Thursday, January 12, 2023

Quiz post: do either or both of these patients have high lateral OMI / South African flag sign?

 Written by Pendell Meyers, edits by Smith

Two patients presented with acute chest pain/pressure. Here are their ECGs:

Patient 1:

Patient 2:

See below for "answers", and below that for both cases.


Patient 1 shows very subtle high lateral OMI, South African flag sign. She had an acute LAD OMI in the process of reperfusion, see case below.

Patient 2 has a normal variant ECG which mimics high lateral OMI, and ruled out for MI, see case below.

Here is the South African Flag sign (Figure by Ken Grauer — with the original 12-lead from Patient 1 attached below — See his Comment from the April 8, 2022 post in Dr. Smith's ECG Blog for more on this sign).

Patient 1:

A woman in her 60s presented with 10 days of intermittent chest tightness. The pain occurs anywhere from once a day to multiple times a day, lasting 10-15 minutes before resolving. It occurs both at rest and with exertion. It most recently occurred at about 1600 this afternoon and lasted 15 minutes. She is reportedly pain free on arrival, when this ECG is obtained:

Triage 1627

Sinus rhythm, normal QRS (except poor R wave progression), perhaps the tiniest possible STE in aVL, tiny STE in V2, awkwardly straight ST segment morphology in I and aVL and V2, concern for increased area under the T waves in aVL, V2, with reciprocal STD and negative hyperacute T waves in III and aVF. All very very subtle.

ECG read as: "Shows T wave inversions in the inferior leads and less than 1mm STE in V2, without STEMI criteria." So the patient was placed back in the waiting room like many others. Aspirin was given.

She was still waiting in the waiting room when her initial high sensitivity troponin T from triage returned at 989 ng/L (reference range for women less than 12 ng/L).

She was then taken back into a room and reevaluated, and still she reported no active symptoms.

A repeat ECG was done at 1918:

Interval improvement/resolution, without yet definitive reperfusion T wave inversions. In the setting of improved symptoms, the interval change supports reperfusion. If the patient continues to have reperfusion, then we would expect progressive terminal T wave inversion then full T wave inversion over time in the future ECGs.

Second troponin T resulted at 1,318 ng/L.

Chest x-ray was read as normal. CT pulmonary angiogram was negative for pulmonary embolism.

Heparin was started.

A third troponin around 4 hours later was down to 756 ng/L.

Next morning 6AM:

What do you think?

Reocclusion! Instead of the expected progression of reperfusion findings, we see signs of LAD OMI here with hyperacute T waves from V2-V6. Limb leads have low voltage and some artifact, but I and aVL are "up" with likely some reciprocal "down" findings in III and aVF, but this is difficult to see with the artifact and voltage.

It is critically important to recognize these T waves as hyperacute in the precordial leads!

There is no mention of whether the patient had any pain at this time.

Cath was done at around 9AM:

Culprit lesion mid-LAD, 99% stenosis, pre-intervention TIMI flow not listed, PCI performed with TIMI 3 flow and 0% stenosis resulting. Other vessels had scattered 20-30% stenoses.

No further troponins were measured.

About 1 hour after cath, 10AM

Soon after PCI, we start to see some deflation of some T waves in precordial leads, with some leads showing the beginning of terminal T wave inversion.

Echo done later that day showed EF 45%, with akinesis of the mid-apical anteroseptal, inferoseptal, and apical myocardium. Also akinesis of the apical lateral and inferior myocardium, and hypokinesis of the mid-apical anterior and anterolateral myocardium. Normal RV, no significant valvular stenosis or regurgitation. 

Day 3

Oddly, not much change from 2 days prior, still only the beginnings of terminal T wave inversion, with precordial T waves still overall too inflated compared to normal. It is possible that she was experiencing reocclusion/reperfusion or downstream showering of emboli (No reflow). But we don't have enough information to be sure.

1 month later:

Clear reperfusion findings, with preserved R waves.

5 months later:

Almost back to normal.

Patient 2:

A man in his 30s had sudden chest pressure that started after having an argument. The pain had been present constantly about 12 hours since then. He also complained of feeling hot and nauseous before a syncopal event approximately one hour ago.

