Sunday, December 6, 2020

The Diagnosis of OMI does not depend on the ECG. But if you recognize it, that's great.

An elderly woman presented with 4 days of waxing and waning epigastric/substernal chest pain, worse on the day she presented.  She described the pain as a constant chest pressure, 6/10, without radiation to left arm, jaw or back, and without change in with breathing or movement.

Here is her ED ECG:

This was read as non-specific.  What do you think?

I found this case while looking through a stack of ECGs, without clinical information.  

I immediately thought "Acute LAD occlusion."  Why?  

There are QS-waves in V2-V4.  These suggest old anterior MI, or subacute MI.  But as we've described many times, old MI does not have large T-waves!  The T/QRS ratio in V4 is 6/10 = 0.6.  If any single ratio in V1-V4 is greater than 0.36, it is acute MI, not subacute and not old.  

Notice I said the LAD is occluded, but there is nearly zero ST Elevation!  

This is why we need to change the name of acute MI due to acute coronary occlusion from STEMI to OMI.

In fact, there was an old ECG available from 16 days prior.  Here it is:

This confirms that the QS-waves are new, as are the large T-waves.

The patient was treated with aspirin and nitroglycerin, but she had persistent pain.

The first troponin returned at 1,950 ng/L.  This, in the context of persistent pain, is all but diagnostic of acute coronary occlusion even without the ECG.  The fact that the troponin is so high is consistent with the prolonged pain (either infarct within the last few days, with acute re-infarction now, or with a single prolonged insult of at least 6 hours).

Thus, the diagnosis of OMI can be made without the ECG (unlike the diagnosis of STEMI).

An ECG recorded after troponin returned, 1.5 hours after the first, is here:

The T-waves are much less tall and there is the beginning of terminal T-wave inversion.
This is reminiscent of Wellens' waves, but different
In Wellens' syndrome, there are preserved R-waves and the pain is always gone.  
V2-V4 show probable persistent occlusion with evolution of transmural infarct.  
V5 and V6 are indeed typical of Wellens, with preserved R-waves.

At this point, the cath lab can be activated even if the ECG findings are not recognized.  It is clearly ACS, with elevated troponin and uncontrolled pain.   

This was not done immediately.  She was started on heparin.

A formal echo was done immediately by the cardiologist, which showed mild systolic dysfunction with evidence of large wall motion abnormality in the LAD vascular territory.

This was the note: 

"Patient continues to have chest pain 5-8 out of 10 along with shortness of breath.  Overall, presentation is consistent with late presenting acute anterior ST elevation myocardial infarction with ongoing chest pain and shortness of breath.  Chest x-ray showed evidence of pulmonary vascular congestion consistent with early form of heart failure."


"Overall, patient does have high risk acute MI involving the LAD with mild systolic dysfunction with evidence of heart failure, elevated proBNP at 2791 and ongoing chest pain.  This would be an indication for emergent coronary angiogram and percutaneous intervention."

So she went for emergent angiogram.


Culprit: 95%, severely calcific lesion in mid-LAD with TIMI-I flow on initial angiography.

No peak troponin was measured.  I suspect it was very high.

Learning Points:
1. Emergent angiography plus/minus PCI is indicated in OMI.
2. OMI can be diagnosed without the ECG: 
        a.) Refractory chest pain with elevated troponin is an indication for emergent reperfusion.
        b.) Persistent Chest pain and new wall motion abnormality is likewise and indication for emergent reperfusion.
        c.) Persistent chest pain and occlusion or near occlusion seen on emergent CT coronary angiogram
3. In this OMI case, as in most, the ECG showed OMI even if the physician cannot see it.  
4. "It is not the ECG that is nonspecific; it is the interpreter who is nonspecific."

See this abstract we wrote for the American Heart Association Meeting (the manuscript is under review):

Critical Result: Sensitivity, specificity, and accuracy of STEMI criteria vs Expert 1 for OMI among all 808 patients were 41% vs 86%, 94% vs 91%, and 77% vs 89%


  1. Our medical director (Paramedic FF Department) had a conversation with one of our cardiologists. I was able to provide questions. The response I got regarding why not use sgarbosa was responded with “sgarbosa is difficult for most physicians”. It would be great to have studies like this article using Paramedics showing that they can better recognize patients needing prehospital cath. Or maybe advocating for a prehospital ECG alert that is likely ACS. As it is, if it’s really obvious with good clinical correlation I just pretend not to see the LBBB so that our cardiologist can see the ecg when I activate via our cell phone app. They can shut it down there if they want.

  2. G’day,
    Great post and article! Quick question though, I’m a huge proponent of using OMI over STEMI, but if the outcomes are similar, is reaching the diagnosis 1.5hrs earlier using OMI as important as it intuitively seems?

  3. G’day,
    Great post and article, though I do have one question. I’m a huge proponent of OMI over STEMI, but if there’s no difference in outcomes, is diagnosing occlusion 1.5hrs earlier as beneficial as it intuitively seems? Or is it a case of more trials being needed to find the benefit?

  4. G’day,
    Great post and article, though I do have one question. I’m a huge proponent of OMI over STEMI, but if there’s no difference in outcomes, is diagnosing occlusion 1.5hrs earlier as beneficial as it intuitively seems? Or is it a case of more trials being needed to find the benefit?

    1. Any individual case has many variables. But if you had a large population of persistent occlusion, half with a delay of 1.5 hours and half without, the % who die in the delay group would be higher. Make sense?

  5. Paramedic here. How do you know that the complexes in V2-V4 are QS waves? Is it morphology? Poor R wave progression? Something else? I couldn't find a good definition/explanation online.

    1. QS-waves means a single negative deflection, without any R-wave or r-wave before or after that negative deflection.

  6. is there any significance to the t wave amplitude in II, III, and aVF? specifically, could it be indicative of a wrap around LAD and ischemia. this is a finding I see in several of your cases, but sometimes it seems I still appreciate something that isnt significant.

  7. Steve...

    This is the first time I have seen this formula used for something other than distinguishing between a ventricular aneurysm and an acute MI. Are others using it? Has its use in this manner been validated?

    Jerry W. Jones MD FACEP FAAEM

    1. Jerry, I think that is exactly what I did here. With QS-waves, one must entertain old MI. The large T-waves show that it is either acute OMI superimposed on old MI, or subacute OMI

  8. Steve...

    I understand what you are saying, but my question is whether or not a persistent ST elevation is required (i.e., ventricular aneurysm) to use this formula. That is the context that I thought this formula was used in. I see far more examples of this scenario than cases of persistent STE.

    1. Jerry, it's most important use is to differentiate patients with any ST Elevation who could have either LV aneurysm or acute OMI. If they have QS-waves, the old MI is quite possible. But our studies showed that all patients with QS-waves due to old MI have small T-waves. So it does apply here. --STeve


DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

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