Dr. Smith's ECG Blog

Instructive ECGs in Emergency Medicine Clinical Content

Associate Editors:
— Pendell Meyers & Ken Grauer (2018)
— Jesse McLaren & Emre Aslanger (2022)
— Willy Frick (2024) — Sam Ghali (2025)

editors

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.

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):

Abstract 12682: Accuracy of Expert Electrocardiography versus ST-Segment Elevation Myocardial Infarction Criteria for Diagnosis of Acute Coronary Occlusion Myocardial Infarction

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%

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