The above ECGs with zero clinical history, and I replied "Interesting, I'm leaning toward this being a normal variant which mimics high lateral OMI. History and more info?"

(I later sent it to Dr. Smith with no info, who said "I suspect this is not an OMI")

Even though there is STE in I and aVL (probably 1 mm each, meeting STEMI criteria), and reciprocal STD in III with a down-up T wave, prior experience helps me to match this ECG with prior normal variants that have tricked me into thinking high lateral OMI. It is hard to describe why.

Two serial high sensitivity troponin T returned at 9 ng/L (reference range for males is less than 20 ng/L). No other acute pathology was discovered. He was discharged home.

Smith noteI believe I can identify some of the features which my pattern recognition recognized:

1. The R-wave in I and aVL in the "No MI" ECG is relatively large, with a low STE to R-wave ratio

2. The "No-MI" ECG has lots of upward concavity to the ST segment

3. The "No-MI" ECG has J-point notching in I and aVL

4. In the OMI case, there is STD in aVF in addition to lead III.

5. In the OMI case, there is Q wave in V2 preceding the subtle STE; in the "No-MI" case, there is an R-wave with substantial amplitude.

Here are the limb leads side by side (left OMI, right normal variant)

Here are their precordial leads side by side:

See these other relevant cases:

True Positive ST elevation in aVL vs. False Positive ST elevation in aVL

Even when the story is obvious, with intractable pain, the STEMI paradigm can cause preventable delays

See other "Quiz Posts":

Learning Points

It takes dedicated learning and observation of outcomes and serial ECGs to learn how to distinguish subtle OMI patterns from OMI mimics like the cases above.

It is critical to understand the OMI progression of ECG findings to know when a reperfused OMI has reoccluded, like in case 2 above.

ECG findings do not define what happened to a patient. OMI is not defined by the ECG, although expertise at reading the ECG greatly help identify OMI with high specificity and as soon as possible.

My Comment by KEN GRAUER, MD (1/12/2023):
The “beauty” of cases like the one presented today by Dr. Meyers — is that it provides a "tracing-to-tracing" comparison — in which one ECG clearly suggests acute OMI ( = ECG #1 in Figure-1) — and the other, is much more likely to be a repolarization variant (albeit impossible on the sole basis of ECG #2 to definitively rule out something acute).
  • Drs. Meyers and Smith highlight in their above discussion how they each intuitively knew (by pattern recognition) to suspect acute OMI for ECG #1 — and to suspect a repolarization variant for ECG #2. I focus my comment on why I immediately felt the same

Figure-1: The initial tracings in today’s case from Patient #1 and Patient #2. (To improve visualization — I've digitized the ECG from Patient #2 using PMcardio).

My Thoughts on ECG #2:
Beginning with the tracing that we all felt represented a repolarization variant ( = ECG #2) — the rhythm is sinus at ~65-70/minute. All intervals and the axis are normal — and there is no chamber enlargement.

Regarding Q-R-S-T Changes:
  • Small and narrow Q waves are present in lateral leads I, aVL — and possibly in V5,V6. These most probably are all normal septal q waves.
  • R wave progression in ECG #2 is appropriate — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V2-to-V4.

  • The ST-T wave finding that probably “caught the eye” of most readers — is the ST elevation in high-lateral leads I and aVL. As per Dr. Smith — I also thought this high-lateral ST elevation to most likely be the result of a repolarization variant because: i) The ST segment has an upward concavity shape (ie, “smiley” configuration)ii) The amount of J-point ST elevation is modest when one considers the amplitude of the R wave in these leads; iii) Although not frankly notched — there is some subtle terminal slurring of the QRS in several leads with ST elevation, as is commonly seen with repolarization variants (RED arrows in ECG #2); iv) The q waves in leads I and aVL are narrow and not deep, when one considers the amplitude of the R wave in these leads; andv) I see neither reciprocal changes in the inferior leads — nor acute changes in the chest leads. Instead — there is excellent R wave progression, with a 9 mm R wave already by lead V2.

