Friday, May 6, 2016

Abnormal ST-T in V1-V3. What is it? Many interesting and informative twists to this case.

A middle-aged woman with a history of CAD and stents, but also a history of several subsequent visits for non-cardiac chest pain, called 911 for chest pain of 5+ hours duration.

The medics recorded this ECG at time zero:
Note the downsloping ST depression in V1-V3, with down-up T-waves in V2 and V3.

Down-up T-waves in right precordial leads during chest pain is likely posterior MI.

When I showed this to a resident, she asked if these are Wellens' waves.  I pointed out that Wellens waves are 1) up-down and 2) after resolution of pain.  And they indicated, of course, LAD thrombus with a reperfused artery (good flow), whereas this is indicative of no or low flow to the posterior wall.  I did add that subendocardial ischemia is also possible.

The medics gave NTG, and the chest pain resolved. This was recorded at time 12 minutes:
Now V2 and V3 have a long flat ST segment with a tiny upright T-wave.  This is also highly suspicious for posterior MI, probably resolving.
V5 and V6 appear to have smaller T-waves now as well.

The patient was brought to the ED, at which time she had pain again, and this ECG was recorded at time 30 minutes (nearly 6 hours after onset of pain):
New but subtle downsloping ST depression with down-up T-waves in V2 and V3.
Interestingly, limb leads are not very helpful here.

The patient's chest was quite tender, and the initial contemporary troponin was below the level of detection (0.010 ng/mL).

I activated our "Pathway B."  Pathway B is intermediate between "admit for serial troponins" and "activate the cath lab (Pathway A)".  That means I call the cardiologist on call, and he/she gets further evaluation going immediately.

The interventionalist came down immediately and talked to the patient, looked at the ECG, and decided to take her to the cath lab.


100% In-stent Occlusion of a large circumflex, easy to cross with wire.  There was no collateral filling.  A stent was placed.

However, it is very puzzling:

All serial troponins remained below the LoD!

But to the angiographer the lesion was not a chronic total occlusion.

The echocardiogram showed a new inferolateral wall motion abnormality, but it was only hypokinesis, not akinesis, and the EF was 60%.  One cardiologist did not initially see the WMA.  This suggests either ischemia with stunning (unstable angina) or small infarct.

Here is the post procedure ECG, 5 hours after PCI:
ST segments and T-waves are mostly normalized, supporting acute ischemia on the previous ECGs

The patient had no more of what she describes as her "heart attack" type chest pain.

This was recorded the next day:
Fairly normal

Coronary thrombosis is a Dynamic process!

The artery opens and closes spontaneously.  Thrombus propagates and lyses (remember there is endogenous tPA).  If the occlusion is brief, then there is no infarct and troponins are negative.  There might still be stunning from ischemia with a WMA.  Then if it occludes again just prior to the angiogram, the angiogram shows 100% occlusion, even if it has only been brief.

This appears to be a case of unstable angina due to coronary occlusion that was complete at the time of the angiogram, though opening and closing prior to the angiogram.

Alternatively (and I think less likely), it could be that she had her MI more than 2 weeks prior and all troponins are now negative.  The lesion might still be easy to cross with the wire.  She would have a wall motion abnormality.  However, with no collateral circulation and a total occlusion, there should be a dense wall motion abnormality (but it was not dense).  If this hypothesis is correct, then she was having post-infarct angina (but that begs the question of why?  Where was the new angina/ischemia originating from?)

Unstable angina still exists.  And it may have an occluded artery at angiogram.

My next post will show another example of unstable angina due to occlusion, with all negative troponins.

In our UTropIA study (see here at of about 2000 consecutive ED patients who had troponin ordered, we measured both contemporary and high sensitivity troponins (Abbott Architect Troponin I) and found that one of 9 STEMI patients (there were quite a few more patients who had ECGs diagnostic of occlusion but that did not meet STEMI criteria) had an initially undetectable high sensitivity troponin.  About half had an initial hs trop below the 99% reference value.


  1. Thanks a lot, what about ECG before angigram, 6 hours after chest is there new ST elevation in lead 1 and subtle elevation in AVL which resolve in ECG after angiogram ?

    1. Atif,
      I'm not convinced, but maybe.

  2. Thanks a lot, what about ECG before angigram, 6 hours after chest is there new ST elevation in lead 1 and subtle elevation in AVL which resolve in ECG after angiogram ?

  3. GREAT case. The “Pearl” (and the image to engrave in one’s memory) — is the biphasic T wave in leads V2,V3 (in the 1st ECG) when this picture is seen in a patient with new chest pain. THANKS for presenting.

  4. Hi Dr. Smith,

    Would it be accurate to say that both the T wave symmetry and size of the T waves in relation to the R wave amplitude/QRS voltage in leads II, III, and aVF are suggestive of inferior wall ischemia? When reading the first strips posted and noting the likelihood of posterior involvement my eyes immediately went to the inferior leads next, though I did notice there were no reciprocal ST changes in I or aVL.

    1. Eric,
      Good eye. Yes. And the repeat ECG pain-free shows T inversion in III.

    2. If I may add to Eric Jackson's astute observation that I was not initially impressed by the T waves in leads II and aVF in the 1st ECG at Time Zero — but, that in view of the clearly abnormal biphasic T wave in leads V2,V3 — in THAT context, more careful scrutiny of the T wave (esp. in lead II) — suggests it is probably a bit “fatter” at its peak and wider at is base than-it-should be given QRS amplitude in this lead (despite lack of anything definitive in aVL) — so a subtle-but-probably real finding (that is supported by subsequent serial tracings).

  5. Not only does unstable angina still exist, I think it's surprising how often the patients can present with frank ST-elevation ("injury") while they are having their ischemic symptoms. I haven't been around too long but I get the sense that even just 10 or 15 years ago most practitioners didn't realize that a good percentage of UA could present with ST-elevation. Back then a STEMI was a STEMI and pretty much only a STEMI could produce ischemic ST-elevation (excepting coronary vasospasm of course). I feel like people knew that UA could progress to STEMI but it wasn't commonly recognized that the reason why those patients were at high risk of that progression was because they were actually experiencing intermittent STEMI that just wasn't picked up. Am I understanding the tone of that time correctly?

    1. Vince,
      I'll show a great example of that in my next post.

    2. Vince — being "of that time" ... I know that in years past I did not pick up the often intermittent nature of spontaneous opening-and-closing that may repetitively occur during the course of an acutely evolving stemi ... By the meticulous nature of Dr. Smith's diligent work illustrating serial tracings on numerous actual cases in his various ECG Blog posts — what you say has become quite clear. THANKS Steve!

  6. It is fantansic,I have learnt a lot from you.

  7. Thanks Dr Smith ,I have been keeping on with your blog for one year and I have learnt a lot from you,
    I am your big fan in China. Thank you !
    About this post,I aslo have a differnet oppion about these ECGs .
    I truely agree that the most prominent changes lied in the V2-3 leads which is the reciprocal changes to the posterior hyperacte T wave and the some extent ST elevation ,but the T wave in I ,avL ,V5 ,V6 (dynamic changes)are all hyperacute T waves in my oppion; besides, the T wave change in III lead was discordant to the II lead .All above changes pointed to the culprit lesion LCA.


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