Thursday, January 22, 2015

Subtle Anterior STEMI Superimposed on Anterior LV Aneurysm Morphology

A male in his early 30s was playing soccer when the ball hit him in the chest.  At some point after this, he began having chest pain.  The pain radiated into the L arm, and was 8/10 in severity. The pain was similar to pain he had with a previous STEMI, for which he received a bare metal stent in the LAD a couple years prior.  He was on no medications.  
BP was 160/100. 

Here was his first ED ECG with 8/10 pain:
There is sinus rhythm.  There is minimal ST Elevation in anterior leads.  There is a QS-wave in V2, due to the old anterior MI.  The T-wave is taller than expected for old MI.  In V4, the T-wave size is far out of proportion to the QRS.  There is minimal STE in aVL with reciprocal ST depression in lead III.

Here is the last ECG from 3 years prior:
There are QS-waves in V2 and V3.  The terminal part of the T-wave in V3 is inverted, and the T-wave in V2 is not tall.
This is typical of LV aneurysm morphology (persistent ST elevation after previous MI)

We have derived and validated a rule to differentiate "LV aneurysm" ST elevation from STEMI (just finishing validation manuscript).  The rule depends on the principle that acute STEMI has a tall T-wave and LV aneurysm does not.  There are two versions:

In the first rule, if there is any single T/QRS ratio in V1-V4 that is greater than 0.36, it is likely STEMI:  for the ECG from 3 years prior, that would be lead V2.  At 5mm/21mm, the ratio is less than 0.36 and would indicate LV aneurysm.  But for the first acute ECG above, lead V2 is 8.5/15 which is 0.56 and would NOT indicate LV aneurysm.

In the second rule, one takes the sum of T-wave amplitudes in V1-V4 and divides by the sum of the QRS amplitude in V1-V4.  A value less than 22 indicates LV aneurysm.  In the second ECG from 3 years ago, that comes to 10/47 = 0.215, consistent with LVA.


Records showed that his STEMI was anterior and resulted in an EF of 40%, an anterior wall motion abnormality, and peak troponin I of over 100 ng/mL.

He was given sublingual NTG with some pain relief.  Here is the second ECG 13 minutes after the first, with 6/10 pain:
There is decreasing T-wave amplitude, consistent with some reperfusion.  

The cath lab was activated.  The interventionalist did not think the ECGs were different from before, but he was glad to take the patient for an angiogram.

In the meantime, the patient was given aspirin, clopidogrel, and a heparin bolus.  While waiting for cath, a NTG drip was started.

At 27 minutes after the first ECG, the patient had 5/10 pain on a Nitroglycerine drip at 200 mcg/min, with a BP of 130/80, and had this ECG recorded:
The T-waves are beginning to invert.  This is consistent with some reperfusion.


There was an in-stent thrombosis in the mid LAD with with 90% thrombotic occlusion and an embolism to the distal LAD.  Plain old balloon angioplasty (POBA) was performed, and the patient was put on aggressive antiplatelet and antithrombotic therapy.

Here is the post cath ECG:
T-waves are fully inverted now.

The troponin peaked at 12 ng/mL (not very high).  The formal echo showed dense anterior, septal, and apical wall motion abnormality, with an EF of only 29%.  This probably indicates "stunning," and there will probably be recovery of wall motion and EF, as reperfusion was quick.

Stunning may take up to 6 weeks to recover.

Learning Points

1. T-wave height correlates with acute infarction.
2. Absence of tall or large upright T-waves in the presence of QS-waves correlates with large old infarction, or LV Aneurysm morphology.
3. Acute STEMI can be superimposed on LV aneurysm morphology.  When it is, the T-wave turns upright with higher amplitude.  


  1. what is the cause of this patients old STEMI and now in stent thrombosis? he is in his early 30s...

  2. GREAT case that is highly insightful for SEVERAL reasons:

    i) Hard to believe the cardiologist did not think ECG-1 was different from ECG-2 (which was the baseline from 3 years prior). There should be NO DOUBT that there are acute changes on ECG-1! Simple lead-by-lead comparison in the chest leads shows MARKED increase in T wave amplitude in virtually all leads despite no more than minimal difference in r wave progression. As per Dr. Smith - these tall upright T waves are clearly worrisome because they are relatively "fat" peaked T waves. In addition, there is: i) a different kind of ST elevation in lead aVL (still shows the residual Q wave - but now with a similar upright hyperacute T wave as in the chest leads); and ii) there is clearly reciprocal ST depression in BOTH leads III and aVF which was not present 3 years earlier - AND lead II is ALSO different (it is now showing a straight ST segment that previously was rounded). Taken together in a patient with new chest pain - these changes are diagnostic of a new event.

    IN AIDDITION - I find it fascinating that in ECG-1 - there is a NEW sharp r' deflection after the QS in both lead V3 and V4 that was not present 3 years earlier - AND which goes away in later ECGs after acute reperfusion. My "theory" is that this r' deflection is real and perhaps reflects a similar phenomenon as is seen with DeWinter T waves. There isn't the usual J-point depression of DeWinter T waves (because the J-point "baseline" from the LV aneurysm is elevated) - but there IS a sharp dip after the r' that then rises to disproportionately tall T waves from this patient with acute LAD occlusion.

    THANKS for presenting! - :)

  3. He was in his 20's when he had the first STEMI. It is a common myth that young people don't get atherosclerotic plaque rupture with MI. But they do. Just not as commonly as older people. He had no risk factors.

  4. Did the chock with the ball make the rupture of the plaque and then the new MI ?
    Thanks a lot for your incredible blog, always so useful !

    1. It has to be a coincidence! You just have to be careful with these so-called "red herrings"!


  5. Steve,
    I find evolution of T-waves in the peri-occlusion setting to be very fascinating. That subtle terminal T-wave inversions in V2 + V3 on the 3rd ECG during this present visit do appear to be a sign of reperfusion (vs just on-going, persistent, fixed occlusion), since the ST-Elevation in V4 has lessened, the size of the T-Waves in V4-V6 have diminished, as have the T-wave amplitudes in I & AVL(as well as the T-wave morphology in these latter two leads)

    Another great case!


  6. Great post.
    Good analysis Ken

    1. @ AKS — THANK YOU. Glad this was helpful — :)


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