A man in his 30s with chest pain. How was he managed? What if they had used the Queen of Hearts?

Written by Pendell Meyers

A man in his late 30s with history of hypertension, tobacco use, and obesity presented to the Emergency Department for acute chest pain which started approximately 3 hours prior to arrival, in the setting of a very stressful situation. The pain radiated down both arms, 10/10 in severity. He stated it did not feel like his prior episodes of reflux. Vitals were within normal limits except some hypertension. 

Triage ECG:

And here she explains her assessment:

The ECG was read as simply "No ST elevation." Which is true.

The initial high sensitivity troponin I returned at around 3300 ng/L. No repeat ECG was done at this time.

CT pulmonary angiogram (unnecessary, often done while missing OMI) was unremarkable.

The diagnosis of "NSTEMI" was made. The physician initiated routine transfer to the local PCI center. Cardiology refused to be the admitting physician because it was "NSTEMI", and forced the ED physician to admit the patient to the hospitalist. 

Of course, there was terrible boarding and the patient was considered non-emergent (NSTEMI), and so could not leave the ED for some time. 

Watch what happens in real life to NSTEMIs with refractory chest pain:

"During ED course patient received 2 sublingual nitro with no improvement in his pain. I discuss this with cardiology who requested treating his hypertension with metoprolol 25 mg PO which mildly improved his pressure to 130 systolic. Patient received 4mg morphine which improved symptoms to 3 out of 10. Repeat ECG shows no changes."

Here is that repeat ECG below, around 3 hours after triage:

Repeat troponin during delay rose to 18,700 ng/L. 

Overnight the patient finally got transferred to the PCI center. 

On arrival the repeat troponin was greater than 25,000 ng/L (the upper limit of reporting in this case). None further were ordered.

Here is the ECG the next morning 8am:

Subacute OMI but still ongoing.

Angiogram around 9am:

Culprit lesion mid LAD 100% stenosis TIMI 0

TIMI 3 after PCI

Severe apical dyskinesis, severe anteroapical akinesis. LV EF 35%.

Scattered other nonobstructive CAD.

Last ECG:

Final Diagnosis: "NSTEMI"

This patient will likely suffer heart failure and early death due to the diagnosis of "NSTEMI"

Learning Points:

Despite NSTEMI guidelines recommending emergent angiography for NSTEMI patients with refractory ischemic symptoms, this is simply not done in many systems, and this has been recorded in a study as well.

Instead, pain is numbed and thus ischemia is obscured with opioids, excuses like hypertension are blamed, and unnecessary CT pulmonary angiograms are focused on. The result is systematic misdiagnosis and delay in treatment for OMI patients with NSTEMI. Once in a while they die during the hospitalization, but I fear that many more like this patient survive for now to develop lifelong increased morbidity and mortality from heart failure.

This patient does not show up in the STEMI registry, and the time to reperfusion will likely not be identified as the problem that it was.

The STEMI registry will show very high sensitivity of the ECG for STEMI, obscuring the fact the STEMI has low sensitivity for OMI

Queen of Hearts sees it easily, like readers of the blog would.

Even if you don't have the skill or the technology to see this on the ECG, OMI is a clinical diagnosis that happens to your patients that you must be able to understand and diagnose it better than the current STEMI/NSTEMI paradigm.

YOU TOO CAN HAVE 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.

Here you will sign up for the Queen of Hearts on the Telegram app:

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

 

Or, you can get the PM Cardio app with Queen of Hearts function through this QR code.

When you register on the app, you need to say you are from a supported country in the EU.  You will get 5 free reports.  After that, it is $30 per month.

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MY Comment, by KEN GRAUER, MD (1/20/2024):

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Today's unfortunate story reviews a case of deWinter T waves that was totally missed. We’ve reviewed multiple variations on this theme in Dr. Smith’s ECG Blog (See My Comment at the bottom of the page in the October 6, 2023 post — and the April 17, 2023 post — to name just two). 

• What regularly impresses me about this clinical entity (that predicts impending and/or ongoing LAD OMI) — is that depending on when during the process a given ECG is obtained — the ECG “picture” of deWinter T waves may vary in a number of ways from the 8 clinical ECG examples presented in the original NEJM manuscript by deWinter et al (Figure-1).
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• Today’s case presents yet another variation — in that what represents clear indication of a deWinter T wave in lead V2 of today's initial ECG — then goes on to manifest a more traditional evolution of an anterior OMI without additional deWinter T waves.

Figure-1: The deWinter T Wave Pattern, as first described by Robbert J. de Winter et al in N Engl J Med 359:2071-2073, 2008. ECGs for the 8 patients shown here were obtained between 26 and 141 minutes after the onset of symptoms. (See My Comment in the April 17, 2023 post for more on this pattern).

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Today's Initial ECG:

As we have stressed on many occasions — the importance of recognizing deWinter T waves, is that in a patient with severe, new-onset CP (Chest Pain), as in today's case — the diagnosis of an acute OMI until proven otherwise should be instantly made the moment the ECG picture in lead V2 of today's initial ECG is seen (within the RED rectangle in Figure-2).

• More than just a QS pattern in lead V2 — there has been loss of r wave from lead V1, with initial fragmentation of this QRS complex (ie, more than just a QS — lead V2 manifests a qrS complex). R wave progression is limited throughout the remainder of the chest leads — with r waves remaining small and transition delayed until lead V5-to-V6.
• That the T wave in lead V2 is hyperacute can be recognized from across the room. This hugely disproportionate T wave could easily "swallow up" the tiny QRS in this lead — and is all but screaming, "Take me to the cath lab — my LAD is acutely occluded!"
• Although most of the time with deWinter T waves — giant T waves are seen in more than a single lead — the T waves in leads V3-thru-V6 are nevertheless hyperacute (BLUE arrows in these leads highlighting disproportionate increase in size, with "fatter"-than-expected T wave peaks for each of these leads).
• ST-T wave changes in the limb leads are more subtle — but still present. Although not appreciably elevated — the shape of the ST-T waves in leads I and aVL looks acute. In this context — I interpreted the straightening of the ST segments in leads III and aVF as a reciprocal change.
• 
  
• BOTTOM Line: In this patient with severe new-onset CP — I interpreted the dramatic disproportionality of the T wave in lead V2, in association with much more subtle but nevertheless still hyperacute T wave appearance in the remaining chest leads as consistent with a deWinter T wave pattern. In association with reciprocal inferior lead changes and the fragmented qrS in lead V2, followed by poor R wave progression — ongoing infarction has to be assumed until proven otherwise. Prompt cath with PCI is needed (with this decision justified even before doing repeat ECGs and before learning that troponin was so markedly elevated).

Figure-2: I've labeled the initial ECG in today's case.