Did the machine miss something big?

I'm going out on a limb here, since I don't have the cath report yet. But I'm getting it soon, so we will have some closure on this!

The case:
A 68 year old male called 911 for "10/10" chest pain, and took aspirin before EMS arrival. Nitroglycerin was given by the medic, but it dropped the BP. Some normal saline took care of that, and transport was expedited.

The first ECG:

Computer interpretation: "Widespread ST-T abnormality suggests myocardial injury/ischemia"

Literally seconds later, the monitor showed a burst of activity:

A repeat ECG then showed:

No further events enlivened transport to the tertiary-level, primary-PCI facility.

So what does the first ECG show?
This ECG suggests a proximal LAD occlusion in two different ways, and justifies cath-lab activation, in my view.

The first pattern is likely familiar to astute 12-lead ECG readers. There is widespread depression throughout the ECG (II, III, aVF, and V3-V6), and ST elevation in aVR. Such a pattern indicates either severe 3-vessel disease or severe occlusion of the left main artery.

The second indication of LAD occlusion is not as well-known. Note the upsloping pattern of ST depression in the precordial leads.  This is distinct from the horizontal or downsloping pattern that you often find with a posterior AMI.

For example, this posterior MI demonstrates horizontal ST depression:

Source

Another example of a posterior MI shows a downsloping pattern of the ST segment:

Source

By contrast, in our ECG we have a sharply upsloping ST segment. Furthermore, it terminates in a tall, fairly sharp, T-wave.

DeWinter "waves"
Back in 2008, de Winter and a few other authors described a ECG pattern that they had seen in 2% of anterior AMIs. Interesting, all of the patients with this pattern had occlusions of the LAD in the proximal region - a very serious blockage that could infarct a good chunk of myocardium.

[T]he ST segment showed a 1- to 3-mm upsloping ST-segment depression at the J point in leads V₁ to V₆ that continued into tall, positive symmetrical T waves. The QRS complexes were usually not widened or were only slightly widened, and in some there was a loss of precordial R-wave progression. In most patients there was a 1- to 2-mm ST-elevation in lead aVR

They offered 8 examples of the precordial ST-T pattern:

Interesting looking ST segments and T-waves! Comparing these examples to our patient, looking at a blow-up of the precordial leads:

Upsloping ST-segment depression? Check.
Tall, positive, symmetrical T waves? Check.
Loss of R-wave progression? Check.
Normal-width T-wave? Check.
ST-elevation in aVR? Check.

So even without the 20/20 hindsight that blogging affords me, I'm anticipating a proximal LAD occlusion.

The final ECG
It appears the ST segments have normalized - both the ST elevation in aVR, and the ST depressions in multiple leads have returned to baseline. Even though this spontaneous reperfusion is an encouraging development, the patient still requires emergent angiography in my opinion, given the high likelihood of a dangerous, unstable lesion.

The Bottom Line
There - you know what I know now. Do you see anything that points to an alternative diagnosis, another concomitant problem, or different management?

I'll dig up the final results, and and them in the comments in a few days.