Troponin I, Serum
Exclusion diagnosis of acute myocardial infarction
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Troponin is a complex that regulates the contraction of striated muscle. It consists of 3 subunits (C, T, and I) that are located periodically along the thin filament of the myofibrils. Troponin I inhibits actomyosin ATPase.
Troponin I is an inhibitory protein and exhibits in 3 isoforms: cardiac muscle, slow-twitch skeletal muscle, and fast-twitch skeletal muscle. The cardiac form of troponin I has 31 amino acid residues on its N-terminal, not present in the skeletal forms, which allow for specific polyclonal and monoclonal antibody development. The cardiac specificity of this isoform improves the accuracy of diagnosis in patients with acute or chronic skeletal muscle injury and possible concomitant myocardial injury.
Troponin I is the only troponin isotope present in the myocardium and is not expressed during any developmental stage in skeletal muscle. Troponin I is released into the bloodstream within hours of the onset of symptoms of myocardial infarction or ischemic damage. It can be detected at 3 to 6 hours following onset of chest pain with peak concentrations at 12 to 16 hours, and remains elevated for 5 to 9 days.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
< or =0.04 ng/mL
Reference values have not been established for patients <17 years of age.
There are, on occasions, elevations of cardiac troponin T (cTnT) which we use clinically which can be due to skeletal muscle disease. One way to unmask such elevations is to measure cardiac troponin I (cTnI), which will be normal in that circumstance. In addition, at times there are interferences that can cause spurious increases or decreases in cTnT values. Conceptually, these same interferences can occur with cTnI but in any given case, the likelihood of having both assays be confounded in that way is highly unusual. Thus, potential false-positives would be unmasked by a normal cTnI and false-negatives by an elevated value.
A reference range study was conducted using the ADVIA Centaur TnI-Ultra assay based on guidance from the Clinical and Laboratory Standards Institute (CLSI) Protocol C28-A2.25. The study, which used 1,845 fresh serum, lithium heparin plasma, and EDTA plasma samples from 648 apparently healthy individuals ranging from 17 to 91 years of age, demonstrated a 99th percentile of 0.04 ng/mL (mcg/L).(1)
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
A positive troponin result is not always indicative of myocardial infarction. Other conditions resulting in myocardial cell damage can contribute to elevated cardiac troponin I levels. These conditions include, but are not limited to, myocarditis, cardiac surgery, angina, unstable angina, congestive heart failure, and noncardiac-related causes, such as, renal failure and pulmonary embolism.
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
1. Package insert: Siemens Centaur XP, TnI, 04744371 Rev H, 2008-09
2. Apple F: Acute myocardial infarction and coronary reperfusion: serum cardiac markers for the 1990s. Am J Clin Pathol 1992;97:217-226
3. Adams JE 3rd, Bodor GS, Davila-Romain VG, et al: Cardiac troponin I: A marker for cardiac injury. Circulation 1993;88:101-106
4. Corin SJ, Jushasz O, Zhu L, et al: Structure and expression of the human slow twitch skeletal muscle troponin I gene. J Biol Chem 1994;269:10651-10659