Why you should use the Queen of Hearts and record serial ECGs more often. If you wait for troponin.....

This was sent to me by a French colleague, Olivier Peyronie

"Yesterday we received a 62 yo man with diabetes, hypertension and smoker. He reported typical chest pain since 4H AM and arrived at our ED at 10h with ongoing chest pain. The first ECG (10h14) showed TWI in inferior leads."

Time zero:

What do you think?

Queen of Hearts Diagnosis: Not OMI with High Confidence (but in French!)

French for "Not OMI"

First troponin was 290 (hh-TnT, <14).

"Despite the very elevated first troponin, cardiologist ordered a 2nd troponin...I really don't understand why...."

Second ECG (14h58, I think we should have performed earlier...) showed STD in V2-V3. 

4 hours 44 minutes later:

What do you think?

 

Now there is ST depression in V2-V4.  This is diagnostic of posterior OMI.

Queen of Hearts diagnosed OMI with high confidence:

The queen of hearts transforms 6 x 2 ECGs into 3 x 4 ECG.

You can see that the overall interpretation is derived from lead-specific interpretations in V2 and V3 

(ST depression maximal in V1-V4, vs. V5-6, is 97% specific for OMI!)

"The patient was transferred to cardiology at the referral hospital (we don't have cardiology in our hospital)."

"Unfortunately, the cardiologist waited until the next day to refer the patient for angiography and intervention because patient did not meet criteria for "STEMI"."

"Finally they changed their mind (I don't know the reason) and coronarography was performed at 2h AM (22h after the pain started)."

"The coronary angiography showed a 100% ostial main (obtuse) marginal occlusion!"

"Dominant right coronary, atherosclerotic and calcified. Presence of a single coronary lesion: occlusion of the ostial main marginal. Successful primary angioplasty of the mid-circumflex artery towards the main marginal branch with the implantation of a drug-eluting stent. Good angiographic result. Complete revascularization."

The echocardiogram shows a preserved left ventricular ejection fraction (LVEF) of 55% with marked basal and mid inferolateral and basal anterolateral hypokinesia.

Peak troponin: 128,000 ng/L.  This is an enormous posterior infarct!

And Olivier finishes with this commentary:

"Yet another example in favor of abandoning STEMI criteria for diagnosing OMI. And the absurdity of requesting several troponins when the pain is typical and, moreover, the first troponin is already positive without any another valid reason."

Smith: and all you need is the Queen of Hearts to easily make the diagnosis.  Olivier has it, as it is approved in the European Union.  Waiting for the FDA.

Click here to sign up for Queen of Hearts Access.

Smith commentary:

1. You must record frequent serial ECGs for patients with chest pain. Every 15 minutes!

2. You must be an expert OMI ECG reader (very difficult) or use the Queen of Hearts.  

3. If you don't have near perfect ECG interpretation, then, in order to know whether your patient with persistent chest pain has esophageal pain or acute MI, you will need to wait for 1-2 troponins while myocardium dies, irreversibly.

4. Even if you fail to recognized OMI on the ECG and need to wait for troponins, if they return elevated, that is an indication for emergent cath lab activation regardless of the ECG.

5.  The sad fact is that, although the guidelines state clearly that MI with persistent symptoms should go to the cath lab in "less than 2 hours" (both AHA/ACC guidelines and Eur Soc Cardiology guidelines), this guideline is rarely followed (6% of the time in Lupu's study - see reference below) 

Lupu L, Taha L, Banai A, Shmueli H, Borohovitz A, Matetzky S, Gabarin M, Shuvy M, Beigel R, Orvin K, et al. Immediate and early percutaneous coronary intervention in very high-risk and high-risk non-ST segment elevation myocardial infarction patients. Clin. Cardiol. [Internet]. 2022;Available from: https://onlinelibrary.wiley.com/doi/10.1002/clc.23781   

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MY Comment, by KEN GRAUER, MD (10/22/2024):

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Today's case provides yet one more example of how the recognition of acute coronary occlusion was needlessly delayed for over a day. 

• For clarity in Figure-1 — I've consolidated and labeled the 2 tracings in today's case, which I've put together to facilitate comparison.

Figure-1: Comparison between today's initial ECG — and the repeat ECG obtained 4+ hours later.

