Epigastric pain radiating to the chest for 18 hours. ECG makes the Dx. Troponin makes the Dx. CT makes the Dx!

I was shown this ECG with no other information:

What do you think?
Hint: try to see through the artifact!

I answered immediately: “High lateral MI with posterior MI. OMI.” (Occlusion Myocardial Infarction)

I asked, “Did the patient present with chest pain?”

Here is the history: “A middle-aged male complained of about 18 hours of epigastric pain that radiated to the chest.  He also had an apparently new facial droop of equal duration.  A stroke code was called, NIH stroke scale was only 1, and attention was turned to the chest pain.”  BP was 148/83.

How did I make this ECG diagnosis?

There is subtle STE in aVL with reciprocal STD in II, III, aVF, and STD in V3 and V4.

While there are ECGs that have STE in aVL with reciprocal STD in II, III, aVF in the absence of OMI, they do not also have STD in right precordial leads.  Furthermore, the morphology here is perfect for OMI.

(See the bottom of the post for 3 ECGs from this week with STE aVL and STD III, for which my answer was “no ischemia.”)

They performed a point of care cardiac ultrasound (parasternal short axis):

What do you think?

Notice the upper right (septum) contracts much more vigorously than the lower right and right (lateral wall)

The physician did not appreciate this because he was thinking about the patient’s pain combined with the facial droop, and so he appropriately obtained a chest CT aortogram to look for aortic dissection.  It did not show dissection, but did show the following images of his heart:

LV on the right. Lower right wall has dark area where there is no contrast in the myocardium (no perfusion)

These show hypoperfusion of the lateral and posterior walls.
Dark areas have no contrast because they are not perfused.

Our radiology chief, Gopal Punjabi, is a CT genius.  He loves to use Spectral CT, and has a spectral CT blog: https://www.ctspectral.com/

He applied spectral CT:

Anterior is to the left, and posterior is to the right
See the dark parts of the posterior wall.  This means there is no contrast there.  It is transmural infarction.

He diagnosed acute MI from his CT reading room. 

For more cases of CT diagnosis of myocardial ischemia via perfusion defect (all by Dr. Punjabi), see here:

A middle-aged man with severe syncope, diffuse weakness

Case continued
At the very same time that the radiologist was calling to alert of acute MI, the first troponin I returned at 39.4 ng/mL (very high).  In almost any scenario, a troponin this high (even without the ECG and CT) should be considered diagnostic of OMI until proven otherwise by angiography.  The presence of acute refractory chest pain is an indication for emergent angiography regardless of the ECG or any imaging evidence of ischemia.

Could it be something else?  Possible, but unlikely.  Myocarditis, takotsubo, type 2 MI and others almost never have troponin this high.

IV nitroglycerine was started.  Aspirin and heparin were given.

A 2nd ECG was obtained later while the patient had ongoing pain:

OMI looks more obvious

Cardiology was consulted.

A second troponin returned at 55.6 ng/mL.  Pain continued.  A third troponin returned at 57.1 ng/mL.  Pain continued.

The ED physicians decided to give nitroglycerin.

The BP dropped to 96/54 and the pain did not go away (even though hydromorphone was also given — this can only do harm by masking the pain).  

A 4th troponin returned at 63.8 ng/mL and the patient was taken to angiogram.

At angiogram, he had a 100% occluded circumflex.

It was opened and stented.

The troponin peaked 2.5 hours after the angiogram, and 12 hours after arrival, at 135.6 ng/mL.  This is very high.

Echo next day:

Normal left ventricular size, mild concentric LV hypertrophy, and normal systolic function.
The estimated left ventricular ejection fraction is 60%.
Regional wall motion abnormality-inferolateral, hypokinetic.

(Fortunately, the patient’s EF remained quite good.)
Here is the post PCI ECG:
STE and STD remain

Learning points:
1. Learn to recognize STE elevation in aVL, with reciprocal STD in inferior leads.
2. Learn to differentiate it from look-alikes (see below)
3. Pay attention to perfusion of the heart with contrast on CT scan.
4. Very high troponin is almost always a type 1 MI due to OMI
5. Use echo to help the diagnosis.

High Lateral Mimics

Here is a previous post on STE in aVL, and when reflects high lateral OMI and when it does not
True Positive ST elevation in aVL vs. False Positive ST elevation in aVL

These are some other ECGs I was shown this week in patients with chest pain:

There is STE in aVL, with reciprocal STD in III
What do you think?

There is STE in aVL, with reciprocal STD in III. What do you think?

There is STE in aVL, with reciprocal STD in III
What do you think?

My immediate response to all was “normal.” And they were normal.  They just do not have the “look” of ischemia.  I’m sure Ken Grauer can tell us exactly what makes these non-ischemic when, in contrast, the one at the top of the post is indeed ischemic and we can recognize it as such.  All I can say is that they are a face I can recognize.

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