Guess the culprit with ST Elevation in posterior leads

A middle aged man had off and on chest pain for 2 weeks, then 2 hours of more severe and constant pain.

Here was his ED ECG, which was identical to the prehospital ECG.  He did not get prehospital activation.

What do you think?

There is sinus rhythm with ST depression in I, II, aVF and V2-V6.  It is maximal in V3 and V4.  This usually means posterior MI, whether the T-wave is upright or not.

There is also some ST elevation in aVR, which must be present whenever there is ST depression in I and II (a lead between I and II is (-) aVR, opposite aVR; if ST segments in I and II are negative, then they must also be negative in the lead that is between them [(-) aVR].  If (-) aVR has ST depression, then aVR must have ST elevation.

ST Elevation in aVR is not the same as STE in other leads because there is no underlying myocardial wall; there are only atria!  So STE in aVR is reciprocal to ST depression elsewhere.

ST vector

In this ECG, the ST vector is both posterior (away from V3 and V4), upward, away from aVF, and rightward (away from I, II, V5, V6 and towards aVR.  It is mostly posterior, as the greatest ST depression is in V3 and V4.

When the ST vector is primarily posterior, the diagnosis is usually posterior STEMI.
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I just read Ken's comments before publishing.

He wrote below that there is 2 mm of STE in aVR.  I did not and do not measure it that way.

So I went back to the original ECG and magnified it:

I put the top of the line just under the QRS onset, and the J-point, for both complexes

As you can see, the STE in aVR is indeed 1 mm, not 2 mmThe ST depression in V3 and V4 is much more pronounced than the STE in aVR.
Contrary to what Ken stated, the ST vector remains mostly posterior

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What about subendocardial ischemia?

Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall.  This has been shown in multiple studies of stress testing, in which the location of the ST depression does not correlate with the subsequent angiogram.

So if there is subendocardial ischemia due to an LAD lesion, the ST depression is not usually in the "anterior" precordial leads.  It is more often in II, V5, and V6.  ST depression due to a circumflex (lateral wall ischemia) or RCA (inferior subendocardial ischemia) similarly will not reliably localize.  It is possible that there will be ST depression in those locations, but not necessarily.

Conversely, if there is ST depression in the inferior leads, it does not mean there is "inferior ischemia;" it is far more likely to be reciprocal to ST elevation due to subepicardial ischemia (transmural, often extremely subtle) in aVL.

Similarly, STD in aVL is usually reciprocal to inferior ST elevation, not "lateral ischemia."

Likewise, ST depression in V2-V4 is most commonly reciprocal to ST elevation due to subepicardial (transmural) ischemia of the posterior wall.

ST depression maximal in V5 and V6 cannot be reciprocal to subepicardial, transmural ischemia under aVR because, as stated above, there is no ventricular myocardium beneath that lead, no STEMI under aVR.

Thus, ST depression maximal in V5, V6 is subendocardial ischemia.

Clinical Course 

I activated the cath lab.

Out of curiosity, I recorded posterior leads (Here, V4-V6 are really V7-V9 on the back):

V3 = V7, V4 = V8, V6 = V9
Notice the voltage is very small.
This is because the electrical impulse is impeded by air (lung)
The voltage of QRS and of ST segments fall proportionately.
Thus, the 0.5 mm of ST elevation in lead V9 (labelled V6) meets "criteria" for posterior MI.
You can also see that V3 still has much STD.
Had there been zero STE in V9, but persistent STD in V3, I would have called V9 a false negative!

Diagnosis: Posterior MI, right?


Just prior to transport, the patient became confused and agitated and, although blood pressure and pulse were OK, I was worried about cardiogenic shock.  We intubated him.

Cath lab
The BP was 70/40 on arrival to the cath lab and received a balloon pump and norepinephrine.

Angiogram

Left main: Severe calcific stenosis of ostial and distal left main. 

LCX: chronically occluded and filled by right to left and left to left collaterals. 

LAD: large caliber vessel with severe calcific stenosis of the proximal LAD with TIMI2 flow. There are large caliber diagonal branches with no significant stenosis. Mid LAD has another area of focal moderate stenosis. 

