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Brief Communication |
Department of Medicine III, University of Heidelberg, Im Neuenheimer Feld 410, Heidelberg, Germany;
aaddress correspondence to this author at: Department of Medicine III, University of Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany. Fax +49–6221–56–33679; e-mail: evangelos_giannitsis{at}med.uni-heidelberg.de.
Abstract
Background: Using a new precommercial high-sensitivity cardiac troponin T (hsTnT) assay, we evaluated whether hsTnT increases after reversible myocardial ischemia.
Methods: In 195 patients undergoing nuclear stress testing (ST) using single-photon emission computed tomography (SPECT) for suspected ischemic heart disease, we measured hsTnT before and 18 min, 4 h, and 24 h after the stress test. Thirty patients were excluded before ST because of cardiac troponin T (cTnT) >30 ng/L (0.03 µg/L) as measured by the fourth-generation commercial test. Another 65 patients were excluded because of a combination of fixed and reversible perfusion defects (PDs) after SPECT.
Results: We studied 18 patients with reversible PDs, 41 patients with fixed PDs, and 41 patients without any PDs. Of these 100 patients, 61 received dynamic ST and 39 pharmacological ST. Median baseline hsTnT concentrations (25th, 75th percentile) were comparable in patients with reversible, fixed, and no PDs [5.57 (2.47, 12.60), 8.01 (4.55, 12.44), and 6.90 (4.63, 10.59) ng/L, respectively]. After ST, median hsTnT concentrations did not change in the reversible, fixed, or no PD groups from baseline to 18 min [–0.41 (–0.81, 0.01), 0.01 (–0.75, 0.79), and 0.36 (–0.42, 1.01) ng/L] or from baseline to 4 h [–0.56 (–1.82, 0.74), 0.24 (–0.60, 1.45), and 0.23 (–0.99, 1.15) ng/L]. Median baseline hsTnT concentrations tended to be higher in patients undergoing pharmacological vs dynamic ST; however, there were no significant increases in hsTnT concentrations after either type of ST.
Conclusions: Elevation of cTnT is rather a consequence of irreversible myocyte death than reversible myocardial ischemia after exercise or pharmacologic myocardial ischemia.
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