Monday, January 8, 2018

High ST Elevation in a Patient with Acute Chest Pain

I was shown this ECG of a 50-something with acute chest pain:
What do you think?
















I replied that this ST Elevation in precordial leads was normal variant STE.

Why did I say so?

1.  One can see that the QT interval is short (in fact, the computer measured it accurately at 285 ms.  With Bazett correction, that comes to a QTc of 381 ms (RR interval = 560 ms).  This computer has a proprietary algorithm (Veritas) that calculated a QTc of 349 ms.  In any case, this is a pretty short QTc for acute anterior STEMI.
2.  There are very prominent J-waves in V4 and V5.
3.  The R-wave amplitude is high.

3-variable formula: use 5.0 mm for STE60V3 = 21.94 (low value, indicating probably not STEMI)
4-variable formula:                                           = 17.0   (again, low value)

Go here for explanation of formulas:

12 Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion


There is also some fairly prominent PR segment depression in multiple leads, so pericarditis is possible.

V5 and V6 have a fairly high ST/T ratio, which favors pericarditis over early repol.

Further history: Patient presented with terrible pressure-like chest pain that woke him from sleep just prior to arrival. He had been having intermittent chest pain the last four days that he thought was his GERD. It resolved with acetaminophen but kept recurring. No reliable triggers. His pain at presentation was 10/10, mostly in his epigastrium, but radiating to his throat and back and worse when he is laying down or takes a deep breath.

There was an ECG from one month prior for comparison:
QTc 397
This also has normal variant STE, but not as much as above

31 minutes later another ECG was recorded:
QTc = 365
Now there is significantly less ST Elevation now


Due to profound ST Elevation that is dynamic and changed from previous, the cath lab was activated.

Outcome

All coronaries were clean.

He was admitted and all troponins were below the level of detection.

The patient underwent a CT scan to rule out pulmonary embolism.

Here are the scan results:

Impression:  
1. Pneumomediastinum (almost certainly secondary to large perforation in
cervical esophagus) and findings concerning for extensive mediastinitis.
2. Small pericardial effusion.
3. Small right pleural effusion with overlying consolidation concerning
for infection or aspiration.
4. No evidence of pulmonary embolism

Diagnosis: esophageal perforation with mediastinitis and probable pericarditis (this does not necessarily mean the ECG represents pericarditis -- maybe and maybe not).

Conclusion

The ECG findings could be due to either dynamic early repolarization (normal variant ST elevation), or to pericarditis, or to a combination of the 2 entities.

Yes, normal variant ST elevation can be dynamic:

Increasing ST elevation. STEMI vs. dynamic early repolarization vs. pericarditis.



Alternatively, the ECG could represent pericarditis superimposed on early repol.  There certainly was pericarditis, but that does not mean the ECG findings were due to pericarditis.

This paradox is extremely well illustrated in this brilliant post

I do believe that in this age of very sensitive troponins (cTn) that pericarditis that results in ST Elevation will have at least detectable troponins.  We used to differentiate pericarditis from myocarditis using elevation of cTn.  There is no literature on this topic.  This article by my friend Pierre Taboulet is the closest I can find, but was published in 2000, many years before the age of highly sensitive troponins:

Serum cardiac troponin I and ST-segment elevation in patients with acute pericarditis










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