Extract

Monoclonal antibody–based immunoassays for measurement of cardiac troponins T and I, (cTnT and cTnI, respectively)2 were first described approximately 25 years ago (1, 2). Their promise was a more accurate diagnosis of acute myocardial infarction (AMI) due to improved tissue specificity. The advantages of cardiac specificity were realized soon after the clinical trials started, but an unexpected finding, increases of cTnT and cTnI that occurred “too early” in patients without traditional diagnostic criteria of AMI, was initially believed to compromise the biomarkers' diagnostic specificity. Further clinical studies established the real cause of these findings: minor myocardial damage. These new discoveries, made possible by cTn measurement, led to the redefinition of myocardial infarction (3), and the eventual new clinical diagnostic category of acute coronary syndromes (ACS). In the new diagnostic paradigm, AMI is a subset of ACS, and both conditions can be diagnosed by cTnT and cTnI increases above predetermined cutpoint values. Further evolution of the diagnosis of ischemic myocardial injury has identified 7 types of AMI (4), an unexpected development in the early years of troponin use.

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