Abstract
Summary 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.
Highlights
Coronary artery disease (CAD) is the most frequent cause of mortality in developed countries, accounting for nearly 12.8% of all deaths
The data shows that dipyridamole stress testing does not trigger release of troponin in patients with and without inducible reversible ischemia
After exclusion of ongoing acute coronary syndrome (ACS) during Emergency Department (ED) evaluation (i.e., no diagnostic ECG variation, and no rise-and-fall of troponin – troponin being determined with AccuTnI (Beckman Coulter Inc, Chaska, Minnesota, USA) – at time 0, 6 and 12 hours), were challenged with a provocative test consisting of both basal and pharmacological stress echocardiography using dipyridamole as a stressor agent
Summary
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 aimed to establish whether or not dipyridamole stress echocardiography elicits release of troponin I (TnI) and T (TnT), as reliable biomarkers of myocardiocyte injury. At no time point the concentration of either HS-TnI or HS-TnT was significantly different among patients with negative or positive stress test. Ni u jednom trenutku merenja koncentracije HS-TnI i HSTnT se nisu razlikovale izme|u pacijenata sa negativnim ili pozitivnim rezultatom stres-testa.
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