Two patients with chest pain. Do either of them need emergent reperfusion? Both? Neither?

 Written by Pendell Meyers

Here is a quick comparison / quiz post. It will be easy for long time blog readers. The two ECGs below are both from middle aged patients with acute chest pain. Do either, neither, or both patients have an ECG diagnostic of OMI, warranting emergent reperfusion therapy?

Patient #1:

Patient #2:

Distinguishing subtle OMI from normal variant ST elevation can be a difficult but important skill that is achieved through supervised pattern memorization and recognition. As in the cases above, the distinction CANNOT BE MADE BY AMOUNT OF MILLIMETERS. 

Patient #1 has a totally normal, normal variant ECG. There is no OMI. There is about 1mm of STE in all inferior leads (importantly without any reciprocal STD or TWI in aVL), and additional STE in V4-V6. There are J waves. None of the T waves are hyperacute. It is NOT inferolateral OMI. It is certainly NOT evidence of pericarditis. It is normal. The patient ruled out for AMI with serial troponins.

Patient #2 has unequivocal (i.e., definite!) acute inferoposterior OMI. There is maybe 1mm of STE in lead III, and only a touch of STE in II and aVF, but with diagnostic reciprocal STD in aVL (unexplained by the normal QRS complex). The inferior T waves are subtly hyperacute, because the diagnostic context tells me that their area is increased from what the baseline must be. The diagnosis is made even easier by the concomitant posterior OMI, evidenced by STD maximal in V2-V3 and unexplained by the normal QRS complex. The ECG is diagnostic of inferoposterior acute transmural injury, almost certainly due to acute thrombotic coronary occlusion or near occlusion (once in a while, another etiology such as occlusive spasm etc. will achieve the same physiologic occlusion).

Patient #2 sadly had a delay to identification of her acute RCA occlusion because her ECG "didn't meet STEMI criteria". No posterior leads were ever done (as is common in these missed cases). The RCA was eventually stented. She survived the hospitalization and likely has increased long term mortality and morbidity compared to her outcome with immediate reperfusion. 

Learning Points:

Side-by-side comparison of definitive OMI and its mimics is the key to unlocking the pattern recognition needed to become as accurate as possible at the reperfusion decision. 

In many cases, the differentiation of OMI from OMI mimic has nothing to do with which one has more millimeters of STE. Everything is proportional, and there is no reason why OMI "owes us" 1mm in two consecutive leads. It is a totally unsupported expectation that has no equivalent in other modern approaches to acute deadly pathologies we see in acute care medicine.

Patient #2 does not meet STEMI criteria. Yet she would have benefitted from emergent reperfusion. With targeted training and observation of actual outcomes, anyone can learn to identify this. One day these cases will be just a regrettable part of the past management of ACS.

Posterior OMI is most easily seen by maximal STD in V1-V4 that is otherwise unexplained by abnormal QRS morphology. Posterior leads are unreliable, have smaller overall voltage, and simply ARE NOT PERFORMED in actual practice in the routinely missed posterior OMI cases that happen every day.

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Comment by KEN GRAUER, MD (9/9/2022):

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Today's blog post by Dr. Meyers provides a simple but instructive teaching exercise! For clarity — I've reproduced in Figure-1 the ECGs from both of the middle-aged patients presented in today's post, each of whom came to the ED with new-onset chest pain.

• I had not seen these tracings before. I'll add the following thoughts to the excellent comments by Dr. Meyers.

Figure-1: I've labeled the 2 ECGs in today's case (See text).

MY Thoughts on the ECGs in Figure-1:

To emphasize — When a patient of "the right age" presents to the ED with new-onset chest pain — the onus falls on us to prove that there is no OMI, rather than the other way around.

• This is different than when a younger adult presents to an ambulatory office with less typical symptoms — in which case the prevalence of acute coronary disease is decidedly less, and equivocal ECG findings are less likely to indicate acute disease.
• While definitely present — I thought the abnormal ECG findings in the tracing from Patient #2 were subtle. That said, given the history — acute OMI had to be assumed until proven otherwise.

