Acute MI from LAD occlusion, or early repolarization?

3 hours of chest pain. Is it STEMI or is it normal (or early repolarization)?

Read Answer Below



This ECG looks quite normal, with only moderate ST elevation, upward concavity, good R-wave amplitude.  There is no ST depression or T-wave inversion.

But one easily identified characteristic makes the ST elevation unlikely to be from early repolarization: the computerized QTc is 455 milliseconds. In my study of early repolarization (ER) (n=167), only 2 of 167 (2%) cases of ER had a QTc greater than 455ms. The mean QTc was 394ms, compared to 420ms for MI (n=125) from LAD occlusion. Conversely, only 4% of LAD occlusion, vs. 40% of ER, had a QTc less than 380 ms. These clues were not appreciated by the clinicians. A very astute interpreter would not that the T-waves are also too symmetric to be early repol, which should have a steeper downslope than upslope, as demonstrated here:

The clinicians did not appreciate these subtle differences.

The patient continued to have chest pain.  70 minutes later, they repeated the ECG, which is shown here:

Note that now there are tiny Q-waves in V2-V4, making this unequivocally diagnostic of acute STEMI. 

These subtle Q-waves were not appreciated, but the clinicians were astute and ordered a stat echocardiogram, which confirmed anterior wall motion abnormality. The patient was taken to the cath lab and had a 100% LAD occlusion.

After reperfusion, the patients baseline ST-T complex was revealed. This is probably what they would have looked like prior to the LAD occlusion:

For those who want some more detail on differentiating ER from MI, see below:

Also useful was the mean (from V2-V4) R-wave amplitude, at a cutoff of 5 mm, with values less than 5 mm likely to represent MI. Interestingly, mean ST elevation (no matter how it was measured) was not as good a differentiator as the mean R-wave amplitude, but if mean R-wave was less than 5 mm OR the mean ST elevation (V2-V4, as measured at the J-point, STEJ) was greater than or equal to 2 mm, then it was very likely to be MI and very unlikely to be ER.

Even better was a formula derived with logistic regression, which also included the QTc :
(1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc in milliseconds) - (0.326 x RA in V4 in mm), where RA is R-wave amplitude and STE60 is ST elevation at 60ms after the J-point relative to the PR interval.

If the value of the formula is greater than or equal to 23.4, it is MI (Sens, spec, accuracy all around 90%); if less, then it's ER.

For the first ECG, STE60, V3 = 2.5mm, QTc = 455, and RA V4 = 17, so: (1.196 x 2.5) + (0.059 x 455) - ( 0.326 x 17) = 24.29; this is barely greater than 23.4, thus consistent with MI but also further illustrating that this ECG is very difficult.

Two cases of ST depression

NSTEMI with subtle ST depression.

EKG from 11-12. Symptoms on 11-12 were also subtle, but present for 5 days, so if a single troponin was sent, it might have been positive. Pt. returned 2 days later (11-14) with similarly difficult symptoms [right neck pain, bilateral foot swelling (due to increase in amlodipine dose), recurrent abd pain (CT 2 days earlier had shown massive amount of stool), BRBPR and heme positive stools, and an aside that this abdominal pain goes up "into my esophagus and left neck." The ECG shown is from 11-12 and is the most diagnostic, with ST depression in V4 and V5. V3 is slightly negative. There is also a long QTc (484ms) and large T waves in V2-V4. These "hyperacute" T waves can be due to acute LAD ischemia OR due to posterior reperfusion (patient is pain free, posterior wall motion abnormality, posterior artery). In this case it is the latter. REMEMBER: in V2 and V3, there is almost always some ST elevation. Absence of ST elevation may be relative depression. A troponin on 11-14 was 2.0 and going down. It might have been much more elevated if measured on 11-12. The ECG pon 11-14 had very minimal ST depression. Cath showed occluded RCA and large OM, 80% LAD (severe 3-vessel disease).

