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EnglishBackground: 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 bio-markers 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 echocar-diography 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). Cardio specific 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.
| Titolo: | Dipyridamole stress echocardiography does not trigger release of highly-sensitive troponin I and T. |
| Autori: | |
| Data di pubblicazione: | 2014 |
| Rivista: | |
| 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 bio-markers 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 echocar-diography 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). Cardio specific 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. |
| Handle: | http://hdl.handle.net/11562/788765 |
| Appare nelle tipologie: | 01.01 Articolo in Rivista |
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