High-Sensitivity Cardiac Troponin for Screening Large Populations of Healthy People: Is There Risk?

Imagine a biomarker that is able to diagnose acute myocardial infarction (MI)3 with high clinical sensitivity and within 2 h of the onset of ischemic symptoms. Imagine that the same biomarker can rule out an MI with almost 100% negative predictive value by using multiple measurements taken over a 2- to 3-h period. Imagine that the biomarker can also risk-stratify symptomatic and stable acute coronary syndrome (ACS) patients for both short-term (during admission) and long-term (over 6 months to 2 years) major adverse cardiac events by using the same measurements. Imagine thinking, beyond ACS, that the biomarker can also identify nonischemic pathologies that have caused the myocardial injury, thus identifying these individuals as belonging to a group at higher risk than ACS patients. The story gets better—no hype. Imagine this biomarker can stand alone—without the cumbersome weight of a multiple-biomarker strategy—as a predictor of major adverse cardiac events in individuals within the general population. So what is this biomarker, and is it being used in clinical practice? What is the evidence to convince laboratory scientists and clinicians that they should drop everything and add this test to their laboratory test menu?In the year 1995 the first cardiac troponin assay, for cardiac troponin T (cTnT), was cleared [510(k)] by the US Food and Drug Administration (FDA) as an aid for the diagnosis of MI. In 1996, the FDA cleared cTnI. I often wonder why it took 20 years for this cardiac-specific marker to get to the market. Once these markers were FDA cleared, and with the rapid development and availability of immunoassays for both cTnT and cTnI, data regarding their clinical utility quickly accumulated in the evidence-based literature (1). In 1999, the clinical chemistry community, followed by the cardiology community in 2000, recommended cardiac troponin as the definitive biomarker …