Troponin T (TnT) is a component of the contractile apparatus of the striated musculature. Although the function of TnT is the same in all striated muscles, TnT originating exclusively from the myocardium (cardiac TnT, molecular weight 39.7 kD) clearly differs from skeletal muscle TnT. As a result of its high tissue‑specificity, cardiac troponin T (cTnT) is a cardiospecific, highly sensitive marker for myocardial damage. In cases of acute myocardial infarction (AMI), troponin T levels in serum rise about 3‑4 hours after the occurrence of cardiac symptoms and can remain elevated for up to 14 days.
Troponin T is an independent prognostic marker which can predict the near‑, mid‑ and even long‑term outcome of patients with acute coronary syndrome (ACS). In addition, four multicenter trials involving more than 7000 patients have shown that troponin T is also useful to identify patients that benefit from anti‑thrombotic therapy (GPIIb/IIIa inhibitors, low molecular weight heparin).
Because it has been proven that cardiac troponin is an independent marker which best predicts the outcome of patients with ACS and is a useful tool in guiding anti‑thrombotic therapy, the joint committee of the European Society of Cardiology (ESC) and American College of Cardiology (ACC) redefined myocardial infarction (MI). According to this new definition, MI is diagnosed when blood levels of cardiac troponin are above the 99 th percentile of reference limit (of a healthy population) in the clinical setting of acute ischemia. The imprecision (coefficient of variation) at the 99 th percentile for each troponin assay should be defined as less than or equal to 10 %.
Thus, patients with ACS and elevated cardiac troponin and/or CK‑MB are considered to have experienced a non - ST - elevation MI (NSTEMI); whereas the diagnosis of unstable angina is established if cardiac troponin and CK‑MB are within the reference range. This redefinition of MI is now also part of the new ACC/AHA guidelines for the management of patients with unstable angina and NSTEMI.
Based on the redefinition of myocardial infarction several recommendations have been published concerning the role of cardiac troponin testing in patients with ACS.
Myocardial cell injury leading to elevated troponin T concentrations in the blood can also occur in other clinical settings like congestive heart failure, cardiomyopathy, myocarditis, heart contusion, renal failure, lung embolism, stroke, left ventricular dysfunction in septic shock, and interventional therapy like cardiac surgery, non - cardiac surgery, PTCA, and drug‑induced cardiotoxicity. In many of these cases – in particular in patients with renal failure – increased levels of cardiac troponin T identify patients with poorer prognosis. In summary, elevated troponin levels are indicative of myocardial injury, but elevations are not synonymous with an ischemic mechanism of injury. The term MI should be used when there is evidence of cardiac damage, as detected by marker proteins in a clinical setting consistent with myocardial ischemia. If the clinical circumstance suggests that an ischemic mechanism is unlikely, other causes of cardiac injury should be pursued.