THE SECOND CASE is ST depression from hypokalemia. The patient was a 17 year old with syncope. She has tachycardia of unknown etiology. There is diffuse ST depression. There is no CP or SOB. I guessed it would be 2.4, but it was actually 3.0. There is more ST depression than one usually finds with a K of 3.0. Notice there is a bump just before the P wave (leads II, III, V3-V5). One might be tempted to call this a T-wave. But it is a U-wave. The ECG completely normalized with K supplementation.

ST elevation MI in the setting of a paced rhythm

ST elevation MI in the setting of a paced rhythm from hqmeded.com on Vimeo.

t wave inversion

t wave inversion from hqmeded.com on Vimeo.

Is this Wellens' syndrome??? No! It is old MI with persistent ST elevation (LV aneurysm morphology)

This 53 year old man presented with increasingly frequent episodes of chest pain, the longest lasting for 10 minutes. He was from Africa and had never seen a U.S. physician, but his doctor in Africa had told him something about blockages in his heart. His last pain was 3 days prior.

Note that there is terminal T wave inversion in V2 and V3, suggesting Wellens' syndrome. However, in this case there is no R-wave remaining. Wellens' syndrome should have a well developed R-wave. Wellens' syndrome is dangerous because there is a large amount of anterior wall myocardium that is viable but at risk. Here, the absence of any R-wave makes it highly likely that this man has already lost his anterior wall; thus, there is little more at risk. When I saw him, I suspected that this represented old MI, not acute MI. It could also represent subacute or evolving MI that is so far along that the anterior wall is nearly completely infarcted. So this could be an infarct that is12 hours old or 12 years, but is highly unlikely to represent acute MI; more accurately, it is unlikely to represent acute "injury."

FYI: "Infarction" is a misnomer for ST elevation MI because infarction implies irreversible death. The ST elevation implies myocardium at risk of infarction but still alive. Therefore, "injury" is the most appropriate term. The height of the T-wave in acute MI is the best predictor of whether the injured or "at risk" myocardium is salvagable: the larger and higher the T-wave, the more myocardium is salvageable.

A single troponin was negative. We did an ED emergency physician performed bedside ECHO that showed an apical wall motion abnormality. We then set him up for an outpatient stress sestamibi. He went today and it showed a large fixed infarct with apical dyskinesis, or LV aneurysm. He did not have any inducible ischemia. He will follow up in Cardiology clinic.

Below is an example of true Wellens'. Wellens' occurs when an area of STEMI (which goes unrecorded by an EKG) gets reperfused. You're seeing the after effects of an occlusion which is now reperfused. The T inversions are also called "reperfusion T waves" because they happen after therapeutic Reperfusion therapy for STEMI. In the case of Wellens', there was no EKG recorded at the time of occlusion. The first EKG was only recorded after the perfusion restored itself spontaneously and the pain resolved. That is why EVERY PATIENT in the Wellens' studies was pain free at the time of the EKG AND had either an open artery or collateral flow.  Additionally, Wellens' has preserved R-waves because only a small amount of myocardium is infarcted.

This is Wellens' Type A (terminal T wave inversion). Type A will evolve into Type B (deep symmetric T wave inversion) over hours. If it does not evolve or resolve, it is not Wellens'.

LV aneurysm (persistent ST elevation after previous MI) in the setting of RBBB

65 yo male with recent rule out presents with unrelated complaint but also states he is SOB.

What are the worrisome EKG findings, and what is the differential diagnosis? What is the most likely diagnosis? What info would you like to have to make a decision?

LV aneurysm with Right Bundle Branch Block

This is a really hard one. But we had a patient 10 years ago who received tPA twice for an EKG like this before we reali zed that it was old MI with persistent ST elevation. LV aneurysm (persistent ST elevation after old MI) usually has no (or minimal) R-wave. But RBBB automatically provides an R' wave, which makes it difficult to realize that the anterior wall is dead. Additionally, RBBB with acute MI can look very similar. That is why, before you diagnose RBBB with acute MI, you should see if there is a previous EKG. In this case, the previous EKG was found and looked pretty identical. Previous echos confirmed dense anterior, septal, and apical wall motion abnormality with akinesis (I don't think there was dyskinesis).

