Does echocardiographic stress test induced release of hsTnT and TnI II?

Background: Cardiac troponins (cTn) are considered as the best biomarkers for detection of
myocardial cell injury. In this study, cTnT and cTnI were measured by new commercially
available high-sensitive methods in patients undergoing brief exercise- or pharmacologicinduced
stress. Our aim was to compare cTnT and cTnI levels before and after the stress tests,
in the patients with or without reversible ischemia.
Materials and Methods: Fifty patients (28 men and 22 women) underwent an echographic
stress test (ST) for suspected ischemic heart disease. Of these 50 patients, 28 received
pharmacological ST (dobutamine injection) and 22 dynamic ST (bicycle exercise). The
patients were subdivided into two groups according to the presence or absence of documented
transient reversible ischemia: 14 with reversible ischemia ( mean age: 67.71±9.66 y) and 36
without ischemia ( mean age: 63.17±11.72 y).
In all patients, cTnT and cTnI concentrations were measured by high sensitive methods
(hsTnT, Roche Diagnostics and TnI II, Abbott Diagnostics) on heparin plasma immediately
before (T0) and after ST (T1).The lower detection limit of these assays was 0.005μg/L for
hsTnT and 0.01μg/L for TnI II.
The protocol was approved by the ethics committee of the University of Liège (Belgium). All
patients gave informed consent. All statistical analyses were performed using Medcalc
version 8.1 for Windows. P value <0.05 was regarded as statistically significant.
Results:
There was no significant difference between hsTnT concentrations at T0 and T1, neither in
the whole patient group, nor in the subgroups of subjects who received pharmacological ST or
dynamic ST. The same was true for TnI II.
Although there was no change in hsTnT levels during test in ischemic and in non ischemic
patients, the latter tend to demonstrate higher median T0 levels (25th, 75th percentiles) than the
others [0.011 (0.007, 0.029) vs 0.007 (0.0047, 0.1125) ng/ml, p=0.09]. They also showed
higher median T1 levels [0.014 (0.065, 0.03) vs 0.007 (0.003, 0.0102) ng/ml, p=0.08]. Higher
TnI II levels were also recorded in ischemic patients as compared to non ischemic patients at
T0[ 0.014 (0.0072; 0.0265) vs 0.005 (0.003; 0.01) ng/ml, p=0.08] and T1[ 0.013 (0.0085-
0.03) vs 0.006 (0.0035-0.008) ng/ml, p=0.08]. Also, TnI II levels did not change during test in
both subgroups.
Conclusions:
Measurement of cardiac troponins by high sensitive methods did not allow to detect
significant release of biomarkers from the heart during exercise-or pharmacologic-induced
ST, even in patients who demonstrated reversible myocardial ischemia. The type of test –
pharmacological or dynamic - was without effect. The patients with induced transient
ischemia had however higher troponin T and I levels at baseline, this difference remaining
during test.