The ECG from Patient #1:

As per Dr. Meyers — there is ST elevation in both the inferior and lateral chest leads (V4,V5,V6). Features in favor that this ST elevation which is present in 6/12 leads is benign, include the following:

• The shape of this ST elevation has an upward concavity (ie, "smiley"-configuration — as suggested by the curved BLUE lines in the inferior leads).
• There is J-point notching characteristic of a repolarization variant (BLUE arrows in leads II,V4,V5). Also present is slurring on the downstroke of the R wave in leads III and aVF — which is another characteristic of repolarization variants.
• The shape of the ST elevation in all 6 leads that manifest this finding is virtually identical (whereas acute OMI tends to localize its abnormal ST-T wave findings).
• There are no reciprocal changes. Given predominant negativity of the QRS in lead aVL — the isoelectric (or perhaps tiny amount of T inversion) that we see in lead aVL is a common and normal finding (attributed to the physiologic finding that the T wave axis commonly follows the QRS axis in the frontal plane).
• R wave progression is normal. The QTc is not prolonged.
• 
  
• Bottom Line: Although there is some ST elevation in 6/12 leads — the appearance of this ECG looks benign. As per Dr. Meyers, the overall picture is consistant with a repolarization variant (For more on Early Repolarization and its variant patterns — Please see the May 23, 2022 post in Dr. Smith's blog by Dr. McLaren — with my detailed comment at the bottom of the page).
• 
  
• P.S. Did you notice that there is PR depression in multiple leads (II,III,aVF; V4,5,6)? While I always look for PR depression when contemplating a diagnosis of acute pericarditis — I have found this to be a nonspecific finding (ie, I've seen PR depression with acute MI and with normal variants).  

The ECG from Patient #2:

In reviewing the ECG from Patient #2 — my "eye" was immediately drawn to the abrupt and straightened ST segment "takeoff" in lead III (as suggested by the angled RED line in this lead).

• Although subtle — this is a "real" finding (especially in a "high-prevalence" middle-aged adult who presents to the ED with new-onset chest pain).
• Note how this ST segment "straightening" differs in shape from the upwardly-curved ST segment in the inferior leads of Patient #1 (curved BLUE lines in the inferior leads).

PEARL #1: When looking for subtle clues of acute OMI — I find it extremely helpful to first identify those 1 or 2 or 3 leads that I feel definitely show abnormal ST-T wave findings. Once I do — it often becomes easier to identify other leads that show even more subtle-but-real abnormal findings.

• The other lead in the ECG from Patient #2 that is definitely abnormal — is lead V2. Normally, there is a small amount of upward-sloping ST elevation in anterior leads V2 and V3 (as we saw for the ever-so-slightly elevated ST segment in lead V2 for Patient #1). The ST segment should not be depressed in lead V2 — as it definitely is in the V2 lead for Patient #2.
• 
  
• PEARL #2: As I've emphasized on many occasions in Dr. Smith's ECG Blog — I have found the Mirror Test to be an extremely helpful visual aid for recognizing the special shape of anterior ST depression seen in association with acute posterior OMI (See My Comment in the January 3, 2022 post in Dr. Smith's ECG Blog — for illustration on how to apply the Mirror Test).
• 
  
• Doesn't the Mirror-Image view of lead V2 that I show in Figure-1 look like an acute MI? (This mirror-image view of the anterior leads — provides insight as to what is occurring in the oppositely located posterior wall).
• Early transition (with a disproportionately tall R wave already in lead V2) — is another finding suggestive of posterior infarction.

Additional Abnormal ST-T Wave Findings:

In response to slight-but-real ST elevation in the inferior leads (with "straightening" of the ST segment takeoff in lead III) — there is reciprocal ST depression in lateral leads I and aVL.

• As opposed to the predominantly negative QRS complex in lead aVL from Patient #1 — there is a substantial R wave in lead aVL of the ECG from Patient #2 — such that the T wave inversion we see (RED arrow in lead aVL) is not normal. In addition — there is J-point ST depression with ST flattening in lead I (RED arrow in this lead).
• 
  
• Bottom Line: In the context of a middle-aged patient with new-onset chest pain — the ST-T wave changes in these 5 leads is strongly suggestive of acute infero-postero OMI until proven otherwise.