How important are old ECGs in Non-obvious cases of potential OMI?

In the last post, we saw how important old ECGs are in assessing the current ECG in a patient without atypical presentation (in this previous case, the patient had no chest pain, and the apparent inferior OMI did not have reciprocal ST depression in lead aVL).  

Here is that last post: A 90-something with acute stroke. She has no chest symptoms. What is the diagnosis?

Here is another new case in which the previous ECGs were crucial:

A 60-something male had sudden crushing chest pain.  He stated he had never had this before.  Here is his first prehospital ECG:

1st Prehospital ECG

What do you think?

There is what could be hyperacute T-waves in V1 and V2.  There is some ST depression in V5,6 which suggest the "Swirl" pattern.  [If you are not certain what "Swirl" is, see here: Precordial Swirl -- 20 cases of Swirl or Look-Alikes]

Here the PM Cardio Queen of Hearts AI app gives her interpretation:

With explainability, here you can see which leads are informing that interpretation:

We (Pendell Meyers and I) taught the Queen by labeling ECG as either "Active" OMI or "Reperfused" OMI (and also as "Acute" or "Subacute" and with high or low confidence.  So there were 8 categories of OMI.  

However, she does not (yet) make use of those training classifications to differentiate active from reperfused.  So when she sees what appear to be reperfusion (Wellens') waves, as there are in aVL and V3, she reports "OMI".  

We who know ischemic ECGs know that really when T-wave inversion is specific for coronary thrombosis that it indicates reperfusion of the artery, not active occlusion.

Future versions of the Queen will differenitate between "Active" and "Reperfusd."  I personally can hardly wait for that future version!

Here is the 2nd prehospital, 14 minutes later

Now, lead aVL looks particularly worrisome (it looks as if it is re-occluding), with less T-wave inversion and increasing ST Elevation, and with inferior reciprocal ST depression.

The cath lab was activated by the medics.  The patient was given sublingual NTG and the pain resolved.

Here is the first ED ECG recorded, now pain free after sublingual Nitro:

There is what appears to be a reperfusion T-wave in I and aVL.

The emergency physician was skeptical and believed the ECG to be a mimic, a false positive.  

So they looked into the patient's chart.

Here is what they found:

The patient was recently seen in 2 months prior for concerns of ACS and was admitted for diagnosis of "NSTEMI, but all troponins were undetectable) 

Here is his ECG from 5 months prior:

Very similar

Here is the ECG from the presentation 2 months prior:

Looks very similar to above ECGs

Here is an ECG from the same presentation 2 months prior, now 30 minutes after the first:

After seeing all of these, the providers de-activated the cath lab.  

Outcome:

All 4 serial hs troponin I, out to 6 hours, were undetectable.

Formal Echo on this visit after ruling out by troponins:

Normal estimated left ventricular ejection fraction; 66%.

No wall motion abnormality identified.

Normal LV cavity size with moderately increased wall thickness.

Learning Point:

1. If you have old ECGs available, seek them out and compare today's ECGs to those old one.

The Queen of Hearts has not yet been trained to compare with previous or with serial ECGs.  That is coming in the future with further training.

The Queen of Hearts AI app will hopefully be FDA approved in Q1 of 2024.  It is already approved in Europe.

YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!!  (THE PM CARDIO OMI AI APP)

If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

https://share-eu1.hsforms.com/18cAH0ZK0RoiVG3RjC5dYdwfyfsg

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My Comment by KEN GRAUER, MD (11/14/2023):

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One of the most helpful clinical clues in support that an acute cardiac event is ongoing — is the finding of "dynamic" ECG changes. 

• As is often emphasized on Dr. Smith's ECG Blog — the evolution of an acute OMI is not necessarily static — but may be "dynamic". By this, it is meant that even before treatment with thrombolytic agents and/or PCI — the acutely occluded "culprit" artery may spontaneously reperfuse. When this happens — it will typically be accompanied by reduced ST elevation and reduced (or relieved) chest pain.
• BUT — What spontaneous reopens — might just as easily spontaneously reclose — sometimes passing through this process of spontaneous reopening — followed by reclosure — then reopening — multiple times until the vessel's final state is attained.
• 
  
• THEREFORE — In a patient who presents with new CP (Chest Pain) — ST-T wave changes that are correlated to changes in the presence and relative severity of symptoms is indication of dynamic ST-T wave changes that suggest acute evolution of an OMI in progress. (For examples of this phenomenon — See My Comment in the February 14, 2018 — July 21, 2020 — and December 22, 2022 posts in Dr. Smith's ECG Blog).

The CAVEAT — As invaluable as recognition of dynamic ST-T wave changes may be in support of an acute cardiac event in a patient who presents with new CP — this ECG finding is not perfect.

• From a clinical standpoint — detection of dynamic ST-T wave changes that are correlated to changing severity of CP signal a need to assume acute OMI until proven otherwise.
• That said — We've published examples of occasional exceptions, when repolarization variants or some other form of cardiac pathology (ie, myocarditis) and not acute OMI turned out to be the cause of dynamic ST-T wave changes. (For examples of such exceptions — See My Comment in the January 9, 2019 — August 22, 2020 — and June 30, 2023 posts in Dr. Smith's ECG Blog).

