Inferior ST depression in ACS is reciprocal to ST elevation in aVL

For this topic, see also this post: http://hqmeded-ecg.blogspot.com/2009/01/st-depression-limited-to-inferior-leads.html This 72 yo male with h/o HTN, hyperlipidemia, and CAD, and h/o 4-vessel CABG 17 years prior presented with 8 hours of substernal chest pain radiating to upper back. Here is his initial ECG:

Notice there is ST segment depression in II, III, and aVF. The QRS is normal, so any ST segment abnormality cannot be blamed on the QRS (i.e., ST depression is "primary", not "secondary," and the ddx of this is ischemia, hypokalemia, digoxin, and normal variant). The ST depression is somewhat "scooped" in appearance, suggesting hypoK or digoxin, but the QTc is 423 ms, so hypokalemia is unlikely (usually > 450 ms) and the patient was not taking Digoxin.

ST depression of subendocardial ischemia does not "localize". That is to say, for example, that "inferior" ST depression does not represent inferior subendocardial ischemia. When there is inferior ST depression from ischemia, it is invariably reciprocal to ST elevation in aVL (i.e., the high lateral wall). So if we look at aVL, there is indeed some ST elevation, about 0.5 mm. This is actually a significant amount of ST elevation because the R-wave is only 2 mm, and this is common in aVL.

Furthermore, there is subtle ST depression in lead V3 (0.5 mm). There should NEVER be ST depression in leads V2 and V3, there is usually some amount of ST elevation. 0.5 mm of ST depression is likely to be 1.0-1.5 mm of relative ST depression.

A colleague showed me this and I said that, because there is ST elevation in aVL and ST depression in V3, it is probably an obtuse marginal (OM) branch (of the circumflex) or near-occlusion.

Appropriate management is to treat maximally for ischemia with ASA, heparin or enoxaparin (depending on institutional preference), clopidogrel if institutionally acceptable and epitifibatide if not. If the pain does not resolve, go urgently to the cath lab. If the pain and ECG findings resolve, then next day cath is acceptable.

The patient had initial symptom control and was put in the ICU, but symptoms recurred and were refractory, so he was taken urgently to cath and was found to have ACS of the saphenous vein graft to the obtuse marginal. This was stented, and flow was TIMI-III after the procedure. Pre-procedure flow was not documented, but pain was resolved afterwards. Troponin I peaked at 8.5 ng/ml. Post-procedure ECG showed prominent T-wave inversion in aVL (analogous to Wellens' T-waves in the anterior leads). Notice the ST depression in V3 is gone, but the ST elevation in aVL is more pronounced, as is the reciprocal ST depression.