This is really good Prehospital, ED, and Cardiology care. Inferior de Winter's T-waves.

A 50-something y.o. male with history of previous acute MI and stent was shoveling snow.  Shortly thereafter he had the onset of tight chest pain across the front of his chest, without radiation, but associated with diaphoresis and nausea without vomiting. It felt similar to his prior heart attack 9 years ago. He called EMS immediately. 

Here is his first prehospital ECG: 

What do you see?

There is ST depression maximal in V3, and also in inferior leads.  There is minimal T-wave inversion in aVL, by itself a soft sign of inferior MI.  Are the T-waves large?  Does this inferior ST depression with large T-waves represent inferior de Winter's waves?  

So this is an inferior-posterior OMI, very subtle.

Inferior De Winter's waves have been reported before by Sunil Karna

The medics immediately recognized ischemic ST depression. They gave aspirin and sublingual nitroglycerine.  The pain resolved and they recorded another ECG:

The ST depression is gone.  

In fact, one might not have recognized those hyperacute T-waves on the initial ECG until comparing with the next resolved ECG, where the inferior T-waves are now much smaller than they were.  

The T-wave inversion in aVL is also gone.

Medics recognized that this was an acute MI and alerted the ED, even though they did not activate the cath lab.

Thus, when the patient arrived, cardiology had been notified and was in the ED when the patient arrived (it was a weekday during daytime hours).

Another ECG was recorded in the ED:

Completely normal

The initial troponin was below the Limit of Detection.

The ECGs were inspected by the team and the cardiologist, and the cath lab was activated. 

Heparin and ticagrelor were administered. 

Dynamic ST-T changes are a sign of unstable thrombus that is at risk of occluding at any moment!

Angiogram:

Culprit is 99% thrombotic stenosis in the proximal LCX at the take off of OM1.  It was opened and stented.

Also: Co-Culprit is 95% stenosis in the proximal RCA.

LCx: LCX is a Large vessel.

LCX is a co-dominant vessel.

Which wall was affected?  It was the inferior wall.  Both the circumflex and the RCA supply the inferior wall, and they were co-culprits.  There were hyperacute T-waves, and ST depression in inferior leads during ischemia. 

So that initial ECG is manifesting inferior de Winter's T-waves.

Again, these culprits are at risk of re-occlusion at any moment.  But rapid recognition and treatment prevented such an outcome.

Troponin profile (contemporary 4th generation Abbott Architect, URL = 0.030 ng/mL):

Troponin results return approximately 1 hour after the time listed.  Therefore, you can see that, if they had waited for troponins, it would have been 4 more hours before the diagnosis of acute MI would be made.

Had an iSTAT troponin been used, it would have been 7 hours, as its URL is 0.080 ng/mL.

Here is the next day ECG:

No change

Echocardiogram done that day:

The estimated left ventricular ejection fraction is 64%.

There is no left ventricular wall motion abnormality identified.

Almost zero damage done to the myocardium!  By either troponin or echo.

Meyers comment: This is what near-perfect care looks like for Occlusion MI. If everything is done perfectly and immediately, often there would be no such thing as STEMI because it would never get to that stage, but instead would be prevented from happening altogether, as in this case.