A 50-Something Male with 2 hours of Chest discomfort

This ECG was texted to me in real time, but I did not notice the message until about an hour after it came. 

"50 + yo. Concerning history, known CAD"

Recorded 2 hours after pain onset:

What do you think?

This was my response:

"This looks like a worrisome EKG. It looks like an Occlusion MI (OMI), but I am not 100% certain. But by now you must have a repeat ECG.  Can I see it?"

Pendell Meyers had an identical response when I sent it to him.

PM Cardio AI algorithm said "OMI with high confidence"

Explanation: There is subtle ST Elevation in inferior leads, with a hyperacute T-wave in III, reciprocal STD in aVL with an inverted T-wave in aVL, as well as an inverted T-wave in V2, and up-sloping ST segments in V5,6 with a biphasic (up-down) T-wave.

The first hs troponin I was barely detectable at 4 ng/L.

He sent me an old one from 2 years prior:

The STE is now known to be new.  

This makes the first one diagnostic.

There is some LVH vs. Benign T-wave inversion in V3-V6.

A repeat ECG was recorded 80 minutes after the first, at 200 minutes after pain onset:

There are dynamic changes.  Confirms that the first one is diagnostic.

The cath lab was activated.  The interventionalist asked for another troponin, which shortly returned at 66 ng/L.

Another ECG was recorded while waiting for the cath team (it was nighttime). This was at 140 minutes after presentation, or 260 minutes after pain onset:

Similar to the 80 minutes ECG.

Angiogram:

Culprit for the patient's inferior ECG changes and non-ST elevation myocardial infarction is a 100% acute thrombotic occlusion of the proximal RCA.

It was opened and stented.

Formal bubble contrast echo:

The estimated left ventricular ejection fraction 57%.

Regional wall motion abnormality-inferolateral.

Regional wall motion abnormality-inferior.

No further troponins were measured.

Here is a next AM ECG:

Now there are new inferior Q-waves.  

There is deeper T-wave inversion in V3-V6 than on the baseline ECG above.

The patient was diagnosed with a"Non-STEMI."

To me, that is a meaningless diagnosis.  

Here is the main learning point:

The infarct was due to an occluded artery (Occlusion MI, OMI).  In 30% of OMI, there is no significant ST Elevation.  They should be called Occlusion MI.

Traditionally, Occlusion MI (OMI) myocardial infarctions that are not STEMI are called NonSTEMI.  They have large infarcts and high mortality.

Likewise, Non-Occlusion MI (Non-OMI, or NOMI) (artery is not occluded) myocardial infarctions are given the same name (Non-STEMI) even though they are qualitatively different: they have small infarct size and FAR lower mortality that NonSTEMI-OMI.  

Calling BOTH of these very different pathologies by the same name ("Non-STEMI") simply because of one very inaccurate ECG characteristic (presence of absence of ST elevation) obscures the reality of the underlying pathology and its danger.

Call these what they are:  Occlusion MI!

Other Learning Points:

1. Learn to recognize subtle OMI

2. Door to opening is dependent upon recognition of these subtle findings.

3. The first troponin is not helpful to allay your concerns

4. The PM Cardio Bot (AI ECG OMI interpretation) is amazingly accurate and we hope it will be available to all soon.

5. RCA occlusion can (and often does) affect the lateral wall, manifesting in V5 and V6.  

6. In fact, when inferior OMI does manifest in V5,6, there is still always STD in aVL (in our study, this was true in 33/33 cases; this is because aVL is high lateral and V5,6 are more inferior)

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My Comment by KEN GRAUER, MD (3/19/2023):

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Interesting case presented above by Dr. Smith — that emphasizes important points about the OMI Paradigm. I focus My Comment on some additional aspects of this approach.

• For ease of comparison in Figure-1 — I’ve reproduced the first 3 tracings in today’s case.

What Is It About the 1st ECG?

