Thursday, May 23, 2013

24 yo woman with chest pain the morning after binge drinking: Is it Pericarditis?


A 24 yo with no past medical history and no risk factors except for tobacco smoking presented with chest pain.  The pain started in her left chest at 6:20 AM and radiated up through her arms and into her back. She admitted to drinking heavily the previous night and returned home about 1:30 or 2 AM.  She had multiple episodes of vomiting overnight. She's never had chest pain like this before.  BP was 140/100 and pulse of 93.  There was no rub on exam.

Here is her prehospital ECG at 0720:
Sinus rhythm.  Inferior and lateral ST elevation with reciprocal ST depression in aVL.  There is no significant PR segment depression

She was given 2 sublingual NTG and her pain improved from 10/10 to 7/10, and continued to improve.  Here is her first ED ECG at 0748:
Not much change except for less STE in lateral leads.

Chest X-ray confirmed absence of Boerhaave's syndrome.

Some might suspect pericarditis in a young person with diffuse ST elevation.  However, you diagnose pericarditis at your peril!  I believe pericarditis is over diagnosed, even in the literature, and that many cases assumed to be pericarditis in the past would not be proved to be Acute MI.  This is conjecture based on many cases that I have seen, not based on peer-reviewed evidence.

Furthermore, in our study of benign inferior ST elevation vs. inferior STEMI, ST depression in aVL was nearly perfect in diagnosing MI.

I activated the cath lab immediately.

3 cardiologist came to the ED and opined that this was pericarditis.  I told them that with STD in aVL it is acute MI until proven otherwise.

They insisted on doing an echo first.  A bedside echo performed by a world expert, Dr. Richard Asinger, showed no effusion, and he could not discern a wall motion abnormality.  The patients pain was almost gone by this time.

While waiting for the team, we recorded another ECG at 0826:
Again, not much change.



And a right sided ECG at 0827:
This appears to show right sided ST elevation, though perhaps not a full mm.  This strongly suggests an RV infarct.  

At cath, the culprit was a proximal LAD lesion (open, with TIMI-3 flow)!  It had embolized to the distal LAD, which was a "type III" or "wraparound" LAD supplying the inferor wall.  So this was an antero-infero-lateral MI.  The proximal lesion was stented and the distal was treated with antiplatelet and antithrombotic therapy.

The next day she has reperfusion T-waves in the anterior leads, as well as inferior and  lateral leads:
Looks like Wellens' syndrome in anterior leads, because it is analogous.  There is also what I call inferior and lateral "Wellens'", as there are repefusion T-waves (T-wave inversion) in all these locations

Formal Echo later showed moderate hypokinesis of the septum and dense hypokinesis of the apex and inferior wall.  Peak troponin I was 24 ng/ml.

We always look for explanations when young people have MI.  "They must have done cocaine."  "They must have high cholesterol."  But sometimes coronary atherosclerosis is accelerated, or there is one focal lesion, without good reason.  Her lipids were: LDL 139, VLDL 10, HDL 70, total cholesterol 219.

Lessons:

1) Myocardial Infarction does occur in young women!  They need not have a lot of risk factors or take cocaine.  In young women with STEMI, the diagnosis is more often missed or delayed than in any other demographic group, probably because of the bias that leads us to say, as my chief of EM always expresses it: "Nah, couldn't be."  MI is much more common in young people, including women, than previously recognized.  Many MI in very young women may be due to spontaneous coronary dissection, but this is not the most common etiology.  If the ECG is diagnostic, as in this case, believe it!  Do not try to convince yourself that it "couldn't be."

There was an important article published in fall of 2012 showing that young women with STEMI have longer Door to Balloon times and higher mortality.  There are a couple smaller studies with the same findings here and here.

2) You diagnose pericarditis at your peril

3) Absence of Wall motion abnormality may be misleading, especially if the pain and/or ECG abnormalities have resolved.  In this case, the difference between the informal and formal echo was the use of Definity contrast.


21 comments:

  1. The other thing going for MI over pericarditis is that the ST elevation in III is> than in II, whereas in pericarditis the ST elevation in II is usually greater than in III. Not a hard and fast rule but it all adds to the weight of evidence

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    1. This is an old rule which has not panned out and is not well supported by our data or others. For II can be greater than III if the QRS axis is between 60 and 90 degrees. Many MI have an axis between 60 and 90, and these all have ST depression in aVL. That is why ST depression in aVL is far more accurate.

