Myocardial Ischemia Induced by Rapid Atrial Pacing Causes Troponin T Release Detectable by a Highly Sensitive Assay: Insights From a Coronary Sinus Sampling Study
What are the kinetics of myocardial release of cardiac troponin T (cTnT) during induced ischemia with rapid atrial pacing and its correlation with objective indicators of ischemia?
Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple time points during and after incremental rapid atrial pacing. cTnT was quantified using both a standard and a precommercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing. Between-group comparisons were performed using the Wilcoxon signed rank test.
cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 minutes after termination of rapid atrial pacing (p < 0.0001), changes that were mirrored at 180 minutes in peripheral blood (5.1-11.8 pg/ml, p < 0.0001). Although peripheral cTnT concentrations tended to be higher at 180 minutes following pacing for patients with CAD and lactate elution (n = 7) when compared with those without either marker (n = 5) (25.0 pg/ml vs. 10.2 pg/ml, p = 0.10), relative (1.7-fold vs. 5.2-fold) and absolute (6.8 pg/ml vs. 8.8 pg/ml, p = 0.50) changes were not different between groups.
The authors concluded that brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work.
The study demonstrates that significant absolute and relative increases of TnT, as measured by the highly sensitive assay, may be detected even among patients without biochemical evidence of ischemia or significant CAD. Furthermore, small increases in cTnT may be expected following periods of increased myocardial work, even among patients without clinical signs of myocardial ischemia or obstructive CAD, and assessment of dynamic changes in cTnT, particularly below the threshold for myocardial infarction definition, may not accurately discriminate increases in cTnT caused by myocardial ischemia from other causes of troponin release. Given the concern about decreased specificity, additional research is needed before highly sensitive troponin assays are widely adopted into clinical practice in the management of patients with chest pain syndromes.
Keywords: Coronary Artery Disease, Myocardial Infarction, Infarction, Myocardial Ischemia, Biological Markers, Troponin T
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