MY Thoughts on Today's CASE:

The history is extremely concerning = a 62-year old man with risk factors, who was apparently awakened at night for new-onset, severe CP (Chest Pain). This persisted for 6 hours — at which time ECG #1 was obtained.

• By definition — this worrisome history immediately places this patient in a higher-risk likelihood for having an acute event. Clinically — this means we need to pay even more attention to seemingly subtle ECG changes.
• The above said — the fact that this patient has now had CP for ~6 hours — means that even if he is having an acute event — his initial ECG might show any of a variety of ECG changes — from acute ST elevation — to reperfusion T wave inversion — to various (subtle) degrees of "pseudonormalization" (if spontaneous reperfusion of a "culprit" artery has just occurred).
• KEY Point: Notation of the presence and relative severity CP at the time each ECG is recorded (easily followed by using a CP "scale" from 1-to-10) — could provide invaluable insight as to the likely status of a "culprit" vessel (ie, Did this patient's CP improve since when it awakened him from sleep? — or — Is his CP now at its worst?).

ECG #1 — shows such subtle but-definitely-present changes in multiple leads:

• The rhythm is sinus at 80-85/minute. Intervals (PR-QRS-QTc) are normal. The frontal plane axis is leftward — but not leftward enough to qualify as LAHB (since the QRS is not predominantly negative in lead II). There is no chamber enlargement.
• There are small, narrow Q waves in leads I, aVL. Whether these are normal septal q waves — or something more — is not initially apparent.
• R wave progression is normal.

In a higher-risk patient with new CP — leads I and aVL caught my "eye", as there is subtle straightening of the ST segment takeoff in both of these high-lateral leads.

• That this finding in leads I and aVL is likely to be "real" — is supported by ST segment coving and T wave inversion in leads III and aVF (with ST flattening in the 3rd inferior lead = lead II).
• Further support of an acute ongoing event is provided in lead V2 — which manifests a disproportionately "bulky" T wave, that is clearly "fatter"-than-it-should-be at its peak given the size of the QRS in this lead (BLUE arrow in V2).
• As we often note in Dr. Smith's ECG Blog — there normally should be slight, upward sloping ST elevation in leads V2 and V3. The YELLOW arrow indicates a lack of this slight normal ST elevation in lead V3.
• The remaining 4 chest leads (V1; V4,5,6) — all show abnormal ST segment flattening. 

Impression of ECG #1: Although ECG changes in this initial tracing are subtle (and criteria for a STEMI are clearly not met) — 11/12 leads show ST-T wave abnormalities in this higher-risk patient. I was therefore suspicious of a postero-lateral OMI — which would localize the "culprit" artery to the LCx (Left Circumflex).

• I wondered if the "bulky" upright T wave in lead V2 might be the result of some spontaneous reperfusion (which is why it would be so helpful to find out if the patient's CP had decreased).

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ECG #2 — was only obtained 4+ hours after ECG #1 ...

• As per Dr. Peyronie — the initial ECG should have been repeated much sooner! In a patient with ongoing CP who is actively evolving an OMI — repeating the ECG within 10-to-20 minutes will often show significant change.

Comparing the 2 tracings in today's case:

• When ECG changes are subtle — it is important to compare serial ECGs side-by-side. When this is not done — subtle changes will be missed.
• Leads I and aVL now show subtle-but-real ST elevation.
• Leads II and aVF now show slight ST depression.
• The upright, "bulky" T wave in lead V2 — is now disproportionately taller than it was in ECG #1 — and there is now slight J-point ST depression that was not present earlier.
• Perhaps the most decisive ST-T wave change between ECG #1 and ECG #2 — is seen in lead V3, which now clearly shows ST segment straightening and definite ST depression that was not seen previously (YELLOW arrows).

Putting It All Together: 

If after seeing ECG #1 there was doubt about the diagnosis of acute postero-lateral OMI (presumed LCx "culprit" ) — the ECG should have been repeated within 20 minutes.

• The above said — Comparison between ECG #1 and #2 suggests subtle-but-real "dynamic" ST-T wave changes that confirm the diagnosis of acute OMI and the need for prompt cath with PCI.
• I wonder if the reason for repeating the ECG 4+ hours after the initial tracing — was because of an increase in CP? The new (albeit subtle) ST elevation in leads I,aVL — and the above noted changes in leads V2,V3 — suggest that if there had been some spontaneous reperfusion, that the "culprit" artery was again reoccluding.