Serial quantitative measurements of cardiac troponin I or T have become the cornerstone for diagnosis of myocardial infarction (MI) and are useful for stratifying risk and guiding management of patients with suspected acute coronary syndrome(1). This clinical case reminds us that in addition to documenting values exceeding a specified cutpoint, a rise and/or fall in the biomarker is essential for establishing the diagnosis. Cardiac troponin is a marker of cardiac injury, not etiology. Many non-MI conditions may cause troponin increases, and analytical false positives are also possible. Although cardiac troponin measurements are central for assessment of patients with suspected acute coronary syndrome, MI is a clinical diagnosis, and other nonlaboratory data are essential.
The presence of antibodies that affect cardiac biomarker results was documented in the 1970s and 1980s, when antibodies to CK-BB were identified as an interference with some CK-MB methods. Antibodies against other species, e.g., HAMA, can cause a positive interference with immunoassay reagents for cardiac markers. Autoantibodies that react with cardiac troponin can cause either negative interference(2) or positive interference, as was seen in this case. An important point made in this case was that autoantibodies against cardiac troponin can occur in about 10% of healthy individuals. The common occurrence of such autoantibodies in healthy individuals compels us to be very thoughtful when establishing 99th percentile cutpoints for MI and risk assessment in reference control populations, as recommended in MI redefinition and guideline documents(1)(3).
Coronary heart disease remains the most common cause of death in the Western world, and approximately 6–9 million patients with suspected acute coronary syndrome present annually to emergency departments in the US alone. Given the central role of cardiac troponin measurements, laboratories should be prepared to investigate potential interferences by having on hand heterophile blocking tubes, stocking protein A columns, and/or arranging access to alternative cardiac troponin methods.
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Authors’ Disclosures of Potential Conflicts of Interest: No authors declared any potential conflicts of interest.
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- © 2010 The American Association for Clinical Chemistry