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A previously healthy 53 yo woman was transferred to a receiving hospital in cardiogenic shock.
pH was 6.9 and K was normal.
Here was the ECG:
Usually shark fin is in one coronary distribution and represents massive ST elevation that is as high as the peak of the R-wave and therefore fuses the R-wave and ST segment.
So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution.
It is often confused with a wide QRS due to conditions such as hyperkalemia. But it is very distinct from hyperkalemia (and anything else, including VT), and such confusion can only be due to lack of familiarity, because, if you look closely, its morpholgoy is very different from anything else.
So this is STEMI, right?
Which artery?
There is ST Elevation in every lead except aVR (STD in aVR).
Well, don't we see diffuse ST Elevation in Myo-pericarditis (with STD in aVR)? Could this be myopericarditis?
The patient was hypothermic at 90 degrees F (32.2 C) and she was positive for influenza. Her troponin I was 500.01 ng/mL (equivalent to a high sensitivity troponin I of 500,000 ng/L). This is among the highest troponin I of which I have ever heard.
Her ejection fraction was 10%.
She was taken to the cath lab and her coronaries were clean!!
There was no MRI, but the presumptive diagnosis is myocarditis.
Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. Here is what he wrote:
"This is a marker of coronary perfusion pressure in the context of severe elevated in LVEDP outside the range of coronary auto regulation. I have seen this pattern in severe acute AI also." In other words, the severely increased end diastolic pressure from the extremely poor LV function caused by the myocarditis results in extremely poor coronary perfusion pressure.
A previously healthy 53 yo woman was transferred to a receiving hospital in cardiogenic shock.
pH was 6.9 and K was normal.
Here was the ECG:
 |
| There is sinus tachycardia. This is "Shark Fin" morphology. Shark Fin has also been called: "Giant R-wave" "Triangular QRS-ST-T waveform" |
Usually shark fin is in one coronary distribution and represents massive ST elevation that is as high as the peak of the R-wave and therefore fuses the R-wave and ST segment.
So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution.
It is often confused with a wide QRS due to conditions such as hyperkalemia. But it is very distinct from hyperkalemia (and anything else, including VT), and such confusion can only be due to lack of familiarity, because, if you look closely, its morpholgoy is very different from anything else.
So this is STEMI, right?
Which artery?
There is ST Elevation in every lead except aVR (STD in aVR).
Well, don't we see diffuse ST Elevation in Myo-pericarditis (with STD in aVR)? Could this be myopericarditis?
The patient was hypothermic at 90 degrees F (32.2 C) and she was positive for influenza. Her troponin I was 500.01 ng/mL (equivalent to a high sensitivity troponin I of 500,000 ng/L). This is among the highest troponin I of which I have ever heard.
Her ejection fraction was 10%.
She was taken to the cath lab and her coronaries were clean!!
There was no MRI, but the presumptive diagnosis is myocarditis.
Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. Here is what he wrote:
"This is a marker of coronary perfusion pressure in the context of severe elevated in LVEDP outside the range of coronary auto regulation. I have seen this pattern in severe acute AI also." In other words, the severely increased end diastolic pressure from the extremely poor LV function caused by the myocarditis results in extremely poor coronary perfusion pressure.
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MY Comment by KEN GRAUER, MD (2/16/2020):
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As per the title by Dr. Smith — this case was not what I thought. I did recognize the Shark Fin morphology of dramatic ST elevation. Shark Fin morphology has been shown on Dr. Smith’s blog a number of times, including:
- In the June 11, 2018 post —
- In the October 4, 2019 post —
- In the November 22, 2019 post —
- in the January, 24, 2020 post —
PEARL — What I did not appreciate when I reviewed this case — was that among the many potential etiologies of acute myocarditis was HypoThermia!
- I have summarized the major etiologic categories of acute myocarditis and inflammatory cardiomyopathies. A more complete listing of specific etiologic agents can be found on the source I used to prepare Figure-1 (Kühl Uwe & Schultheiss Heinz-Peter: Myocarditis — Deutsches Ärzteblatt Int. 109 (20):361-368, 2012 — CLICK HERE).
- Referring to Figure-1 — this 53-year old woman who presented in extremis with cardiogenic shock and an initial pH = 6.9, had at least 2 potential etiologies for developing acute myocarditis: i) Profound hypothermia (core temperature = 90°F = 32.2°C); and, ii) She tested positive for influenza.
 |
| Figure-1: Potential etiologic categories of acute myocarditis (See text). |
Our THANKS to Dr. Smith for presenting this case!
Could it be Takotsubo Cardiomyopathy?
ReplyDeleteGood question. It says cath was clean — and if Takotsubo, this would have shown up on cath.
DeleteNice case! Thanks a lots for is sharing it with us. The rhythm is clearly sinus, heart rate is about 120 bpm. Initially, when I have seen this tracing, I immediately thought about the possibility of OMI, because "shark fin" morphology, but so I have realized that there are no reciprocal changes, Q waves. Rather than, there are diffuse STE with STD in aVR, therefore I have taken in doubt if this tracing was really OMI.
ReplyDelete@ Unknown — THANKS for your comment! You have highlighted 1 of the many important learning points from this case! — :)
Delete1)The findings in leads V4-6 may suggest wide QRS but the leads 1-3 clearly shows where the QRS ends and the elevated ST segment begins.
ReplyDelete2)If the elevated ST segment begins from the R or R' and is continuously down-sloping as in this case, don't think of MI but non-MI conditions, which there are many including Brugada syndrome, acquired Brugada ECG pattern, RV dilation, metabolic or electrolyte problems, transiently after a shock to the precordium, etc.
3)My prediction is that there is no myocarditis and the myocardial biopsy would not show any inflammation. This is a transient ECG manifestations of conditions I mentioned above.
K. Wang.
Hello again K. Just now seeing your 3rd comment. YES — Leads V1,2,3 are the "tip-off" regarding duration of the QRS complex! — :) — Otherwise, I think you may be correct regarding your points 2) and 3) — but I don't know that there is follow-up on this case. In any event — I thought it a fascinating case! THANKS as always for your comments! — :)
DeleteI should have included hypothermia in the list of conditions causing this kind of ST elevation in my comment above.
ReplyDeleteK. Wang.
Hi K. I wrote My Comment late last night — and don't know if it appeared before or after what you write above. Would have been nice to gain access to serial tracings as this patients underlying conditionS were treated — :)
DeleteI am curious as to how long the ST elevation lasted.
ReplyDeleteK. Wang.
Hi K! Yes — The 1st thing I asked when I saw this case was WHAT did this patient's ECG look like as core temperature normalized! There are a number of things going on in this case (ie, Flu and/or sepsis — hypothermia — myocarditis) — and which entity contributed to what degree to producing these dramatic ECG changes would have been extremely interesting to follow with repeat tracings as the patient’s clinical condition improved — :)
DeleteWhat about 2 type of myocardium infarction?
ReplyDelete@ Unknown — I'm happy to add Type 2 MI to the list of entities/possible things going on in this case (ie, Flu and/or sepsis — hypotherma — myocarditis — Type 2 MI). That said, I suspect ( = my opinion) that most of what we see on the ECG in this case is not the result of Type 2 MI ...
DeleteIt could indeed be type II MI in the sense explained by our chief of cards:
Delete"This is a marker of coronary perfusion pressure in the context of severe elevated in LVEDP outside the range of coronary auto regulation. I have seen this pattern in severe acute AI also." In other words, the severely increased end diastolic pressure from the extremely poor LV function caused by the myocarditis results in extremely poor coronary perfusion pressure.