Friday, March 14, 2014

Pseudonormalization of Wellens' Waves

A male in his 60's complained of intermittent chest pain all day.  He was vague as to whether there was active chest pain, but it was definitely better at the time I talked to him.

Here is his initial ECG:
There is minimal ST elevation and there are subtle T-wave inversions in V2-V5, highly suggestive of Wellens' syndrome.  
Is the ST Elevation normal? Very low R-wave amplitude suggests NOT.  See formula here:

The QTc was 380
ST Elevation at 60 ms after the J-point in lead V3 = 1.5 mm
R-wave amplitude in V4 = 2.5
QRS V2 = 15.5 mm
3-variable formula = 23.4 (equals cutoff of 23.4, consistent with LAD occlusion)

4-variable formula = 18.34 (above 18.2, consistent with LAD occlusion)
In Wellens' syndrome, the artery is open.  T-wave inversion, as I've pointed out countless times (and hope I'm not belaboring) is indicative of reperfusion of the infarct-related vessel.

So this, along with the resolving chest pain, appears to be a reperfusing LAD occlusion.

BP was elevated, pulse lowered to 45.  He received ASA, Plavix 600mg, Heparin, and a Nitro drip.

As a matter of course, I ordered another ECG 15 minutes later:
The increasing T Wave inversion is Diagnostic of LAD ACS.


Once the diagnosis is made, the patient must go to the cath lab if pain cannot be controlled or the ECG shows any evidence of re-occlusion.  Re-occlusion is diagnosed by pseudonormalization of the T-wave (becoming upright).

Then the patient stated his pain was increased to perhaps 4/10.

I ordered another ECG:
The T-waves are now upright and there is slightly more ST elevation (though this by no means meets "STEMI" criteria - these critieria are very insensitive for LAD occlusion)If you apply the early repol/LAD occlusion formula (see sidebar Excel applet), using a computerized QTc of 413, the value is 26.6, which is significantly greateer than 23.4 and confirms the diagnosis of LAD occlusion.

I immediately activated the cath lab.  Because this was a highly unstable lesion, in discussion with the interventionalist, we gave a load and drip of eptifibated (Integrilin).

A bedside Echo of course showed an anterior wall motion abnormality.

His pain again subsided.

A 4th ECG was recorded, pain free:
Reperfusion T-waves are again present.





The artery is open again.

The patient went to cath and had a distal LAD 99% stenosis with thrombus and TIMI-2 flow.

Initial troponin I returned at 1.5 ng/ml.  Peak was 8.1 ng/ml.



Lesson:

1. Pay attention to T-wave inversions
2. Obtain serial ECGs
3. Patients with objective evidence of ACS whose pain and ECG abnormalities cannot be controlled must go for emergent PCI
4. LAD occlusion may be very subtle, with minimal ST elevation
5. T-wave inversion is a sign of reperfusion and open artery.
6. Normalization of T-waves in this context is "Pseudonormalization" and is diagnostic of re-occlusion






9 comments:

  1. I promise that you're not belaboring this discussion, the principles of reperfusion and re-occlusion need continuous emphasis!

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  2. Does the ECG show RBBB?(and if so, does it have any clinical relevance in this pacient?)

    ReplyDelete
    Replies
    1. There is an insignificant incomplete right bundle branch block.

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    2. So, does that mean the inverted T wave in V1 is a normal variant or is it related to Wellens' syndrome?(because in the first ECG you state there is T wave inversion in V2-V5).Also the amplitude of the T-wave inversion in V1 doesn't seem to change from the first to the second ECG.

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    3. T wave inversion in V1 is normal

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  3. If TWI represents reperfusion, how should we interpret the T-wave inversions typically seen in aVL in the early course of an inferior infarct?

    http://ekgumem.tumblr.com/post/84127411939/whats-a-better-predictor-of-acs-than-the

    ReplyDelete
    Replies
    1. Great question. The T-wave inversion in lead ABL in inferior my is reciprocal to a hyperacute T-wave in lead three. In this case, it does not imply reperfusion.

      Delete

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