Myocardial Ischemia Induced by Rapid Atrial Pacing Causes Troponin T Release Detectable by a Highly Sensitive Assay

The purpose of this study was to assess whether (1) very small increases in troponin T, measured by a new highly sensitive assay for cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis and (2) serial changes can discriminate ischemia from other causes of cTnT release. A new hs-cTnT assay offers greater sensitivity than current assays. Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple timepoints during and after incremental rapid atrial pacing. cTnT was quantified using a standard and pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary atherosclerosis and myocardial lactate release with pacing. cTnT concentrations in CS blood increased from a median of 6.8 to 15.6pg/mL 60-minutes after termination of rapid atrial pacing (p<0.0001), changes that were mirrored at 180-minutes in peripheral blood (5.1 to 11.8pg/mL p<0.0001)]. Although peripheral cTnT concentrations tended to be higher at 180-minutes following pacing for patients with atherosclerosis and lactate elution (n=7) when compared to those without either marker (n=5) (25.0 vs. 10.2pg/mL, p=0.10), relative (1.7- vs 5.2-fold) and absolute (6.8 vs 8.8pg/mL, p=0.50) changes were similar between groups. Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive atherosclerosis. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.