WHY was the initial ECG in today’s case immediately recognized by Drs. Smith and Meyers as “worrisome”? My thoughts on seeing this tracing  ( = ECG #1 in Figure-1) — were as follows:

• The “final diagnosis” in today’s case was a "Non-STEMI" — despite a cardiac cath that showed a proximal RCA occlusion. As per Dr. Smith — diagnosing today's case in that way indicates a misunderstanding of the pathophysiology involved. The reason the initial ECG is so concerning — is that it already suggests high likelihood of OMI ( = Occlusion-based MI) in this 50-ish year old man who presents with a 2-hour history of new chest pain.
• To realize — Assessment of ECG #1 is complicated by knowing: i) That today’s patient has a history of documented CAD; and, ii) The lack of a prior tracing for comparison at the time the initial ECG was interpreted. That said — the 1 lead in ECG #1 that has to be assumed acute until proven otherwise — is lead aVL (within the RED rectangle in ECG #1). Today’s patient is having new chest pain — the R wave in lead aVL is tiny, but it is preceded by a disproportionately deep Q wave (considering the small amplitude of the R in aVL) — the ST segment in lead aVL is coved, and the inverted T wave in this lead is clearly hypervoluminous (and disproportionate compared to the small size of the QRS in this lead).
• In support of our presumption that ST-T wave changes in lead aVL are acute in this patient with new chest pain — is the mirror-image opposite ST-T wave picture in lead III (ie, There is slight-but-real ST elevation — straightening of the ST segment takeoff — and a “fatter”-than-it-should-be hyperacute T wave in this lead).
• 
  
• To EMPHASIZE: ST-T wave abnormalities are also present in most other leads in ECG #1 — but they are clearly more subtle, and difficult to declare as “acute” in this patient with known coronary disease in the absence of a prior ECG for comparison.
• 
  
• Editorial Comment: As per Dr. Smith — It is encouraging to see that the PMcardio AI interpretation of ECG #1 was made with high confidence for the diagnosis of acute coronary occlusion (because the PMcardio AI program was able to recognize the hyperacute findings in leads III and aVL). This signals tremendous improvement in the ability of computerized programming using Artificial Intelligence to “learn” when properly “taught” (ie, programmed) — how to detect acute coronary occlusion at an early point in the process, even without ST elevation.

Figure-1: Comparison between the first 3 ECGs in today’s case.

What We Learn from the Prior Tracing?

As per Dr. Smith — as soon as a prior ECG from today’s patient became available — the diagnosis of an acute (presumably ongoing) cardiac event was confirmed. 

• To EMPHASIZE: We are not told the circumstances under which ECG #2 was obtained. As a result — we do not know if ECG #2 represents a stable “baseline” tracing — or whether it might have been obtained during a period of ischemia in this patient with a history of known coronary disease. That said — we do know that ECG #2 was the last ECG on file prior to this patient’s presentation to the ED on the day of admission. As a result (as per Dr. Smith) — this confirms that the ST-T wave changes in the limb leads of ECG #1 are new since the last ECG was recorded.

Looking Closer at ECG #1 vs ECG #2:

Sinus rhythm is present in both ECG #1 and ECG #2, albeit the heart rate is slightly slower in ECG #1. It’s important to note that both the frontal plane axis, as well as the sequence of R wave progression and QRS amplitudes — are different in the 2 tracings. That said — I completely agree with Dr. Smith that compared to the prior tracing — acute changes are seen on ECG #1:

• The change in frontal plane axis between the 2 tracings should not be expected to result in the disproportionate, hypervoluminous T wave inversion that we see in lead aVL of ECG #1. It should also not result in the hyperacute-appearing upright T waves seen in leads III and aVF of ECG #1, that were so flattened in the prior tracing.

