How much time are you willing to wait for OMI to become STEMI (if it ever does)?

Written by Pendell Meyers, few edits by Smith

A man in his 60s with history of stroke and hypertension but no known heart disease presented with chest pain that started on the morning of presentation at around 8am.

Here is his triage ECG when he presented at 1657:

What do you think?

There is sinus rhythm with normal QRS complex and ST depression in V2-V5, maximal in V3-V4. There is no ST depression in V6, II, III, or aVF, and no significant ST elevation in aVR, all confirming that the ST vector is not consistent with diffuse subendocardial ischemia, but rather a focal ST vector pointed at the posterior wall. It is posterior OMI until proven otherwise.

This ECG is quite obvious for long-time readers, and you may think this far too easy to be presented on this blog.

But in actual practice, similar patients are routinely missed and under-treated, as you will see as this case progresses. "Posterior STEMI" may not even technically exist according to the current (2013) ACC/AHA STEMI guidelines, as it is not described as a "STEMI equivalent" and the only relevant statement in the guidelines is: "In addition, ST depression in 2 precordial leads (V1-V4) may indicate transmural posterior injury."  JACC 61(4):e78-140; page e83.

Furthermore, the term "STEMI equivalent" has no reliable or definable meaning except between two practitioners who both agree on the list of entities that they believe are STEMI equivalents and can agree on how to identify it.

It is true that other documents occasionally describe "abnormal ST segment elevation" in the posterior leads (commonly accepted criteria is 0.5 mm in just one lead V7-9), but as far as I can tell all of these documents specifically avoid calling this condition STEMI and specifically avoid using any terminology similar to "STEMI equivalent."  The once exception I have found is the NCDR guidelines, which actually do give a definition: "ST elevation in the posterior chest leads (V7 through V9), or ST depression that is maximal in V1-V3, without ST segment elevation in other leads, demonstrating posterobasal myocardial infarction, is considered a STEMI equivalent and qualifies the patient for reperfusion therapy." I find this definition problematic because the maximal STD in posterior OMI frequently extends out to V4 rather than V3.

So it is very unclear to me whether or not "posterior STEMI" is actually a recognized entity under our current guidelines. It is my opinion that this lack of clarity is part of the reason why patients with posterior OMI are frequently underecognized and undertreated. Regardless of its formality, the more important problem is that it is certainly not recognized in widespread current practice.


Back to the case:


As is unfortunately common practice, a repeat ECG was only performed after the initial troponin T returned elevated at 0.19 ng/mL 1.5 hours after arrival.

1833:

Persistent posterior injury. The ST depression which was present in V5-V6 is now gone, which may be either resolution or relative ST elevation of the lateral wall (which would be common with posterior involvement), either way it is dynamic and further proves the existence of ACS.

This was interpreted as "no significant change." Cardiology was called, but elected not to take the patient to the cath lab for some reason, but instead simply admitted him.

The second troponin returned at 0.25 ng/mL. There is no mention of whether the patient had ongoing symptoms. The records show that heparin drip had been ordered in addition to aspirin which had already been given.

The third troponin returned at 22:05 at 0.92ng/mL. A repeat ECG is recorded at 2333, along with a posterior ECG minutes later:

Leads labelled V4-V6 are actually V7-V9 on the posterior thorax. Obvious inferoposterior STEMI.

At this time, just before midnight, the cath lab was activated. The acute finding is reported as a 100% thrombotic lesion of the proximal left circumflex (TIMI 0 flow). In the views below, I would have guessed that this vessel was a ramus intermedius as it seems to be the middle vessel of a trifurcation of the left main, but I will simply defer to the true angiographers. See the occlusion here:

Here is the ECG after intervention showing resolution:



The peak troponin T was 2.35 ng/mL (fairly large MI). The patient had no further complications. Unfortunately an echo was not available.

I hope you are surprised at this case, but I fear that most readers recognize this as the sad reality that exists across many institutions as of 2019. I attribute this mostly to the inadequate current paradigm of myocardial infarction which inspires failure for all such cases that are not obvious according to the STEMI criteria. If this case were an acute occlusion of ANY other important artery (say for example, the superior mesenteric artery, or the middle cerebral artery), 7 hours from arrival to diagnosis despite ongoing evidence of occlusion would be seen as an important and unacceptable delay to diagnosis. Yet in our STEMI vs. NSTEMI paradigm this is simply not understood as an emergent arterial occlusion syndrome. "Time is muscle," but somehow only for occlusions that cause STEMIs, not for occlusions that are more subtle.

Hopefully fixing the paradigm by reframing this disease as an acute arterial occlusion will help people understand this problem. This patient had an Occlusion MI (OMI) and needed emergent reperfusion therapy. It is common sense that such patients have a higher probability of survival and of myocardial preservation if such an OMI is reperfused early, and there is no study that contradicts this notion.

Cases like this will be carefully quantified and studied in our ongoing retrospective study designed to quantify the difference in accuracy between advanced ECG interpretation and the current STEMI criteria. Specifically, cases such as this one will detail the difference in time between diagnosis of Occlusion MI by expert ECG interpreter vs. the current STEMI criteria. This case, for example, would be nearly 7 hours of ischemic time between arrival and cath lab activation.

How much time are you willing to wait for OMI to become "STEMI" (if it ever does)?

