Rapid atrial pacing increased coronary sinus cTnT concentrations from 6.8 to 15.6 pg/ml (p<0.0001), with similar absolute changes in patients with and without objective evidence of ischemia.
Observational
Does incremental rapid atrial pacing cause detectable troponin T release using a highly sensitive assay in patients referred for diagnostic catheterization?
19 patients referred for diagnostic catheterization
Incremental rapid atrial pacing with serial coronary sinus and peripheral plasma sampling
Baseline (prior to pacing) and comparison between patients with CAD and lactate elution (n=7) versus those without either marker (n=5)
Changes in troponin T concentrations measured by a highly sensitive assay (hs-cTnT) during and after pacingsurrogate
Brief periods of increased myocardial work and ischemia cause low-level troponin T release detectable by highly sensitive assays, even without frank infarction or obstructive CAD.
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. Keywords: ischemia, troponin T, cardiac biomarkers, coronary artery disease, rapid pacing
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Aslan T. Turer
Tayo Addo
Justin L. Martin
Journal of the American College of Cardiology
Harvard University
Brigham and Women's Hospital
Massachusetts General Hospital
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Turer et al. (Wed,) conducted a observational in Patients referred for diagnostic catheterization (n=19). Rapid atrial pacing vs. Baseline (prior to pacing) was evaluated on cTnT concentrations in coronary sinus blood at 60 min (p=<0.0001). Rapid atrial pacing increased coronary sinus cTnT concentrations from 6.8 to 15.6 pg/ml (p<0.0001), with similar absolute changes in patients with and without objective evidence of ischemia.
www.synapsesocial.com/papers/69e7e9c0536d4ca0393ca20f — DOI: https://doi.org/10.1016/j.jacc.2010.11.066
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