Patient with STEMI (-) OMI is now pain free. Is there need for emergent cath lab activation?

I was reading through a stack of ECGs to put in the formal interpretation, and came across this one:


This was my interpretation without having any clinical information:

"There is suspicion for evolving infarction in inferior, lateral, and posterior walls." ("Evolving" means that it has been going on for some time, is not very acute, probably subacute) 

Then I went into the patient's chart:

This was a 50-something female who presented from an outside hospital in the very early hours with "NSTEMI." The patient started having pain the previous evening.  She reported that she was leaving work the previous afternoon when she started having nausea and diaphoresis.  She was able to get home and shortly after returning home started having numbness of her left arm.  2 hours later, she had onset of chest pain.  She went to the ED:

This ECG (ECG 1) was recorded at the outside hospital: time zero

There is minimal STE in inferior leads, with reciprocal ST depression in aVL.  There is a downsloping ST segment in lead V2 and a bit of ST depression in lead V3.  In this clinical situation, this is diagnostic of inferior-posterior OMI.  If I saw this, I could activate the cath lab.


She was given some nitro and heparin, which resolved her pain.  The pain continued to wax and wane. Troponin I returned at 1.38 ng/mL.  

Another ECG (ECG 2) was recorded at 1 hour after arrival:

The findings are still present.  The ECG continues to show ischemia even in the absence of chest pain.

Believe the ECG: ischemia is often clinically silent.

Instead of undergoing emergent angiogram, she was transferred to our hospital and was pain free on transfer and had continued free in the ED.

She had this ECG (ECG 3) recorded at about 12 hours after onset of symptoms (the same one I saw, posted above):

The ischemic findings are significantly improved compared to those at the outside hospital (ECGs 2 and 3), but it still shows evolving infarction.

Her initial troponin I here was 4.12 ng/mL (contemporary troponin).  A rising troponin does not by itself mean that there is continued occlusion.  Infarction that occurred hours ago but is now no longer ischemic will still have a rising troponin because elevated troponin is a delayed signal (whereas ECG ischemia is instantaneous, real time).  

And this ECG does show ongoing ischemia, in spite of absence of chest pain.

A bedside echo (not shown) revealed a clear posterior wall motion abnormality.  What does this mean?  This confirms the ECG interpretation of ischemia and posterior infarction but echocardiogram is also a delayed signal!  Myocardium that was ischemic, but is no longer ischemic, often continues to be akinetic or hypokinetic ("myocardial stunning") for hours/days/weeks.  If it was ischemic, but only a small amount sustained infarction, that wall motion will recover over hours/days/weeks.  So we expect to see a wall motion abnormality whether there is ongoing ischemia or not.  In other words, the echo does NOT tell you whether the patient needs the cath lab now in order to save myocardium.

The repeat troponin I was 3.99 ng/mL, reflecting a steady state.  Does the absence of a rise imply that there is no more ischemia?  Not necessarily.  The troponin does not easily make it into the circulation when there is 100% occlusion; it is trapped.  It is not until the artery is opened that it gets "flushed out" (my words).

Here, the ECG does still show ischemia, though diminished.  Is it diminished because the artery is opening?  Or is it diminished because much of the ischemic myocardium at risk has already infarcted and therefore no longer manifests ischemic findings?  I believe the latter: the amount of viable myocardium is diminishing.

The absence of pain can be falsely reassuring. 

She went for PCI at about 5 hours after arrival here, which would be a total of 14 hours after arrival at the outside hospital (very delayed).  

Angiogram

Mid LAD with indeterminate disease in mid vessel.

Mid RCA described as mid subsection with 65% stenosis.

Left Circumflex (LCx): LCX is a Large vessel.  LCX is a co-dominant vessel.
OM 1 (branch of circumflex) is a large size vessel supplying the posterior wall.  It is 100% occluded in the Proximal segment of the vessel.

It was opened and stented.

Here is the post PCI ECG:

Q-waves and T-wave inversion in inferior leads and lateral leads: manifestations of significant loss of myocardium and reperfusion.  Notice the large T-wave in V2.  This is a posterior reperfusion T-wave.  Reperfusion of the posterior wall results in T-wave inversion in posterior leads, which is recorded as an INCREASE in T-wave amplitude on anterior placed leads.

There was only one more troponin measured, and that was late:

Highest measured troponin is 40.19 ng/mL.  This is a pretty large infarct, fairly average for a STEMI and much larger than a typical Non Occlusion MI (NonSTEMI with open artery)
There was no mention on angiogram of collaterals supplying the affected myocardium, and this later rise in troponin shows that there it was NOT sufficient.

Echocardiogram:
The estimated left ventricular ejection fraction is 51 %.
Regional wall motion abnormality-inferior .
Regional wall motion abnormality-inferolateral.

While it is possible that these wall motion abnormalities (WMA) are due to "stunning" (ischemic myocardium that will recover), this is unlikely with this very elevated troponin.  Most of this WMA is due to infarcted, not stunned, myocardium. The only way to know for certain would be to record a "convalescent" echo at about 6 weeks, which was not done.


Learning Points
There are a number of randomized trials of "early" cath lab activation for NonSTEMI.  All which included patients whose chest pain was persistent AND which took patients at < 2 hours after ED arrival showed a benefit.  In other words, if the patients still has pain and they truly go very quickly, there is benefit.  Patients without ongoing chest pain (which includes our patient here) did not have proven overall benefit unless they had a GRACE score above 140 (TIMACS and VERDICT trials). 

So there is no proof that a patient like this needs to go to the cath lab.  But the ECG is diagnostic of OMI (Occlusion) and it has not resolved along with the pain.  There is no study which randomized patients with OMI without collateral circulation to emergent vs. delayed angiogram, and I suspect none could be done.