In the Chest Leads of ECG #2:

• Voltage criteria for LVH are satisfied in lead V6 (R wave in V6 ≥18mm). R wave amplitude is also unexpectedly tall in leads V4,V5. ST-T waves especially in lateral chest leads V4,V5,V6 — manifest the typical appearance of LV “strain” (ie, slight J-point ST depression — with asymmetric, slowly downsloping ST segment that terminates in a more rapid rise back to the baseline). [For more on "My Take" regarding the ECG diagnosis of LVH and "strain" — Please see My Comment at the bottom of the page in the June 20, 2020 post of Dr. Smith’s ECG Blog].
• 
  
• NOTE #1: While LVH does not generally result in the slight J-point depression, ST segment flattening, and down-up terminal T wave seen in lead V3 of ECG #2 — this could still be a longstanding finding from LVH in a patient with surprisingly tall R waves beginning in lead V3.
• NOTE #2: The ST segment coving with shallow but symmetric T wave inversion in leads V2-thru-V6 — does represent some ST elevation that has occurred in leads V3-thru-V6 of ECG #1, when one considers that there was slight-but-real ST depression on the prior tracing!
• 
  
• PEARL: New ST-T wave elevation or depression is often much harder to assess when a baseline tracing shows ST-T wave abnormalities from LVH with “strain” and/or in a patient with ECG abnormalities from preexisting coronary disease (and today’s patient had LVH and known coronary disease).

What Do We Learn from ECG #3?

As per Dr. Smith — the repeat ECG in today’s case ( = ECG #3 — done 80 minutes after ECG #1 when chest pain returned) — confirmed the diagnosis of acute coronary occlusion because of dynamic ST-T wave changes compared to ECG #1.

• Q waves are now present in each of the inferior leads in ECG #3. 
• The ST-T waves in leads III and aVF of ECG #3 — are now clearly more hyperacute than they were in ECG #1 (ie, there is now definite ST elevation — with T waves that are obviously much “fatter”-at-their-peak than they were in ECG #1 ).
• Support that these changes in leads III and aVF are real — is forthcoming from the equally dynamic change in the ST-T wave in lead aVL of ECG #3 (that now shows J-point ST depression — with a “fatter” T wave at its nadir).
• 
  
• NOTE #3: I thought ECG #3 localized the “culprit” artery to the proximal RCA because: i) ST-T wave elevation and hyperacuity were now pronounced in leads III and aVF — but lacking in lead II; — ii) Reciprocal ST-T wave changes were equally marked in lead aVL (more so than in lead I); — and, iii) There was now slight ST elevation with a prominent upright T wave in lead V1 — which in a patient with RCA OMI suggests that there may be acute RV involvement.
• 
  
• Elsewhere in the chest leads — artifact precludes drawing conclusions about ST-T wave changes in leads V4,V5 of ECG #3 — but the ST coving and sharp T wave inversion in lead V3 (compared to the appearance of lead V3 in ECG #1) — is another dynamic change in this repeat ECG.

BOTTOM LINE regarding Today’s CASE:

In 2023, given the current state of our knowledge — the discharge diagnosis that was given for this case (ie, that of a Non-STEMI) — is meaningless and misleading. Instead — Cardiac cath proved there was acute occlusion of the proximal RCA. 

• In context with the presenting history — the diagnosis of acute OMI was strongly suggested as soon as the initial ECG was recorded. 
• The need for prompt cath and PCI was firmly established as soon as this initial ECG was compared with the prior tracing ( = ECG #2).
• The follow-up ECG (done 80 minutes after ECG #1, when chest pain returned) — was diagnostic of acute OMI, removing doubt about acute occlusion until proven otherwise by prompt cath.
• The normal initial troponin is not unexpected, and does nothing to dissuade the diagnosis of acute OMI.
• Multiple serial ECGs should have been obtained long before 80 minutes after the initial ECG was recorded (Doing so would have established the diagnosis of acute occlusion that much sooner).
• There is no “magic” to prompt diagnosis of OMI in cases such as today’s — since even AI (by use the PMcardio interpretation program) is now able to establish “with high confidence” from the initial ECG that OMI is occurring.
• I don’t understand continued use by all-too-many clinicians (including cardiologists) — of the outdated, meaningless and misleading term “Non-STEMI” — even after cardiac cath proof that acute occlusion did occur.