Tuesday, July 1, 2014

Head On Motor Vehicle Collision. ST depression. Myocardial Contusion?

A woman in her 40's was involved in a head-on motor vehicle collision.  EMS noted a facial droop. On arrival she was hypertensive but other vitals were normal.  She did complain of back and neck pain, chest pain, and SOB.  She also had a facial droop as noted by medics.  This droop was apparently new.

An ECG was recorded:
This shows diffuse ST depression (diffuse subendocardial ischemia) in leads I, II, aVF an V3 to V6, with reciprocal ST elevation in aVR and V1.  This is diagnostic of subendocardial ischemia or injury.  

The ECG was repeated 36 minutes later:
The findings are improving


Is this:

1. Myocardial contusion?
2. Stress Cardiomyopathy?
3. ACS?
4. Type II (demand ischemia) from stable coronary disease with stress?

She was found on CT to have a subacute middle cerebral infarct.  Other workup and imaging did not show any serious injuries.

She was admitted and underwent serial troponins.  All were negative.  In fact, they were undetectable with the Abbott Architect (contemporary, sensitive, but NOT high sensitivity) troponin I.  Limit of detection (LOD) = 0.010 ng/mL.   All values were less than 0.010 ng/mL.

An ECG was recorded the next AM:
Finding are almost completely resolved, but there is residual ST depression


An echocardiogram was normal with an EF of 82%.

She underwent an adenosine nuclear stress test:

"Myocardial perfusion imaging with pharmacologic vasodilatation demonstrated small to moderate size, mild to moderate intensity reversible perfusion defect involving the distal myocardial segment of the anterior and anterosptal walls with minimal involvement of the apex. There was no breast shift artifact to explain the difference between the rest and stress images. There was 1-1.5 millimeter horizontal ST depression in the inferior and lateral leads during regadenoson (an A2A adenosine receptor agonist that is a coronary vasodilator) infusion along with some chest tightness, nausea, and diaphoresis that resolved during recovery. These findings are suggestive of possible flow-limiting lesion in the distal LAD territory."

This is a notable learning point, other than just ischemia: note that the ST depression was "inferior and lateral" but the ischemia by ultrasound was anterior!  This illustrates a well-known phenomenon that subendocardial ischemic ST depression does not localize.

Thus, she underwent angiography:

There was a critical 95% stenosis of the left main coronary artery.

She then underwent CABG.  The outcome was good.

Final diagnosis:

ST depression due to diffuse subendocardial ischemia triggered by stress in the setting of a very tight, fixed stenosis of the left main.  This was not ACS, not stress cardiomyopathy, and not myocardial contusion.


Lesson:

In spite of severe subendocardial ischemia of the entire heart, all contemporary troponins were negative. This highlights the importance of an ECG in trauma, and the importance of following up on the ECG findings in spite of negative troponins.  What would the result of high sensitivity troponins have been?  We have no idea.

This also shows how diffuse ST elevation with ST elevation in aVR is NOT due to Left Main occlusion.  It is due to left main insufficiency.  Occlusion nearly universally causes death and has the findings of simultaneous STEMI of anterior, lateral, and posterior walls.

For a detailed explanation of ST elevation in aVR, in both STEMI and NonSTEMI


9 comments:

  1. very nice case. It was the last DD in my differentiaL dignosis!!!!

    ReplyDelete
  2. what about a co-culprit cerebrogenic cardiac disfunction?
    literature reports various ecg changes (i would point to that upper limit PT and QTc prolongation) or ST abnormalities occurring in 22% 33% of patients with stroke.

    http://www.ncbi.nlm.nih.gov/pubmed/8316185
    http://stroke.ahajournals.org/content/5/6/775.full.pdf

    best wishes

    PS
    i did not get that memory T wave inversion

    ReplyDelete
    Replies
    1. when stroke causes these findings, it is generally a very large stroke. This was a very tiny one only causing some facial assymetry.

      Delete
  3. Dr Magnus ByrödJuly 3, 2014 at 2:29 PM

    Very interesting case. As i have understood it from dr Mattus blog, ST-elevation in aVR would suggest occlusion:
    http://ekgumem.tumblr.com/post/17948970835/lead-avr-deserves-your-respect-episode

    There is also quite a few referenses in the shownotes like Rokos supporting this:
    http://www.ahjonline.com/article/S0002-8703%2810%2900758-1/fulltext

    Am i missunderstanding this, or is it more a case of different opinions? Would be really interesting to hear your thoughts on this!

    ReplyDelete
    Replies
    1. This is a widespread misunderstanding throughout the literature. I am trying to dispel this persistent myth, that in fact is both wrong and makes no sense electrocardiographically.

      Read the last section of my article here. It is on ST elevation in aVR, in both STEMI and NonSTEMI:
      http://link.springer.com/article/10.1007/s40138-012-0003-1#page-2

      Let me know if the link does not work. It should.

      Steve Smith

      Delete
    2. Dr Magnus ByrödJuly 4, 2014 at 11:52 AM

      Thanks for the link, works fine!

      I guess the most important thing is what you do about these patients. Dr Mattu suggests urgent cath and that you stay of clopidogrel since there is a high chance of CABG, which seems reasonable. Would you send a patient straight to cath lab or try medical treatment first if they presented to the ED with this ECG and complaining of chest pain(without car accident)?

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    3. I think immediate cath is optimal, but if there are resource limitations, it is acceptable to try medical therapy first: aspirin, heparin, Nitro, GP IIb-IIIa. If ischemia persists, then cath. If chest pain and ST depression resolve, then put on continuous 12-lead ST segment monitoring and cath next day.

      Delete
  4. Can I suspect RV mi from the 1st ecg?

    ReplyDelete
    Replies
    1. Not in this case. You should suspect it if there is inferior MI, in which case STE in V1 is due to subepicardial ischemia beneath the V1 lead (of the RV). In this case, there is diffuse subendocardial ischemia, giving an ST depression vector away from lead V1, which causes reciprocal ST elevation in V1 !! (as well as aVR). Confusing, I know. I hope you understand my explanation.

      Delete