Saturday, October 29, 2011

Wellens' syndrome, no culprit, what happened?

A 55 yo male with h/o smoking complained of 4 days of intermittent chest pain lasting up to a few hours each day.  He presented to the ED pain free and had the following ECG at 1332:

There is a suggestion of terminal T-wave inversion in V2, highly suggestive for early Wellens' syndrome.  There is T-wave inversion in I and aVL diagnostic of ACS.

The first troponin returned with "minor increase" on a qualitative troponin I, so another quantitative troponin was sent and it was elevated at 0.325 ng/ml.  The patient remained pain free.  Another ECG was recorded at 1555:
The T-wave inversion is more pronounced in V2, an evolution diagnostic of Wellens' syndrome.  TWI in aVL again is clearly ischemic.
See here for classic evolution of Wellens' waves.

The patient was admitted to the hospital late on a Friday, and put on antithrombotics and antiplatelet agents.  His troponin I peaked at 1.05 ng/ml that day.

On day 2, he had an echo which was suggestive of anterior wall motion abnormality.  He had no ECGs that day.

Sunday AM at 0800, he had another episode of severe chest pain, waxing and waning.  He had the following ECG recorded, and it is unclear whether he was having the pain at the time of the ECG.

Now there are deeper and more symmetric Wellens' waves.  Is this just evolution of the waves seen 2 days ago?  Or did something new happen?

Troponin rose again that day (day 3).  So the patient was taken to the cath lab.  He had no culprit, but a 50-60% narrowing of the proximal LAD.  Fractional Flow Reserve was performed across the lesion and it was 0.88 to 0.90 (negative, showing no blockage of flow).  Intravascular ultrasound revealed that the lesion had a minimal luminal diameter of 2.3 mm but a large plaque burden.  Nevertheless, it did not appear to the angiographer to be the cause of the symptoms.

The patient went back to the wards.  He had an identical episode of pain the next morning (day 4).  It turns out that the patient was on an ST segment monitor and it had not been checked on day 3 after the previous episode of pain.  So the interventionalist went and had it printed out.  Here it is, a 12-lead monitor strip:
Obvious anterolateral STEMI.

This illustrates what Wellens' syndrome is: it is always recorded when the patient is pain free, after an episode of chest pain.  The artery is always open but there is an LAD lesion that is at high risk of re-occlusion (as in this case).  Wellens' is the aftermath of occlusion that has reperfused.  The inverted T-waves are "reperfusion T-waves."

In this case there was no clear LAD lesion.  This was probably spasm, but could have been an unseen thrombotic event.  They went back and stented the LAD and all symptoms have resolved.


  1. GREAT case with typical superb Steve Smith meticulous follow-up with excellent teaching point at the end! ST segment monitor strips are truly impressive and establish without doubt your diagnosis. That said - I'll raise the point that the first two tracings above are subtle and perhaps less than diagnostic by themselves of Wellens syndrome. Lead aVL is clearly abnormal in both tracings - but the hint of T inversion in V1,V2,V3 is minimal (though present) and the slope of the downslope of the T in these leads isn't that steep on these initial two tracings. Lead I is nonspecific. So - clearly suspicious that something acute is going on given the history and lead aVL's appearance - and the 3rd and 4th tracings document in context and comparison that this was indeed Wellens all along. GREAT case! (as usual by Dr. Smith) - with to me important teaching points of how lead aVL is sometimes a key lead suggesting ongoing acute evolution (even when other findings are subtle/minimal) - and how great follow-up (per Dr. Smith) can be used to elucidate the fascinating evolution that unfolded in this case. THANKS for sharing!

  2. Dr. Smith,
    If we classify wellens sign as aftermath of reperfusion, why is that if there is wellens sign on ecg, it is obvious that LAD would be more than 50% blocked, we haven't opened the artery, stenosis is still there where as in anterior STEMi it occurs after we have already reperfused the artery.

    1. It takes greater than 80% narrowing to cause ischemia at rest. In Wellens', the artery was occluded, or nearly so, during the chest pain. It was occluded by thrombosis at ruptured plaque at the site of a stenosis. The thrombus lyses, but the stenosis remains and adequate flow is re-established, resolving the chest pain. But the plaque remains hot and at risk for recurrent thrombosis and re-occlusion.
      Steve Smith

  3. Dr.Smith
    Can we say that there are Hyperacute T waves in II , III , AVF which become somehow bigger from ECG1 to ECG3.This is more pronounced in III lead, esp. if we compare T wave to QRS complex and in the contex of T-wave inversion in I and AVL .And may be I am mistaken but there is a little bit of poor R-wave propagation from V1 to V3 .

    1. Viktor,
      The "hyperacute" T-waves inferior are not actually hyperacute T-waves. They are reciprocal to the reperfusion (inverted T-waves, and increasingly so) in the high lateral area. If pain is ongoing and inferior T-waves are becoming larger, then they may be hyperacute. If pain is waning or gone and inferior T-waves are enlarging, then they are reciprocally enlarged T-waves.