Monday, August 7, 2017

A 50-Something w Chest Pain, Anterior STE, and no Evolution on 3 Serial ECGs over 30 minutes, (-) POCUS

This is a 50-something with no previous medical history who presented to triage at time zero after 3 hours of substernal chest pain associated with diaphoresis.  There was some positional component to the pain.  The pain was stuttering.  

Here is the initial ECG at t = 5 minutes:
computer QTc = 385
What do you think?
There was no old ECG available for comparison

There is ST Elevation in V2-V4, all consistent with normal variant (also called early repolarization) or with acute anterior MI. There is upward concavity in all of V2-V6, no terminal QRS distortion, no Q-waves, and no T-wave inversion, but there is suspicious ST depression in lead III, reciprocal to some STE in lead aVL.  

This ST depression is not diagnostic, but very worrisome.  

Lead V3 looks particularly worrisome for anterior MI, as the T-wave size is out of proportion to the QRS.  

If you apply either of the formulas (3- or 4- variable), they both come up negative because of the high R-wave voltage in V4.

The right thing to do is serial ECGs and immediate echo. 

A bedside echo was done but not recorded.  The interpretation was "without effusion, no large RV, normal aortic root / distal aorta."  Presence of wall motion abnormality was not commented upon in the chart, but the MD told me verbally that he did not see one.

 Here is the next ECG at T = 19 minutes:
computer QTc = 400
Not a lot of difference, and the formulas remain negative.

He was started on a nitroglycerin drip and the pain slightly improved.

Another ECG was recorded at T = 35 minutes
QTc = 383
Now there is some sagging ST depression in lead aVF, very suspicious

Troponin I drawn at t = 14 minutes returned T = 58 minutes with a value of 0.036 ng/mL (slightly above 99% level of 0.030 ng/mL).  A D dimer was negative.

This elevated troponin, in a patient with ongoing pain and a negative D dimer, is certainly enough evidence to activate the cath lab

Another ECG was recorded at t = 68 minutes

QTc = 387
This one finally shows some definite evolution, with increasing STE in V3

The cath lab was activated at this point, and a 100% LAD occlusion was found and opened and stented.

Here is the ECG the next AM:
Reperfusion T-waves, with persistent ST Elevation

The troponin peaked at 85.5 ng/mL

The next day echo showed EF of 56% with a wall motion abnormality of the distal septum, anterior wall and apex.

In writing this up, I found an old prehospital ECG that had not been found at the time:

There is nearly zero baseline ST Elevation.
There is no baseline inferior ST depression
Although even early repolarization can change some from month to month and year to year, this much change without ischemia is highly unlikely.

Learning Points:

1. Early repolarization and Anterior MI can look nearly exactly alike, even when the ST elevation is new and definitely the result of ischemia, as in this case.

2.  The formulas should mostly convince you that what you thought was early repol is in fact anterior MI.  They do have false negatives and it is dangerous to assume that, if negative, early repolarization is assured.

3.  Inferior ST depression is good evidence that anterior ST elevation is NOT due to early repolarization.

4.  While evolution of STE over the ensuing hour after the first ECG is strong evidence of coronary occlusion, the absence of evolution (though helpful) does not rule it out!  Other modalities (echo, troponin, and sometimes angiogram) are necessary.

5. Anyone with ST Elevation that is due to ischemia will have a wall motion abnormality. Since we now know that this was new, ischemic, ST Elevation, there had to have been a WMA!!  But it was not seen on the POCUS.  These may be very difficult to see, especially without contrast. 

That is why I always say that you must have a contrast exam done by an expert in order to rule out coronary occlusion.

False negative wall motion abnormalities:

1. Not done with contrast.
2. Not done by an expert.
3. Done after resolution of pain
4. Done after resolution of ECG abnormalities.
5. Coronary distribution is too small (new acute occlusion of a large epicardial coronary artery without collateral circulation will always produce a wall motion abnormality)

3. and 4.: Although the myocardium may remain stunned for quite a long time, it may also completely recover as the ischemia resolves and the ST segment recovers. Only trust the echo if it is done during the symptoms and ECG findings.


  1. > diaphoresis < -very bad, > ongoing chest pain < -bad, changing ecg's -not good even if subtle..
    old stuff doesn't change in front of you

    2 bads and a not good = issues

    2 of the most "in your face" signs & symptoms diaphoresis and persistent chest pain

    great case illustrating the importance of clinical signs and symptoms providing context
    and this picture sheds a lot of context on the ecgs and angio

  2. Thank you! Great case for sure. Oleg Lykov MD from Kyiv,Ukraine


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