Tuesday, June 17, 2014

Dynamic T-wave inversion (apparent Wellens' waves), all troponins negative: Unstable Angina

This middle-aged woman presented with increasing intermittent substernal chest discomfort similar to her GERD, but not relieved by the usual therapies.  She was given an aspirin.  She had the following ECG recorded in the ED:
A very astute physician read this as "biphasic T-waves in V3 and V4."  There is also T-wave inversion in aVL.  This is very suggestive of Wellens' syndrome with a proximal LAD lesion.

A subsequent ECG was recorded:
Not much changed

The patient was admitted to observation.  Her troponins [Ortho Clinical Diagnostics, Limit of detection is 0.012 mcg/L, 99% reference value ("positive" troponin) of 0.034 mcg/L] were less than 0.012, then 0.015, then less than 0.012.  

The ECG findings were not commented upon by the inpatient team, and the patient technically "ruled out" for MI.  After a careful evaluation that did not suggest an ischemic etiology, she was sent home without a stress test and with a diagnosis of "reflux."

2 weeks later, the patient presented with the same symptoms, happening 5 times between 6 AM and noon, never lasting longer than 15-20 minutes.  Here was here initial ECG with pain:
This time there are full blown Wellens'-like T-waves in V2-V5, I, and aVL, nearly diagnostic of a proximal LAD stenosis.  

Then the pain resolved 25 minutes later, and this ECG was recorded:
There are PVCs, but the Wellens' T-waves have resolved.  This is typical of unstable angina: when there is infarction, the T-waves will evolve by becoming deeper and more symmetric over many hours' time.  See link below.

She was started her on heparin and eptifibatide.  105 minutes later (it is uncertain whether the patient had another episode of pain that she did not report). 
Wellens' waves are back

The next day at 7 AM this was recorded:
Wellens' T-waves are again less prominent

Troponins never became "positive:"  The first level was "normal," the second was "normal," then 3rd was 0.021, 4th 0.029, 5th 0.032, never climbing above the 99% reference value of 0.034 mcg/L.

Such a rise under the 99th percentile is highly suggestive of, but not diagnostic of, ischemia.  With contemporary troponins, the 10% coefficient of variation (10% CV) is not low enough to be certain that these are real differences, though they probably are.  High sensitivity troponins have very low 10% CV and can accurately measure changes below the 99% level. They may help diagnose unstable angina in the future.

Case continued

Later that day, the patient underwent an angiogram and had a 95% stenosis of the proximal LAD with thrombus, and another of the first diagonal off the LAD.  Both were stented.


This is NOT Wellens' syndrome.

In Wellens' syndrome, the T-waves are inverted when the patient is pain-free.  The underlying pathology is that during the pain, the artery was occluded and there was (unrecorded) ST elevation.  After reperfusion, when the patient is pain-free, if there is some infarction, the terminal part of the T-waves invert (Wellens' Pattern A).  Over time, the T-wave inversion evolves to become deeper and more symmetric (Wellens' Pattern B).

This case is distinct from Wellens' syndrome.  This ischemic T-wave inversion is during the most ischemic phase but without complete occlusion and ST elevation. The T-waves normalize when the ischemia resolves.  There is no evolution of T-wave inversion because there was little or no infarction.

Here is typical Wellens' evolution:


When these T-waves normalize, it is NOT pseudonormalization:

In this case, the T-waves were dynamic, inverting, then normalizing.  One might be tempted to call these normalizing T-waves "pseudonormalization."  But this term is the name for the becoming-upright of a T-wave when the artery is re-occluding.  See these posts:

In this case, the ischemia is resolving without significant infarction, so that the T-waves truly normalize.

1) Even ACS with negative troponins may be strongly suspected by ECG analysis.
2) Troponin rise and fall, even below the 99th percentile, strongly suggests ACS
3) Dynamic T-waves are an infrequent but potentially important sign of ACS.


  1. Nice case. Thank you. Were there also some parietal hipokinesia ? Very low troponin , could be explained by ischemic cascade? Do you use eptifibatide up-stream?

    1. Alenia, I occasionally use eptifibatide upstream if it is very high risk (like Wellens' is) AND the patient is not going immediately to cath. I'm not sure what you mean by "parietal hipokinesia" or "ischemic cascade". The low troponin indicates a very small amount of myocardial necrosis, but does not meet the standard definition of MI (at least one value above the 99th %ile.).
      Steve Smith

    2. send to: dr.smiths.ecg.blog@gmail.com Two things help it get posted: 1) it must be unique, interesting, accurate, 2) the more finished the product, the less work I have to put into it. My time is very limited and I can't put up as many posts as I would like, though I have endless material

      Steve Smith

  2. Alenia,
    I use eptifibatide in very high risk patients (like Wellens') who are not going immediately to cath. The low troponins were due to very small amount of ischemic cellular infarct (necrosis, death), but were not high enough to meet the standard definition of MI, in which at least one value must be above the 99th %ile.
    Steve Smith

  3. What if someone want to contribute to this blog ? or to send ecgs.

    1. send to: dr.smiths.ecg.blog@gmail.com Two things help it get posted: 1) it must be unique, interesting, accurate, 2) the more finished the product, the less work I have to put into it. My time is very limited and I can't put up as many posts as I would like, though I have endless material

  4. Dear dr. Smith,

    On a side note, is it true that 'inferior wellens' suggests near coronary occlusion of RCA/RCx? Thought you mentioned this in one of your blog posts, but I could'nt find it.

    Kind regards,

    1. Emil,
      Yes. I call them reperfusion T-waves. They signify previous occlusion with spontaneous reperfusion, at which time the T-waves turn down. This is the pathyphysiology of Wellens and it occurs in any coronary distribution.

  5. Hi dr Smith.
    Thank you for this great case as usual.
    Just one question: she is slightly tachycardic on both occasions. Do you know if there's any reason why? Ischaemia doesn't contribute to tachycardia.

    1. Thanks! Well, only tachy by definition if you use 90 as your cutoff. I usually use 100. But I agree that is a bit faster than most stable patients with ACS. And I don't remember the details of the case well enough now to answer.


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