"Seizure" in a 60 year old male

This 60 yo male had an apparent tonic clonic seizure.  He had no history of seizures.  He was unconscious for 8 minutes and slowly awoke in the ambulance, complaining of nausea only.  First responders found him to be very tachycardic, confused, perserverating and with no memory of the event.  There was tongue biting.  Lightheadedness continued.

The tachycardia was gone by the time paramedics arrived.

He had a prehospital ECG:

What do you think?

Interpretation.  There is terminal T-wave inversion in V2, highly suggestive of Wellens' pattern.  But syncope or seizure alone, without chest pain, is not enough to call it Wellens syndrome.  

There might also be some subtle ST depression, suggestive of de Winter or Precordial Swirl pattern.

Without chest pain, the pretest probability is not very high.

Here is the Queen's interpretation (the Queen always assumes a fairly high pretest probability of OMI):

This version of the Queen (version 1) does not differentiate between active and reperfused OMI.  So she will call Wellens' ECG "OMI".

With explainability:

She also sees that terminal T wave inversion.

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He arrived in the ED and had another ECG recorded because of the abnormal prehospital EKG: 

Here was the ED ECG:

Now: obvious classic Wellens' morphology Pattern A (terminal T-wave inversion), but only in lead V2.  

Upsloping ST segment with sharp downturn into negative T-wave.

Notice also the slight STE in aVL with terminal T-wave inversion, and reciprocally upright large T-waves in inferior leads.

Further review of systems with the patient fully awake revealed that the patient had been having chest pain on and off all week.

The ECG in the context of intermittent/resolved chest pain suggests proximal LAD lesion with open artery.  With the chest pain history, this is now Wellens' syndrome.  It is likely that the patient had ventricular tachyardia as a cause of prolonged syncope.  

Head CT was normal, as were electrolytes.

Here is the Queen of Hearts interpretation:

Again, this version of the Queen (version 1) does not differentiate between active and reperfused OMI.  So she will call a Wellens' ECG "OMI".

 Initial trop I = 1848 ng/L, up to 4533 at 6 hours.

Echo

The estimated left ventricular ejection fraction is 40 %. 

Regional wall motion abnormality-distal septum anterior and apex akinetic large.

Regional wall motion abnormality-distal inferior wall .

Angiogram

"Culprit Lesion (s): Uncertain culprit, as the myocardial territory served by the apical LAD is disproportionately large compared to troponin elevation. Diagonal branch supplying collaterals to the apical LAD could also represent a culprit."

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Smith comment: It is not contradictory to have a large territory at risk and a relatively low troponin when it is Wellens' syndrome.  This is a syndrome of spontaneous reperfusion and if the occlusion is of short duration, there is not a lot of infarction.  In Wellens' syndrome, there can be a huge territiory at risk and a troponin just barely elevated.

Here is a case in which the peak troponin was only 364 ng/L.  It can be much lower.

First ED ECG is Wellens' (pain free). What do you think the prehospital ECG showed (with pain)?

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Cardiology: culprits for the patient's non-ST elevation myocardial infarction and syncopal event with possible arrhythmic etiology include occlusion of the distal LAD (chronicity uncertain) and severe stenosis of the proximal first diagonal branch.

Successful PCI of the distal and mid LAD.

Successful PCI of the ostial/proximal first diagonal branch.

Excellent angiographic results with TIMI-3 antegrade flow throughout the LAD territory