I had a recent comment on this post, which was put up 7 years ago (850 posts since then!). I was reminded of it. And so I thought I would repost it.
Case
This is a 48 y.o. male with a history of Bipolar disorder, polysubstance abuse, spontaneous pneumothorax x2, who presents for chest pain x 4 hours. The patient was in his usual state of health until this afternoon when he noticed the gradual onset of bilateral chest pain. He had a relapse of crack use this AM. He describes the pain as bilateral, radiating to the left arm, worsening over time, and associated with mild SOB and also some pleuritic chest pain. There is no relation of pain to exertion or meals, and no associated diaphoresis, nausea or vomiting. No recent long sedentary periods. No recent trauma, but has been doing more manual labor than usual. Pt has not had chest pain with crack use before.
Here is his initial ECG:
Here I place them on the same page for better comparison:
Here I have magnified II, III, aVF, and aVL for better comparison:
Here I have magnified V1-V3 for better comparison:
The Emergency physician started therapy for NSTEMI. The first troponin returned at 2.25 ng/mL. The cardiology fellow then opined that this was myopericardititis and instructed to stop the heparin. However, myopericarditis is a diagnosis of exclusion and much less common than acute MI. One must undertake treatment for ACS, including an angiogram. Only if the angiogram is normal would one then consider myocarditis and probably obtain an MRI.
The reciprocal ST depression in lead aVL and the T-wave enlargement in V2 and V3 are all but diagnostic of MI.
Follow up:
The troponin I peaked at 23.6 ng/mL. The echo showed an inferior and anterior wall motion abnormality. Thus, it was not pericarditis, though myocarditis is possible.. Angiogram showed a ruptured plaque in the proximal LAD, with distal embolization of thrombus to the apex. This was a "type III," or "wraparound" LAD which supplies both anterior and inferior walls. This accounts for the transient hyperacute T-waves in anterior leads and for the ST elevation in inferior leads.
Even without the angiogram, the rapid rise and fall of troponin is highly suggestive of MI, not myopericarditis.
The stenosis was minimal, and the ACS occurred in the setting of cocaine use, so the therapy was eptifibatide and heparin for 72 hours, with no PCI.
Learning Points
1) Pericarditis should never be assumed when there is even a hint of reciprocal ST depression. Only localized pericarditis (most pericarditis is "diffuse" inflammation of the entire pericardium) ever has reciprocal ST depression, and localized pericarditis is very rare. I suspect that many cases of "localized pericarditis" are really STEMI that went undiagnosed.
2) Wraparound or Type III LAD ACS mimics pericarditis because it leads to diffuse ST elevation.
Case
This is a 48 y.o. male with a history of Bipolar disorder, polysubstance abuse, spontaneous pneumothorax x2, who presents for chest pain x 4 hours. The patient was in his usual state of health until this afternoon when he noticed the gradual onset of bilateral chest pain. He had a relapse of crack use this AM. He describes the pain as bilateral, radiating to the left arm, worsening over time, and associated with mild SOB and also some pleuritic chest pain. There is no relation of pain to exertion or meals, and no associated diaphoresis, nausea or vomiting. No recent long sedentary periods. No recent trauma, but has been doing more manual labor than usual. Pt has not had chest pain with crack use before.
Here is his initial ECG:
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Here I have magnified II, III, aVF, and aVL for better comparison:
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|
The reciprocal ST depression in lead aVL and the T-wave enlargement in V2 and V3 are all but diagnostic of MI.
Follow up:
The troponin I peaked at 23.6 ng/mL. The echo showed an inferior and anterior wall motion abnormality. Thus, it was not pericarditis, though myocarditis is possible.. Angiogram showed a ruptured plaque in the proximal LAD, with distal embolization of thrombus to the apex. This was a "type III," or "wraparound" LAD which supplies both anterior and inferior walls. This accounts for the transient hyperacute T-waves in anterior leads and for the ST elevation in inferior leads.
Even without the angiogram, the rapid rise and fall of troponin is highly suggestive of MI, not myopericarditis.
The stenosis was minimal, and the ACS occurred in the setting of cocaine use, so the therapy was eptifibatide and heparin for 72 hours, with no PCI.