RCA: Moderate caliber with moderate to severe stenosis of the proximal to mild RCA. It gives epicardial collaterals to OM1 and OM2
All arteries had at least TIMI-2 flow, so this does not appear to be OMI to the posterior wall

Intervention: on Left Main and LAD

Next day

The highest troponin I recorded was 13.7 ng/mL.  

Echo:
Normal LV size, normal LV wall thickness, mildly to moderately reduced LV
systolic function. Estimated EF 42%.
Wall motion abnormality - anterior, anteroseptal, apex
Wall motion abnormality - lateral (not posterior) 

I suspect that "lateral" means the lateral wall that has always been called lateral, and not the posterior wall that is now also called "lateral" on echo.  

In other words, I believe this ultrasound result refers to the lateral wall that is recorded by I, aVL, V5, V6; terminology has changed such that anything that is either posterior or lateral is now called "lateral."  This is unfortunate in my view, as it complicates the retrospective analysis of the ECG!!  Lateral can now include the wall that is detected by STE in I, aVL, V5, V6, but now also the wall detected by ST Depression in V2-V4)


Interpretation:

It seems that in this case is an exception to the rule that if the ST depression is maximal in V2-V4 that it is a posterior MI.  Subendocardial ischemia does not localize, but that does not mean that subendocardial ischemia of the anterior wall (LAD) cannot manifest with STD in the anterior leads.  Only that it need not!

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MY Comment by KEN GRAUER, MD (4/24/2020):

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Prediction of a “culprit lesion” is an imperfect science. Striving to envision what prompt cardiac catheterization is likely to reveal in a patient with acute cardiac chest pain is enticing to the ECG enthusiast, and it does enhance clinical assessment and optimal management. But a more important goal is knowing when to (and when not to) activate the cath lab.

• The cath lab was not activated in the prehospital setting in this case — despite a prehospital tracing identical to the initial ECG in the ED, that I have reproduced for clarity in Figure-1.

Figure-1: The initial ECG in this case (See text).

On seeing ECG #1 — Dr. Smith promptly activated the cath lab. THIS was the correct response — which was borne out a little bit later by sudden deterioration in the patient’s condition as efforts were being made to expedite transport to the cath lab.

MY THOUGHTS on ECG #1: I interpreted ECG #1 a bit differently than Dr. Smith. Clearly (as per Dr. Smith) — ST segment depression is maximal in leads V3 and V4 — and this finding should always suggest the possibility of acute posterior MI. This is especially true in ECG #1 because: i) the SHAPE of the depressed ST segment in the anterior leads here is consistent with a positive “Mirror Test” (Please see My Comment at the bottom of the February 16, 2019 post in Dr. Smith’s ECG Blog); and, ii) the R wave becomes relatively tall sooner-than-expected by lead V3 in ECG #1 (ie, potentially the mirror-image of an enlarging Q wave in the posterior lead distribution). That said:

• I thought ST segment flattening and depression in ECG #1 was quite generalized — and quite marked in no less than 8 of the 12 leads (ie, ≥1-1.5mm ST depression in leads I, II, aVF, and V2-thru-V6).
• The amount of ST elevation in lead aVR is marked (ie, ≥2 mm).
• Instead of seeing at least some ST depression in lead V1 (as is typically seen with acute posterior MI) — there is slight ST elevation. This can occur, if what would have been ST depression in lead V1 is countered by ST elevation from associated acute RV involvement — yet there is no sign of acute inferior ST elevation (as I’d expect if there was acute proximal RCA occlusion causing RV infarction).
• My Impression: While I thought acute posterior MI was a definite possibility — I favored the more nonspecific conclusion of diffuse subendocardial ischemia — which in this middle-aged man with increasingly severe chest pain, could be due to any of several possibilities: i) severe LMain disease; ii) severe proximal LAD disease; and/or, iii) severe multi-vessel coronary disease.
• BOTTOM Line: It really does not matter which of the above possibilities is the cause of the ECG findings we see in Figure-1. Regardless of the cause — the clinical situation cries out for prompt cardiac catheterization — which fortunately was expeditiously accomplished by Dr. Smith.