Thursday, August 12, 2010

35 yo woman with LAD occlusion manifesting with only hyperacute Ts and inferior ST depression, also missed by computer

Click here for other cases of missed STEMI.
Click here for cases of early repolarization vs. LAD occlusion

A 35 yo woman had the sudden onset of epigastric pain, more severe and different from her usual acid-related pain. She presented ambulatory. She had an ECG ordered by the triage nurse. The patient and the ECG were placed in a far-away room.


The computerized ECG read was:

"Minimal ST depression, inferior leads" and
"ST Elev, Probable normal early repolarization pattern."

This ECG is diagnostic of STEMI: the T-waves in V2 and V3 tower over the entire QRS. As described in 3 previous cases, inferior ST depression is due to high lateral STEMI (see this post and this post):


Early repolarization always has prominent R-waves in V2-V4. This is not early repol.

Because of a variety of issues, the physician did not see this ECG immediately. Had the computer read "ischemia" or "AMI", the tech would have brought it immediately to his attention. He did not rush to see it because it was a 35 year old woman with atypical symptoms. When he did see it, he recognized STEMI immediately.

The next ECG showed anterior Q-waves. She did go to the cath lab with some delay and had an ostial LAD occlusion that was opened. She had a subsequent EF of 50%.

  • Anyone, of any age or sex can have MI.
  • Do not trust the computer.
  • You must read the ECG yourself.
  • Have a system to review all ECGs that have been recorded.

Earlier posts on early repolarization use the application of a regression equation to differentiate early repol from anterior STEMI. See this post (which also includes an example of serial ECGs, this post (which also demonstrates straightening of the ST segment, and this post (which also shows serial ECGs improving after a reperfused LAD occlusion).



I have also derived a simpler rule but which may not work as well in cases of very low or very high QTc:

If 2 of 3 of these are positive, then it is anterior STEMI over early repol with a sensitivity and specificity of 90%:

1) R-wave in V4 less than 13 mm
2) computerized QTc greater than 392 ms
3) ST elevation at 60 ms after the J-point greater than 2 mm
Here is another example that points out the use of serial ECGs when the diagnosis is in question:

Wednesday, August 11, 2010

ST depression does not localize: 2 cases of "inferior" ST depression diagnostic of high lateral STEMI

Case 1:

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).
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Thus, this ECG is diagnostic of occlusion of a vessel supplying the high lateral wall.
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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.
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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.
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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.

Case 2.

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.
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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.
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A second ECG, after stabilization, was recorded:



The peaked T waves have resolved, and there is less tachycardia, but the ST depression in II, III, aVF persists. There is definite ST elevation in aVL.

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This was not acted upon.

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[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]
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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:

http://hqmeded-ecg.blogspot.com/2009/01/st-depression-limited-to-inferior-leads.html

Anterior Hyperacute T-waves diagnostic of LAD Occlusion

This series of ECGs from a patient with LAD occlusion shows hyperacute T waves in precordial leads, as well as ST elevation in V1-V3 and aVL. The second ECG was 16 minutes after the first and shows markedly increased ST elevation. The patient was taken for rapid PCI. The third ECG is post-reperfusion.









Monday, August 2, 2010

New upright T-wave that is NOT pseudonormalization

A 79 yo female presented with crescendo angina. She has a history of anterior STEMI a few years ago treated with tPA. She has DM, HTN, and smokes. She was pain free at the time of this ECG (ECG #1):

There is one mm of ST elevation in each of V1-V3, along with deep QS-waves and upright but not large or tall T-waves in V1-V3. This is typical "LV aneurysm" morphology (otherwise known as persistent ST elevation after old MI). This typically has a low T/QRS ratio..

It is always wise to compare with a previous ECG, but only with knowledge of the normal evolution of post-MI ECGs. Here are the previous ECGs:

ECG #2 is the last ECG, recorded after resolution of the previous anterior STEMI shown below.
T-waves are inverted and QS-waves are present. This is a typical ECG of post transmural MI, with shallow T-wave inversion in right precordial leads V1-V3. Non-STEMIs have deeper T-wave inversion and preservation of some R-wave, often a QR-wave. (There is deeper T inversion in V4-V6.)
ECG #3 is the one obviously diagnostic of anterior STEMI (before evolution to the LV aneurysm morphology above:
Obvious anterior STEMI

Why are the T-waves upright now (ECG #1)? Is it pseudonormalization? No:

In the normal evolution (over months) of the post-MI ECG, T inversion (usually) becomes upright. On the other hand, pseudonormalization happens acutely (within the first week or two), usually after a reperfused MI and is due to re-occlusion. The T-waves are large and hyperacute.

Thus, we expect that the T inversion after an MI will be resolved if we get an ECG much later.
So ECG #1 is not due to pseudonormalization. If the patient has ongoing symptoms (unlike this one), serial ECGs are indicated because hyperacute T-waves and ST elevation may develop, but this ECG#1 represents the expected ECG evolution of this patient with previous transmural MI. This patient ruled out for MI by troponin.
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