Clinical Information

Cardiac troponin-I (TnI) is a regulatory subunit of the troponin complex associated with the actin thin filament within cardiac muscle cells. TnI, in conjunction with troponin-C and troponin-T, plays an integral role in the regulation of muscle contraction.

Clinical studies have demonstrated the release of cardiac troponin-I (cTnI) into the blood stream within hours following myocardial infarction (MI) or ischemic damage. Elevated levels of cTnI (above the values established for non-MI specimens) are detectable in serum within 4 to 6 hours after the onset of chest pain, reach peak concentrations in approximately 8 to 28 hours, and remain elevated for 3 to 10 days following MI.

High sensitivity troponin (hs-Tni) assays have been defined as those which can achieve less than or equal to 10% CV at the 99th percentile of a healthy population and are capable of detecting troponin in greater than 50% of both men and women individually. These assays can detect levels of troponin within 3 hours after the onset of chest pain.

Cardiac troponin is the preferred biomarker for the detection of myocardial injury based on improved sensitivity and superior tissue-specificity compared to other available biomarkers of necrosis, including CK-MB, myoglobin, lactate dehydrogenase, and others. The high specificity of troponin measurements is beneficial in identifying cardiac injury for clinical conditions involving skeletal muscle injury resulting from surgery, trauma, extensive exercise, or muscular disease. High tissue specificity of cardiac troponin, however, should not be confused with the specificity for the mechanism of injury (e.g., MI vs. myocarditis).

An elevated troponin value alone is not sufficient to make the diagnosis of myocardial infarction. Serial sampling is recommended to detect the temporal rise and fall of troponin levels characteristic of MI. In addition, other markers such as CK-MB can be used in conjunction with troponin-I results in aiding the diagnosis of MI.

Several major studies have shown that troponin is also useful as a predictor of cardiac risk in patients with unstable angina. Previous studies showed that during a 30-day follow-up, patients with acute coronary syndromes (including unstable angina) were at greater risk of progressing to MI if troponin is elevated. Results from the PRISM trial showed that elevated troponin levels could help to identify patients with unstable angina who had additional cardiac risk (especially within the first 72 hours after onset of symptoms) and who could benefit from treatment with a glycoprotein IIb/IIIa-receptor antagonist. Thus, troponin can play an important role in identifying patients with acute coronary syndromes who are at greater risk for cardiac events.