Clinical Lab Handbook

Container/Tube: Light green-top (lithium heparin) gel tube-Hemolyzed specimen is not acceptable.

Specimen Volume: 2.5 mL of heparinized plasma

Collection Instructions: Spin down immediately.

Chemiluminescence Immunoassay

An immunometric immunoassay technique is used, which involves the simultaneous reaction of cardiac Troponin I present in the sample with a biotinylated antibody (mouse monoclonal anti-cTnI)) and a horseradish peroxidase (HRP)-labeled antibody conjugate (mouse monoclonal anti-cTnI)). The antigen-antibody complex is captured by streptavidin on the wells. Unbound materials are removed by washing.

The bound HRP conjugate is measured by a luminescent reaction. A reagent containing luminogenic substrates (a luminol derivative and a peracid salt) and an electron transfer agent, is added to the wells. The HRP in the bound conjugate catalyzes the oxidation of the luminol derivative, producing light. The electron transfer agent (a substituted acetanilide) increases the level of light produced and prolongs its emission. The light signals are read by the system. The amount of HRP conjugate bound is directly proportional to the concentration of cTnI present.

Cardiac Troponin I measurement aids in the diagnosis of acute myocardial infarction and in the risk stratification of patients with non-ST-segment elevation acute coronary syndromes with respect to relative risk of mortality, myocardial infarction (MI) or increased probability of ischemic events requiring urgent revascularization procedures.

Troponin I (TnI) is a protein normally found in muscle tissue that, in conjunction with Troponin T and Troponin C, regulates the calcium dependent interaction of actin and myosin. Three isotypes of TnI have been identified: one associated with fast-twitch skeletal muscle, one with slow-twitch skeletal muscle and one with cardiac muscle. The cardiac form has an additional 31 amino acid residues at the N terminus and is the only troponin isoform present in the myocardium.

Clinical studies have demonstrated that cardiac Troponin I (cTnI) is detectable in the bloodstream 4–6 hours after an acute myocardial infarct (AMI) and remains elevated for several days thereafter. Thus, cTnI elevation covers the diagnostic windows of both creatine kinase-MB (CK-MB) and lactate dehydrogenase. Further studies have indicated that cTnI has a higher clinical specificity for myocardial injury than does CK-MB.

Other conditions resulting in myocardial cell damage can contribute to elevated cTnI levels. Published studies have documented that these conditions include, but are not limited to, sepsis, congestive heart failure, hypertension with left ventricular hypertrophy, hemodynamic compromise, myocarditis, mechanical injury including cardiac surgery, defibrillation and cardiac toxins such as anthracyclines. Factors such as these should be considered when interpreting results from any cTnI test method.

Because of its cardiac specificity and sensitivity, cTnI has been used as a reliable marker in evaluating patients with unstable angina and non-ST segment elevation acute coronary syndrome (ACS). Previous clinical studies of patients with ACS have shown that minor increases in cTnI values provide important prognostic information about the short and long term risk of death. Ultimately, the assessment of the prognosis can be useful in identifying patients most likely to benefit from specific therapeutic interventions.

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