56 year old male had 5/10 chest pain for several hours, then presented to the ED in the middle of the night with 1/10 pain.

A 56 year old male with PMHx significant for hypertension had chest pain for several hours, then presented to the ED in the middle of the night.

He reported chest pain that developed several hours prior to arrival and was 5/10 in intensity.  The pain was located in the mid to left chest and developed after riding his bike.   There was associated fatigue when symptoms developed and mild shortness of breath at onset of chest pain however that has since resolved.  

The patient states he experienced similar 7/10 chest pain 2 days prior when he had to hurry to catch the bus.  He states he experienced shortness of breath and chest pain with exertion and once he sat on the bus his symptoms slowly resolved. 

He presented on this day because it did not go away.

Here is his first ECG (1/10 pain):

Smith: sinus rhythm with RBBB and normal ST-T.  No ischemia.

An ECG from 4 years prior was the same.

The Queen of Hearts interpreted "OMI with Low confidence".  This surprises me, but the Queen often sees things that I cannot see.  On the other hand, I have also seen quite a few false positive Queen interpretations in the presence of RBBB.

The explainability map is here:

It seems that part of the diagnosis of OMI is due to T-wave inversion in V4 and V5.  In RBBB, the T-wave should be normally upright, so this is indeed abnormal.

Case Continued

The first hs troponin I returned at 139 ng/L.

Management: The clinical scenario with a troponin of 139 makes the diagnosis of acute MI.  However, I would not activate the cath lab immediately.  Rather, I would manage medically.  If that did not resolve the symptoms, then I would activate the cath lab.  In the absence of clear ECG signs of OMI, one should always start with aspirin and NTG, perhaps intravenous NTG, and see if the pain can be managed.  Do not give opiate analgesics!!  They only mask the underlying pathology.

Aspirin and heparin were given, but no NTG.

Case continued

Another ECG was recorded 3 hours later, still 1/10 pain:

There is sinus bradycardia with RBBB.  There is minimal STE in I and aVL, but this can be quite normal in RBBB.  There is some minimal reciprocal STD in inferior leads.   There is some STD in V1-V3, but this is normal discordant STD in RBBB.  There is minimal STD in V4-V6, but it does not have an ischemic appearance.  There is some non-specific new T-wave inversion in inferior leads; this could be due to inferior reperfusion.  But there are also new Q-waves, stronly suggesting new infarction.

Overall interpretation: this does not look like OMI to me.  

A bedside cardiac ultrasound performed by a true EM expert (Robert Reardon, who wrote the cardiac ultrasound chapter in Ma and Mateer) showed an inferior wall motion abnormality.

This is a conundrum, because it is clear that the patient is having an acute MI, the ECG is dynamic, but the pain is very mild and there is no ECG evidence of active transmural ischemia.  An inferior wall motion abnormality does NOT say that there is active ischemia because previous ischemia will result in persistent wall motion abnormality (stunning).  

We already know that the patient is suffering an acute MI.  We already know that the ischemia is ongoing, though mild (because of the persistent pain).

Only the ECG and presence or absence of pain can tell you what is happening right now.

Again, I would give NTG and re-assess.

Case continued:

A 2nd troponin I returned at 744 ng/L.  So we know there is myocardial infarction and the patient has persistent pain, but it is very mild.

A rising troponin does NOT mean that there is active ischemia.  Troponin tells you what was happening hours ago, not what is happening now.  Again, active presence of ischemia (or absence) and the ECG are the only evidence you have of the present ischemic condition of the myocardium.

Sublingual NTG was given and the pain completely resolved, from 1/10 to 0/10.

3rd ECG at 4 hours, pain free:

ECG is dynamic, since the ischemia is dynamic.  Q-waves are even more pronounced.

Troponin profile

See how the troponins rise even after 3 AM when the ischemia is apparently gone.

No further trops were measured, even after PCI

So we don't know how high they would have gone

Echo the next AM showed dense inferior WMA.

Angiogram:

Culprit for the patient's non-ST elevation myocardial infarction is a thrombotic occlusion of the proximal RCA

Incidentally noted mid LAD occlusion that is suspected to be chronic given heavy proximal calcification and relatively well-developed left to left collaterals.

The culprit was opened and stented.

Learning points:

You must remember that if someone has a brief episode of ischemia, or for a few hours, and then it goes away, that the wall motion abnormality will remain (the myocardium is “stunned”).  Of course if there is infarction, there will also be persistent wall motion abnormality.  Similarly, the troponin that was released during the ischemia will keep rising even though the ischemia is now gone.  

ONLY the ECG and presence or absence of pain tells you the ischemic state of the myocardium at any moment.

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