I was shown this ECG of a 50-something with acute chest pain:
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:
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:
31 minutes later another ECG was recorded:
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:
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:
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| 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
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:
Superb case with LOTS of room for speculation, albeit with a number of still unanswered questions. I’ll make some speculations. ECG #1 is not the ECG of acute infarction for the reasons discussed by Dr. Smith. But I submit that this 1st ECG is clearly consistent with acute Pericarditis because of the pattern of diffuse ST elevation that is clearly more marked (and more diffuse) than is usually seen with early repolarization — occurring in association with prominent PR segment depression in many leads, with PR elevation in lead aVR. That said, Dr. Smith has often emphasized that “one diagnoses acute pericarditis at your peril” — so caution (and careful clinical correlation) is essential before jumping to that diagnosis. True pericarditis is less common than is generally appreciated, and there clearly is a tendency toward overdiagnosing early repolarization variants as “pericarditis”. That said, we DO have the luxury of an ECG on this patient taken 1 month earlier — and comparison between the 1-month earlier and new ECG is telling. Not only is the relative amount of ST elevation much less in the 1-month earlier tracing — but PR depression is practically nonexistent (and there was no PR elevation in aVR) — AND — a less-used ECG sign known as Spodick’s sign was NOT present 1 month earlier, but IS present on the new ECG. Spodick’s Sign is a downsloping of the TP (or entire QRS-TP) segment that may be present in a number of leads with acute pericarditis. I’ll note that despite the world-renowned expertise of Dr. David Spodick on the topic of pericarditis — to me, this sign is often subjective and suboptimally reproducible, so that I never depend upon it in the ECG diagnosis of acute pericarditis. That said, in this case — Spodick’s Sign was absent 1 month earlier, and is now unmistakably present in the new ECG. Because of the poor sensitivity and poor specificity of PR depression in the ECG diagnosis of acute pericarditis — I also rarely use this as a deciding feature in my assessment. But once again, PR depression was essentially absent 1 month earlier, and now is unmistakably present on the new ECG. To me, this combination of serial changes with new development of PR depression + Spodick’s sign + dramatic increase in the amount of diffuse ST elevation compared to the ECG done just 1 month earlier — in association with new symptoms — strongly suggests that a significant component of these signs on the new ECG are indeed the result of acute pericarditis. That said, the amount of ST elevation did substantially decrease in the ECG done just 31 minutes after the 1st ECG — and that is consistent with early repolarization (but not acute pericarditis). Bottom Line: I suspect there is baseline early repolarization in this patient that manifests some element of dynamic change AND in addition, there has been superposition of a series of new ECG changes as a result of acute pericarditis. All in all, a fascinating case!
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