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  2. First of all I would like to thank you Dr. Smith for all of you excellent posts and teachings. I am an RN and I work in Huntington, WV. It is very bothersome to me that most people immediately say pericarditis d/t age. I have personally seen a 24,26,30 year olds with true stemi's unrelated to stimulants. Sadly most of the physicians in our ER would jump straight to pericarditis even after seeing young people with AMI. There have been a few instances one very recent where I begged a physician to activate the cath lab for an EKG that was transmitted to us from the volunteer fire department I am a part of. This was an obvious anterior/lateral mi with depression in inferior leads and this pt was 55 years old! So,you can imagine when a young person presents with CP and ekg changes. So,again thank you for your posts and teachings on up to date electrocardiography findings. I wish more of our physicians were like you. It makes ER work a lot easier when you aren't arguing with a physician over an ekg.

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    1. Dane, I'm glad you're advocating for your patients!

      Steve Smith

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  3. Dr. Smith,

    Dr. Amal Mattu has a number of EKG of the Week videos on pericarditis, and he constantly stresses that if there is any ST depression, it is a STEMI. In this case there was clear depression in aVL from the first EKG. What are your thoughts on this?

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    1. I completely concur on that: any ST depression anywhere (except for aVR!!), and it is NOT pericarditis. aVR is reciprocal to the other leads and is always an exception.

      Steve Smith

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  4. This might be the reference you were looking for http://www.ncbi.nlm.nih.gov/m/pubmed/22748404/.
    Great case. Would have you performed a full workup if the ECG was normal?

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    1. That is the reference! Thanks. If the ECG were normal, I would not have pursued it further. When patients have a low pretest probability, I generally stop with the ECG.

      Steve Smith

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    2. I might have ordered a single troponin, or maybe not. I often stop at a normal ECG in low risk patients.

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    3. Agree: low pretest probability patients might even be harmed by a conventional workup since stress tests have too many false positives. May I ask what would be in your opinion a reasonable test threshold for ACS?

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    4. That is a very big question and depends on so many factors: age, risk factors, quality and location of pain/discomfort etc. Sometimes an ECG is enough, sometimes serial ECGs. sometimes one troponin suffices, sometimes serial trops. Sometimes a formal echo, or stress test, or angiogram. Too complex for this forum!

      Steve

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    5. Thanks for your time. I've learnt so many things from your blog and I want to to use this opportunity to express my thankfulness.

      Mattia Quarta

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  5. We had a really similar story.
    She was 22. She had a similar ECG changes.
    Our first theory was pericarditis, but we saw apical wall motion abnormality on the echo, but no efflusion. Than we thought, it could be Takatsubo (she had broken up with her boyfriend, and had lost her job on the previouse day). We performed the angio and we found an LAD occlusion.
    It was a real shock for me!

    Moreover her first Troponin was negative, and she had higher WBC, CRP results.

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    1. This comment has been removed by the author.

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    2. Thanks for sharing! The initial troponin is usually negative in acute STEMI.

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  6. is there any correlation between the localization of MI ( or ocluded artery) and the amount of Troponins ?

    Lotfi Djilali Bensekrane

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    1. There is a loose correlation: LAD MI is usually larger than other territories, especially if proximal LAD. So, in general, troponins are higher also.

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  7. There is a recent article on theheart.org that hits many of the points you mentioned: Girl trouble: Rising tide of STEMI in young women "clearly not acceptable" http://www.theheart.org/article/1542051.do?utm_medium=email&utm_source=20130523_heartwire&utm_campaign=newsletter

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  8. excellent presentation, and comments. thanks, steve

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  9. This is a big surprise to me because until now I have just thought RVMI is only caused by RCA occlusion, but in this case, it is due to distal wraparound LAD... Dr. Smith, could you explain how a distal wraparound LAD occlusion can lead to RVMI? Thank you.

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    1. You are correct. This was NOT an RV infarct. The ECG looks like it, but it turned out to be an LAD LV anterior MI with wraparound to inferior wall. The differential diagnosis of inferior MI with STE in V1-V3 is RCA with RV MI vs. LAD with wraparound.

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