Cardiac Troponin: The basics from St. Emlyn’s

T E N N I S (3)

Do you remember when it took three days to ‘rule in’ or ‘rule out’ an acute myocardial infarction (AMI)?  When I was a medical student doing my first clinical attachments, I remember doing ward rounds on the CCU seeing patients with suspected AMI.  The way they were managed is a million miles from what we do now.  Back then, patients would have serial ECGs and then be admitted for cardiac enzyme evaluation over the course of the next 3 days.  We’d measure CK, AST and LDH.  ‘CK’ was the so-called ‘early marker’, which would rise early after the start of an AMI.  Today we use CK as a marker of skeletal muscle damage (e.g. rhabdomyolysis).  AST and LDH (today we think of these as liver function tests, I know) were the ‘late markers’ – and by late I really mean late – we might see a rise on days 2 and 3, for example.

Could you imagine for a second, in today’s world, ruling out AMI because their CK and LFTs were normal?  It’s completely unthinkable.  That’s how much cardiac troponin has changed our practice.  We rely on it so completely to diagnose AMI.  And yet, it’s one of the most misunderstood tests in medicine.  Given how much we use it, I guess we feel that we all should know lots about this test.  But doctors still have so many questions.  Here are just a few:

  • What is cardiac troponin?
  • Why is it a marker of AMI?
  • What else causes a raised troponin and how?
  • Should we be doing troponins at 3 hours, 6 hours, 12 hours?  What’s the difference and what’s the evidence?
  • What is a ‘delta troponin’?
  • What do you need to ‘rule in’ AMI?
  • How do you use cardiac troponin in patients with renal failure?

This is just a brief list.  With the research I do in this area and my experience developing protocols/guidelines, people get in touch to ask questions like this quite a lot.  There are loads of questions that people ask – but there are lots of themes in common.  We thought it was about time we produced a handy run down in the true spirit of #FOAMed.

Take a listen to Part 1 of our troponin podcast.  While Simon and Iain have been prolifically churning out spectacular stuff for some time now, this is my debut on the St. Emlyn’s podcast.  I really enjoyed talking about troponin with Iain – and I hope we covered some useful stuff.

We’ll cover more in part 2, when we’ll move on to discussing high sensitivity troponins, what they are, how to use them and how to speak the troponin lingo.  Please get in touch if there’s anything we haven’t covered that you’d like us to, or if there’s anything you’d like us to elaborate on some more!

Rick

5 Comments

  1. srrezaie

    Hello Rick,
    So I want to be sure I am clear on what you were saying….specifically regarding the time between troponins.

    1. There have been slew of studies now (i.e. ASPECT, ADAPT, APACE) all looking at different troponin assays recommending 2 hours between testing. These patients of course were all TIMI = 0 and ECG with no new ischemic changes….or very low risk patients.

    2. The AHA/ACC recommends 6 – 8 hour testing between troponins in chest pain patients.

    3. So my specific question is this….does the AHA/ACC guidelines need to be updated to q2hours or are we supposed to be doing 6 hrs in patients who are not low risk?

    I realize the type of troponin assay you have will make a difference in this, but lets just say for arguments sake that a person has a contemporary or sensitive troponin assay. Not all institutions have the high sensitivity troponins yet… 😉 Great podcast, and great topic.

    Salim

    Reply
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