Sunday, January 31, 2016

The Electrocardiographically Silent Circumflex Artery

A 39 yo otherwise healthy man with no risk factors was walking at the mall when he developed chest pressure.  He presented to the ED after 30 minutes, now also feeling weak.  He was diaphoretic.  Here was his initial ECG:
There is sinus rhythm.  There is abnormal T-wave inversion in V2 which is abnormal and very suspicious There is minimal, nondiagnostic ST elevation in inferior leads with possibly a suggestion of reciprocal ST depression in aVL.  There are thin and normal inferior Q-waves. Thus, there are some suspicious abnormalities, but no definite signs of ischemia.   There is also minimal, nondiagnostic ST elevation in V5 and V6. 
Because of persistent symptoms, another ECG was recorded 30 minutes later:
There is only one new finding on this ECG which suggests ischemia.  It is very subtle but real.  What is it?  

See V3, where there is now some ST depression.  The previous ECG has a small amount of appropriate ST elevation in V3; any ST depression in a young male is abnormal, especially if changed from previous.  This is worrisome when combined with the abnormal T-wave in V2.

Let's look at both V3's, magnified:
The later ECG (bottom panel) shows minimal ST depression in V3.  The top shows minimal ST elevation (normal).  The difference is significant and highly suggests posterior ischemia.

This abnormality in V3 was apparently not seen by the treating MD, who is a nationally recognized expert in STEMI care (showing how difficult these diagnoses can be).

The initial troponin was negative. The patient was admitted to telemetry.  At 4 AM, his second troponin returned at 1.8 ng/mL.  Another ECG was recorded:
T-waves in V2 and V3 are now upright and larger, evolving. 
Are these posterior reperfusion T-waves?

He went for cath at 6 AM because of ongoing symptoms and a "positive" troponin.  He had an occluded OM-2 that was opened and stented.  

Troponin I peaked at 99 ng/mL (large MI)!

So this is a NonSTEMI, right?  Technically, yes, because there is not 1 mm of STE in 2 consecutive leads.  But the definition misses the point.  It is a coronary occlusion with a substantial myocardial territory at risk, that showed only very subtle ST changes.

Should you activate the cath lab for this?

Not from the ECG alone.  However, if you notice the ST depression, you then realize that this is ischemic chest pain, not esophageal spasm.  Once you know that the chest pain is ischemic in origin, and you cannot control it medically, then you must go urgently to the cath lab.

The patient should be treated with NTG, Aspirin (and clopidogrel, if your institution allows), metoprolol, antithrombotics, and GP IIb IIIa inhibitors.  If the pain persists, and the ST depression persists, then talk to your interventionalist immediately.

Here is the followup ECG:
The ST abnormalities have resolved.  There are new inferior Q-waves diagnostic of inferior MI.  The R-wave is increased in V2, consistent with posterior (now called lateral, to my dismay) MI (analog of a Q-wave).  There is no apparent resolution of the minimal and non-diagnostic inferior ST elevation.
Notice the T-waves are smaller in V5 and V6 now.

I don't have all the data on this case, and do not know if there is an inferior wall motion abnormality, or if this OM-2 supplied the inferior wall.  It  probably did, as evidenced by the Q-waves; but it is very interesting that during the acute phase, there were no diagnostic ST changes in inferior leads, and the minimal ST elevation that was present did not evolve.

Many MIs are electrocardiographically "silent," especially when in the circumflex territory.  I do wonder whether, in the studies that show this phenomenon, if an ECG expert evaluated the ECG for the subtle signs of ischemia.  I suspect that many or most that are thought to be "silent" are really just "subtle."  But many show nothing!

Here are more electrocardiographically subtle MI.

Why is the lateral wall, and the circumflex artery territory, electrocardiographically silent?

1. The lateral wall stretches far around to the posterior wall.  I, aVL, V5, and V6 just don't go posterior enough.  Posterior leads may help with this.
2. As you go lateral, the heart has more lung between it and the chest wall, so lead strength is buffered by air.

Anterior ST depression can help with assessing the posterior wall.   The combination of 1) accepting a lower threshold in lateral leads (0.5 mm), 2) considering ST depression in V1-V4 as posterior STEMI, and 3) using posterior leads at a threshold of 0.5 mm, will all improve the sensitivity.


  1. There were (almost) no changes in inferior leads. But the apparently reciprocal change in aVR was easier to spot. Or am I wrong trying to interpret this?

    1. aVR is the mirror image of an imaginary lead situated between I and II. So if you don't see any ST elevation in I and/or II, there is no ST depression in aVR. Remember that, among limb leads, only I and II are even measured by the machine. All the other limb leads are calculated ("derived") from I and II. Perhaps you are better at "seeing" ST depression that ST elevation, in which case aVR is more useful to you.
      Steve Smith

  2. ... 3) using posterior leads: why not here finally ?

    thanks Dr Smith (le meilleur)


    1. Al
      I can't answer that because I wasn't there. It might have helped, or might not. We'll never know.
      Better to recognize the new ST depression and realize that this is ACS. And that any ACS that can't be controlled medically should go to the cath lab.

  3. This case made me think a lot.
    I must admit I missed the V3 ST depression which is not normal in this context since we should expect a “male pattern” and thus the opposite.
    By the way, this MI is very large since maybe there is involvement of lateral wall since in ECG #4 the R waves in I, AVL and V5-V6 are lower in comparison with the first ECG. Isn’t it?
    A really very, very tough ECG.
    Mario Parrinello

    1. Mario,
      That is true, but could be due to lead placement.
      Steve Smith


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