PEARL #1: Rather than the ST elevation in leads I and aVL — what concerned me more was the appearance of the ST-T wave in leads III and V2. In my experience, the best clue to ST elevation that reflects acute OMI — is the presence of suspicious ST-T wave findings in multiple other leads.
  • Although the ST-T wave in lead III is depressed — this is not necessarily abnormal as an isolated finding (ie, when it is not seen in the other inferior leads). The fact that the QRS in lead III is both tiny and fragmented renders it not surprising that there is also some shallow ST depression. As a result — I was not convinced that the isolated ST depression in lead III represented a “reciprocal” change.
  • The ST segment takeoff in lead V2 is of potential concern — because this ST takeoff is straighter-than-usual, in that it lacks the usual gradual upsloping appearance. There is also slight ST elevation in lead V2. That said — I did not see ST-T wave changes of concern in the other 5 chest leads. Instead — I thought it possible that the ST-T wave in lead V2 might represent a “transition lead" — in that it occurs between the ST coving and T wave inversion in lead V1 — and the small amplitude T wave in lead V3.

  • To Emphasize: Given that Patient #2 presented with chest pain — I did not feel that I could rule out an acute event solely on the basis of ECG #2. That said — I thought it more likely than not that ECG #2 was in Dr. Meyers' words, a "mimic" — and probably did not represent an acute process.

My Thoughts on ECG #1:
The rhythm in ECG #1 is sinus at ~70/minute. All intervals and the axis is normal. There is no chamber enlargement. Instead — there is diffuse low voltage.

Regarding Q-R-S-T Changes:
  • There is a QS complex in leads V1 and V2 of ECG #1
  • A tiny initial r wave is seen in lead III — so instead of a Q wave, there is an rSR' complex in lead III.
  • A small r wave is seen in lead V3 — but R wave progression is clearly delayed, as transition does not occur until between leads V5-to-V6.

 The lead that "caught my eye" in ECG #1 — is lead III. The shape and disproportionate size of the ST-T depression in lead III is simply not "normal" — especially in a patient who presents with new chest pain. Once at least 1 lead is identified as clearly not being "normal" — it becomes easier to recognize more subtle abnormalities in neighboring leads.
  • There is subtle-but-real ST-T wave depression in the other 2 inferior leads ( = leads II and aVF). In support that these inferior lead ST-T wave findings may be acute — is the shape of the ST segments in high-lateral leads I and aVL (ie, the ST segment takeoff is straightened in these leads, with a hint of ST coving).

  • In the chest leads, in addition to the QS in leads V1 and V2 — there is slight ST elevation and definite straightening of the ST segment takeoff in lead V2. In a patient with chest pain — this is simply not a "normal" ST-T wave in lead V2.
  • In contrast — none of the other chest leads manifest any ST elevation at all. Instead — lead V1 and leads V3-thru-V6 are remarkable for the nonspecific ST-T wave flattening in each of these leads.

PEARL #3: The ST-T wave appearance in ECG #1 brings to mind the possibility of the South African Flag pattern — in which there is ST elevation (or hyperacute T waves) in lateral limb leads I and aVL — reciprocal ST-T wave depression in lead III — and ST elevation in lead V2, but not in any of the other chest leads. As we have reported on a number of posts in Dr. Smith's ECG Blog (Please see my comment at the bottom of the page in the April 8, 2022 post) — the South African Flag pattern suggests that there may be acute OMI of either the 1st or 2nd Diagonal Branch of the LAD.
  • Alternatively — some patients with acute LAD OMI may present early on with ST elevation limited in the chest leads to lead V2 — with ST elevation (or hyperacute T waves) only later developing in other chest leads (as turned out to be the case in this 2nd Patient).

PEARL #4: In favor of acute OMI for ECG #2 until proven otherwise is: i) The finding of definitely abnormal ST-T waves in lead III and lead V2ii) The QS complexes in leads V1 and V2, with delayed transition showing no more than tiny initial r waves until lead V5; andiii) Abnormal ST-T waves in this patient with new chest pain in no less than 11/12 leads (ie, in leads I,aVL; II,III,aVF; and in all 6 chest leads)!

PEARL #5: It is worthwhile to keep in mind that the ECG finding of low voltage in a patient with acute OMI may be very relevant — as among the list of causes of low voltage is extensive acute MI with depressed LV function from myocardial "stunning" (For more on the causes and clinical significance of low voltage — Please see My Comment at the bottom of the page in the November 12, 2020 post in Dr. Smith's ECG Blog).

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