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IMPACT OF CLONAL HEMATOPOIESIS ON SECONDARY CARDIAC INJURY AFTER ISCHEMIC STROKE
Markus Winklerand 16 co-authors
Charité - Universitätsmedizin Berlin, Department of Experimental Neurology
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-092
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Date TBA
Board: PS04-08PM-092
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Poster Board
PS04-08PM-092
Poster
View posterAbstract
Clonal haematopoiesis describes a clonal expansion of haematopoietic stem cells driven by mutations in epigenetic and DNA repair–associated genes, such as tet2. Patients carrying Tet2-CHIP have an increased risk for cardiovascular events. Stroke–heart syndrome refers to stroke-induced cardiac injury and dysfunction mediated by neurohumoral and inflammatory pathways. In this preclinical study, we aimed to analyse the impact of tet2-CHIP on stroke–heart syndrome.
Unilaterally irradiated mice reconstituted with either WT or tet2-knockout bone marrow were subjected to 30-min middle cerebral artery occlusion or sham surgery at 7 months of age. Using echocardiography, we analysed cardiac function and structure at baseline as well as on days 7 and 26 after ischaemic stroke. Troponin T levels were measured on days 7 and 28. Heart tissue underwent full spectrum flow cytometry based immunophenotyping after perfusion.
Echocardiographic data showed a reduction in ejection fraction and cardiac output exclusively in tet2-CHIP mice after stroke, which progressed over time. We observed indications of mild diastolic dysfunction alongside hypertrophic changes. These observations were accompanied by an expansion of Tet2-knockout leukocytes in the blood.
Our data suggest an exacerbated stroke–heart syndrome in tet2-CHIP mice following ischemic stroke, likely driven by proinflammatory changes associated with clonal haematopoiesis. Future interventional studies will evaluate immunomodulatory approaches to attenuate stroke-induced heart failure.
Unilaterally irradiated mice reconstituted with either WT or tet2-knockout bone marrow were subjected to 30-min middle cerebral artery occlusion or sham surgery at 7 months of age. Using echocardiography, we analysed cardiac function and structure at baseline as well as on days 7 and 26 after ischaemic stroke. Troponin T levels were measured on days 7 and 28. Heart tissue underwent full spectrum flow cytometry based immunophenotyping after perfusion.
Echocardiographic data showed a reduction in ejection fraction and cardiac output exclusively in tet2-CHIP mice after stroke, which progressed over time. We observed indications of mild diastolic dysfunction alongside hypertrophic changes. These observations were accompanied by an expansion of Tet2-knockout leukocytes in the blood.
Our data suggest an exacerbated stroke–heart syndrome in tet2-CHIP mice following ischemic stroke, likely driven by proinflammatory changes associated with clonal haematopoiesis. Future interventional studies will evaluate immunomodulatory approaches to attenuate stroke-induced heart failure.
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