Abstract

To the Editor: Cardiac troponin is the standard biomarker for detection of myocardial injury. An increase of cardiac troponin >99th percentile by use of a sufficiently sensitive and precise assay is required to diagnose acute myocardial infarction (MI)1 and is increasingly measured by use of high-sensitivity cardiac troponin T (hs-cTnT) and hs-cTnI assays outside the US. In patients with stable coronary artery disease (SCAD), hs-cTnT can be detected in >80% of patients (1), with values above the 99th percentile in approximately 11% of patients (2). Increasing concentrations of hs-cTnT and hs-cTnI above the 99th percentile are also associated with an increased risk of adverse cardiovascular events (2, 3). The mechanisms underlying cardiac troponin increase remain unclear, but may include silent plaque rupture, inducible ischemia, anatomic burden of CAD, cardiac structural abnormalities, or impaired left ventricular (LV) function (4, 5). We evaluated serial changes in hs-cTnT (Elecsys 2010, Roche Diagnostics, detection limit 3 ng/L, 10% CV 13.5 ng/L, 99th percentile value of 14 ng/L) (6), sensitive cTnI, (S-cTnI) (TnI Ultra, Advia Centaur, Siemens Healthcare Diagnostics, detection limit 0.006 μg/L, 10% CV 0.045 μg/L, level 2 assay) (7, 8), heart fatty acid binding protein (HFABP) (Evidence Investigator, Randox Laboratories, 99th percentile 5.8 μg/L, CV 5%) (9), and N-terminal pro–B-type natriuretic peptide (NT-pro-BNP) (Elecsys 2010, Roche Diagnostics, CV 3.2%–2.4% 175–4962 ng/L with an analytic range 5–35 000 ng/L) (10) in outpatients referred for exercise echocardiography with suspected angina pectoris and normal resting LV function (ejection fraction >50%) without overt cardiac structural abnormality. Blood …

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