Comment from K. Wang:

Very clinically important point is being made by this case as usual. What is "STEMI"? It's an ECG manifestation of transmural MI from an occluded coronary artery registered in the ECG leads FACING the infarcted ventricular wall. Yes, a transmural MI occurs in the posterior wall, too,  The only reason we don't see ST elevation in the "routine" 12 lead ECG is because it does not include posterior chest leads, which are the leads FACING the infarcted wall. Do we have to take posterior chest leads to see it then? No, we already have it . It's in the anterior chest leads registered reciprocally, i.e. upside down, as ST depression. If one wants to confirm it, just pick up the tracing, turn it upside down and look at it against light. There, one sees typical STEMI to one's satisfaction. I agree with Dr. Smith that, if current ACC guidelines are not clear about posterior STEMI, it should be clarified for better patient care.

K. Wang.

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Comment by KEN GRAUER, MD (2/16/2019):

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The importance of early recognition of an acute OMI (instead of waiting until it becomes a “stemi” ) can not be overstated! The consequences of failing to appreciate this critical concept is made painfully evident in this case by Dr. Meyers — in which it took over 6 hours until this man with new chest pain was finally taken to the cath lab. Superb review (above) by Dr. Meyers about the details of this case. I focus My Comments on 3 of the ECGs that were shown in this case (Figure-1).

Figure-1: The 1st, 3rd and 4th ECGs shown in this case (See text). 

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The crux of this case — is the failure to appreciate that acute posterior OMI was clearly evident in the initial ED ECG ( = ECG #1). The abnormal findings in ECG #1 are localized (ie, ST depression in leads V2-thru-V5) — and, in the setting of new chest pain — ECG #1 should be interpreted as acute posterior OMI until proven otherwise. Had the treating clinicians recognized these concepts — they would have: i) obtained a 2nd ECG long before 18:33 (~ 1 1/2 hours after ECG #1 was done); and, ii) they would have advocated for activating the cath lab.

• SUGGESTION: Consider use of the “Mirror Test”. I’ve been teaching this concept for over 36 years (since including it in my first ECG publication that I wrote in 1983). The mirror test is a simple visual aid: It helps the clinician recognize acute posterior infarction. The mirror test is based on the concept that none of the standard 12 leads directly view the posterior wall of the LV — BUT — the anterior leads provide a mirror image of electrical activity in the posterior wall. By simply inverting a standard 12-lead ECG, and then holding it up to the light — you can easily visualize the “mirror-image” of leads V1, V2 and V3. It should be readily apparent that the mirror-image view of leads V2 and V3 in ECG #1 (just to the right of ECG #1 in Figure-1) — shows a QRST complex that is almost shouting out, “I’m having an acute posterior OMI (ie, large Q waves; coved ST elevation and symmetric T wave inversion in this mirror-image). With a little bit of practice — use of the Mirror Test should facilitate near-instant recognition of subtle changes such as the slightly-taller-than-expected anterior R waves in leads V2 and V3 of ECG #1 (which “become” Q waves in the mirror image view) — and the “shelf-like” shape (ie, nearly straight) ST depression in leads V2,V3 of ECG #1 (which “becomes” ST elevation in the mirror-image view).

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ECG #2 (which is not shown in Figure-1) — was done ~1 1/2 hours after ECG #1. It showed slightly less ST depression than was seen in ECG #1 — but no sign of ST elevation (ie, no “stemi” ).

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Review of ECGs #3 and #4 is especially interesting. ECG #3 was done 6+ hours after ECG #1. It shows downward slanting and slightly greater ST depression in a number of chest leads compared to ECG #1 — but still NO ST elevation in the inferior leads, and NO reciprocal ST depression in lead aVL.

• ECG #4 was done just a few minutes after ECG #3 for the purpose of directly assessing posterior leads V7, V8 and V9. These posterior leads show obvious ST elevation. But DID YOU SEE that this 4th ECG (done just minutes after ECG #3) now shows: i) ST elevation in leads III and aVF that was not present in ECG #3; ii) reciprocal ST depression in lead aVL that was not present earlier; and, iii) significantly more ST-T depression in leads V1, V2, V3 compared to what was seen JUST MINUTES EARLIER in these same leads in ECG #3. This means we are just now in ECG #4 catching acute evolutionary changes, that are evolving in front of us over these very few minutes between the time when ECGs #3 and 4 were done.
• KEY POINT —Although many providers advocate for doing posterior leads when looking for acute posterior involvement — realize that the magnitude of ST elevation that you are likely to see in posterior leads with acute posterior infarction is usually modest. The reason the amount of ST elevation in leads V7, V8 and V9 in ECG #4 is as large as it is — is because this ECG #4 was obtained during the very moments that acute evolution was developing (ie, Note there is now inferior lead ST elevation in ECG #4 — and note how profound is the downsloping ST depression in leads V2 and V3).
• Finally — Note how obvious acute posterior infarction is in the Mirror Test of leads V1, V2, V3 in ECG #4 (insert to the right of ECG #4 in Figure-1). While use of posterior leads (V7,V8,V9) clearly showed ST elevation in ECG #4 — Are posterior leads really needed to make the diagnosis of a STEMI in this case? I am not saying that you should never do posterior leads — but rather, that with a little bit of practice — it’s possible to make the diagnosis of acute posterior OMI much more quickly by just using the standard 12 lead ECG. COMMENT — I don’t think I’ve seen a case in which posterior leads told me something that I did not immediately know from use of the standard 12-lead ECG (with Mirror Test of the anterior leads).

Our THANKS to Drs. Meyers and Smith for presenting this highly insightful case.

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FOR MORE:

• For another example of the Mirror Test— CLICK HERE.