Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay: insights from a coronary sinus sampling study

Abstract

Objectives: The purpose of this study was to assess whether: 1) very small increases in troponin T, measured by a new highly sensitive cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis; and 2) serial changes can discriminate ischemia from other causes of cardiac troponin T (cTnT) release.

Background: A new hs-cTnT assay offers greater sensitivity than current assays.

Methods: 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 pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing.

Results: cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 min after termination of rapid atrial pacing (p < 0.0001), changes that were mirrored at 180 min in peripheral blood (5.1 to 11.8 pg/ml, p < 0.0001). Although peripheral cTnT concentrations tended to be higher at 180 min 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.

Conclusions: 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 CAD. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.

Figure 1. Study schema

Figure 2. Median levels of cTnT measured by the hs-cTnT assay in the coronary sinus and in peripheral blood in the entire study population

An early rise in cTnT was observed in response to rapid pacing, which was eventually mirrored in the peripheral blood. The p-values refer to changes in biomarker levels across timepoints for both coronary sinus and peripheral samples.

Figure 3. Median levels of cTnT measured by the hs-cTnT assay from the coronary sinus following pacing-stress stratified by the presence or absence of CAD and lactate elution

At baseline there were significant differences in cTnT concentrations which diminished over time following pacing. The p-values refer to changes in biomarker levels across timepoints for each group.

Figure 4. Median levels of cTnT in peripheral blood measured by the hs-cTnT assay following pacing-stress stratified by the presence or absence of CAD and lactate elution

At baseline there were significant differences in cTnT concentrations between the CAD+ and CAD− groups. Following pacing, significant and similar increases were observed in each group. The p-values refer to changes in biomarker levels across timepoints for each group.