An all too common question in my cardiac courses relates to a common (up to 70%) situation where a patient with chronic kidney disease (CKD) returns a positive Troponin .
So
Why does my renal patient have an elevated Troponin level in the absence of an acute MI?
...
Let's recap some basic cardiac sell physiology.
Inside heart muscle cells (cardiomyocytes) exists tiny molecular protein machines called sarcomeres. They look stripy under the microscope which is why heart tissue is often called striated muscle. Striated means stripe like.
These sarcomeres contain complex protein filaments that change shape (shortening and lengthening) in shape when electrically stimulated.
Called Actin and Myosin filaments, the action of shortening is what causes the muscle cell to contract.
Now actin and myosin are glued together with a protein called Troponin. Three types, Troponin I, T and C
.
Troponin T and I are cardiac muscle specific.
Now visualise this. The sarcomeres with all these Troponin, Actin and Myosin proteins are "locked" away inside heart cells. Not in blood/serum, but inside cells.
If you think of them as the yoke of an egg. The only way a yoke can leak out, is if the egg breaks. Likewise, the only way Troponin can leak out is when the cardiac cell is damaged.
Enter a myocardial infarction (MI). As heart cells die and break open like eggs, they leak their contents onto the interstitial fluid, then, because the cardiac tissue injury causes inflammation and subsequent increase in capillary permeability, the large troponin proteins diffuse (leach) into the blood stream. Hence, a Troponin rise is detected in serum. It is not quick, it leaks slowly into the blood stream, and peaks at about 9 hours after injury to heart cells.
Measured in nanograms/L or micrograms/L depending on the path lab at your facility, Troponin rise it diagnostic when recorded to be greater than 15ng/L (on newest assays), or 0.04mcg/L on older assays or IStat machines.
Commonly clinicians report false positives. In patients who live in areas where there are high rodent numbers (esp mice), these individuals can have developed anti-mouse antibodies due to high rodent exposure. Their rodent antibody rich blood can cross react with the various Troponin assays in the lab, returning false elevated Troponin values.
Commonly, renal patients with CKD will have elevations in Troponin in their blood which can confuse the diagnostic value of a CKD patient's chest pain presentation. But why? Why if there was no acute cardiac damage, could Troponin leak?
Well it does. Chronic kidney disease patients often have a chronic elevation in Urea in their blood. This uraemia is damaging to cardiac and other muscle tissue. Slow chronic insidious erosion of heart tissue allows troponin to continually leak like a dripping tap, elevating the baseline level of Troponin. A sharp rise is still diagnostic, but a one off elevation that is slightly over the threshold of 0.04mcg is not diagnostic of an acute event in these renal patients. We'd admit for serial cardiac Troponin levels to watch for rise over the 9-12 hours.
We cover all this interesting stuff in our #Cardiac, #ARRR #PirateSeminar, and #AcuteDeterioration
Seminars. Check them all out here www.ect4health.com.au/whatswww.ect4health.com.au/whats
