Sunday, February 12, 2012

Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-equivalents.

Here are some basic concepts before we get into the ECGs:
  • STEMI and NonSTEMI are arbitrary terms that may confuse the clinician.
  • "STEMI" should mean "coronary occlusion" (or near occlusion, without good collateral circulation -- in other words, it needs thrombolytics or emergent angiogram with PCI).  
  • NonSTEMI should mean "MI without occlusion."
  • "STEMI-equivalent" is a good term for "coronary occlusion".
  • Many STEMI-equivalents have no significant ST elevation, as you may have seen from many of my posts.
  • In some STEMI-equivalents (posterior STEMI, lateral  STEMI, posterolateral STEMI), ST depression is the only, or most visible, feature of the ECG.
  • So how do we tell if ST depression represents a STEMI-equivalent or NonSTEMI/subendocardial ischemia?
  • As I see it, there are 5 primary patterns of ST depression.  I outline them below and demonstrate them to show which are STEMI equivalents and which are NonSTEMI.
  • NonSTEMIs/subendocardial ischemia may need immediate angiogram and PCI (or emergent CABG) if the patient is hemodynamically unstable or if the ischemia (as measured by chest pain and ECG findings) cannot be controlled medically (aspirin, GP IIb IIIa inhibitor, antithrombotic, nitroglycerin).
  • NonSTEMIs should never get thrombolytic therapy.
  • Clopidogrel should probably be avoided in NonSTEMIs that have a high likelihood of needing CABG (ST elevation in aVR)
ST elevation axis (vector) is the opposite of the ST depression vector, though not necessarily the same magnitude (millivolts or millimeters).  Once you understand this, it makes everything simple.  It is worth a few moments to concentrate and learn it.

First, there are countless ways ischemic ST depression (STD) presents.  Check here, for instance. 

But I like to classify 5 primary STD patterns in ACS in which there is ST depression without any significant ST elevation.  Some are STEMI-equivalents, and some are Non-STEMI.  The diagnosis depends on the ST axis.  Which direction does ST elevation go?  Sometimes it is better to ask: what is the opposite of the ST depression vector?

If the ST depression is directly anterior (V1-V4), then the ST elevation axis is directly posterior, and there is a high likelihood of posterior STEMI.

If the ST depression vector is inferior and leftward, there is a lot of ST depression in inferior and left lateral leads, and corresponding ST elevation in aVR (superior and rightward), towards the base (top) of the heart. (There may also be ST elevation in right sided leads but NOT due to RV MI).   Unless there is a concomitant anterior STEMI (high occlusion resulting in STEMI of anterior and basal walls), STE in aVR is not a STEMI in lead aVR; rather the STE in aVR is reciprocal to a leftward and inferior ST depression axis caused by diffuse subendocardial ischemia.

  • Thus, an ST elevation axis that is anterior, posterior, inferior, or left lateral is likely to be a STEMI-equivalent.  Anterior-Superior axis (anterior STE + V1 and aVR) is also STEMI
  • An ST axis which is rightward (ST depression V3-V6) or superior (ST elevation in aVR) is likely to be a NonSTEMI. 

In all this, it is important to realize that ST depression does not localize subendocardial  ischemia.  On the other hand, reciprocal ST depression does help to localize the area with ST elevation.   For instance, if there is ST depression in V4-V6, it does not necessarily mean that the ischemia is of the lateral wall.  The ischemia might be in that location, but not necessarily.

This is a mystery I cannot explain, but has been proven by comparing ECG findings to angiography.


1. Severe subendocardial ischemia, nonlocalized: Diffuse ST depression, including leads I, II, aVF, III, V3-V6, with STE in aVR.  This one was severe acute left main stenosis.  One might also find this in severe 3 vessel disease with ACS.

A patient who lives through Left Main Occlusion is not common.  Acute left main ACS with critical stenosis is the much more common issue, and this causes subendocardial ischemia.  So no thrombolytics.  Both severe 3 vessel ACS and acute left main ACS are likely to need CABG and thus you might want to avoid clopidogrel.  So the fact that 3 vessel ACS and left main cannot be differentiated on the ECG is not so important.

ST elevation is in aVR.  The ST axis is towards aVR, but this does not mean there is STEMI in aVR!  Instead, this elevation is reciprocal to global subendocardial ischemia with the negative ST axis inferior and lateral, towards the apex (I, II, aVF, III, V3-V6).  There is no occluded artery here.  There is no STEMI.  The precordial ST depression is not maximal in precordial leads V1-V4, therefore there is no posterior ST axis and no posterior STEMI.
2. Isolated posterior STEMI: Leads V1-V4 primarily 

Standard 12-lead ECG:
ST depression is limited to precordial leads and is maximal in V2-V4 precordial leads.  Thus the ST axis is posterior.

