Friday, May 31, 2013

Woman in her 60's with 1 hour of chest pain

A woman in her 60's with h/o DM and HTN complains of 1 hour of sudden onset chest pain.  Here is her prehospital ECG:

Sinus rhythm.  Computerized QTc is 422.  What do you think?

There is ST segment elevation (STE) at the J-point, 1.0 mm in lead V2 and 1.5 mm in lead V3, relative to the PR segment (PQ junction).  This does not meet the most commonly used "criteria" for diagnosis of anterior ST elevation MI (see below).  So is this normal variant ST elevation?  Or is it abnormal?  Is it early repolarization?  Could it be anterior STEMI?

Remember that normal variant ST elevation is less common as age increases.

The standard "criteria" are (1): At least 2 Consecutive Leads With ST elevation of:
V1, V4-V6: 1 mm  
V2, V3:   for men over 40 yo: 2 mm
                for men under 40 yo: 2.5 mm
                for women, any age: 1.5 mm 

"The threshold value for abnormal J-point elevation in V2 and V3 recommended in that part is 0.2 mV for men 40 years of age and older and 0.25 mV for men less than 40 years of age. The recommended threshold value for adult women in V2 and V3 is 0.15 mV. The threshold recommended for abnormal J-point elevation for men and women in all other standard leads is 0.1 mV. These threshold values appear to be an appropriate compromise for practical clinical use in the evaluation of ST elevation."

We found these criteria to be very insensitive and nonspecific in differentiating subtle anterior STEMI from early repol.  However, if we use the formula for differentiating early repolarization from subtle LAD occlusion (see sidebar of this blog for excel applet), and use these numbers: 
1. STE at 60 ms after the J-point in lead V3 = 2.0 mm, 
2. QTc = 422 ms, and 
3. R-wave amplitude in lead V4 = 4mm, 
 --we get a value of  25.99 (greater than 23.4 correlates highly with LAD occlusion).  It is the relatively long QT interval and the low R-wave amplitude which make this likely to be STEMI.

Case continued:

The medics (and computer) interpreted the ECG as normal and brought the patient to the ED without alerting me.  By protocol, an ED ECG was recorded and this ECG was brought to me:
Now there is slightly more ST elevation, the QTc is slightly longer at 427ms, and lateral precordial T-waves are larger.
This is the first ECG that I saw and it is clearly diagnostic of LAD occlusion, with anterolateral STEMI.  I immediately activated the cath lab.  The formula value for this is now 27.2 (STE60V3=2.5, QTc=427, RAV4=3)

While waiting for the cath lab, we did a bedside echo and the anterior wall motion abnormality was very subtle and would not have helped with the diagnosis.

She went to the cath lab and had an ostial occlusion of a type III (wraparound) LAD to the inferior wall.  There was a large ramus intermedius (artery between the LAD and circ which functions like a large first diagnonal) which supplied the lateral wall.

Subsequent formal echo with Definity contrast showed an akinetic distal septum anterior and apex as well as akinetic distal inferior wall, so there was a dense MI.  The peak troponin was 257 ng/mL, so this was a large anterior MI.

The inferior wall involvement does not show on the ECG and I find this difficult to explain.

Here is the ECG 2 days later:
Interestingly, the T-wave inversion is consistent with only anterolateral (not antero-infero-lateral) MI.  And T inversions in I and aVL are present in spite of absence of clear evidence of injury on the previous ECGs.


1. Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized  Electrocardiology. J Am Coll Cardiol. 2009;53:1003-1011.


  1. Thank you for explaining the anomaly, very interesting.

  2. Steve- this is an excellent case. A few observations:

    You write "T inversions in I and aVL are present in spite of absence of clear evidence of injury on the previous ECGs".

    1. If you look closely there is indeed subtle ST-Elevations in I & AVL on the prehospital ECG.
    2. The T-Waves in the leads are clearly Hyperacute. The shear fact that they are upright given the remainder of the ECG (which is consistent with acute occlusion) implies direct injury. (as opposed to reciprocal hyperacute T-Waves that are inverted)
    3. In light of the above, the 3rd ECG makes complete sense in terms of global reperfusion T-wave morphology.
    4. I suspect there was no persistent lateral echo wall motion thanks to the Ramus Intermedius.
    5. I presume also that the akinetic distal inferior wall may not have large enough to cause inferior STEMI findings.


    1. Sam,
      I do not see any ST elevation on the prehospital EKGs.
      I think that the reason there is no ST elevation in either AVL or in III is that this was both inferior and high lateral. They cancel each other out.


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