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The improved analytical characteristics of both sensitive and high-sensitivity assays for cardiac troponins I (cTnI)3 and T (cTnT) have substantially increased the diagnostic sensitivity for early detection of acute myocardial infarction (AMI) (1–3). With the ability to detect small increases in circulating cardiac troponins, any cause of myocardial injury will now produce a substantially greater number of analytically true positive findings not detectable by earlier generations of cardiac troponin assays (3–6). This evolution has led to a decrease in diagnostic specificity for the diagnosis of AMI, a concern to many clinicians who may incorrectly equate any increased cardiac troponin value to an AMI (7, 8). Observational studies, although conducted predominately with prior-generation assays, have consistently demonstrated that any increase in cardiac troponin due to almost any mechanism of myocardial injury carries an association with worse outcomes (3, 7). Nevertheless, because diagnostic specificity is pivotal to appropriate therapy, pragmatic approaches are needed to sustain diagnostic specificity with sensitive and high-sensitivity assays for cardiac troponin. In this issue of Clinical Chemistry, Mueller and colleagues (9) report on their experience with one such approach that uses the change in cardiac troponin over time (δ).

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