Submitted by Alex Bracey, with edits by Meyers and Smith
A man in his 50s with history of type B aortic dissection with prior TEVAR experienced acute onset chest pain at rest and presented to the Emergency Department.
Here is his ECG on arrival:
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| What do you think? |
Here is a prior ECG on file (presumed baseline):
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There is sinus rhythm with minimal STD in V5, V6, II, III, aVF. There is the tiniest amount of STE in aVL, but the T wave is not hyperacute (instead there is a terminal inversion). I would call this ECG consistent with subendocardial ischemia, but also the question of possible high lateral OMI (for which I am not yet convinced and would need serial ECGs, echo, etc.).
The team was worried foremost for possible aortic dissection given his history and presentation. He was neurologically intact with ongoing pain, without obvious vascular signs.
A CT aortogram was performed and is shown below:
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| This was read as an acute type A aortic dissection. |
He was transferred to a surgical center for management.
On arrival he complained of increasing chest pain, and a repeat ECG was ordered:
This ECG shows interval increased severity of diffuse subendocardial ischemia (non-occlusion ischemia). There is now STD from V3-V5 (maximal in V5 slightly greater than V4), as well as leads I, III, aVF, I (maximal in II), with obligatory reciprocal STE in aVR. I see no signs of superimposed high lateral OMI which we were considering from the first ECG.
Knowing that the patient has aortic dissection, the most likely explanation is that the dissection is involving, but not fully occluding, the left main (or potentially both left main and RCA). Potentially this supply/demand mismatch could be due to increased demand from hypertension, pain, etc., but typically these etiologies alone would not produce the severity of ECG findings seen above.
He underwent surgery and survived.
See many more cases of diffuse STD with reciprocal STE in aVR:
See many more cases of diffuse STD with reciprocal STE in aVR:
"I would call this ECG consistent with subendocardial ischemia, but also the question of possible high lateral OMI (for which I am not yet convinced and would need serial ECGs, echo, etc.)."
ReplyDeleteI'm surprise about the conclusion. I see quite enough STE in I / AVL and mirror effect in inferior to call an OMI.
What I see is
Maybe you're right? These are difficult and I've been wrong before in every possible way on cases like this. In my opinion there are subtle LAD/LCX subtotal occlusion patterns that have both a tiny vector of OMI findings, superimposed on simultaneous diffuse subendocardial ischemia, which could look just like this case at first. The STD vector includes II, III, aVF, V5, V6, and could conceivably have some reciprocal small STE in aVL (I cannot tell which is primary vs secondary). I would not have been surprised if the serial ECGs had indeed developed into high lateral and or anterior clear OMI. But in real practice I don't think I would have called the first one specific for high lateral OMI (but I work in a system with absolutely zero tolerance for any false positive activation, zero tolerance for the idea of an NSTEMI who needs the cath lab, etc. In Steve's hospital the mindset is very different). Also, I am of course biased now because I know the outcome. Thanks for your comment!
Deleteexcellent case, and presentation, Alex! thank you all three.
ReplyDeletetom