Friday, April 14, 2017

What is the culprit artery? Not what you think.

An elderly woman who was quite healthy except for some chronic renal insufficiency and hypertension had 3 days of classic angina lasting only 10-15 minutes at a time, but which became more constant on the day of presentation.

She called 911.  Medics palpated a pulse of 80 and a BP of 140 systolic, and recorded this prehospital ECG (day 1):

Atrial Fibrillation at a rate of about 120.
Profound ST depression: leads I, II, III, aVF, V3-V6.
There is STE in aVR (reciprocal ST elevation, reciprocal to the ST depression)
This is classic diffuse subendocardial ischemia.

She was given a sublingual nitroglycerin and her BP dropped to 80 systolic.

On arrival, she still had chest pressure and this ECG was recorded:
Atrial fibrillation with rapid ventricular response
Diffuse ST depression, as with prehospital ECG

Is the ischemia a result of atrial fib with RVR, or is atrial fib with RVR just exacerbating ischemia whose source is acute coronary syndrome?

The history is highly suggestive of ACS.

The patient was given a diltiazem bolus and drip, her pulse slowed, and her chest pain completely resolved.  Another ECG was recorded:
Atrial Fib with a controlled rate
The ST Depression is mostly resolved with this slower rate

The first troponin was, not surprisingly, elevated at 1.07 ng/mL.  

The blood pressure was well maintained.  The patient was started on heparin and aspirin, and coronary angiography was planned for the next morning but also with plans to take her emergently to the cath lab if her pain recurred or if the ST depression recurred.

She did well overnight.  The troponin peaked on day 2 at 3.0 ng/mL (expected with complete resolution of ischemia -- this rise is due to ischemia that occurred before the rate control).

The ECG showed near complete resolution of ischemia on day 2:
Now converted to sinus rhythm.
Only minimal residual ST depression

Formal Echo showed a subtle inferior wall motion abnormality.

For various reasons, partly due to her calculated risk of angiography, she did not go to the cath lab that day.

The next day (day 3), the pain recurred and another ECG was recorded:
Inferior-posterior-and lateral subtle STEMI

At this point, she went emergently to the cath lab and had a circumflex occlusion with thrombus.

Comment 1:

You thought it was going to be LAD or Left Main, right?  It certainly could have been.  But it is important to remember that ischemic ST depression does not localize.  When there is diffuse subendocardial ischemia, it can be due to any culprit artery.  This is proven in stress testing, in which the location of the ST depression during stress does not predict the stenosed artery.  Why is this?  Uncertain.

In this case, the thrombus in the circumflex on day 1 was non-occlusive, resulting in subendocardial ischemia that manifested as ST depression in many leads.  It is tempting to say that the ST depression was "posterior STEMI" on these initial ECGs, but that is not so.  The ST depression was not V1-V3 (as in posterior STEMI), but rather V3-V6 (which is what is seen in subendocardial ischemia).  Furthermore, there was ST depression in I, II, III, and aVF.  The ST depression vector was inferior and anterior, with a reciprocal ST elevation vector that is superior (resulting in STE in aVR).

2 days later, when the artery completely occludes, real STEMI results, with an ST elevation vector towards inferior and posterior walls.  Complete occlusion reverses the ST vector! 

Comment 2:

This is a great example of how the dichotomy between STEMI and Non-STEMI is false.  They are both due to thrombus in the coronary artery and both are very dangerous.  STEMI and NonSTEMI exist on a spectrum.  Thrombus can lyse and propagate, and NonSTEMI can convert to STEMI.


  1. can we make electrical cardioversion first?

  2. Excellent explanation. Always loved the way you make ECG learning easy. Can you please through some light on Tombstoning Ecgs?


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