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Invited Commentary
December 17, 2018

Gaming, Upcoding, Fraud, and the Stubborn Persistence of Unstable Angina

Author Affiliations
  • 1Cardiovascular Division, Washington University School of Medicine, St Louis, Missouri
JAMA Intern Med. Published online December 17, 2018. doi:10.1001/jamainternmed.2018.5967

Unstable angina (UA), previously known as crescendo or preinfarction angina, is one of the acute coronary syndromes (ACS) that includes non–ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation MI (STEMI). Unstable angina is unique among the ACS in that, despite clinical evidence of myocardial ischemia, biomarkers of myocardial necrosis are not elevated.1 Symptoms and signs of ischemia are usually controlled by antianginal medications, systemic anticoagulation, and antiplatelet therapy but coronary angiography and revascularization, usually by percutaneous coronary intervention (PCI) are generally performed on an urgent or semiurgent basis to prevent progression to MI. In the early 1990s, in an era that preceded widespread use of troponin assays, UA was one of the most common reasons for hospital admission.1 With the introduction of more sensitive troponin biomarkers, an increasing proportion of patients previously diagnosed with UA began being reclassified as NSTEMI based on elevation of biomarkers. For example, in the TIMI 3 trial, conducted between 1989 and 1992, 25% of patients classified as UA based on absent creatine kinase (CK)-MB measurements had conventional cardiac specific troponin I (cTnI) levels of 0.4 ng/mL or more (to convert to µg/L, multiply by 1.0), a relatively high cutoff compared with current standards.2 The reclassification of patients with UA to NSTEMI has continued because the upper reference limit (URL) has been adjusted downward in recognition of the increased risk of adverse events with even minimal troponin elevations.1 With the introduction of more sensitive troponin assays beginning in around 2010, the number of patients who present with an ACS without a rise in detectable troponin has continued to decline. In a post hoc analysis of the PROTECT-TIMI 30 trial, published in 2009, 82% of patients with typical features of UA including rest pain exceeded the URL of a high-sensitivity assay by 8 hours, thus shifting their diagnosis to NSTEMI.3 As a result, in 2013, Braunwald and Morrow proposed it was time to prepare a requiem for UA, and they concluded that “it is not clear that ACS events can occur without some increase in circulating cTn when measured by a high-sensitivity assay.”1(p2455)

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