Posterior ECG: Leads V4-V6 replaced by leads V7-V9:
ST elevation in V7-V9 confirms posterior STEMI.  There was a circumflex occlusion.

3. Posterolateral STEMI: Precordial leads V1-V3 +/-V4 with STD in II, III, aVF, but no ST depression in I and minimal STE in aVL

Example 1:
The ST axis is away from inferior and anterior leads, and so is posterior and superior.  With a bit of ST elevation in aVL, it is also lateral.

Example 2:

There is ST Elevation here, in aVL, but it is much less obvious than the ST depression  in inferior leads and in V2, V3.

4. Subendocardial ischemia, non-localized, usually not as severe as #1 above: ST Depression in V3,V4-V6.  ST axis is rightward, with little posterior or inferior components.

77 yo presented with pulmonary edema.  Troponin I peaked at 6.7 ng/ml.  There was an inferoposterior wall motion abnormality.  All arteries were diseased but there was no obvious culprit.  This is not a posterior STEMI.  This is a NonSTEMI.

In this case, the ST axis is perpendicular to III and  aVF and towards aVR, and away from I and II (leading to ST depression in I and II).  So it is upward and rightward.  If this were inferior STEMI, the ST axis would be towards III and aVF (which also give ST depression in I and aVL).

5. Isolated High Lateral STEMI: II, III, aVF only (ST Depression is reciprocal to minimal STE in aVL)

Example 1.
Acute Circumflex occlusion (also old inferior MI with Q-waves, and early repol giving anterior STE)

Example 2.
Acute First Diagonal Occlusion.

Example 3.
This patient presented with DKA and an acute STEMI with first diagonal occlusion.  The peaked T-waves are due to hyperkalemia, which was immediately treated.  Notice that the ST elevation in aVL is far less obvious than the reciprocal ST depression in II, III, aVF.  The ST axis is towards aVL and away from inferior leads; thus there is ST depression in inferior leads.  There was a 100% acute occlusion of the first diagonal, with peak troponin I of 110 ng/ml, new lateral wall motion abnormality, and ejection fraction decreased to 55%.


  1. Great post Dr. Smith!
    a couple of questions:

    Using this reasoning, if the vector of ST elevation was anterior and also inferior, would that imply a "wraparound" LAD occlusion that also supplied part of the inferior wall?

    If the vector of ST elevation was more or less anterior, you would have ST depression in the inferior leads if the axis of elevation was also superior (towards aVL), but you could have no reciprocal ST depression if the axis of elevation was directly anterior? is that correct then?


  2. That is correct. Indeed, if there are opposing forces, they may cancel each other out, or attenuate each other. Anterolateral STEMI with a wraparound LAD, for instance: the STE in aVL can attenuate the STE in III. Posterior STEMI can attenuate the anterior STE in V1 caused by RV MI.

  3. Thank you for this attention to detail on ST-depression Dr. Smith! I'm afraid for many of us we were simply taught that it was "ischemia".

  4. The LM case is NOT an occlusion and NOT a STEMI equivalent. The vast majority of LM ACS is acute stenosis with subendocardial ischemia. LM occlusions rarely make it to the ED alive.

    Here are the Vereckei references:

    1. Vereckei A, Duray G, Szenasi G, Altemose GT, Miller JM. Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur Heart J 2007; 28:589-600.
    2. Vereckei A, Duray G, Szenasi G, Altemose GT, Miller JM. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm 2008; 5:89-98.

  5. Perhaps this is just me, but..

    ECG #2 of 9, the first ECG under 2.Isolated Posterior STEMI- looks to me like there is ST Depression in I, maybe in aVL, and definitely convex STE in aVR.

    Can you explain this or am I seeing things?

    Thank you so much for the wonderful teaching points!


  6. That's why I say "primarily". The ST axis is not directly posterior, but also a bit rightward.

  7. Great interpretation and breakdown of subendocardial ischemia vs occlusion etc.. I am going to share this and I look forward to reading more in the future.

  8. Great work !!!
    However, I have a question: When we look at the ST depression, do we just concentrate on the maximal ST depression?
    For example, in case 4 under subendocardial ischemia not as severe as #1, I noticed some ST depression in I and avL albeit the ST depression is only a little bit. So in this case, do we just concentrate on the obvious ST depression in V3-V6? As I have read, ST depression in avL even though only for a little points towards inferior STEMI. So am I just imagining? Please enlighten.


    1. Again, look at the ST axis. In this case, it is perpendicular to III and aVF and towards aVR, and away from I and II (leading to ST depression in I and II). So it is upward and rightward. If this were inferior STEMI, the ST axis would be towards III and aVF (which also give ST depression in I and aVL).

