sometimes provide the “mirror image” of lateral precordial leads. We see classic LV “strain” in lead aVL - but not in V5,V6. I suspect the beginning T inversion in V6 would become more typical LV “strain” IF one did posterior leads (V7,8,9) - and that might be reasonable to do when assessing a patient like this. But if we do a “mirror test” on the QRS and ST-T waves in leads V1,V2,V3 - you would get the mirror-image opposite, or LVH + “strain” with deep T inversion - the kind you may see in EITHER marked LVH and/or ischemia. All that said - this is NOT the usual “LVH pattern” you see in a 30-year old UNLESS there is significant underlying predisposing disease. So I’m very curious about this patient’s HTN history. Very longstanding and severe? Associated with renal disease? I’d almost bet it is given her ECG.

    v) Great that you could do an Echo to confirm good LV function! - as this is another strong point against ACS. My point in bringing out the above re likely severe and longstanding LVH - is that knowing this would clearly enhance my comfort level interpreting this ECG as more than likely exactly what you describe - namely, marked LVH leading to an ant. stemi-mimic.

    Again - GREAT teaching case. I think the overall ECG pattern plus presumed history of severe longstanding hypertension for this woman in her 30’s overwhelming favor the conclusion you arrived at. THANKS for presenting!

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    1. Ken, all excellent points! I try to be brief (because of my own time limitations, and also so that people will not get overwhelmed) and would have made many of the same points had I written more. And I also must refrain from giving too much detail for identification purposes. Suffice it to say that, as you say, she had severe hypertension with resulting renal insufficiency.
      Thanks for the great comments!
      Steve

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