A middle-aged woman called 911 for burning chest pain and dyspnea. Here is her prehospital ECG:
The computer did not read STEMI, but medics were very suspicious and brought the patient to the critical care area.
An ED ECG was immediately recorded:
The cath lab was activated.
History:
The patient states she has had 3 days of burning chest pain and SOB. She thinks she has the flu and states that she is currently pain free.
These are her first vital signs:
101/65
127
18
100.3
A bedside cardiac ultrasound was done:
Here is the parasternal long axis:
There is a moderate size pericardial effusion and some collapse of the RV
Here is the short axis:
Technique is not optimal, but there appears to be a lateral wall motion abnormality and poor ejection fraction.
With the prolonged pain and pericardial fluid, there was concern for subacute MI with myocardial rupture, and also for myocarditis/pericarditis.
Clinical course:
The angiogram was normal.
Here is the post cath ECG:
A formal echo showed:
Decreased left ventricular systolic performance moderate .
The first troponin I returned at 33.7 ng/mL (33,700 ng/L)
3 hours: 30 ng/mL
8 hours: 32 ng/mL
10 hours: 43 ng/mL
44 hours: 16 ng/mL
ECG 2 days later:
Echo 2 days later:
 |
| There is clearly acute myocardial injury with ST elevation in high lateral leads. |
The computer did not read STEMI, but medics were very suspicious and brought the patient to the critical care area.
An ED ECG was immediately recorded:
 |
| There is sinus tachycardia. There is clear high lateral and posterior injury. |
The cath lab was activated.
History:
The patient states she has had 3 days of burning chest pain and SOB. She thinks she has the flu and states that she is currently pain free.
These are her first vital signs:
101/65
127
18
100.3
A bedside cardiac ultrasound was done:
Here is the parasternal long axis:
There is a moderate size pericardial effusion and some collapse of the RV
Here is the short axis:
Technique is not optimal, but there appears to be a lateral wall motion abnormality and poor ejection fraction.
With the prolonged pain and pericardial fluid, there was concern for subacute MI with myocardial rupture, and also for myocarditis/pericarditis.
Clinical course:
The angiogram was normal.
Here is the post cath ECG:
 |
| Even more ST elevation, and ST depression reciprocal to injury of the posterior wall |
A formal echo showed:
Decreased left ventricular systolic performance moderate .
Regional wall motion abnormality-lateral .
Regional wall motion abnormality-inferolateral .
Regional wall motion abnormality-anterolateral probable.
The estimated left ventricular ejection fraction is 35 %The first troponin I returned at 33.7 ng/mL (33,700 ng/L)
3 hours: 30 ng/mL
8 hours: 32 ng/mL
10 hours: 43 ng/mL
44 hours: 16 ng/mL
ECG 2 days later:
Echo 2 days later:
Sinus tachycardia of 125-130 bpm.
Normal left ventricular size, mild hypertrophy and severe systolic dysfunction.
The estimated left ventricular ejection fraction is 25-30 % (visually estimated).
The patient became quite ill from cardiogenic shock due to myocarditis.
The patient became quite ill from cardiogenic shock due to myocarditis.
Learning Point
This case demonstrates that it is all but impossible to differentiate between acute MI and myocarditis.
Both may have:
1. ECG: Focal ST elevation with reciprocal ST depression
2. Echo: Focal wall motion abnormality
3. Very high troponin
4. Pericardial fluid (common in myo-pericarditis), possible in subacute MI if there is either postinfarction pericarditis or myocardial rupture
With the presence of fever, one might suspect myocarditis, but it would be dangerous to make any conclusions before studying the coronaries.
This case demonstrates that it is all but impossible to differentiate between acute MI and myocarditis.
Both may have:
1. ECG: Focal ST elevation with reciprocal ST depression
2. Echo: Focal wall motion abnormality
3. Very high troponin
4. Pericardial fluid (common in myo-pericarditis), possible in subacute MI if there is either postinfarction pericarditis or myocardial rupture
With the presence of fever, one might suspect myocarditis, but it would be dangerous to make any conclusions before studying the coronaries.
at the end could we say (maybe after MRI) focal (postero-lateral) MyoPericarditis (or better
ReplyDeletePeriMyocarditis because of decreased EF - M. Imazio) ?
merci beaucoup Dr Smith !
Al
Al,
DeleteMRI would clinch the diagnosis. Otherwise, it could possibly be a false negative cath.
Thanks,
Steve
interesting and educative case.
ReplyDeleteThanks Dr. Smith
GREAT case skillfully presented (as always). I initially thought we were dealing with acute left circumflex occlusion given isolated and marked ST elevation in leads I,aVL (with loss of R wave in these leads) plus “telltale” reciprocal ST depression (mirror-image in III compared to aVL) — at least until the cath came back normal — at which point acute myopericarditis became the diagnosis by exclusion. BUT, all the clues WERE there from the start = “flu-like syndrome” (that the patient insisted she had) + low-grade fever + “burning” chest pain that resolved at the time she was seen. In retrospect we might ask if the degree of ST segment deviation in the limb leads after 3 days of symptoms wasn’t a bit disproportionate considering loss of high lateral R wave (and the QS in aVL) — but given how much more common acute coronary occlusion is compared to localized acute myopericarditis — there is clearly a tendency to “assume” acute STEMI rather than the less commonly thought about localized myocarditis … So this case is an EXCELLENT reminder not to forget acute myopericarditis in the differential. And, as William Osler always said, “Listen to the patient and he/she will tell you the diagnosis” (ie, think acute myocarditis esp. with an abnormal ECG + recent flu-like illness). THANKS for presenting!
ReplyDeleteP.S. I think there is a typo under your learning point. You said it was impossible to differentiate between “acute MI and pericarditis” but perhaps meant to say acute MI “and myocarditis (or perimyocarditis)” …
Thanks, Ken, especially for catching that typo (which I corrected)!
DeleteAnother very interesting case.
ReplyDeleteThe present case is very interesting not only because of the difficulties on the differential diagnosis between STEMI and myocarditis (ECG first) but also on the management.
Due to the presence of pericardial effusion with some echo signs of tamponade, there is the real risk of subacute miocardial rupture or ‘simple’ tamponade.
How did they manage the patient before angiogram? Did the patient receive aspirin, P2Y12, antigoagulants or did the clinicians wait for the result of the angiogram? Many thanks.
Mario Parrinello
Mario,
DeleteVery good question. Yes, they did give aspirin, P2Y12 inhibitor, and heparin. Given the fever and "flu" and pericardial effusion, I think I would wait for the angiogram to give those medications. But even if the angio showed occlusion, hemopericardium could be present. I think, however, that it is unlikely to be hemopericardium as there is no evidence of clot in the percicardium. With hemopericardium, there is usually some fluid and some echogenic clot.
Steve