Classic LV aneurysm (persistent ST elevation after previous MI)

70 yo with h/o MI, recent CABG, has acute onset of chest pain.

What are the worrisome EKG findings, and what is the differential diagnosis? What is the most likely diagnosis? What info would you like to have to make a decision?

Answer

There are deep QS waves in V1 and V2, and tiny R-waves in V3 and V4. With ST elevation in V1-V3, one must always entertain the possibility of acute MI in this patient with CP. The differential is wider, however, and mostly includes "old MI with persistent ST elevation," otherwise known as "left ventricular aneurysm morphology". This morphology is very common after an old and completed or nearly completed anterior MI. By complete, that is to say that there was no early reperfusion (spontaneous or therapy related). It was, in the old terminology, a "transmural" infarction. More accurately, there was a substantial mass of myocardium that died (infarcted, meaning irreversibly). Very often, such large anterior MI result in persistent ST elevation and they may or may not have a demonstrable "LV aneurysm" by echo. Echocardiographically, this is called "diastolic dyskinesia", meaning that the infarcted territory is thinned out and bulges even in diastole. Much of the time, there is only "akinesis", meaning no contraction of that territory. The important point is that old MI frequently has persistent ST elevation.

This is an example of "old MI with persistent ST elevation". So how do you differentiate old MI from acute MI? First, there are deep QS waves. Although anterior MI may have Q waves very early after onset, these are always QR waves (Q waves followed by an R-wave). The fact that there are zero anterior forces should lead you to think that there is no remaining anterior wall left to infarct. Second, in acute MI, as long as there is significant viable myocardium, the T wave is usually upright; remember that acute MI has large T waves. Lastly, acute infarction should have not only an upright T wave, but a prominent one. The "hyperacute T wave" is not simply a phenomenon of early infarction; it is simply more visible early on.

If you want a rule, I derived one a few years ago (AJEM 23(3):279-287; May 2005). Comparing proven acute LAD occlusion to patients with proven old MI and diastolic dysfunction and ST elevation, I found that the T/QRS ratio in any one of leads V1-V4 was almost always higher than 0.36 in acute MI, and almost always lower in LV aneurysm. Better was a T amplitude (V1+V2+V3+V4) / QRS amplitude (V1+V2+V3+V4) <> 0.22. The only acute MI's missed by this rule had at least 6 hours since symptoms onset.

I cannot tell from this ECG if it is 12 hours or 12 years since the MI. But looking through the records, I found that he had an old anterior MI with anterior apical akinesis.

He did have improvement of pain on a nitro drip, so we admitted to the CCU. He ruled out for MI.

ST depression: is it ischemia? No, hypokalemia.

This patient presented with alcohol intoxication and possible overdose. No ischemic symptoms.

Rate 71

PR 224

QRSD 90

QT 424

QTc 461

There is ST depression in V4-V6 (minimal). She is in alcohol intoxicated: high risk for hypokalemia.

Differential of ST depression is:

Secondary to abnormal QRS (LVH, LBBB, RBBB, etc.)

Primary ischemia

Hypokalemia

Digoxin

Normal variant.

This patient had a K of 2.8. Difficult case because she does not have prominent U waves (though they are there). I just finished a study of patients with proven hypokalemia compared to a control group. The QTc was the single best differentiator, with 450 ms the best cutoff. ST depression had good specificity but very poor sensitivity. Prominent U-waves were specific but not sensitive, and presence of any U-wave was sensitive but not specific. The best combination of factors was: Subjective diagnosis + QTc > 450 + Prominent U-waves, vs. none of the 3, with sensitivity of 86%, specificity of 100%, and accuracy of 92%. This held true when the subjective interpretation was done by residents who had had a short tutorial by me.