NSTEMIs that are pain free are a heterogeneous group, including many without ongoing infarction (Non-OMI), but also including OMI with ongoing infarction.  It just makes sense that if there is an occlusion with ongoing infarction, symptom free or not, the patient needs the cath lab now.  This case is a great example.  

I would argue that the patient should have undergone immediate cath at the outside hospital, before transfer.    There will definitely be many who disagree with me on that because they don't want a possible false positive cath lab activation.  But could it possibly be false positive even if the artery is open and the patient needs a stent tomorrow?  Why not tonight?

Here is another example case of a patient with complete LAD occlusion but without symptoms:

Why we need continuous 12-lead ST segment monitoring in Wellens' syndrome

If you knew the patient had an occlusion, even if asymptomatic, would you want to delay?


I summarize the trials of "early" vs. delayed intervention for NonSTEMI here:

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MY Comment by KEN GRAUER, MD (10/2/2020):

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I can totally relate to the circumstances under which Dr. Smith came upon the 1st ECG shown in today’s case — which appeared in a “stack” of ECGs to be read. During the years I was faced with a similar task (ie, interpreting all ECGs in a large ambulatory clinic) — I always found it especially challenging to have to complete my interpretation of the “stack” of tracings in front of me in minimal time without the benefit of any clinical history.

• I never had time to inquire about the history and management rendered for each of the patients whose ECGs appeared in the large stack in front of me. Instead — I had to be selective by limiting which tracings I needed to pull the chart on.

The 1st ECG shown in today’s case is an instructive example of just that type of ECG that one needs to look up the chart on.

• PEARL — The KEY criterion I used to optimize my time-efficiency in working through a “stack” of tracings without the benefit of any history — was my recognition of subtle ECG findings of potential clinical importance that I thought might be missed by other providers. This is precisely what Dr. Smith so astutely did in today's case.

In his discussion above — Dr. Smith correlates interpretation of the serial tracings in today’s case with clinical events. I limit my comments to the 1st tracing shown above that appeared in that “stack” of tracings for Dr. Smith to read.

• WHY did Dr. Smith need to pull the chart after seeing ECG #1? (For clarity — I’ve reproduced this 1st ECG in Figure-1).

Figure-1: The 1st ECG shown in today’s case (See text).

WHY Did Dr. Smith Pull the Chart?

Please take another LOOK at ECG #1. Remember the circumstances: YOU are asked to interpret this tracing without the benefit of any history.

• WHY should ECG #1 be of concern?

MY Thoughts on ECG #1: — The rhythm is sinus at 85-90/minute. All intervals appear normal. There is a leftward axis — but not leftward enough to qualify for LAHB (ie, the QRS complex is still predominantly positive in lead II). There is no chamber enlargement. Regarding Q-R-S-T Changes:

• There are tiny septal Q waves in leads I and aVL. These are not significant. There are no other Q waves (ie, there is a tiny initial positive deflection in each of the inferior leads).
• Regarding R Wave Progression — Transition occurs early, with a predominantly positive deflection (R wave) as early as in lead V2. This is relevant to today’s case! (See below).

Regarding ST-T Wave Changes — These are subtle — but definitely present! I illustrate my concerns in Figure-2 by the addition of BLUE lines to 10 of the leads and by addition of a mirror-image of 1 complex from lead V2.

• Take another LOOK at lead V2 in Figure-1. This is the one lead that most caught my attention in ECG #1. There is subtle-but-real ST depression in lead V2 that just should not be there. The mirror-image view of lead V2 in Figure-2 facilitates seeing why. In the inverted (mirror-image) view — the prematurely tall R wave in lead V2 becomes a deep Q wave — and the subtle ST depression becomes coved ST elevation. (For more on use of the Mirror-Test for facilitating recognition of posterior MI — SEE My Comment at the bottom of the September 28, 2020 post in Dr. Smith’s ECG Blog).

Once I recognized these abnormalities in lead V2 — I looked closely at the rest of the ECG.

• Acute (or subacute) posterior MI is often accompanied by signs of inferior infarction. ST segments in each of the inferior leads show abnormal straightening (BLUE lines) — with suggestion of slight ST elevation and a hint of ST coving in lead aVF (The J-points in leads III and aVF “look” elevated — even though the amount of actual ST elevation is minimal).
• That these subtle inferior lead ST-T wave changes are real — is supported by the shallow ST segment scooping seen in lead aVL (which looks like the mirror-image of the ST coving noted in lead aVF).
• The other high-lateral lead ( = lead I) is not normal. White there is no ST segment deviation in lead I — the ST segment is uncharacteristically flat.
• Subtle-but-real ST segment coving is also suggested in lateral chest leads V5 and V6.
• The remaining chest leads ( = leads V1, V3 and V4) all show subtle ST segment straightening (BLUE lines in these leads).

Clinical IMPRESSION: All of the above findings in ECG #1 are subtle! I didn’t think ECG #1 looked like an MI that just happened — but the ECG findings I describe above could reflect a subacute MI (ie, onset within recent hours).

• I thought the appearance of the QRS complex and ST-T wave in lead V2 was clearly abnormal. While no single other lead by itself looked acute — there are subtle-but-real ST-T wave abnormalities in no less than 11/12 leads on this tracing.
• BOTTOM Line: This is a tracing for which we would need to pull the chart to find out the History and what happened to the patient! Clearly, more information than this single tracing is needed for clinical decision-making. Dr. Smith’s detailed account (above) tells the rest.

Figure-2: I've labeled key findings in ECG #1. No less than 11/12 leads show subtle-but-real ST-T wave abnormalities (BLUE lines + the mirror-image insert in lead V2). Taken together — these ECG findings must prompt concern!