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Troponin elevation in acute ischemic stroke (TRELAS)--protocol of a prospective observational trial
Jan F Scheitz1, Hans-Christian Mochmann, Christian H Nolte
1Center for Stroke Research Berlin, Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany. jan-friedrich.scheitz@charite.de
Insights
Elevated cardiac troponin T (cTnT) in acute ischemic stroke patients is common. The TRELAS study investigates its cause to guide clinical management and improve patient outcomes.
Area of Science:
- Cardiology
- Neurology
- Biomarkers
Background:
- Elevated cardiac troponin T (cTnT) is frequent in acute ischemic stroke (AIS) and predicts poor outcomes.
- The cause of cTnT elevation in AIS is uncertain, potentially due to co-morbid coronary artery disease or neurogenic cardiac damage.
- This uncertainty complicates the diagnostic and therapeutic management of AIS patients with elevated cTnT.
Purpose of the Study:
- To investigate the frequency and underlying pathomechanism of cTnT elevation in AIS patients.
- To provide guidance for clinical practice regarding the workup of AIS patients with elevated cTnT.
- To clarify the pathophysiologic concepts of co-morbid cardiac damage in AIS.
Main Methods:
- Prospective observational trial (TRELAS) screening AIS patients for cTnT elevation.
- cTnT levels measured on admission and the following day; elevated levels trigger coronary angiography within 72 hours.
- Comparison of angiographic findings with matched Non-ST-Elevation myocardial infarction patients to identify obstructive coronary artery disease.
Main Results:
- The study aims to determine the primary endpoint: occurrence of culprit lesions in coronary angiograms indicating obstructive coronary artery disease.
- Secondary endpoints include stroke localization and cardiac dysfunction suggestive of stroke-induced damage.
- The findings will establish the frequency and etiology of cTnT elevation in AIS.
Conclusions:
- The TRELAS study will prospectively determine the frequency and etiology of troponin elevation in a large AIS cohort.
- Findings are expected to clarify pathophysiologic concepts of cardiac damage in AIS.
- Results will provide a basis for clinical recommendations for cardiac workup in AIS patients.
Background:
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.
Methods/Design:
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.
Discussion:
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:
clinicaltrials.gov NCT01263964.
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