Wednesday, June 29, 2022

When Normal is only Pseudo-Normal, it can deceive the caregivers.

An Aussie friend down under sent me this case. 


A 70-something male presented with sharp stabbing central CP.  Here is the initial ECG with 7/10 CP:

Normal


The pain was resolving, and another ECG was recorded with 3/10 CP:

Normal, but compared to the first, the T-waves in V2 and V3 are not as tall.  Hmm.......


The pain completely resolved:

What do you think?







Now there is an all-but-diagnostic terminal T-wave inversion in V2.  This is very subtle Wellens'.


The patient then developed 8/10 stabbing CP again:

The T-wave in V2 is again upright, indicating re-occlusion of the LAD.  There is also less T-wave inversion in aVL, so it is likely a proximal LAD.  There are subtle ST-T abnormalities in III, V5, and V6 as well.  
This is "Pseudonormalization" because it looks normal but it is not!!

The patient again became pain free:

Now there are unequivocal Wellens' pattern A waves (terminal T-wave inversion, biphasic up-down) in V2 and V3.  The T-wave is again deeper in aVL

Here is the high sensitivity troponin I profile (99% URL = 20 ng/L):

0852    8

1215    10

1730     8

2030     12

0535     12


The patient had chest pain again at 24 hours after presentation:

On its own, this ECG appears almost completely normal (for those with sharp eyes, there is abnormal ischemic ST depression in inferior and lateral precordial leads.  However, compared with all previous ECG, the T-waves are now upright, and there is much more ST Elevation than on any previous ECG.
Thus: Pseudonormalization AGAIN!

There is again Reocclusion.  I don't believe this was recognized as Re-occlusion because another troponin was measured, which returned at 30 ng/L (now elevated).  

Then this was recorded at 26 hours, without any intervention:

The ST elevation is resolved.  The T-wave is now normal.  There are Wellen's inverted waves in aVL.

Fortunately, the LAD spontaneously reperfused.  Otherwise, there would have been a lot of myocardial loss.

Here is the angiogram:

The Proximal LAD has an ulcerated plaque with 90% stenosis and there is TIMI II-III flow.  
There was successful PCI.


Here is the entire progression again.  Be sure to click on the image to enlarge it!!




Learning Points

1. Wellens' is reperfusion of OMI

2. The artery is has "hot" thrombus which can propagate and/or lyse, over and over.

3. This is really a Transient STEMI (better: Transient OMI, as it never meets STEMI criteria!)

4. Wellens' implies some (sometime tiny) amount of myocardial loss (infarction) and therefore some change in troponin.  In this case, it did rise by 4 ng/L, which is a significant rise (i.e., not due to natural variation or laboratory imprecision), but it did NOT rise above the 99th percentile, so this was unstable angina, until the later re-occlusion at which point the troponin DID rise above the 99th percentile and it was a type I MI.

5.  The re-occlusion was missed because the ECG looks nearly normal during LAD Occlusion.  The best clue that it was occluded was to look carefully for the VERY SPECIFIC changes (some changes in ECGs are not specific, but this morphology is very specific!)

6.  Optimally, patients with Wellens' would go immediately to angiography, because that hot thrombus is a transient STEMI.  Transient STEMI frequently need to go to the cath lab in the middle of the night if they don't go immediately

See this post:

Timing of revascularization in patients with transient STEMI: a randomized clinical trial

7. If you don't take them right away, they should get continuous 12-lead ST segment monitoring.

See these posts:

Why we need continuous 12-lead ST segment monitoring in Wellens' syndrome






===================================
Comment by KEN GRAUER, MD (6/29/2022):
===================================
Illustrative case presented by Dr. Smith that emphasizes once again the following important concepts:
  • That part of the definition of Wellens' Syndrome requires a history of the patient having had chest pain — that has now resolved!
  • That there is a spectrum of ECG changes that may be seen with Wellens' Syndrome — including extremely subtle findings (as evidenced by the terminal T wave inversion in lead V2 of the 3rd ECG shown above). This could have been all-too-easy to overlook had the clinician not integrated the history with new development of this terminal T wave inversion at the time that the patient's chest pain had totally resolved!

  • Subtle cases like the one presented today "tell a story" — that may only become clear through sequential clinical correlation of serial tracings — in which the timing of ECGs — the presence and relative severity of patient symptoms — of serial troponin values (and of bedside Echo if done) — are all integrated.
  • Understanding all parts of the story explains how concepts such as "pseudo-normalization" of the ECG — and reocclusion of the "culprit" vessel — can easily be overlooked.

We have emphasized the importance of serial ECG comparison on numerous occasions in Dr. Smith's ECG Blog. For reference — I'll just cite 3 posts in which I focused on the "art" of serial ECG comparison in My Comment ( = the November 15, 2018 post — the June 28, 2018 post, in which Dr. Smith worked through another Wellens' Syndrome evolution  — and the August 20, 2020 post).
  • For clarity — I wanted to focus on just 1 of the 7 tracings shown today — which is the 4th ECG that was done (Figure-1). As discussed above by Dr. Smith — this 4th tracing was obtained in associated with the recurrence of chest pain (described by the patient as "8/10 and stabbing"). Without careful serial ECG comparison with the 3 previous tracings — the clinical significance of the ECG findings on this 4th ECG could easily be overlooked!
  • The fact that the patient's chest pain symptoms returned (with even greater severity than they had been) — in association with an element of "pseudo-normalization" (ie, the "tell-tale" terminal T wave inversion in lead V2 had been replaced by an upright T wave) — was diagnostic in this context of proximal LAD reocclusion.

The other point to emphasize about the ECG in Figure-1 — is that it is not a normal tracing.
  • Although there is no more than the most minimal ST depression — there is definite ST segment flattening — with an abrupt angulation at the junction of the flattened ST segments with the T wave that follows (RED lines in leads I,II; V4,V5,V6 in Figure-1). These are not normal ST-T waves.
  • What this ST segment flattening and angulation at the T wave junction means — is another matter. It depends. I've seen similar ST-T waves countless times in the thousands of primary care ECGs I interpreted in years past. By itself — it is purely a nonspecific finding, which can at times represent a subtle sign of underlying coronary disease — but at other times may be devoid of clinical significance.
  • That said — in the context of today's serial tracings — this ST segment flattening and abrupt angulation was clearly increased in ECG #4 compared to the 3 prior ECGs in today's case. Together with loss of the terminal T wave inversion in lead V2 of ECG #3 — this made for that many more leads in ECG #4 indicative of "dynamic" ST-T wave changes despite seeming "pseudo-normalization".

Figure-1: This is the 4th ECG shown in today's case — obtained shortly after the patient's chest pain returned (described as "8/10" and "stabbing" ).













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