Chest pain and Transient ST Elevation

A 56 year old diabetic male with family history of young MI and prior CAD with stent was awoken by typical substernal chest pain.  He had this ECG recorded.   

Sinus Rhythm.  ST elevation with upward concavity in V1-V6.  Upright T in V1 > T in V6 (a soft sign of anterior STEMI, but also found in early repol in 14% of cases).  QTc is 411 ms.  RW in amplitude in V4 is 15.5 mm.  ST elevation at 60 ms after the J-point in lead V3 is 4mm (the first complex should be used because of downsloping baseline).  Plug these values into the formula at the right, and you get a value of 23.98, greater than 23.4 so very likely to be anterior STEMI.

Here are precordial leads enlarged:

Strictly speaking, the formula should not be used because there is terminal QRS distortion, which by itself makes STEMI almost certain: "Emergence of the J point ≥50% of the R wave in leads with qR configuration, or disappearance of the S wave in leads with an Rs configuration)"

They gave him nitro and morphine and his pain resolved.  The ED ECG is below, 27 minutes after the prehospital ECG, and few minutes after resolution of pain.  

Pretty much normal

The ED physician activated the cath lab and the cardiologists were in disagreement but took the patient to the cath lab.

He had a 95% thrombotic LAD that was stented.  Troponin I peaked at 2.4 ng/ml.

Here is his 30 hour ECG:

Sinus with PVC.  Classic Wellens' syndrome ECG

These things are clear: 

1. During the prehospital ECG, the LAD was occluded, or flow was limited to the point where there was ST elevation (injury due to subepicardial, transmural, ischemia)

2. The pain resolved (a key criterion for Wellens')

3. The repeat ECG was normal

4. The artery had clearly reperfused and had adequate flow to the anterior wall (another key criterion for Wellens')

5. The patient needed an angiogram and PCI at some point

6. The next day ECG was identical to Wellens' ECG

This is a great demonstration of something I have promoted for years, but without proof: 

That Wellens' syncdrome is the result of the aftermath of spontaneously reperfused LAD occlusion that went unrecorded during the episode of pain.  

This idea is supported by these characteristics of Wellens' syndrome:

1. Wellens' syndrome is always after resolution of pain

2. There are always preserved R-waves

3. The LAD is always open, or there is good colllateral flow

4. The T-wave inversion of Wellens' is identical to the pattern of T-wave inversion that occurs after therapeutic reperfusion of LAD occlusion.

    See this study by Doevendans et al.

    See this study by Wehrens et al.

5. Cases like this

Emergent Cath Lab Activation Questions

1. Should the cath lab be emergently activated for Transient ST Elevation?  

2. Should it be activated emergently for Wellens' syndrome?

I don't think there is any evidence-based answer to these questions.  I would argue that Wellens syndrome is a result of transient ST elevation that was not recorded.  However, the artery is open.  Both conditions are very high risk for re-occlusion.  

The standard answer for someone who had that ST elevation recorded (Question 1), as in this case, is to go to the cath lab.  Here is what can happens if you make the mistake I did and do not activate the cath lab.

The standard answer for Question 2 would be "No", but I would argue strongly that it is very high risk and it requires maximum antiplatelet and antithrombotic therapy and continuous 12-lead ST segment monitoring.  One cannot depend on symptoms to guide the recording of subsequent ECGs, and I will show an example of this in the next post.