Wednesday, March 20, 2013

Septal STEMI with lateral ST depression, then has collateral reperfusion resulting in Wellens' waves

A middle-aged male presented with 1.5 hours of 8/10 chest pain associated with diaphoresis and vomiting.  He has a prior history of untreated hypertension and hyperlipidemia, and is a current smoker.

He called 911. Prehospital vitals were normal, and there was no change in pain with 2 sublingual NTG.  Here is his first ED ECG, at time zero. The preshospital ECG was identical and the computer in both cases read "nonspecific ST-T abnormalities."
Zero hours.  There is STE in V1 and V2, and ST depression in I, aVL, V5, and V6.  Is it normal variant STE?  Or is it anterior STEMI?  As in a recently posted case, ST depression in the lateral leads should not be seen in normal variant STE.  Because of this ST depression, STEMI should be diagnosed until proven otherwise, and the STE equation should not be used; if it were used, with STE60V3 = 2, QTc = 412ms, RAV4 = 20mm, the value would be 20.18 (less than 23.4 would indicate normal variant).  The equation is falsely negative because most of the ischemia is in the septum, not the anterior wall, so that STE in V3 is not high and R-wave amplitude in V4 is not affected.

In this case, there was a previous ECG to compare with (and the patient's last echocardiogram was totally normal as well)

Previous ECG had no ST elevation or depression.  This confirms that the STE is new ischemia and that this is STEMI.
The STEMI was not recognized, the patient was put on a nitroglycerine drip (as well as aspirin, heparin, and clopidogrel), and pain continued.  A subsequent ECG was recorded at 1 hour:
1 hour.  The T-waves in V1-V3 are inverting and in V4-V6 are flattening.  This is some evidence of reperfusion; is it Wellens'?

The ECG has the appearance of Wellens' waves, but the patient is not pain free, so it is not Wellens' syndrome.  Continued pain in the context of definite ischemia is an indication for urgent angiography and PCI.

The patient was still having pain after up-titration of nitro when this ECG was recorded at 2.5 hours after presentation:
2.5 hours.  Wellens' waves are evolving.
Rather than going urgently to the cath lab, an immediate echo was recorded, which showed moderately decreased LV function with an EF of 40%, and a new wall motion abnormality of the distal septum, anterior, and inferior walls, and apex.

The patient was taken for angiogram which showed total occlusion of a type III (wraparound) LAD at the takeoff of a large 1st diagonal.  However, the LAD was filling via left to left and right to left collaterals.  The LAD was opened and stented.

The troponin I peaked at 40 ng/ml.  The collateral circulation explains the Wellens' waves, but it did not fully restore perfusion and so the patient had continued pain.  Collateral circulation was likely fostered by nitroglycerine.

Here is the ECG after intervention

Full evolution of Wellen's waves to "type B" deep symmetrical waves.


  1. What if this exact ECG with similar history was seen in an older patient with longstanding hypertension? In such a case can we attribute such changes in lateral leads as strain equivalent changes of possible LVH? What about using STe/S wave ratio for possibility of LVH? Gives value greater than 25% in V3 = occlusion..?

    1. If it were due to LVH in ANYONE, there would have to be high voltage. By the way, the 25% rule of Armstrong does not work. Read this:


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