Clinical Information

Troponin I, in conjunction with troponin C and troponin T, plays an integral role in the regulation of muscle contraction. Clinical studies have demonstrated the release of cTnI into the blood stream within hours following MI or ischemic injury. High sensitivity assays (such as the one used at KH) can detect elevated levels of Troponin I within 3 hours after the onset of chest pain. Cardiac troponin I reaches peak concentrations in approximately 8 to 28 hours and remains elevated for 3 to 10 days following MI. Cardiac troponin is the preferred biomarker for the detection of myocardial infarction based on improved sensitivity and superior tissue-specificity compared to other available biomarkers of necrosis, including CK-MB, myoglobin, lactate dehydrogenase, and others. The high tissue specificity of Troponin I measurements is beneficial for identifying myocardial infarction in clinical conditions involving skeletal muscle injury resulting from surgery, trauma, extensive exercise, or muscular disease.

High tissue specificity of cTnI, however, should not be confused with the specificity for the mechanism of injury (e.g., MI versus myocarditis). When an increased value for cTnI is encountered in the absence of evidence of myocardial ischemia, other etiologies for cardiac damage should be considered. Elevated troponin levels may be indicative of myocardial injury associated with heart failure, renal failure, chronic renal disease, myocarditis, arrhythmias, pulmonary embolism, or other clinical conditions.

Limitations:

In rare cases, cryoprecipitates can form in specimens stored refridgerated. Cryoprecipitates can cause inconsistent and erroneous results. If cryoprecipitates are suspected, repeat testing on a fresh specimen.