Regina von Rennenberg1, Bob Siegerink2, Ramanan Ganeshan3,2, Kersten Villringer2, Wolfram Doehner2,4,5, Heinrich J Audebert3,2, Matthias Endres3,2,6,7,8, Christian H Nolte3,2,8, Jan F Scheitz3,2,6,8. 1. Klinik für Neurologie, Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Charité-Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany. regina-irene.freiin-von-rennenberg@charite.de. 2. Center for Stroke Research, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Charitéplatz 1, 10117, Berlin, Germany. 3. Klinik für Neurologie, Klinik und Hochschulambulanz für Neurologie, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Charité-Campus Benjamin Franklin, Hindenburgdamm 30, 12203, Berlin, Germany. 4. Berlin-Brandenburg Center for Regenerative Therapies, Charite Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Augustenburger Platz 1, 13353, Berlin, Germany. 5. Medizinische Klinik mit Schwerpunkt Kardiologie, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Campus Virchow-Klinikum, Augustenburger Platz 1, 13353, Berlin, Germany. 6. German Center for Cardiovascular Research (Deutsches Zentrum für Herz-Kreislaufforschung), Partner Site Berlin, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. 7. German Center for Neurodegenerative Diseases (Deutsches Zentrum für Neurodegenerative Erkrankungen), Partner Site Berlin, Charitéplatz 1, 10117, Berlin, Germany. 8. Berlin Institute of Health, Anna-Louisa-Karsch-Str. 2, 10178, Berlin, Germany.
Abstract
INTRODUCTION: Cardiac troponin (hs-cTnT) is a sensitive marker of myocardial injury and has been linked to incident dementia. The underlying mechanism of that observation is still unknown. Given that severity of cerebral small vessel disease is a predictor of cognitive decline, we aimed to explore whether there is an association between hs-cTnT and severity of white matter lesions (WML) as a marker of cerebral small vessel disease in patients with ischemic stroke. METHODS: We analyzed consecutive acute ischemic stroke patients admitted to Charité-University Hospital, Berlin from 2011 to 2013. Severity of WML was graded on 3T-MRI using the age-related white matter severity score (ARWMS). Patients with hs-cTnT elevation suggestive of acute coronary syndrome (ACS) were excluded (hs-cTnT > 52 ng/l or dynamic change of hs-cTnT > 50%, ESC guideline). We performed unadjusted and adjusted quantile regression models to assess the association between increased hs-cTnT (dichotomized at the 99th percentile, 14 ng/l) and severity of WML. RESULTS: A total of 860 patients was analyzed (median age 73 years, 44.8% female, median ARWMS 6). Patients with elevated hs-cTnT had more extensive WML than those without (median ARWMS 8 vs. 5, adjusted beta for 50th percentile 1.12, 95% CI 0.41-1.84). The association between WML and hs-cTnT elevation was strongest in patients with severe WML (adjusted beta 1.77, 95% CI 0.26-3.27 for 80th WML percentile). CONCLUSION: Elevated hs-cTnT levels were associated with extent of WML in acute stroke patients. Further studies are needed to assess whether hs-cTnT can be used to identify stroke patients at risk for cognitive decline.
INTRODUCTION: Cardiac troponin (hs-cTnT) is a sensitive marker of myocardial injury and has been linked to incident dementia. The underlying mechanism of that observation is still unknown. Given that severity of cerebral small vessel disease is a predictor of cognitive decline, we aimed to explore whether there is an association between hs-cTnT and severity of white matter lesions (WML) as a marker of cerebral small vessel disease in patients with ischemic stroke. METHODS: We analyzed consecutive acute ischemic strokepatients admitted to Charité-University Hospital, Berlin from 2011 to 2013. Severity of WML was graded on 3T-MRI using the age-related white matter severity score (ARWMS). Patients with hs-cTnT elevation suggestive of acute coronary syndrome (ACS) were excluded (hs-cTnT > 52 ng/l or dynamic change of hs-cTnT > 50%, ESC guideline). We performed unadjusted and adjusted quantile regression models to assess the association between increased hs-cTnT (dichotomized at the 99th percentile, 14 ng/l) and severity of WML. RESULTS: A total of 860 patients was analyzed (median age 73 years, 44.8% female, median ARWMS 6). Patients with elevated hs-cTnT had more extensive WML than those without (median ARWMS 8 vs. 5, adjusted beta for 50th percentile 1.12, 95% CI 0.41-1.84). The association between WML and hs-cTnT elevation was strongest in patients with severe WML (adjusted beta 1.77, 95% CI 0.26-3.27 for 80th WML percentile). CONCLUSION: Elevated hs-cTnT levels were associated with extent of WML in acute strokepatients. Further studies are needed to assess whether hs-cTnT can be used to identify strokepatients at risk for cognitive decline.
Entities:
Keywords:
Cardiac troponin; Cerebral white matter lesions; Cognitive impairment; Stroke
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