A middle-aged woman presented with what is described as a burning feeling in her chest which the physician said was "very atypical." It did occur during exercise and radiated to both wrists.
Here is the first ECG:
The computer algorithm might say: "Diffuse ST elevation, consider pericarditis, early repolarization, or myocardial infarction." I don't know what it actually said.
Early repol vs. LAD occlusion
Should we use the LAD-Early Repol calculator?
If you did, and it was negative, it would likely be a false negative. Why?
There is Terminal QRS distortion in V3, which is not a finding of normal variant ST elevation.
What is Terminal QRS distortion?
Terminal QRS distortion is the absence of both an S-wave or a J-wave in either V2 or V3. It is not seen in early repolarization, or is very rare. In the right clinical context, and in the presence of non-diagnostic ST elevation, it is highly suspicious for coronary occlusion.
They did apply the formula, using these measurements: 1.5 mm for STE at 60 ms after the J-point in lead V3, QTc of 437, and R-wave amplitude in V4 of 13. (I would have used 2, 437, 14)
Their numbers resulted in 23.34 (very close to 23.4, but technically negative. I recommend that anything above 22.0 be investigated further)
My measurements would have resulted in 23.6, also very close but positive.
Pericarditis vs. LAD occlusion
I always say "You diagnose pericarditis at your (and your patient's) peril."
Why is this not pericarditis:
1. ST vector: The ST vector in pericarditis should be lateral and inferior and only slightly anterior. The vector here is towards V3.
2. Large T-waves: in pericarditis, the ST elevation is much more pronounced than the T-wave. Here the T-wave is more pronounced, hyperactute.
3. No diagnostic PR depression.
4. Notice there is a Spodick's sign in V3-V5. But this is a worthless sign (see this recent post).
They recorded 2 more ECGs at unknown intervals:
2nd:
3rd:
Fortunately, the troponin came back slightly elevated, and fortunately they did not not attribute that elevation to myocarditis.
The patient was taken to angiography and found to have a 99% thrombotic LAD occlusion.
Here is the first ECG:
The computer algorithm might say: "Diffuse ST elevation, consider pericarditis, early repolarization, or myocardial infarction." I don't know what it actually said.
Early repol vs. LAD occlusion
Should we use the LAD-Early Repol calculator?
If you did, and it was negative, it would likely be a false negative. Why?
There is Terminal QRS distortion in V3, which is not a finding of normal variant ST elevation.
What is Terminal QRS distortion?
Terminal QRS distortion is the absence of both an S-wave or a J-wave in either V2 or V3. It is not seen in early repolarization, or is very rare. In the right clinical context, and in the presence of non-diagnostic ST elevation, it is highly suspicious for coronary occlusion.
They did apply the formula, using these measurements: 1.5 mm for STE at 60 ms after the J-point in lead V3, QTc of 437, and R-wave amplitude in V4 of 13. (I would have used 2, 437, 14)
Their numbers resulted in 23.34 (very close to 23.4, but technically negative. I recommend that anything above 22.0 be investigated further)
My measurements would have resulted in 23.6, also very close but positive.
Pericarditis vs. LAD occlusion
I always say "You diagnose pericarditis at your (and your patient's) peril."
Why is this not pericarditis:
1. ST vector: The ST vector in pericarditis should be lateral and inferior and only slightly anterior. The vector here is towards V3.
2. Large T-waves: in pericarditis, the ST elevation is much more pronounced than the T-wave. Here the T-wave is more pronounced, hyperactute.
3. No diagnostic PR depression.
4. Notice there is a Spodick's sign in V3-V5. But this is a worthless sign (see this recent post).
They recorded 2 more ECGs at unknown intervals:
2nd:
Perhaps some increase in STE |
3rd:
There is slightly increasing ST Elevation |
Fortunately, the troponin came back slightly elevated, and fortunately they did not not attribute that elevation to myocarditis.
The patient was taken to angiography and found to have a 99% thrombotic LAD occlusion.
Steve -
ReplyDeleteIs QRS an independent predictor of occlusion, beyond what we already see here? I.e., if we didn't have a large T-wave, small R, and a straight ST in V3, would QRS distortion be as useful?
Brooks
Brooks,
DeleteYes. there are cases in which the only finding to indicate MI is Terminal QRS distortion.
See this case: http://hqmeded-ecg.blogspot.com/2013/10/terminal-qrs-distortion-due-to-lad.html
The most important point for me is that it is very unusual, or maybe even always absent, in early repolarization.
Steve
nice case ;)
ReplyDeleteGreat case!
ReplyDeleteI suspect the latter two ECGs were taken in very close proximity to the 1st, as the T's are still upright (LAD still closed) yet there is little in the way of natural evolutionary transition from tall R waves to QS waves.
Sam, yes they were not days later, but they were hours later. There was a significant delay to angio.
DeleteSteve
Thanks for sharing this great example.
ReplyDeleteI was re-reviewing your marvellous book and happened to Case 7-4. May be you would consider to share it here for comparison. It is a tough one because of precordial derivations. It has ST vector directed to V2 and terminal QRS distortion in V3, similar to this case. Limb leads have less T voltage and more pericarditis look but if you kindly consider comparing it with this one I would really appreciate it.
Thanks
Emre,
Deletegood pickup! This does not change the thought that when the DDx is between MI and Early Repol, terminal QRS distortion is very good for MI, because in this case, early repol was not part of the differential.
However, it does suggest that pericarditis can have terminal QRSD.
On the other hand, this ECG was presumed to be pericarditis, and I am pretty sure it is, but I don't believe there is angiographic or troponin proof that it was not MI.
Steve
quite cool case... thank you S.
ReplyDelete