Today's case provides yet one more example of how dynamic ST-T wave changes are not an infallible indicator of an acutely evolving OMI.

• For clarity in Figure-1 — I've reproduced the first 3 tracings shown in today's case to illustrate how much ST-T wave changes may vary in this patient who was not having an acute OMI.

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

How Would YOU Interpret the Serial Tracings in Figure-1?

As per Dr. Smith — Today's patient is a 62-year old man who developed sudden, severe CP. Treatment with sublingual NTG relieved his symptoms. EMS arrived — and recorded 2 ECGs. The 3rd tracing in Figure-1 was the initial ED ECG — obtained at a time when the patient's CP had resolved. I'd make the following points:

• ECG #1 — is clearly abnormal. The rhythm is sinus — with normal axis and intervals.
• I added dotted RED lines at the transition between leads V2 and V3 in both of the prehospital ECGs to highlight this common feature in EMS tracings — in which large QRS complexes will often be truncated. We get a better idea of the true S wave amplitude in lead V2 in the initial ED ECG ( = ECG #3) — as shown by the double RED arrow in the bottom tracing in Figure-1.
• NOTE: It's important to be aware of this "automatic truncation" effect so commonly seen in EMS ECGs — because one might otherwise misinterpret the seemingly "large" ST-T wave as disproportionate to a short S wave in ECGs #1 and 2, and therefore presume this to represent a hyperacute T wave (See My Comment in the June 20, 2020 post in Dr. Smith's ECG Blog).

Returning to the serial ECGs in Figure-1:

• Even accounting for truncation of QRS amplitudes in leads V1,V2,V3 of ECG #1 — the ST-T waves are clearly of concern. There appears to be significant ST elevation, especially in lead V1 (somewhat less in lead V2) — followed by a biphasic and terminally negative T wave in lead V2 — with varying degrees of ST depression and T wave inversion in virtually all other leads. In a 62yo man with new CP — the onus falls on us to assume acute OMI until proven otherwise.
• 
  
• 14 minutes later — ECG #2 was recorded by EMS. Lead-by-lead comparison between ECG #1 and ECG #2 shows slight change in axis (Note the much deeper S wave in lead I of ECG #2) — but this is probably not enough to account for the obvious change in ST-T wave appearance in leads I, III and aVL between the 2 tracings.
• In the chest leads — the QRS complex in lead V1 looks entirely different in ECG #2 compared to QRS appearance in ECG #1. That said, R wave progression between these 2 tracings for the remainder of the chest leads is similar. This leads me to believe that the deeper T wave inversion in leads V4,V5,V6 of ECG #2 most probably reflects a real change.
• 
  
• Shortly thereafter, on arrival in the ED — ECG #3 was recorded. Lead-by-lead comparison with ECG #2 — reveals further significant ST-T wave changes, in this patient whose CP has now been totally relieved. Specifically — T wave inversion in leads I and aVL is now clearly deeper than it was in ECG #2 — and the T waves in each of the inferior leads are now prominent and upright, whereas there previously was ST depression in each of these leads. 
• 
  
• BOTTOM Line: In association with a changing severity of symptoms — the serial ECGs in Figure-1 clearly show real ST-T wave changes. In this patient who presented with new CP — this qualifies as "dynamic" ST-T wave change.

CASE Conclusion: As per Dr. Smith — the cath lab was initially activated on the basis of the history of changing symptoms occurring in association with dynamic ST-T wave changes on these 3 serial ECGs shown in Figure-1.

• BUT — Review of this patient's medical chart revealed previous ECGs showing a similar pattern of labile ECG changes. Some patients do this ... that is, show a pattern of labile ST-T wave changes not due to an acute coronary event.
• 
  
• Despite the seemingly worrisome ST-T wave changes on serial tracings shown in Figure-1 — an acute event was definitively ruled out by 4 consecutive negative hs troponins — with further support provided by an Echo showing excellent LV function without wall motion abnormality.
• Echo did show "moderately increased wall thickness" — so LVH is presumably playing a role in the changing ST-T wave appearance seen on this and previous hospital admissions (albeit the ST-T wave changes that we see are not those expected simply from LVH).
• 
  
• FINAL Thought: Looking at the ECG changes seen in the 3 serial tracings shown in Figure-1, in association with the changing severity of this patient's symptoms — I completely agree with the initial decision to activate the cath lab. That said — following review of this patient's chart (that revealed a similar pattern of labile ST-T wave changes on previous admissions) + 4 consecutive negative hs troponin values — an acute event could be definitively ruled out in this patient whose CP had totally resolved. Cancelling cath lab activation was completely appropriate. That said — I would not be at all surprised if frequent future CP episodes occur, that at some point cardiac catheterization does get done.
• 
  
• P.S.: As an incidental note — Did you see the changing QRS morphology in leads III and aVF of ECG #3? (ie, from a QR — to rSR' — to rsR's' morphology). I periodically see this pattern in these 2 leads — which I attribute to the inferior location of Leads III and aVF, such that diaphragmatic motion from normal respiration may result in enough cardiac displacement to alter QRS morphology. I find it helpful to be aware of this phenomenon — since transient Q waves in either of these leads is that much less likely to be a marker of prior infarction.