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Troponin elevation in acute ischemic stroke (TRELAS) - protocol of a prospective observational trial

Jan F Scheitz12*, Hans-Christian Mochmann3, Christian H Nolte12, Karl G Haeusler12, Heinrich J Audebert12, Peter U Heuschmann1, Ulrich Laufs4, Bernhard Witzenbichler3, Heinz-Peter Schultheiss3 and Matthias Endres12

Author affiliations

1 Center for Stroke Research Berlin, Charité - Universitätsmedizin Berlin, 10117 Berlin, Germany

2 Klinik für Neurologie, Charité- Universitätsmedizin Berlin, 10117 Berlin, Germany

3 Medizinische Klinik für Kardiologie und Pulmonologie, Charité - Campus Benjamin Franklin, 12200 Berlin, Germany, Germany

4 Klinik für Innere Medizin III, Kardiologie, Angiologie und Internistische Intensivmedizin, Universitätsklinikum des Saarlandes, 66421 Homburg, Germany

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Citation and License

BMC Neurology 2011, 11:98  doi:10.1186/1471-2377-11-98

Published: 8 August 2011



Levels of the cardiac muscle regulatory protein troponin T (cTnT) are frequently elevated in patients with acute ischemic stroke and elevated cTnT predicts poor outcome and mortality. The pathomechanism of troponin release may relate to co-morbid coronary artery disease and myocardial ischemia or, alternatively, to neurogenic cardiac damage due to autonomic activation after acute ischemic stroke. Therefore, there is uncertainty about how acute ischemic stroke patients with increased cTnT levels should be managed regarding diagnostic and therapeutic workup.


The primary objective of the prospective observational trial TRELAS (TRoponin ELevation in Acute ischemic Stroke) is to investigate the frequency and underlying pathomechanism of cTnT elevation in acute ischemic stroke patients in order to give guidance for clinical practice. All consecutive patients with acute ischemic stroke admitted within 72 hours after symptom onset to the Department of Neurology at the Campus Benjamin Franklin of the University Hospital Charité will be screened for cTnT elevations (i.e. >= 0.05 μg/l) on admission and again on the following day. Patients with increased cTnT will undergo coronary angiography within 72 hours. Diagnostic findings of coronary angiograms will be compared with age- and gender-matched patients presenting with Non-ST-Elevation myocardial infarction to the Department of Cardiology. The primary endpoint of the study will be the occurrence of culprit lesions in the coronary angiogram indicating underlying co-morbid obstructive coronary artery disease. Secondary endpoints will be the localization of stroke in the cerebral imaging and left ventriculographic findings of wall motion abnormalities suggestive of stroke-induced global cardiac dysfunction.


TRELAS will prospectively determine the frequency and possible etiology of troponin elevation in a large cohort of ischemic stroke patients. The findings are expected to contribute to clarify pathophysiologic concepts of co-morbid cardiac damage in ischemic stroke patients and also to provide a basis for clinical recommendations for cardiac workup of such patients.

Trial registration NCT01263964