Troponin I (TnI) is a key regulatory protein of the striated musculature. Although its function in the contractile apparatus is the same in all striated muscles, TnI originating from the myocardium (cardiac TnI, molecular weight 23.9 kD) clearly differs from skeletal muscle TnI. Due to this high tissue‑specificity, cardiac troponin I (cTnI) is a highly sensitive marker for myocardial damage. Cardiac TnI allows to differentiate between skeletal muscle lesions (e.g. rhabdomyolysis and polytraumatism) and myocardial injury.
In cases of acute myocardial infarction (AMI), cTnI levels in serum rise about 3‑6 hours after the onset of cardiac symptoms, peak at 12‑16 hours, and can remain elevated for 4‑9 days. Elevated cTnI levels have also been reported in cases of unstable angina pectoris (UAP) and congestive heart failure (CHF). Cardiac TnI is a well‑established prognostic marker which can predict the near‑, mid‑ and even long‑term outcome of patients with acute coronary syndrome (ACS).
Given that cTnI as well as cardiac troponin T are independent markers which best predict the outcome of patients with ACS, the joint committee of the European Society of Cardiology (ESC) and American College of Cardiology (ACC) redefined myocardial infarction (MI). According to this redefinition, MI is diagnosed when blood levels of cardiac troponin are above the 99 th percentile of the reference limit (of a healthy population) in the clinical setting of acute ischemia. The imprecision (coefficient of variation) at the 99 th percentile for troponin assays is required to be less than or equal to 10 %.
Based on the redefinition of MI several recommendations have been published concerning the role of cardiac troponin testing in patients with ACS.
In patients with UAP and those without evidence of ST segment elevation (NSTEMI) detectable levels of cardiac troponin correlate with higher incidence of mortality. Thus, the measurement of troponin can be useful in the risk stratification of these patients which is also part of the ACC/AHA (American Heart Association) guidelines for the management of patients with UAP and NSTEMI.
In summary, elevated troponin levels point to myocardial injury, but are not necessarily indicative of an ischemic mechanism. 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 considered.