Friday, March 3, 2017

Another 40-something with intermittent chest pain

I was sent this ECG by a resident from elsewhere, with the following information:



"Young previously healthy man with several 10-20 minute episodes of chest pain over the past few hours, asymptomatic on presentation and during this ECG."

"What do you think?"

There are Q-waves in V2 and aVL.  The T-wave in V2 is too large for this Q to be due to old MI.  There is minimal STE in aVL and a proportionally large T-wave, with a reciprocally large T-wave in lead III and a biphasic down-up T-wave in aVF.
There is some STE in V2 and V3, but this cannot be called normal variant because there is a Q-wave in V2 and poor R-wave progression.
All of these are very worrisome for LAD or D1 ischemia.


Here is my response:

"Old MI with superimposed LAD or First Diagonal acute ischemia.  Q-wave in V2, aVL suggest old MI, but T-wave is too large in both to be old.  Alternative is subacute MI of these vessels."

"Please send info."


Case:

This is a 40-something who complained of several 10-20 minute episodes of chest pain over the previous few hours.  He had no prior medical history, but is a smoker with a positive family history of CAD.  He arrived at 7:30 pain free and had this ECG recorded at 7:32.  I will repost it here:
See above description


The first troponin was undetectable (cTnT, < 0.01 ng/mL) and he was sent to the observation unit for serial troponins without recording any more ECGs.


Smith comment: this is not acceptable.  One should at least perform many serial ECGs to look for either resolution or evolution of these T-waves.  Since his pain had resolved and was still gone, one would expect resolution of the large T-waves and minimal ST elevation and this would be diagnostic.

Case continued:

At 8:30 he complained that his pain was returning and another ECG was recorded at 8:42:
This is slightly BETTER than the previous  There are smaller T-waves, and less STE in aVL, and the reciprocally inverted T-wave in III is not as deep.  The down-up T-wave in aVF is now all up.
This ECG represents dynamic ACS

--Proving that serial ECGs recorded in the ED would have shown resolution of the T-waves.  
--Now they are growing larger from what would have been seen on an intervening ECG 


The ECG was interpreted as No Change.


Case continued:

At 8:50 he had "seizure like activity" that resolved (probably an episode of pulseless VT) and was moved to the ICU, where he had this ECG:
Obvious proximal LAD occlusion (STEMI)



Here is his next 12-lead:
Ventricular Fibrillation is not supposed to be captured on a 12-lead ECG!


This is after defibrillation and the patient had a pulse and was awake:
Slow and sick!  Take me to the cath lab!!


This was recorded just before he was taken to the cath lab:


Here is the angiogram:
Proximal LAD occlusion


Here annotated with arrows:




Learning Points:

1. Real ECG findings of coronary occlusion can be extremely subtle!
2. Learn to recognize hyperacute T-waves.
3. Learn to recognize down-up T-waves
4. Learn to recognize the reciprocity between aVL and III
5. Troponins are not reliable for diagnosis of early ischemia/occlusion
6. There is still a role for observation!

4 comments:

  1. Very interesting case and many learning points, as always; thank you! I noticed in the last ECG, recorded before cath lab, ST elevation in lead II (instead of ST depression seen in the ECG showing clear STEMI) and ST-T anomalies resembling DeWinter. Did angio results show a wraparound LAD?

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    Replies
    1. Mario,
      I don't believe it was wraparound. I do think that on the 8:50 ECG, lead II looks like a de Winter's T-wave. Which is pretty interesting because that has only been described in precordial leads.
      Steve

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  2. Indeed very helpful case, and I probably would have missed this finding too. Great to learn from you!
    For your initial response ("Old MI with superimposed LAD or First Diagonal acute ischemia. Q-wave in V2, aVL suggest old MI, but T-wave is too large in both to be old."), is there a single finding you'd consider significant for acute ischemia, or is it the combination of hyperacute T and down-up T-waves? For those of us not seeing hyperacute T-waves on a daily basis, is there any guide you can give to e.g. differentiate from early repol in left vent. hypertrophy? And for the Q-Wave in aVL: I learned that Q-waves need to be in two contiguous leads to be considered "pathologic" (what aVL and V2 are not, as far as I know), but you consider this pathologic and are obviously right in the context of the angiogram. When do you start to consider a Q wave as pathologic?

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    Replies
    1. Not just a combination of hyperacute T and down-up T-waves. There is ST elevation in V2 and V3. Of course that amount of STE can be normal. But when it is normal, there are always well formed R-waves. In this case, there are not. In fact, V2 has a Q-wave. so it cannot be normal variant ST elevation!

      Read my paper here: http://www.annemergmed.com/article/S0196-0644(12)00160-6/pdf

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