      Does that make sense?

      Steve Smith

  9. Flipped T in avl can be a sign of inferior infarct according to mariott according to amal mattu for the first 12 lead for 2.

    Mariott - "may precede the expected changes in inferior leads; may initially bethe only abnormality found on the ECG of a patient with acute inferior MI orischemia"

    1. We've formally studied this, abstract in October Annals of EM, and the best predictor was any ST depression in aVL, with nearly 100% sensitivity and spec for inf STEMI. It was better than TWI in aVL, though that had value (but no value independent of ST depression)

  10. Thank you for the explanations dr. Smith. This STEMI equivalents tell us not to see a ST depression merely as ischemia, as told by old schoolers. Can we still diagnose a patient as having an ischemia, when the ECG shows ST depression not included in these 5 examples ? For instance , ST depression in inferior leads without any ST elevation

    And also, there seems to be a consensus to see a deep ST depression (more than 4 mm) as an infarct. What's your comment on this ?

    1. ST depression isolated to "inferior" leads is almost always reciprocal to a superior ST elevation vector and aVL should be scrutinized for any ST elevation.

      Significant ischemic ST depression almost always has a positive troponin (with rise and/or fall) and is thus MI, especially if at least 2 mm.

      Steve Smith

  11. Many thanks for the explanation !

  12. Thanks for your great explanations.
    I'd like to ask about the posterior STEMI, do you include the R/S >1 in V2-3?

    1. Good Question: R/S ratio is analogous to Q-waves and is a later or chronic finding. It may help to make the diagnosis of acute posterior STEMI, if present, but if absent it is of no help.
      Steve Smith

  13. How to find st axis in lateral wall st depression and where st axis fall in anterior lead st we consider reciprocal changes of dippression as st axis.can one find st exis on ecg for each st depression or we should assume that if v5v6 is showing dippression and the patient is feeling immense symptoms without st axis it rational to consider stems equivalent.or an st axis is necessary.please make topic clear

    1. Dr. Gupta, I am very sorry I don't understand your question. Can you get someone to help you to formulate it more clearly?
      Steve Smith

  14. Dear doctor what is st axis means

    1. The ST axis is the direction that the ST vector points to. If there is ST elevation anterior, then the ST vector is anterior. If the ST elevation is anterior and inferior, then the ST vector is anterior and inferior. If there is ST depression lateral, then the ST elevation vector is in the opposite direction, to the right. OK?

  15. Sir, ECG # 4 of 77 yrs old person having ST depression in V3 to V6. Is there subtle elevation in aVR and V1. If yes then what it signify?

    1. These are manifestations of global subendocardial ischemia, but not as pronounced as in case 1.

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  17. So just bc I have ST Depression on a resting Ecg doesnt mean I have ischemia or CAD? I am so worried I have a blockage or I am going to have a stroke! :(

    1. Any ECG must be evaluated in clinical context = your symptoms. Sometimes there is baseline benign ST depression, but I cannot comment on you. See your doctor.

  18. Kindly make a video if this if possible.. Thank you.. 🙂

  19. Thanks Dr Smith for the amazing blog and all the teaching.
    I do have a question about the 2nd ECG
    On a first look i would have said this is AVR STE with diffuse STD involving V2-6, Lead I, AVL, II and III (using T-P segment as the baseline).
    wouldnt you call it LM insufficiency / TVD with diffuse subendocardial ischemia ??

    1. No. The maximal ST depression is in right (not left) precordial leads. If right, then posterior (the STD is reciprocal to STE posterior Vector). If left, then the STD is primary, and STE in aVR is reciprocal to the ST depression (then it is LM, 3VD, but non-occlusive!) Make sense?

    2. Thanks for your clarification. May I also ask how should we interpret the STE in AVR and the down-sloping STD in Lead I and AVL (in the same ECG). ??

    3. aVR is 120 degrees and 150 degrees opposite aVL and I, respectively. You should expect them to have reciprocal findings.

  20. Dear Dr, thanks for your sharing!
    Is it possible to get anginal symptoms from LM stenosis?
    Our patient came in with a history of episodic chest pain worse with exertion
    The ECG at the emergency department showed significant ST elevation in AVR and ST depression / T wave inversion in I, II, AVF, V3-6
    The patient had already taken TNG and the chest pain soon subsided, with a repeat ECG in 30min showing near complete resolution of all the ST changes.
    Should that be treated as a severe acute left main stenosis and warrant an urgent PCI? Would thrombolytics be less indicated in such cases?

    1. If symptoms and ECG findings are persistent, are due to ACS, and there is no possibility of intervention, only then would thrombolytics be indicated.


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