Clinical utility of Troponin

(Source: Tietz Clinical Chemistry 4th Edition)

Fig: Use of troponin to identify UA from MI

Increase above URL seen after 2-6 hours of onset of AMI and peaks at 48 hours. The initial increase in due to 3-6% cytoplasmic fraction of troponin (CK-MB is 100% cytoplasmic). 

Second, cTnI and cTnT can remain increased upto 4-14 days after AMI. This is due to release from 94% to 97% myofibril bound fraction. Third is very low to undetectable cardiac troponin values from patients without cardiac disease permit the use of lower discriminator concentrations compared with CK-MB for determination of myocardial injury.

Troponin is insufficient for effective early diagnosis as it shows low sensitivity and specificity upto 6 hr after onset of chest pain. But has high clinical sensitivity (>90%) above 8 hours after AMI.

Due to higher cytosolic content cTnT releases earlier than cTnI. In addition cTnT release is biphasic first cytosolic and second is muscle bound. cTnI release is monophasic due to lower free cTnI and also it exist and TIC, IC or free I.

72 hour troponin measurement correlates with infarct size. Since the second phase rise in cTnT occurs within 2-4 days, so if the infarct is severe then this phase is seen but if it is improving this phase is not seen.

Other causes of increase in troponins are hypothyroidism, renal failure, hypertension, rhabdomyolysis, sepsis, pulmonary embolism, etc.