A 63 y.o. female with a past medical history of lupus and MS presents with chest pain and SOB she has never had before, starting approximately 1615. The pain gradually diminished since onset. It was described as pressure, with SOB, and no radiation. There is some reproducibility with palpation, but the pain is not positional or pleuritic. She has no h/o CAD, HTN, or DM. There is no pericardial friction rub. NTG by EMS improved pain. The pain resolved after 1 hour in ED.
Here is her initial ECG at 1954 (3.5 hours after onset of CP):
Inferior MI virtually always has reciprocal ST depression of some amount, or at least T-wave inversion, in aVL.
See this case and this case for patients who were erroneously thought to have pericarditis, whose ECGs had subtle reciprocal ST depression in aVL.
When there is inferior and lateral STEMI or inferior and anteroapical STEMI, the reciprocal ST depression can be attenuated or completely abolished by the lateral ST elevation. Thus, the ECG can look identical to myo- or pericarditis.
The reading by the cardiologist was: "diffuse ST elevation, consider pericarditis." Subsequent ECGs are of little interest, only showing some resolution of ST elevation, but no T-wave inversions or other diagnostic findings.
Clinically, the patient has pain more typical of ischemia. Her initial troponin I was 8.56 ng/ml. Therefore, whatever the process is, it must have been going on longer than 3.5 hours. Subsequently, every 4 hours, the levels were 9.96, 8.96, 8.40, 7.48, 6.62, so there is some rise and fall, though not dramatic. A steady state is typical of myocarditis, whereas a rise and fall is more typical of MI.
The differential diagnosis, then, is myocarditis vs. inferolateral STEMI (most likely).
Echocardiogram showed wall motion abnormalities of the distal anterior wall, apex, and septum as well as the inferior wall. This could be seen in either MI or myocarditis, but favors MI, as myocarditis less frequently has focal myocardial dysfunction.
Her angiogram showed a Type III LAD ("wraparound LAD, that supplies the inferior wall). It had moderate diffuse disease in the distal segment of the vessel, which would be the supply to the inferior wall. There was no definite culprit or thrombus, so no definite explanation of the findings.
Therefore, an MRI was done with gadolinium, to assess for myocarditis.
MRI report
1) Mild to moderately reduced LV function with large apical wall motion
abnormality. Calculated ejection fraction is 45%.
2) Small, discrete focus of transmural enhancement, consistent with
myocardial scarring, in the mid inferior wall of the left ventricle. This
pattern of enhancement is unlikely to be from myocarditis, and is more
suggestive of a small infarct.
Thus, the diagnosis is myocardial infarction of the distal wraparound LAD, with STE in II, aVF, V3-V6.
As I've had more and more experience, I've noticed that most of what is thought to be myo- or pericarditis on the ECG turns out to be MI. As we have better and better tools to make the ultimate diagnosis, we find that cases that should have been diagnosed as MI were diagnosed with pericarditis. That was not the case here, but it did happen here.
Here is her initial ECG at 1954 (3.5 hours after onset of CP):
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See this case and this case for patients who were erroneously thought to have pericarditis, whose ECGs had subtle reciprocal ST depression in aVL.
When there is inferior and lateral STEMI or inferior and anteroapical STEMI, the reciprocal ST depression can be attenuated or completely abolished by the lateral ST elevation. Thus, the ECG can look identical to myo- or pericarditis.
The reading by the cardiologist was: "diffuse ST elevation, consider pericarditis." Subsequent ECGs are of little interest, only showing some resolution of ST elevation, but no T-wave inversions or other diagnostic findings.
Clinically, the patient has pain more typical of ischemia. Her initial troponin I was 8.56 ng/ml. Therefore, whatever the process is, it must have been going on longer than 3.5 hours. Subsequently, every 4 hours, the levels were 9.96, 8.96, 8.40, 7.48, 6.62, so there is some rise and fall, though not dramatic. A steady state is typical of myocarditis, whereas a rise and fall is more typical of MI.
The differential diagnosis, then, is myocarditis vs. inferolateral STEMI (most likely).
Echocardiogram showed wall motion abnormalities of the distal anterior wall, apex, and septum as well as the inferior wall. This could be seen in either MI or myocarditis, but favors MI, as myocarditis less frequently has focal myocardial dysfunction.
Her angiogram showed a Type III LAD ("wraparound LAD, that supplies the inferior wall). It had moderate diffuse disease in the distal segment of the vessel, which would be the supply to the inferior wall. There was no definite culprit or thrombus, so no definite explanation of the findings.
Therefore, an MRI was done with gadolinium, to assess for myocarditis.
MRI report
1) Mild to moderately reduced LV function with large apical wall motion
abnormality. Calculated ejection fraction is 45%.
2) Small, discrete focus of transmural enhancement, consistent with
myocardial scarring, in the mid inferior wall of the left ventricle. This
pattern of enhancement is unlikely to be from myocarditis, and is more
suggestive of a small infarct.
Thus, the diagnosis is myocardial infarction of the distal wraparound LAD, with STE in II, aVF, V3-V6.
As I've had more and more experience, I've noticed that most of what is thought to be myo- or pericarditis on the ECG turns out to be MI. As we have better and better tools to make the ultimate diagnosis, we find that cases that should have been diagnosed as MI were diagnosed with pericarditis. That was not the case here, but it did happen here.
I had a very similar case with one of our docs who called it pericarditis. The major point that I was trying to point out though was 0.5mm of STD in aVF and inverted T-waves in II and III. I tried to explain to him that even though pericarditis is likely, with reciprocal changes it should be proven negative with a cath. He wouldn't activate the cath lab but agreed to administer heparin and plavix. Troponin came back at 8.8 and his cath was clean minus a plaque deposit. Would pericarditis cause that high of a Troponin? His highest troponin was 9.4 and was steadily declined.
ReplyDeleteSo, as with this case, the differential is MYO-carditis vs. infarction. As you can see from this case, the diagnosis of myocarditis may be erroneously made if the cath does not show a definite culprit. You need MRI to make the diagnosis (if you don't believe the ECG!!, which cardiologists do not). On the other hand, if there is no culprit to fix, then is there a big difference? Yes, there is a difference in medical therapy: aspirin, beta blocker, statin, Plavix, etc.
ReplyDeleteThanks for posting these cases , guys! This goes to show , how partial can be the aid of any of our diagnostic tools and how you can't sometimes avoid more "expensive" exams like U/S. So much for the algorithms of hsTrop or the "good knowledge of ecg" many times parroted in the ED and elsewhere. Our teachers at the university were right saying "diseases don't read textbooks".
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