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, itโ€™s simply untrue: if youโ€™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!

"๐˜›๐˜ณ๐˜ฐ๐˜ฑ๐˜ฐ๐˜ฏ๐˜ช๐˜ฏ๐˜ฆ๐˜ฎ๐˜ช๐˜ข" 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 Hereโ€™s a framework for thinking about #tropbumps.

Ask: are there signs of ischemia? If so, you may be facing an โ€œ๐— ๐—œโ€: ๐˜ฎ๐˜บ๐˜ฐ๐˜ค๐˜ข๐˜ณ๐˜ฅ๐˜ช๐˜ข๐˜ญ ๐˜ช๐˜ฏ๐˜ง๐˜ข๐˜ณ๐˜ค๐˜ต๐˜ช๐˜ฐ๐˜ฏ, 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, ๐—น๐—ผ๐—ผ๐—ธ ๐—ณ๐—ผ๐—ฟ ๐˜ƒ๐—ถ๐˜๐—ฎ๐—น ๐˜€๐—ถ๐—ด๐—ป ๐—ฑ๐—ถ๐˜€๐˜๐˜‚๐—ฟ๐—ฏ๐—ฎ๐—ป๐—ฐ๐—ฒ๐˜€.

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 thereโ€™s ๐— ๐—œ๐—ก๐—ข๐—–๐—”.

๐˜ž๐˜ฉ๐˜ข๐˜ต ๐˜ต๐˜ฉ๐˜ฆ ๐˜ฉ๐˜ฆ๐˜ค๐˜ฌ ๐˜ช๐˜ด ๐˜”๐˜๐˜•๐˜–๐˜Š๐˜ˆ?
7/15 ๐˜”๐˜บ๐˜ฐ๐˜ค๐˜ข๐˜ณ๐˜ฅ๐˜ช๐˜ข๐˜ญ ๐˜ช๐˜ฏ๐˜ง๐˜ข๐˜ณ๐˜ค๐˜ต๐˜ช๐˜ฐ๐˜ฏ ๐˜ธ๐˜ช๐˜ต๐˜ฉ ๐˜ฏ๐˜ฐ ๐˜ฐ๐˜ฃ๐˜ด๐˜ต๐˜ณ๐˜ถ๐˜ค๐˜ต๐˜ช๐˜ท๐˜ฆ ๐˜ค๐˜ฐ๐˜ณ๐˜ฐ๐˜ฏ๐˜ข๐˜ณ๐˜บ ๐˜ข๐˜ต๐˜ฉ๐˜ฆ๐˜ณ๐˜ฐ๐˜ด๐˜ค๐˜ญ๐˜ฆ๐˜ณ๐˜ฐ๐˜ด๐˜ช๐˜ด = 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 โ€“ which can even include a STEMI! โ€“ 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 ๐—บ๐˜†๐—ผ๐—ฐ๐—ฎ๐—ฟ๐—ฑ๐—ถ๐—ฎ๐—น ๐—ถ๐—ป๐—ท๐˜‚๐—ฟ๐˜† 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 ๐˜ค๐˜ฉ๐˜ณ๐˜ฐ๐˜ฏ๐˜ช๐˜ค ๐˜ฎ๐˜บ๐˜ฐ๐˜ค๐˜ข๐˜ณ๐˜ฅ๐˜ช๐˜ข๐˜ญ ๐˜ช๐˜ฏ๐˜ซ๐˜ถ๐˜ณ๐˜บ 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?
12/15 โฌ‡๏ธclearance alone doesn't explain the whole picture of asymptomatic troponin elevation in ESRD.

โค๏ธ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?

๐˜›๐˜™๐˜Œ๐˜“๐˜ˆ๐˜š found that patients with ischemic strokes were less likely to have obstructive CAD compared to matched NSTEMI patients. https://pubmed.ncbi.nlm.nih.gov/26933082 
15/15

๐—ง๐—ฎ๐—ธ๐—ฒ๐—ฎ๐˜„๐—ฎ๐˜†๐˜€:
1.Abandon the term โ€œtroponinemiaโ€.
2.Not all troponin elevations are โ€œMIโ€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.
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