Troponin T, High Sensitivity

TROPTHS - NOCO

1 mL serum from SST or Red Top

Temperature	Time
Refrigerated	24 hours

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, the cardiac isoform of TnT originating exclusively from the myocardium (cardiac TnT, molecular weight 39.7 kDa) clearly differs from skeletal muscle TnT. As a result of its high tissue‑specificity, cardiac troponin T (cTnT) is a cardio‑specific, highly sensitive marker for myocardial damage. Cardiac troponin T increases rapidly (i.e. can be detected within 1 hour if using high‑sensitivity assays)1 after acute myocardial infarction (AMI) and may persist up to 2 weeks thereafter. In contrast to ST‑elevation myocardial infarction (STEMI), the diagnosis of non‑ST elevation myocardial infarction (NSTEMI) relies heavily upon elevated cardiac troponin (cTn) concentrations in the appropriate clinical context. The Third Universal Definition of Myocardial Infarction (MI) has confirmed cTn as the biomarker of choice.  Diagnosis of MI is made with acute changes in cTn concentrations with at least one serial sample above the 99th percentile upper reference limit (URL), taken together with evidence of myocardial ischemia (symptoms, electrocardiogram (ECG) changes or imaging results). Various guidelines and publications recommend the optimal imprecision (coefficient of variation) of cTn assays at the 99th percentile upper reference limit be less than or equal to 10 %. The 99th percentile upper reference limit is derived from a reference control group of normal, non‑diseased individuals.  Several guidelines and research activities recognize that improved analytical sensitivity of cTn assays over the last several years has allowed for detection of other etiologies. Chronic cTn elevations can be detected in clinically stable patients such as patients with ischemic or non‑ischemic heart failure,9,10 patients with different forms of cardiomyopathy, renal failure, sepsis  and diabetes.  Elevated concentrations of cTn can also occur in other clinical conditions such as myocarditis,  heart contusion,  pulmonary embolism  and drug‑induced cardiotoxicity. To distinguish between acute and chronic cTn elevations, the Universal Definition of MI stresses the need for serial sampling to observe a rise and/or fall of cTn above the 99th percentile upper reference limit consistent with the clinical assessment, including ischemic symptoms and electrocardiographic changes. Troponin elevations may persist for up to 14 days or occasionally longer.  Other diagnostic tests such as NT‑proBNP and CRP can complement the diagnostic and prognostic information of cTnT in different indications.