Why the study?
Does exercise stress testing induce changes in high-sensitivity cardiac troponin T levels differently in patients with versus without reversible myocardial ischemia?
Does exercise stress testing induce changes in high-sensitivity cardiac troponin T levels differently in patients with versus without reversible myocardial ischemia?
Baseline cTnT levels are higher in patients with reversible myocardial ischemia, but exercise-induced cTnT elevation occurs primarily in patients without reversible ischemia, suggesting other mechanisms drive acute exercise-induced troponin release.
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Exercise-induced cTnT rise occurs mainly without ischemia; hypothesis-generating for non-ischemic mechanisms and should not yet change stress-test interpretation.
Whether reversible ischaemia in patients referred for exercise stress testing and MPI (myocardial perfusion imaging) is associated with changes in circulating cTn (cardiac troponin) levels is controversial. We measured cTnT with a sensitive assay before, immediately after peak exercise and 1.5 and 4.5 h after exercise stress testing in 198 patients referred for MPI. In total, 19 patients were classified as having reversible myocardial ischaemia. cTnT levels were significantly higher in patients with reversible myocardial ischaemia on MPI at baseline, at peak exercise and after 1.5 h, but not at 4.5 h post-exercise. In patients with reversible ischaemia on MPI, cTnT levels did not change significantly after exercise stress testing [11.1 (5.2-14.9) ng/l at baseline compared with 10.5 (7.2-16.3) ng/l at 4.5 h post-exercise, P=0.27; values are medians (interquartile range)]. Conversely, cTnT levels increased significantly during testing in patients without reversible myocardial ischaemia [5.4 (3.0-9.0) ng/l at baseline compared with 7.5 (4.6-12.4) ng/l, P<0.001]. In conclusion, baseline cTnT levels are higher in patients with MPI evidence of reversible myocardial ischaemia than those without reversible ischaemia. However, although cTnT levels increase during exercise stress testing in patients without evidence of reversible ischaemia, this response appears to be blunted in patients with evidence of reversible ischaemia. Mechanisms other than reversible myocardial ischaemia may play a role for acute exercise-induced increases in circulating cTnT levels.
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Røysland et al. (2012) studied this question.
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