Learning Points
1) Pericarditis should never be assumed when there is even a hint of reciprocal ST depression. Only localized pericarditis (most pericarditis is "diffuse" inflammation of the entire pericardium) ever has reciprocal ST depression, and localized pericarditis is very rare. I suspect that many cases of "localized pericarditis" are really STEMI that went undiagnosed.
2) Wraparound or Type III LAD ACS mimics pericarditis because it leads to diffuse ST elevation.
Hi Dr Smith,
ReplyDeleteI notice ST elevation in lead I, Shouldn't there be a reciprocal ST depression in this lead too? or aVL is enough?
Also can ST depression in aVL come with ST elevation in V5,6 ?
Dr. Aleem,
ReplyDeleteExcellent questions. No, lead I frequently has no reciprocal ST depression when it is presnet in aVL because if the ST axis is 90 degrees, the ST segment will be negartive in aVL and isoelectric in I.
If there is inferolateral STEMI, even when there is ST elevation in V5 and V6 there is almost always ST depression in aVL.
Steve Smith
Dear Dr. Smith,
ReplyDeleteThank you for your excellent teaching.
I have read that ST depression may be seen in aVR and V1 acute pericarditis (Punja et al., 2010). Anecdotally, I have observed ST depression in aVR and V1 in at least 2 cases of pericarditis. The most recent patient had diffuse ST elevation in every lead except for aVR and V1, in which there was 1-2 mm of ST depression. This young man went to the cath lab and was found to have pristine coronary arteries. Hw was subsequently diagnosed with myopericarditis. You have mentioned in this posting and in your HQMed contribution that reciprocal ST depression should not be seen in acute pericarditis. In your opinion, does this always apply to aVR and V1?
Thanks,
Nadder
When one says there is no reciprocal ST depression, it always excludes aVR, because aVR is by definition reciprocal: it is opposite nearly all the other leads. So, I should have been more clear. Except for aVR. V1 does often have ST depression in pericarditis (25% in one study, NEJM 295:523. One problem is that all of this literature is old and there is no cath or ultrasound data. The diagnosis would have been difficult to ascertain.
ReplyDeleteDr Smith,
ReplyDeleteI am a nurse/paramedic and have been turned on to your site by Dr EMcrit. I am studying to be an Anesthesia Assistant and I teach paramedics in Florida. I am researching ST segment differentials and would like to know if you could point me in the right direction to distinguish between Myocarditis and Pericarditis.
Thank you in advance,
Chris J (darktrance21@gmail.com)
Hello
ReplyDeleteIt is still a dilema for me when managing pericarditis patients with an elevated Troponin in the ER.
If I have a patient in ER with fever, high Troponin, ST Elevation diffuse do I start anticoagulation therapy directly ? Or I think of pericarditis ? When do I think of left heart catheterization?
assume ACS until proven otherwise. Angiogram!
Deletehello
ReplyDeletecould i ask you a question???
why dose this patient recieve management as NSTEMI , not STEMI
Benjamin,
DeleteIt really was acute coronary occlusion (STEMI has millimeter definition, not met here) and should go for emergent cath just like a STEMI. In my opinion, it was a mistake not to do so. But I was not there. Also, I don't know why there was no stent. I am not an interventionalist, and they have many complex decisions to make in this regard, upon which I am not qualified to comment.
Steve
It’s always nice when you review tracings interpreted years earlier — and see consistency in your message! This initial ECG is timeless in its relevance. The 1st thing that “struck me” was a T wave taller-and-more-peaked-than-it-should-be in lead V2. While contemplating whether the limb leads might or might not be consistent with early repolarization (they of course aren’t, for the reasons Dr. Smith states) — I thought lead V4 was definitive. In a patient with chest pain — I can think of no reason other than acute coronary occlusion for why lead V4 should show more ST elevation than either the chest leads before it (V2,V3) or the chest leads after it (V5,V6). P.S. It is worth a moment noting that leads III and aVL in the Presentation ECG DO show that magical “mirror-image” picture that is so helpful in identifying acute coronary occlusion (ie, scooped even-though-not-really-depressed ST segment in lead aVL — that if “flipped up” will give ST coving [albeit not-really-ST-elevation in lead III). THANKS for reposting this insightful case!
ReplyDeletethanks, Ken!
Delete