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 due to stroke?
3. ACS?
4. Type II (demand ischemia) from stable coronary disease with stress?
5. Aortic dissection affecting both carotid artery and aortic coronary cusps?

--> 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.

ST Elevation in Lead aVR, with diffuse ST depression, does not represent left main occlusion

For a detailed explanation of ST elevation in aVR, in both STEMI and NonSTEMI, see the last section of this article I wrote on the ECG in ACS.