Dipyridamole stress echocardiography does not trigger release of highly-sensitive troponin I and T

Abstract

Background: The patients with episodes of chest pain and no electrocardiographic or biomarker abnormalities are currently monitored and subjected to non-invasive testing. Stress echocardiography is one of the most often used provocative tests, being the most cost and risk-effective imaging technique. Some concerns about this technique have been raised regarding potential drug-induced myocardial injury. Our study hence aimed to establish whether or not dipyridamole stress echocardiography elicits release of troponin I (TnI) and T (TnT), as reliable biomarkers of myocardiocyte injury. Methods: Thirty-two patients, after exclusion of ongoing acute coronary syndrome (ACS) during evaluation in the emergency department (ED), were studied with echocardiography both at the baseline and after pharmacological stress with dipyridamole. Results: All subjects had biomarkers assessment immediately before the stress-test (T1), 1 h from conclusion of the test (T2), and 6 h afterwards (T3). Cardiospecific troponins were assessed with one contemporary-sensitive (TnI) and two highly-sensitive (HS) methods (HS-TnI and HS-TnT). The concentration of TnI, HS-TnI and HS-TnT did not differ throughout the three time points. At no time point the concentration of either HS-TnI or HS-TnT was significantly different among patients with negative or positive stress test. Conclusions: The data shows that dipyridamole stress testing does not trigger release of troponin in patients with and without inducible reversible ischemia.

Keywords

• troponin
• stress test
• echocardiography
• stress echo
• dipyridamole