A man in his 60s woken from sleep by epigastric pain. Would you have been able to correctly diagnose him?

Written by Pendell Meyers

A man in his mid 60s with history of CAD and stents experienced sudden onset epigastric abdominal pain radiating up into his chest at home, waking him from sleep. He called EMS who brought him to the ED. He had active chest pain at the time of triage at 0137 at night, with this triage ECG:

I sent this ECG, without any text at all, to Dr. Smith, and he replied: "LAD OMI with low certainty. V3 is the one that is convincing." 

After his response I sent him the baseline ECG (below), still with no context at all except that this was his prior ECG:

Dr. Smith replied: "Now high certainty. By the way, the formula using QTc of 410 and STE60V3 of 3.5 was 19.4. I bet this LAD occlusion was missed."  (Also, R-wave amplitude in V4 of 12, and QRS in V2 of 16)

I replied: "You're right about both. It was LAD occlusion, and of course it was not seen until about 6 hours later." 

Here is the ECG again: 

The computer QT / QTc is 428 and 461 msec.

Using the computer's QTc of 461 ms instead of Smith's, which was measured by him (at 410 ms) while looking on an iPhone screen, you can see the formula value below.  

There is sinus rhythm with overall normal QRS complexes, normal R wave progression. There is STE in V2-V4, maximal in V3. The T wave in V3 and V4 is likely hyperacute, as it is fat, broad, full, and nearly symmetric in V4. A prior ECG, if available as in this case, would help to confirm or deny whether these are truly hyperacute, and the baseline ECG above shows that they are indeed all new and diagnostic. 

A couple other supportive findings that are not necessary for the diagnosis: 1) there are inferior Q-waves of old MI; this helps to establish the presence of coronary disease. 2) PVC, which also is more likely in patients with old and/or new MI.

See side by side below:

Comparison makes it obvious: huge fat hyperacute T waves in V3-V4.

The computer measurement of the QT might be slightly longer than actuality. But no matter, the formula is grossly positive.

Unfortunately, the ECG was not understood by the provider. Here is the EM decision making:

"The patient's EKG revealed some repolarization abnormalities but no clear signs of a STEMI. The patient's laboratory studies revealed troponin mildly elevated at 25 ng/L but liver enzymes, lipase were normal. Gallbladder ultrasound was negative for stones. Chest x-ray was normal. I ordered  morphine but he refused. I tried a GI cocktail but this did not significantly help. I felt the patient warranted admission for following his cardiac enzymes and EKG."

"ED Diagnoses:

1. Epigastric pain

2. Elevated troponin"

Cardiology was not notified of the patient at all. He was admitted to general medicine floor. No more troponins were ordered by the EM physician.

The hospitalist then came down to the ED to evaluate the patient. Their documented assessment included:

"Epigastric pain with odynophagia. ? gastritis vs. ulcer with recent Goody powder use. Atypical chest pain with elevated troponin. Patient will be started in IV PPI. Consult GI services in a.m. May need endoscopy. Currently denies dark stools. Lipase normal. Stool occult will be obtained. Patient claims 10 years ago when he had stents placed he had witnessed similar symptoms, due to mildly elevated troponin repeat troponin will be obtained. CT angio chest due to concerns of epigastric pain radiating to back, but suspicion for dissection less. No aspirin or lovenox until CT is obtained."

The CT showed no dissection or PE, nor any other acute pathology.

The second troponin returned around 0345, at 1,345 ng/L.

So aspirin and heparin are given, and a repeat ECG was finally ordered and obtained at about 0400:

This was interpreted as "no significant change from initial EKG at 0137."

Obviously it is importantly different, and remains diagnostic of ongoing, progressing LAD OMI. There is new R wave diminution in V3, new pathologic Q waves in V3-V4, new STE in V4. This ECG almost meets STEMI criteria, except that lead V3 in a man older than 40 would require 2.0 mm, whereas he has only 1.5 mm by my zoomed in measurement. V4 certainly has the necessary 1.0 mm.

This ECG was somehow interpreted as no change from the first ED ECG. But due to increased troponin, cardiology was called to see him for "NSTEMI management."

He continued to refuse morphine multiple times during this time period.

Notice how everyone involved (EM, IM, and cardiology) openly and blatantly violate all NSTEMI guidelines that state that NSTEMI with ongoing ischemic symptoms despite medical management requires less than 2 hour angiogram! All of them believe that this is just normal "NSTEMI management." That's because this is how patients are managed in the majority of settings, still, in 2021. The guidelines are simply ignored.

Another troponin was sent, which returned at 5,178 ng/L.

So more ECGs were ordered at 0532 and 0539:

0532:

Ongoing progression of OMI is seen, however at this moment there is small terminal T wave inversion suggesting momentary slight reperfusion. 

0539:

Only 20 minutes later, the T waves have pseudo-normalized, meaning the terminal inversion has been replaced again by hyperacute T waves in V2-V4. The artery is occluded again.

The ECGs before the angiogram are never recognized as a "STEMI" or "OMI".  They never actually meet STEMI criteria. 

The patient finally gets to go to the cath lab at 0744 (more than 6 hours after arrival and immediate what could have been an immediate ECG diagnosis of LAD OMI), where they of course find a complete 100% thrombotic occlusion of the mid LAD, at the site of his prior LAD stent. It is stented with good angiographic result. EF at cath is estimated at 35% with hypokinesis of "inferoapical" myocardium.

All subsequent troponins returned at greater than 25,000 ng/L (our lab's upper reporting limit).

Formal echo confirmed EF of 35-40%, with moderate hypokinesis of the mid-apical inferoseptal, mid-apical inferior, and mid-apical anteroseptal myocardium.

Here are some ECGs over the next few days after cath, showing a huge amount of anterior wall loss, QS waves, LVA morphology, and some amount of tissue saved as evidenced by evolving reperfusion T waves:

This OMI is one of the highest risk for long term morbidity and mortality. 

He survived the hospitalization, with a final diagnosis of "NSTEMI."

Learning Points:

Use the formula.

Learn hyperacute T waves. See thousands of them on this blog.

This case makes it painfully obvious why Khan et al have shown in their meta analysis of more than 40,000 NSTEMI patients, why NSTEMI patients with OMI have double the mortality and worse morbidity, at every time point, than NSTEMI patients without OMI. 

Anyone with high quality ECG training could have shortened his door to balloon time by 6 hours. Anyone who had simply followed the ACC/AHA NSTEMI guidelines could have improved his care by at least 3 hours. But neither of these things is normal in 2021 - not because providers are dumb and evil - because they have been trained that STEMI is what matters. Even when the patient almost/barely meets STEMI criteria as in the repeat ECG before cath above, the STEMI paradigm cripples their minds and prevents them from recognizing evolving changes other than ST elevation. And this patient's long term outcome is the result. This patient happens all over the world, every day. I find and present only a tiny fraction of them.

I can't speak for interventional cardiologists, but EM doctors should not be expected to attain this level of ECG expertise. We have to be good enough at everything, we cannot be expected to be expert at every difficult task. In other areas of imaging that requires intense training and expertise, we have radiologists to help us. We have no such resource for ECGs. Hopefully soon we can make AI that reads ECGs this well or better. Until then, maybe we need an ECG radiologist. Or cardiologists if they would be willing to learn this. Many on Twitter see this case and tell me that they would never let this happen. But in the real world, I have a new case of this to post every day.

Notice how this LAD OMI has no reciprocal STD on the standard 12 lead. Only approximately 50-60% of big obvious anterior STEMIs have reciprocal STD in the inferior leads. When the OMI is harder to see than an obvious STEMI, that number is even less.