Friday, January 6, 2017

LVH with secondary ST depression??

This was sent by Michael Macias (Twitter: @EMedCurious), a 4th year EM resident at Northwestern in Chicago.


An elderly man with end stage renal disease and coronary disease presented with chest pain.

Here is his ECG:
See the computer interpretation above.
What do you think?

Dr. Macias' interpretation is here:

Significant elevation in aVR with diffuse ST depression. Hemoglobin was 7.0 g/dL. I thought this was likely triple vessel disease with subendocardial ischemia, but we activated the cath lab given impressive ECG and his history.

Smith interpretation:

The computer reads LVH with repolarization abnormality. There is high voltage, and you expect some discordant ST depression, but this ST depression, although always discordant, is way out of proportion to the QRS voltage. Moreover, the ST depression is NOT maximal in V5 and V6, as it should be with LVH repolarization abnormalities.

So this is ischemic ST depression.

Whether it is diffuse subendocardial ischemia or posterior STEMI is more problematic.

As the STE is most profound in V3 and V4, NOT V5 and V6, posterior STEMI is more likely. However, the STE in aVR (which is reciprocal STE, reciprocal to the ST depression vector towards the apex), is more typically seen in diffuse subendocardial ischemia. ST depression due to subendocardial ischemia is most commonly caused by demand ischemia. One cause of demand ischemia is severe anemia, but a Hgb of 7.0 does not qualify, especially without any tachycardia.

So this must be assumed to be due to ACS.

In fact, the ST depression in V5 and V6 is not all due to ischemia: it is a combination of LVH repolarization and ischemia; the ischemia component is only one portion and so there is less ischemic STD here than one might at first think. This means that the ischemic ST depression is significantly more profound in V3 and V4.

So this is most likely a posterior STEMI pattern, superimposed on LVH. Activating the cath lab is indicated!


100% acute circumflex occlusion, opened.

Learning Points:

1. Again, the computer algorithm cannot be trusted.
2. Posterior STEMI has more ST Depression in V3 and V4. Subendocardial ischemia is maximal in V5 and V6.
3. Know the expected amount of repolarization abnormality in the presence of LVH.  I don't have a calculated ratio.   Below are two examples of LVH with repolarization abnormalities.  These are both baseline ECGs without any active ischemia.  Notice the proportional amount of ST depression, and that it is maximal in V5 and V6.


  1. Isn't also the horizontal ST depression more likely to be ischemia? (versus downsloping ST depression secondary to LVH)

  2. Isn't the ST depression concordant in V2?

    1. You are quite right. Although there is controversy over whether one should use "area under the curve" (i.e., integral of the waveform) or voltage. I have always used voltage, in which case you're right. But if you use the integral, then there is more area under the R-wave than the S-wave.

  3. NICE case and discussion by Dr. Smith. There is dramatic increased voltage for LVH — but as per Dr. Smith, the J-point ST depression is far more than what one generally sees with LVH. Note there is no less than 5mm of J-point ST depression in leads V4,V5 — as well as the following features that are clearly atypical for LVH + “strain”: i) ST segment coving of the depressed ST segment in leads like II, V4; ii) a very “non-strain-like” appearance to the ST-T wave in lead V3 (with biphasic T wave); iii) very uncharacteristic flat ST depression with terminal T wave positivity in lead V2; iv) overall marked ST depression in no less than 9 of the 12 leads; and v) equally dramatic ST elevation (at least 3-4mm) in lead aVR together with a markedly positive T wave in lead V1. The picture of marked ST-T depression seems too generalized for just LVH with posterior infarction — so my hunch was that this reflects diffuse subendocardial ischemia. While anemia may cause marked ischemic change — it sounds like the low hematocrit may be chronic (the patient has end-stage renal disease) — and the chest pain is acute — so the correct assessment of need for cath lab activation was made. Diffuse ST depression with ST elevation in aVR (and/or in V1) often reflects severe coronary disease (possibly left main and/or proximal LAD or multi-vessel disease) — but this case was due to 100% acute circumflex occlusion. THANKS for presenting!

  4. Agree. What about acute sudden hypertension (200/100)symptomatic (chest pain, headache,flush, vertigo etc) which may change LVH pattern to LVH pattern with STD>2mm mainly in lateral leads (I, aVL, V5,V6)? Is this a mask of CRx occlusion? Sub-endocardial ischemia? Troponine negative.
    Also every time when we have tachycardia >120/min (called "demand ischemia" in this post ;) with LVH pattern is with STD>2mm of course in lateral leads but it could be treated as a "normal" (means in this case non-ischemic) variant (eg subthyreotoxicosis, hyerventilation, psychosis), we do not see STD when the rhythm slow down.

  5. As the STE is most profound in V3 and V4, NOT V5 and V6, posterior STEMI is more likely. -> It means " As the STD is most profound in V3 and V4, NOT ......." ?

  6. Thanks for so useful interpretation!
    I think there is a concordant ST-depression in V2, one more thing suggesting posterior STEMI.

  7. Steve...

    Unusual case!

    The ST elevation in aVR indicates an acute subendocardial ischemia since it approximates an intracavitary lead. However, we typically associate diffuse (in this case, likely circumferential) subendocardial ischemia with either a left main lesion, very proximal LAD lesion or 3-vessel disease. But the cath report only mentions a 100% occlusion of the LCx. Was there any other mention of advanced, but non-occlusive, coronary disease? I'm wondering if all three arteries were severely diseased and the loss of the LCx created a domino effect throughout the coronary vasculature.

    1. Jerry,
      no other artery had more than 50% stenosis and none was a culprit.
      Thanks for the comment!


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