This is a 72 yo male with h/o CABG who presents with 5.5 hours of sudden onset, constant, substernal chest pressure. Here is the initial ECG:
This shows "inferior" ST depression. But stress testing shows us that ST depression does not localize. In other words, when the stress test shows ST depression in an apparent distribution, it does not correlate with the echo, nucleide imaging, or cath. Thus, subendocardial ischemia, for an unknown reason, does not localize. When there is ACS with ST depression due to subendocardial ischemia, it is diffuse (II, III, aVF, V4-V6). If it is focal, one should suspect that it is reciprocal ST depression, reciprocal to ST elevation elsewhere. This is most commonly seen with high lateral STEMI, with reciprocal depression in II, III, aVF. In fact, this ST depression is usually the most obvious finding on the ECG because ST elevation in aVL is rarely pronounced (most commonly because the QRS voltage in aVL is usually very low, and ST voltage cannot exceed QRS voltage).
Thus, this ECG is diagnostic of occlusion of a vessel supplying the high lateral wall.
It does not meet the definition of STEMI because there is not 1 mm of STE. However, this definition is arbitrary. The purpose of the definition is to diagnose coronary occlusion.
The first troponin was 0.82 ng/ml. The findings were not recognized. Subsequent ECGs did not change. The patient was admitted and did not get cath until the following day, at which time the Obtuse Marginal was found to have 90% stenosis with TIMI I-II flow.
The post cath ECG is shown here:
There is now a new Q-wave in aVL, with T-wave inversion. This is diagnostic of completed high lateral MI. Echo showed a new wall motion abnormality. Peak troponin I was 8.6 ng/ml.
This patient presented very ill in DKA and with depressed mental status. He was intubated.
There are peaked T-waves diagnostic of hyperkalemia, but there is also suspicious ST depression in II, III, and aVF. The hyperkalemia was immediately recognized and appropriately treated. However, the significance of the ST depression was not.
It is reasonable to hypothesize that the ST depression is related to demand ischemia (though in such as case it should be diffuse, not localized). If that is the case, it should resolve with therapy and improved hemodynamics and slower heart rate.
A second ECG, after stabilization, was recorded:
This was not acted upon..
[There is also precordial T-wave inversion which was present on previous ECGs and is consistent with "Benign T-wave Inversion (BTWI)" -- I can't remember if I have posted on BTWI before, but will if I have not]
Outcome: the patient had a peak troponin of 110.00 ng/ml (very large) and was taken for angiogram the next day. It showed an occluded first diagonal. Echo showed a lateral wall motion abnormality and the EF was 55%.
For another very subtle example, see this case: