1/15 #MedTwitter: You're admitting a 64YO male with ESRD on HD for hyperkalemia after missing dialysis. A troponin was checked & returned at 0.78 (nl<0.055 ng/mL), similar to his baseline. He is w/osymptoms and EKG is w/o dynamic changes. What would you call this #tropbump?
2/15 Have you ever been taught to think about troponin as being cardiac vs. non-cardiac in origin? Though this may be a nice framework, it’s simply untrue: if you’re measuring cardiac troponin I (cTnI), it is expressed only on myocardium(not skeletal muscle, unlike troponin T).
3/15 The lexicon to describe troponins is confusing!
"𝘛𝘳𝘰𝘱𝘰𝘯𝘪𝘯𝘦𝘮𝘪𝘢" is frequently used but is not very helpful. It is NOT a diagnosis or etiology, and should probably be abandoned as a term altogether.
4/15 Here’s a framework for thinking about #tropbumps.
Ask: are there signs of ischemia? If so, you may be facing an “𝗠𝗜”: 𝘮𝘺𝘰𝘤𝘢𝘳𝘥𝘪𝘢𝘭 𝘪𝘯𝘧𝘢𝘳𝘤𝘵𝘪𝘰𝘯, which can be due to plaque rupture/thrombus (Type 1) or myocardial oxygen demand/supply mismatch (Type 2).
5/15 With type 2 MIs, classically, 𝗹𝗼𝗼𝗸 𝗳𝗼𝗿 𝘃𝗶𝘁𝗮𝗹 𝘀𝗶𝗴𝗻 𝗱𝗶𝘀𝘁𝘂𝗿𝗯𝗮𝗻𝗰𝗲𝘀.
Type 2 MIs can occur in the presence of fixed atherosclerosis, but coronary artherothrombosis is not the underlying cause for troponin elevation.
6/15 And then there’s 𝗠𝗜𝗡𝗢𝗖𝗔.
𝘞𝘩𝘢𝘵 𝘵𝘩𝘦 𝘩𝘦𝘤𝘬 𝘪𝘴 𝘔𝘐𝘕𝘖𝘊𝘈?
7/15 𝘔𝘺𝘰𝘤𝘢𝘳𝘥𝘪𝘢𝘭 𝘪𝘯𝘧𝘢𝘳𝘤𝘵𝘪𝘰𝘯 𝘸𝘪𝘵𝘩 𝘯𝘰 𝘰𝘣𝘴𝘵𝘳𝘶𝘤𝘵𝘪𝘷𝘦 𝘤𝘰𝘳𝘰𝘯𝘢𝘳𝘺 𝘢𝘵𝘩𝘦𝘳𝘰𝘴𝘤𝘭𝘦𝘳𝘰𝘴𝘪𝘴 = MINOCA, and accounts for 6% of MIs. It is much more common in women than men.
8/15 Mechanisms of MINOCA vary, but patients typically present with symptoms of acute MI – which can even include a STEMI! – but are found to have non-obstructive or no CAD and all other causes of myocardial injury are ruled out.
9/15 If your patient has no signs, symptoms, or findings of myocardial ischemia, you are dealing with 𝗺𝘆𝗼𝗰𝗮𝗿𝗱𝗶𝗮𝗹 𝗶𝗻𝗷𝘂𝗿𝘆 w/o ischemia, which comes in 2 flavors: acute or chronic depending on the serial troponin variability.
10/15 In the case of our patient, he most likely has 𝘤𝘩𝘳𝘰𝘯𝘪𝘤 𝘮𝘺𝘰𝘤𝘢𝘳𝘥𝘪𝘢𝘭 𝘪𝘯𝘫𝘶𝘳𝘺 without ischemia.
You may have learned that high troponins in ESRD is from decreased clearance. If that were true, troponins should change pre vs. post dialysis, right?
11/15 The data is mixed here. Some studies show no troponin change pre/post dialysis; others show slight decrease.
pubmed.ncbi.nlm.nih.gov/10085490/
12/15 ⬇️clearance alone doesn't explain the whole picture of asymptomatic troponin elevation in ESRD.
❤️Myocardial microinjury from osmolarity/ion fluxes, preload/afterload changes, calcium deposition are at play as well.
13/15 Ever wonder why patients with stroke can have high troponins? Is it cardioembolic? Or catecholamine mediated?
𝘛𝘙𝘌𝘓𝘈𝘚 found that patients with ischemic strokes were less likely to have obstructive CAD compared to matched NSTEMI patients.
pubmed.ncbi.nlm.nih.gov/26933082
14/15 The study hypothesized catecholamine-mediated ❤️ injury, but was small in size.
More recent studies have suggested possible cardioembolic etiologies (ie. MINOCA).
pubmed.ncbi.nlm.nih.gov/29167390
15/15
𝗧𝗮𝗸𝗲𝗮𝘄𝗮𝘆𝘀:
1.Abandon the term “troponinemia”.
2.Not all troponin elevations are “MI”s. The term MI should be reserved only for ischemic causes.
3.When there are no findings of ischemia, you are dealing with myocardial injury.
What did I miss? @JamesETooley @pablosanchezcas @AshishSarraju @ChadSWeldy @StanfordChiefs @Sharminzi @DrEricStrong @sargsyanz @realjaympatel @cardionerds @CPSolvers
#MedTwitter #FOAMed #MedStudentTwitter
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