Troponin T, Serum
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Troponin T is a myofibrillar protein found in striated musculature. There are 2 types of myofilament, a thick filament containing myosin and a thin filament consisting of 3 different proteins: actin, tropomyosin, and troponin. Troponin is itself a complex of 3 protein subunits: troponin T, troponin I, and troponin C. Troponin T binds the troponin complex to tropomyosin. Troponin I inhibits actomyosin ATPase in relation to the calcium concentration. Troponin C, with its 4 binding sites for calcium, mediates calcium dependency.
In the cytosol, troponin T is found in both free and protein-bound forms. The unbound (free) pool of troponin T is the source of the troponin T released in the early stages of myocardial damage. Bound troponin T is released from the structural elements at a later stage, corresponding with the degradation of myofibrils that occurs in irreversible myocardial damage. The most common cause of cardiac injury is myocardial ischemia, ie, acute myocardial infarction. Troponin T becomes elevated 2 to 4 hours after the onset of myocardial necrosis, and can remain elevated for up to 14 days.
Elevations in troponin T are also seen in patients with unstable angina. The finding of unstable angina and an elevated troponin T are known to have adverse short- and long-term prognoses, as well as a unique beneficial response to an invasive interventional strategy and treatment with the newer antiplatelet agents and low-molecular-weight heparin.
Exclusion diagnosis of acute myocardial infarction
Monitoring acute coronary syndromes and estimating prognosis
Possible utility in monitoring patients with nonischemic causes of cardiac injury
Troponin T is the cardiac marker of choice for the Mayo Health System for the evaluation of patients with possible cardiovascular injury
The upper limit for normal individuals is less than 0.01 ng/mL (undetectable by this method).
For patients who present with acute coronary syndromes, troponin T values greater than or equal to 0.01 ng/mL that are rising make the diagnosis of cardiac injury. Decreasing values are indicative of recent cardiac injury.
Troponin T values greater than or equal to 0.01 ng/mL are a prognostic sign in patients with ischemic heart disease and most other situations. Clinical judgment is necessary to distinguish patients who have ischemic heart disease from those who do not. However, all patients with troponin T values of 0.01 ng/mL and higher are at increased risk for cardiac events relative to patients with undetectable troponin T.
Patients with low level (<0.20 ng/mL) elevations of troponin T and diagnostic uncertainty for acute coronary syndrome should be evaluated by repeat measurements at 3 and 6 hours including a delta between these time points to determine whether this is an acute or more chronic elevation.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
As with all markers of cardiac injury, elevations of troponin T do not in and of themselves indicate the presence of an ischemic mechanism. Many other disease states are associated with elevations of troponin T via mechanisms different from those that cause injury in patients with acute coronary syndromes. These include trauma (eg, contusion, ablation, or pacing), congestive heart failure, hypertension, hypotension (often with arrhythmias), pulmonary embolism, renal failure, and myocarditis.
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.
Clinical References Provides recommendations for further in-depth reading of a clinical nature
Jaffe AS: 2001-A biomarker odyssey. Clin Chim Acta 1999;284:197-211