Troponin in Syncope – Journal Article Review

14 Jun

[Previously posted over here. Originally on a non-medical blog, hence the “basic overview for everyone”]

Here’s a vodcast I did on syncope.

The basic overview for everyone

About 2pm every sunday we have a wee run of ambulances of people who have fainted/passed out/fallen over in church. Religion is bad for you. We can all agree on that.

99% (Warning – made up number alert) of these are what we call syncope, or if we try to be more technical and make it sound like a real disease we say neurcardiogenic syncope of vasovagal. This is largely to make doctors and patients feel better that “I thought it was a faint but I went to the hospital and said it was neurocardiogenic syncope…”

We like to make light of syncope (if you’ll pardon the pun) but in reality it can be tricky. The vast majority of people who fall over, collapse, or have something like a faint then that is exactly what it will be – a faint, a funny turn and of no further consequence. Unfortunately some won’t be. Some will have horrible things happen to them.

As you can imagine most of emergency medicine is like this.

We go to medical school and learn nothing and graduate as doctors and screw up loads and eventually learn something and after a while we get pretty damn good at working out which are just faints and which mean lots of badness.

Some call this clinical gestalt. I figure that this is what we’re paid for.

Most of the time our gestalt is pretty good. Really well people look well… really sick people look sick, fire is hot, ice is cold etc…

The inbetweeners where you’re not sure are the tricky ones. Sometimes we use tests to help us. If I suspect you have a broken wrist I can do an x-ray and then I have a useful answer to my question.

Unfortunately when it comes to syncope we have no such tool or test. ¬†Mainly we have gestalt – we talk to them, hear they’re story and we make an educated guess clinical judgement.

Understandably when we make our guess (ahem…) we err on the side of caution, often this means admitting the patient. When it turns out that the patient is fine then you could say that it was a waste of both hospital and patient time.

The more complex critical appraisal bit

this study from Edinburgh is part of yet another “rule” to help us leave our brains at the door work out who is safe in syncope. In particular it wanted to examine the utility of troponins in making a decision on people with syncope.

I like its conclusion

estimation of troponin I provides little additional benefit to the presenting ECG in identifying patients with syncope due to AMI

however I’m not so keen on how they got there.

They approached patients who presented with syncope to assess eligibility, a quarter were deemed ineligible (by reasonable standards) and 2 thirds of these got enrolled.

My biggest problem comes here: for a study that wants to assess troponins they only managed to do a trop on half of the patients enrolled. I can’t work out if people got troponins at the physicians discretion (in which case it is a selected group of presumably higher risk syncope patients) or if the troponin was part of the protocol (in which case they did a really bad job of following the protocol).

This kind of invalidates a lot of the conclusions if I’ve read it right. How can you make statements about a general syncope population and troponins when only half of the patients got the test? There may have been reasons why these patients didn’t get the test done which makes them different.


Of all who had the trop done there were 4 MIs – all of which had ECG changes. Which is reassuring. If they have a normal ECG then you really shouldn’t have to worry about an MI.

They also found that of the 256 analysed patients, 9% had a bad outcome (their definition of this was slightly more dubious)

And as in lots of other studies, lots of the raised troponins were for non-MI reasons. Hopefully by now we’re learning this – don’t automatically think MI when you see a raised troponin.

Given the constant battle that we find in the NHS to get a patient admitted, the trop is sometimes a useful stick to beat the admitting team with – which is truly terrible practice I know but sometimes you just have to do what you need to get the patient admitted – despite its lack of utility.

I send the vast majority of my syncope patients home after an ECG and history and examination (you know that thing you do where you touch the patient and use the stethoscope thingy – it’s largely useless but it looks good…) In general when there’s something bad happening it’s fairly obvious from the start.

My problem with decision instruments for things like syncope is that it’s too complex a problem to simplify into 4 clinical variables. For ankles this works, for syncope I’m not sure.

3 thoughts on “Troponin in Syncope – Journal Article Review

  1. So my gestalt is probably no better or worse than others. I saw a 35 y/o female the other day. Still hyperventilating on the stretcher after her co-worker started an uncomfortable discussion. She got angry, started yelling and breathing fast. Then fainted. Gestalt: “she goes home. Now.” EKG was normal, nursing had already stated a line and had sent “syncope blood work”. I spent a few minutes calming down the family and the patient, she felt better. With exception to the elevated respiratory rate, her vitals were normal. Even heart rate was 95. I had discharge paperwork typed up when the trop came back 5x the normal limit. Two hours into her observation admission she jumped back into the SVT (AVNRT) that caused the symptoms in the first place and likely, the troponin elevation. So, yeah, she might have still been safe for discharge but she definitely would have been back in the ER 2 hrs later. So I send troponin still—as this is now the second time I’ve seen this. It’s my own little screen for arrhythmia, definitely not a rule out if it’s negative, but when it’s positive it puts to rest most other etiologies, I think.

  2. I agree wholeheartedly with not doing troponins as routine in syncope. Clinical history, exam and ECG should determine whether this is necessary. Using high sensitivity troponins to fish for paroxysmal arrhythmias is not something I would advocate either.

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