Friday, December 22, 2023

Is there OMI on this ECG?

This is a case I had quite a while back. 

The patient with no prior cardiac history presented in the middle of the night with acute chest pain, and had this ECG recorded during active pain: 

I did not see any ischemia on this electrocardiogram. 
It does not look entirely normal, since there are some nonspecific STT abnormalities, such as flattening of the T waves in aVL.  
There is a normal amount of ST elevation in the precordial leads. There are no hyperacute T waves. 
There is no inappropriate ST depression.  But it certainly shows no sign of OMI.

Or does it?
Here is the Queen's interpretation:

Why does she say this?  See the explainability:
She sees large T-waves in V2, V3.  
Is she seeing anterior hyperacute T-waves, or does she see Posterior Reperfusion T-waves?
The patient has active chest pain, so if these are abnormally large T-waves

This is a particularly informative link: 2 Examples of Posterior Reperfusion T-waves

So one might think that, with active pain, there is anterior OMI.

I think the ECG is normal.  I did not think that the T-waves in V2 and V3 are hyperacute and I still do not--I disagree with Ken below--I think they are normal, especially in the context of bradycardia.  They do not have much bulk.  Their apparently excessive length (QT interval) is due to bradycardia.  A corrected QT would be normal.  And it is normal for T-waves in V2 to be taller than the R-wave in V2.

I did not have the Queen at the time.

Case Continued

Patient continued to have uncontrolled pain and trop returned slightly elevated. 

The patient has ongoing symptoms and has an unexplained elevated troponin, so she is having an OMI until proven otherwise.  

Comment: ACS with persistent symptoms is a guideline recommended indication for <2 hour angio (both ACC/AHA and ESC).  The ESC states that patients with suspected ACS should go to the cath lab in <2 hours "regardless of ECG or biomarker evidence of MI!!"  Unfortunately, the only study of compliance with this high-risk ACS guideline showed that this guideline is followed only 6% of the time.  We have shown that morphine is associated with worse outcomes (see learning points below) and have published many blog posts about it, such as this one: Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mass delusion (and Opiate pain relief).

Therefore, we activate the Cath Lab. 

There was a 100% circumflex occlusion that was opened. 

Below are 3 more cases of circumflex occlusion that are normal or near normal, or called normal by the conventional algorithm:



Learning Point:

OMI can be present with a Normal ECG!!  OMI is a clinical diagnosis that includes the ECG.  If the ECG is nondiagnostic, one must use some combination of clinical suspicion, old ECGs, serial ECGs, echo, or simply angiography to be certain that an OMI is not being missed


MY Comment, by KEN GRAUER, MD (12/22/2023):

Interesting "quick" case presented by Dr. Smith. Unfortunately, given occurrence in the past — some details are not available.
  • The BOTTOM Line ( = the important "Take-Home" message in Today's Case) = as per Dr. Smith, since the patient presented with "middle-of-the-night" new CP and Troponins were elevated — that these new and now persistent symptoms with elevated Troponin qualify for prompt cath regardless of what the ECG shows ....

MY Thoughts on the ECG:
For clarity in Figure-1 — I have reproduced today's ECG. In a patient with new CP — I was concerned that the T wave in lead V2 was disproportionate considering R wave amplitude in this lead (within the RED rectangle).
  • The T wave in lead V2 is slightly taller than the corresponding R wave. I thought it to be "fatter"-at-its-peak and slightly wider-at-its-base than expected given the size of the R wave in this lead.
  • By the concept of "neighboring" leads (ie, given my concern that the ST-T wave in lead V2 did not look "normal" to me) in this patient with middle-of-the-night CP — I thought the T wave in lead V3 was also abnormal in appearance (ie, a bit more "hypervoluminous" than I would normally expect given R wave size in this lead).
  • The other "neighboring lead" ( = lead V1) manifests a distinctly upright T wave. While this may be a normal finding in V1 — an upright T wave in lead V1 is not usually this prominent (nor is an upright T wave in lead V1 normally comparable in size to an upright T wave in lead V6, that typically with a narrow QRS, is taller than any upright T wave in lead V1).
  • Other changes on this ECG looked nonspecific to me ...

 — I was not sure what to make of this ECG, other than thinking that this initial tracing was not "normal" in a patient who presents with middle-of-the-night CP. 
  • Learning that the patient had 100% LCx occlusion on cath meant that these ECG findings could not be due to an LAD lesion.
  • Whereas I thought these abnormal-looking upright anterior T waves might represent reperfusion following a posterior OMI — this woud not make sense given the fact that this patient had ongoing CP until PCI, therefore clinically unlikely that there was any reperfusion prior to cardiac cath ...

Figure-1: I've reproduced the initial ECG.

LESSONS to be Learned:
  • As per Dr. Smith — persistent new CP + elevated Troponin is indication for prompt cath — regardless of what the ECG looks like ....

  • In the "Retrospectoscope" (as I review this case done in the distant past) — it appears that the reason for cath was due to the elevated Troponin and persistent CP — which I assume took a certain (unspecified here) amount of time for that elevated troponin to come back ..

  • It also appears that no repeat ECG was done to explore the possibility that the less-than-normal-appearing initial ECG might have been evolving. Had there been a repeat ECG (ie, done within 10-20 minutes of this initial ECG) — then perhaps the indication for cath would have been satisfied sooner than waiting for an elevated Troponin to come back ....
  • No mention was made of any prior tracing. Had there been one — it's possible comparison with today's ECG may have also provided an answer sooner than waiting for an elevated Troponin to come back ...


  1. Great case Steve!

    I agree with all the principles you have emphasized here. Although I must say I agree with Ken! Yes there's bradycardia but the T-waves still catch my eye not only because of their size and morphology but also due to the ST-Takeoff and morphology of the ST segments. I have several questions: Was there a prior ECG for comparison? Were there any repeat ECGs? Do you have any post-cath ECGs? All these would help delineate the electrocardiographic evolution. Also was this a Left-Dominant Coronary Circulation(PDA off the Circ?). Do you have any cath images? Finally, although this wasn't an LAD Occlusion should not cut off the R wave in V4 which appears to be cropped on the original but then not on the digitized version!

    1. I think you are both using the retrospectoscope, and if I had put this in a mix of a hundred ECGs of unknown outcome, you would not have recognized it as OMI. The Queen says OMI because she sees what she thinks are posterior reperfusion T-waves. She calls OMI whenever she sees EITHER and active or a reperfused OMI. But this is during active chest pain and has no evidence whatsoever of active circumflex occlusion.

      This is a repost of a case I put up years ago. I have searched in vain for that blog post without success. I had the EKG in one of my powerpoints, but lost the file on my computer, where the other EKGs were also. There was no old EKG and subsequent EKGs were unrevealing.

      Any OMI you are seeing here is your imagination. Because it wasn't there.


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